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Cancer Research is a biweekly peer-reviewed medical journal published by the American Association for Cancer Research . It covers research on all aspects of cancer and cancer-related biomedical sciences and was established in 1941. The editor-in-chief is Chi Van Dang . [ 1 ] The journal was established in 1916 as the Journal of Cancer Research , was renamed American Journal of Cancer in 1931, and obtained its current name in 1941. The journal is abstracted and indexed in: According to the Journal Citation Reports , the journal has a 2023 impact factor of 12.5. [ 6 ]	https://en.wikipedia.org/wiki/Cancer_Research_(journal)
Cancer Science is a monthly peer-reviewed medical journal covering research in oncology , which is published by Wiley-Blackwell on behalf of the Japanese Cancer Association . Established in 1907, the journal publishes original articles, editorials, and letters to the editor, describing original research in the fields of basic, translational, and clinical cancer research . The editor-in-chief is Kohei Miyazono ( University of Tokyo ). [ 1 ] According to the Journal Citation Reports , the journal has a 2020 impact factor of 6.71, ranking it 50 out of 242 journals in the category "Oncology". [ 2 ] The journal was established in 1907 as the Japanese Journal of Cancer Research by Katsusaburō Yamagiwa ( University of Tokyo ), who first produced tumors in animals by painting tar on their skin. In 1908, he joined the Japanese Foundation for Cancer Research as the first president, and the journal became the official journal of the foundation. [ 3 ] The journal was transferred to the Japanese Cancer Association in 1941 and able to continue its work throughout the Second World War . [ 4 ] The name of the journal obtained its current name in 2003. [ 5 ] The " Cancer Science Young Scientists Award for researchers in Asia" was established for the development of young researchers from the Asian region in the area of cancer research . [ 6 ] This article about an oncology journal is a stub . You can help Wikipedia by expanding it . See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .	https://en.wikipedia.org/wiki/Cancer_Science
Cancer Therapy Advisor (formerly Chemotherapy Advisor ) is an online resource and quarterly medical news publication for oncology healthcare professionals, with updated treatment regimens for patients with cancer and live medical conference coverage. Launched in January 2012, Cancer Therapy Advisor is owned by Haymarket Oncology, a subsidiary of Haymarket Media based in New York City and New Jersey . [ 1 ] This article about a New York newspaper is a stub . You can help Wikipedia by expanding it . This article about an oncology journal is a stub . You can help Wikipedia by expanding it . See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .	https://en.wikipedia.org/wiki/Cancer_Therapy_Advisor
The Journal of the National Cancer Institute ( JNCI ) is a peer-reviewed medical journal covering research in oncology that was established in August 1940. It is published monthly by Oxford University Press and is edited by Patricia A. Ganz . It was merged with Cancer Treatment Reports in January 1988. JNCI used to be the official journal of the U.S. National Cancer Institute (NCI); however, in 1996, the NCI and JNCI agreed to grow apart. Over the next five years, JNCI became independent of the NCI. A related publication is Journal of the National Cancer Institute Monographs ( JNCI Monographs ), established in 1959, which publishes manuscripts from cancer and cancer-related conferences, as well as groups of papers on specific subjects related to cancer. In January 1986, Cancer Treatment Symposia was merged with JNCI Monographs . Additionally, JNCI Cancer Spectrum ( JNCI CS ) is a fully open access journal, which was established in 2017. It is published bimonthly by Oxford University Press and is edited by Ronald Chen . The history of JNCI is linked to that several other journals. A full history of JNCI and JNCI Monographs is presented below. JNCI is indexed and abstracted in: According to the Journal Citation Reports , the journal has a 2014 impact factor of 12.583, ranking it 8th out of 211 journals in the category "Oncology". [ 13 ] JNCI Monographs is indexed and abstracted in	https://en.wikipedia.org/wiki/Cancer_Treatment_Reports
The Journal of the National Cancer Institute ( JNCI ) is a peer-reviewed medical journal covering research in oncology that was established in August 1940. It is published monthly by Oxford University Press and is edited by Patricia A. Ganz . It was merged with Cancer Treatment Reports in January 1988. JNCI used to be the official journal of the U.S. National Cancer Institute (NCI); however, in 1996, the NCI and JNCI agreed to grow apart. Over the next five years, JNCI became independent of the NCI. A related publication is Journal of the National Cancer Institute Monographs ( JNCI Monographs ), established in 1959, which publishes manuscripts from cancer and cancer-related conferences, as well as groups of papers on specific subjects related to cancer. In January 1986, Cancer Treatment Symposia was merged with JNCI Monographs . Additionally, JNCI Cancer Spectrum ( JNCI CS ) is a fully open access journal, which was established in 2017. It is published bimonthly by Oxford University Press and is edited by Ronald Chen . The history of JNCI is linked to that several other journals. A full history of JNCI and JNCI Monographs is presented below. JNCI is indexed and abstracted in: According to the Journal Citation Reports , the journal has a 2014 impact factor of 12.583, ranking it 8th out of 211 journals in the category "Oncology". [ 13 ] JNCI Monographs is indexed and abstracted in	https://en.wikipedia.org/wiki/Cancer_Treatment_Symposia
Cancer and Metastasis Reviews is a quarterly peer-reviewed medical review journal covering oncology and the development of new cancer treatments . It was established in 1982 and is published by Springer Science+Business Media . The editors-in-chief are Kenneth V. Honn ( Wayne State University School of Medicine ) and Avraham Raz ( Barbara Ann Karmanos Cancer Institute ). According to the Journal Citation Reports , the journal has a 2020 impact factor of 9.264. [ 1 ] This article about an oncology journal is a stub . You can help Wikipedia by expanding it . See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .	https://en.wikipedia.org/wiki/Cancer_and_Metastasis_Reviews
Cancer and nausea are associated in about fifty percent of people affected by cancer . [ 1 ] This may be as a result of the cancer itself, or as an effect of the treatment such as chemotherapy , radiation therapy , or other medication such as opiates used for pain relief. About 70–80% of people undergoing chemotherapy experience nausea or vomiting . Nausea and vomiting may also occur in people not receiving treatment, often as a result of the disease involving the gastrointestinal tract , [ 2 ] electrolyte imbalance , or as a result of anxiety . [ 3 ] Nausea and vomiting may be experienced as the most unpleasant side effects of cytotoxic drugs [ 4 ] and may result in patients delaying or refusing further radiotherapy [ 5 ] or chemotherapy. [ 6 ] The strategies of management or therapy of nausea and vomiting depend on the underlying causes. [ 7 ] Medical treatments or conditions associated with a high risk of nausea and/or vomiting include chemotherapy, radiotherapy, and malignant bowel obstruction. [ 8 ] Anticipatory nausea and vomiting may also occur. [ 9 ] Nausea and vomiting may lead to further medical conditions and complications including: dehydration , electrolyte imbalance, malnutrition , and a decrease in quality of life . [ 3 ] Nausea may be defined as an unpleasant sensation of the need to vomit. [ 7 ] It may be accompanied by symptoms such as salivation, feeling faint, and a fast heart rate . [ 7 ] Vomiting is the forceful ejection of stomach contents through the mouth. [ 7 ] Although nausea and vomiting are closely related, some patients experience one symptom without the other and it may be easier to eliminate vomiting than nausea. [ 1 ] The vomiting reflex (also called emesis) is thought to have evolved in many animal species as a protective mechanism against ingested toxins . In humans, the vomiting response may be preceded by an unpleasant sensation termed nausea, but nausea may also occur without vomiting. The central nervous system is the primary site where a number of emetic stimuli (input) are received, processed and efferent signals (output) are generated as a response and sent to various effector organs or tissues, leading to processes that eventually end in vomiting. [ 10 ] The detection of emetic stimuli, the central processing by the brain and the resulting response by organs and tissues that lead to nausea and vomiting are referred to as the emetic pathway or emetic arch. Some medical conditions that arise as a result of cancer or as a complication of its treatment are known to be associated with a high risk of nausea and/or vomiting. These include malignant bowel obstruction (MBO), chemotherapy-induced nausea and vomiting (CINV), anticipatory nausea and vomiting (ANV), and radiotherapy-induced nausea and vomiting (RINV). [ citation needed ] Malignant bowel obstruction (MBO) of the gastrointestinal tract is a common complication of advanced cancer, especially in patients with bowel or gynaecological cancer. These include colorectal cancer , ovarian cancer , breast cancer , and melanoma . [ 8 ] Three percent of all advanced cancers lead to malignant bowel obstruction, and 25 to 50 percent of patients with ovarian cancer experience at least one episode of malignant bowel obstruction. [ 11 ] The mechanisms of action that may lead to nausea in MBO include mechanical compression of the gut, motility disorders, gastrointestinal secretion accumulation, decreased gastrointestinal absorption, and inflammation. [ 12 ] Bowel obstruction and the resulting nausea may also occur as a result of anti-cancer therapy such as radiation, [ 13 ] or adhesion after surgery. [ 14 ] Impaired gastric emptying as a result of bowel obstruction may not respond to drugs alone, and surgical intervention is sometimes the only means of symptom relief. [ 15 ] Some constipating drugs used in cancer therapy such as opioids may cause a slowing of peristalsis of the gut, which may lead to a functional bowel obstruction. [ 12 ] Chemotherapy-induced nausea and vomiting (CINV) is one of the most feared side effects of chemotherapy [ 16 ] and is associated with a significant deterioration in quality of life. [ 17 ] CINV is classified into three categories: [ 16 ] Risk factors that predict the occurrence and severity of CINV include sex and age, with females, younger people and people who have a high pretreatment expectation of nausea being at a higher risk, while people with a history of high alcohol consumption being at a lower risk. [ 10 ] Other person-related variables, such as chemotherapy dose, rate and route of administration, hydration status, prior history of CINV, emesis during pregnancy or motion sickness, tumour burden, concomitant medication and medical conditions also play a role in the degree of CINV experienced by a person. [ 9 ] [ 18 ] By far the most important factor which determines the degree of CINV is the emetogenic potential of the chemotherapeutic agents used. Chemotherapeutic agents are classified into four groups according to their degree of emetogenicity: high, moderate, low and minimal. [ 9 ] The European Society of Medical Oncology (ESMO) and the Multinational Association of Supportive Care in Cancer (MASCC) in 2010 [ 9 ] as well as the American Society of Clinical Oncology (ASCO) (2011) [ 19 ] recommend a prophylaxis to prevent acute vomiting and nausea following chemotherapy with high emetic risk drugs by using a three-drug regimen including a 5-HT3 receptor antagonist , dexamethasone and aprepitant (a neurokinin-1 antagonist ) given before chemotherapy. A common consequence of cancer treatment is the development of anticipatory nausea and vomiting (ANV). [ 20 ] This kind of nausea is usually elicited by the re-exposure of the patients to the clinical context they need to attend to be treated. [ 6 ] Approximately 20% of people undergoing chemotherapy are reported to develop anticipatory nausea and vomiting. Once developed, ANV is difficult to control by pharmacological means. Benzodiazepines are the only drugs that have been found to reduce the occurrence of ANV but their efficacy decreases with time. [ 9 ] Recently, clinical trials suggests that cannabidiolic acid suppresses conditioned gaping (ANV) in shrews. [ 21 ] Because ANV is widely believed to be a learned response , the best approach is to avoid the development of ANV by adequate prophylaxis and treatment of acute vomiting and nausea from the first exposure to therapy. [ 9 ] [ 20 ] Behavioral treatment techniques, such as systematic desensitization , progressive muscle relaxation , and hypnosis have been shown to be effective against ANV. [ 9 ] [ 20 ] The incidence and severity of radiation therapy-induced nausea and vomiting (RINV) depends on a number of factors including therapy related factors such as irradiated site, single and total dose , fractionation , irradiated volume and radiotherapy techniques. Also involved are person related factors such as gender, general health of the person, age, concurrent or recent chemotherapy, alcohol consumption, previous experience of nausea, vomiting, anxiety as well as the tumor stage. The emetogenic potential of radiotherapy is classified into high, moderate, low and minimal risk depending on the site of irradiation: [ 5 ] Nausea and vomiting may have a number of causes in people with cancer. [ 7 ] While more than one cause may exist in the same person stimulating symptoms via more than one pathway, the actual cause of nausea and vomiting may be unknown in some people. The underlying causes of nausea and vomiting may in some cases not be directly related to the cancer. The causes may be categorized as disease-related and treatment-related. [ 22 ] The stimuli which lead to emesis are received and processed in the brain. It is thought that a number of loosely organized neuronal networks within the medulla oblongata probably interact to coordinate the emetic reflex. [ 10 ] Some of the brain stem nuclei which have been identified as important in the coordination of the emetic reflex include the parvicellular reticular formation , the Bötzinger complex and the nucleus tractus solitarii . [ 23 ] The nuclei coordinating emesis had formerly been referred to as the vomiting complex, but it is no longer thought to represent a single anatomical structure. [ 10 ] [ 23 ] Efferent outputs which transmit the information from the brain leading to the motoric response of retching and vomiting include vagal efferents to the esophagus , stomach and intestine as well as spinal somatomotor neurones to the abdominal muscles and phrenic motor neurones (C3–C5) to the diaphragm . Autonomic efferents also supply the heart and airways (vagus), salivary glands ( chorda tympani ) and skin and are responsible for many of the prodromal signs such as salivation and skin pallor. [ 23 ] Nausea and vomiting may be initiated by various stimuli, through different neuronal pathways. A stimulus may act on more than one pathway. [ 23 ] Stimuli and pathways include: Patient reported outcomes (PROs) allow patients to voice their perspective on health and behavioral status through self administered questionnaires. [ 24 ] Cancer and nausea have been measured with the Patient Reported Outcomes Measurement System ( PROMIS ) using surveys with questions such as "in the last 7 days, how severe was your nausea?". [ 24 ] PROs can aid clinicians in tailoring nausea treatment specific to variations in high or low emetogenic chemotherapy from patient to patient. [ 25 ] One notable benefit of PROs is that surveys can be administered electronically, meaning patients who are too sick to go to the doctor can do it from home. [ 26 ] Limitations: While helpful, PROs are subject to bias since they are reported after the symptoms are experienced. [ 25 ] Errors in patients' memories can influence their PROs compared to if they had been asked while experiencing nausea rather than afterwards. [ 25 ] This can lead to ratings which may not accurately reflect how patients perceive their nausea at the moment. [ 25 ] The strategies of management or prevention of nausea and vomiting depend on the underlying causes, whether they are reversible or treatable, stage of the illness, the person's prognosis and other person specific factors. Anti emetic drugs are chosen according to previous effectiveness and side effects. [ 7 ] Drugs that are used in the prophylaxis and therapy of nausea and vomiting in cancer include: Side effects of antiemetic drugs are relatively mild. Depending on the type of drug and dosage prescribed, common side effects may include: headache, constipation, diarrhea, insomnia, agitation, acne, weight loss/weight gain, dizziness, or drowsiness. [ 16 ] In addition, although cannabis has proven extremely beneficial for emetic relief, a small percentage of patients opting to use medical cannabis have shown to become dependent on it after treatment concludes. [ 28 ] Other non-drug measures may include: Palliative care is the active care of people with advanced, progressive illness such as cancer. The World Health Organization (WHO) defines it as an approach that improves the quality of life of patients and their families facing the problems associated with life-threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems (such as nausea or vomiting), physical, psychosocial, and spiritual. [ 33 ] Sometimes it is possible or necessary to provide relief for cancer-caused nausea and vomiting through palliative surgical intervention. Surgery is however not routinely carried out when there are poor prognostic criteria for surgical intervention such as intra-abdominal carcinomatosis, poor performance status and massive ascites . [ 8 ] The surgical approach proves beneficial in affected people with operable lesions, a life expectancy greater than two months and good performance status. [ 12 ] Often a malignant bowel obstruction is the cause of the symptoms in which case the purpose of palliative surgery is to relieve the symptoms of bowel obstruction by means of several procedures including: In 2008, 12.7 million new cancer cases and 7.6 million cancer deaths were estimated worldwide. [ 35 ] Individual: CINV has shown to bring a heavy financial burden on cancer patients. These costs may discourage patients from seeking treatment or purchasing medication despite nausea being one of the most debilitating side effects of chemotherapy. [ 37 ] In addition to hospital fees, studies have found that costs incurred for prescription antiemetics averaged between $100–1400 per chemotherapy cycle depending on the drugs prescribed. [ 37 ] Healthcare system: In addition to patient costs, CINV also takes a heavy financial toll on the healthcare system at large. General cancer symptom management has shown to make up 5% of annual hospital expenses, with the cost of CINV changing with antiemetic treatment. [ 38 ] It was found that people receiving prophylactic treatment posed a significantly lower burden on the healthcare system. In contrast, patients who received no prophylactic treatment were shown to pose a substantial cost to the healthcare system. [ 38 ] These additional costs have shown to be associated with repeated hospital visits and emergency medication for uncontrolled CINV. [ 38 ]	https://en.wikipedia.org/wiki/Cancer_and_nausea
Cancer in adolescents and young adults is cancer which occurs in those between the ages of 15 and 39. [ 1 ] This occurs in about 70,000 people a year in the United States—accounting for about 5 percent of cancers. This is about six times the number of cancers diagnosed in children ages 0–14. [ 1 ] Globally, more than 1.3 million young adults between the ages of 15 and 39 were diagnosed with cancer in 2022, and nearly 378,000 people in this age range died from cancer. [ 2 ] Young adults are more likely than either younger children or older adults to be diagnosed with certain cancers, such as Hodgkin lymphoma , testicular cancer , and some types of sarcomas . In adolescents and young adults 15 to 24 years old, lymphoma , testicular cancer, and thyroid cancer are the most common types, while among 25- to 39-year-olds, breast cancer and melanoma are more common. [ 1 ] [ 3 ] People who are diagnosed with cancer between the ages of 15 and 39 fit the definition of "adolescent and young adults" according to the Report of the Adolescent and Young Adult Oncology Progress Review Group. [ 4 ] While this age range is commonly used in the United States, age ranges used to characterize adolescent and young adult populations in terms of cancer care and research may vary by country, region, or study. [ 5 ] [ 6 ] For example, throughout much of Europe and in Australia, adolescence and young adulthood in terms of cancer is defined as ages 15 through 24, while the age range accepted by the Canadian Cancer Society is 15 through 29. [ 7 ] [ 8 ] The most common cancers among 15- to 39-year-olds worldwide in 2018, determined by estimated age-standardized incidence rates, were: [ 9 ] For some types of cancer, young adults may have better outcomes if treated with pediatric, rather than adult, treatment regimens. Young adults who have a cancer that typically occurs in children and adolescents, such as brain tumors, leukemia, osteosarcoma, and Ewing sarcoma, may fare better if treated by a pediatric oncologist. For example, adolescents and young adults with acute lymphoblastic leukemia (ALL) may have better outcomes if they are treated with pediatric treatment protocols rather than adult treatment protocols. The 5-year survival rates for 15- to 19-year-olds with ALL has risen to 74% as of 2007–2013, from survival rates of around 50% in the early 1990s. This may be due to greater use of treatment protocols for children. [ 10 ] Young adults who have cancers that are more common in adults, such as breast cancer and melanoma, may be better treated by a medical oncologist. [ 11 ] Cancer treatments can affect a person's fertility , with these changes being temporary or permanent. Whether fertility is affected depends on factors such as a person's baseline fertility, age at the time of treatment, the type of cancer and treatment(s), the amount (dose) of treatment, the duration of treatment, the amount of time that has passed since cancer treatment, and other personal health factors. [ 12 ] Cancer treatments may harm reproductive organs and glands that control fertility. Chemotherapy (especially alkylating agents) can affect a female's ovaries, causing them to stop releasing eggs and estrogen, and can damage sperm and sperm-forming cells (germ cells) in young men. Radiation therapy to or near the abdomen, pelvis, or spine can harm nearby reproductive organs. Radiation therapy to the brain can damage the pituitary gland, which controls the function of most other endocrine glands . Surgery for cancers of the reproductive system and for cancers in the pelvic region can harm nearby reproductive tissues and/or nerves or lymph nodes. Hormone therapy (also called endocrine therapy) used to treat cancer can disrupt the menstrual cycle, which may affect female fertility. Hematopoietic stem cell transplantation involves receiving high doses of chemotherapy and/or radiation that may damage a female's ovaries and a male's sperm and sperm-forming cells. [ 12 ] [ 13 ] The American Society of Clinical Oncology encourages oncologists to discuss the possibility of treatment-related infertility, as well as options for preserving fertility, with all people of reproductive age and to provide them with referrals to reproductive specialists. [ 14 ] Females with cancer have fertility preservation options such as oocyte cryopreservation (also called egg cryopreservation or egg freezing), embryo cryopreservation (also called embryo banking or embryo freezing), ovarian shielding (also called gonadal shielding), ovarian tissue cryopreservation (also called ovarian tissue freezing), ovarian transposition (also called oophoropexy), and radical trachelectomy (also called radical cervicectomy). [ 12 ] Males with cancer have fertility preservation options such as semen cryopreservation (also called sperm banking); testicular shielding (also called gonadal shielding), a procedure in which a protective cover is placed on the outside of the body to shield the testicles from scatter radiation to the pelvis when other parts of the body are being treated with radiation; testicular sperm extraction (TESE), a procedure for males who are not able to produce a semen sample; and testicular tissue freezing (also called testicular tissue cryopreservation ) which, for boys who have not gone through puberty and are at high risk of infertility, may be an option. [ 13 ] Adolescents and young adults with cancer have not attained the same improvements in overall survival as either younger children or older adults. [ 15 ] The 5-year survival rate for all invasive adolescent and young adult cancers diagnosed from 2002 to 2006 in the United States was 82.5%. [ 16 ] While this survival rate is comparable to those for children and older adults with cancer during the same time period, survival figures favor younger people with cancer with several cancer types common in both children and adolescent and young adult populations, including acute lymphomas, rhabdomyosarcoma, and Ewing sarcoma. Likewise, older people with cancer fared better than adolescents and young adults in terms of 5-year survival for breast cancer, Kaposi sarcoma, and anal cancer. [ 16 ] To improve low survival rates for some adolescent and young adult cancers, researchers are studying distinct genetic and biologic features of cancer at different ages, differences in treatment approaches and treatment intensity, and possible differences in compliance to treatment, as well as social, behavioral, or other factors affecting young people with cancer. [ 15 ] [ 17 ] Adolescent and young adult with cancer and survivors of cancer report difficulties related to employment, educational attainment, and financial stability—as well as social relationships. [ 18 ] Cancer in adolescents and young adults often differs in terms of signs and symptoms, histology , prognosis, and rates of survivals. Some cancers in adolescents and young adults may have unique genetic and biological features. [ 19 ] For example: A stronger understanding of the different biologic and genomic processes seen in some adolescent and young adult cancers will help to develop new and better treatments for these cancers. [ 19 ] People who reported their cancer treatment was "very intensive" and those who had quit work or school after being diagnosed were more likely to report that cancer negatively affected their work and school after diagnosis, with more than 50% reporting problems with memory and attentiveness. Almost three-quarters of adolescents and young adults with cancer who had been studying or working returned to school or work within one to three years after a diagnosis. Reasons for educational disruption and lower educational attainment given by adolescents and young adults in qualitative interviews included missing school, not taking required tests, and feeling as if they had been "left behind. " [ 18 ] Roughly a third of young adults in the United States reported that cancer had a negative impact on their employment plans. In research that compared young people who had survived cancer with their healthy peers, 33% of adolescents and young adults with cancer were not working compared to 27% of controls. In another US study, 23% of adolescents and young adults with cancer reported unemployment due to health issues compared with 14% of controls. Another national study found that adolescents and young adults who had had cancer reported lower family incomes than their peer-age cohorts without cancer. [ 18 ] Social relationships and educational achievements during the formative adolescent and young adult years are very important, and studies in the United States have documented that a cancer experience can negatively affect the attainment of these goals. Marriage rates were lower among young adults with cancer, and they were more likely to have divorced or separated than peers in an age-related control group. Adolescents and young adults also reported fears about sexual attractiveness due to physical changes as well as fertility-related changes caused by cancer. Young people with cancer whose diagnosis is delayed or takes longer are at increased risk of anxiety, depression and reduced quality of life. [ 21 ] [ 22 ] Adolescents and young adults with cancer expressed a strong desire to connect with other young adults with cancer and survivors from cancer who may have gone through similar experiences for support to cope with these challenges. [ 18 ] Young cancer patients have reported an improvement in their coping abilities due to their participation in an online cancer community. Adolescents and young adults with cancer reported using social media platforms for both "medical and social resources", assisting with relationships and social issues. [ 23 ] They also reported a preference for "tools that facilitate emotional coping of patients and their family." [ 23 ] In general, the uses of social media for healthcare communication include reducing stigma and facilitating dialogue between patients. [ 24 ] According to the European Society for Medical Oncology , cancer patients participating in an online support group reported greater "psycho-social impact—alleviation of seclusion versus induction of anxiety." [ 25 ] During the period from 2000 to 2011, of 40 cancers that are relatively common in both adolescents and young adults in the United States, 7 increased in frequency: acute lymphoblastic leukemia , colorectal cancer, prostate cancer , kidney cancer , testicular cancer, thyroid cancer, and uterine cancer. [ 26 ] Rates of some cancers such as lung cancer and melanoma decreased among adolescents and young adults in the United States during this period. One hypothesis for this decline is the launching of prevention campaigns, such as smoking prevention and skin cancer awareness. [ 26 ] Cervical cancer also declined among adolescents and young adults in the United States, which may be attributable to the introduction of the HPV vaccine. In contrast, rates among older adults declined in 26 types of cancer that also affect adolescents and young adults. Rates among older adults increased only in cancers of the thyroid, kidney, liver, and small intestine. [ 26 ]	https://en.wikipedia.org/wiki/Cancer_in_adolescents_and_young_adults
Cancer prevention is the practice of taking active measures to decrease the incidence of cancer and mortality . [ 1 ] [ 2 ] The practice of prevention depends on both individual efforts to improve lifestyle and seek preventive screening , and socioeconomic or public policy related to cancer prevention. [ 3 ] Globalized cancer prevention is regarded as a critical objective due to its applicability to large populations, reducing long term effects of cancer by promoting proactive health practices and behaviors, and its perceived cost-effectiveness and viability for all socioeconomic classes . [ 2 ] The majority of cancer cases are due to the accumulation of environmental pollution being inherited as epigenetic damage and most of these environmental factors are controllable lifestyle choices. [ 4 ] Greater than a reported 75% of cancer deaths could be prevented by avoiding risk factors including: tobacco , overweight / obesity , an insufficient diet , physical inactivity , alcohol , sexually transmitted infections , and air pollution . [ 5 ] Not all environmental causes are controllable, such as naturally occurring background radiation , and other cases of cancer are caused through hereditary genetic disorders . Current genetic engineering techniques under development may serve as preventive measures in the future. [ 6 ] Future preventive screening measures can be additionally improved by minimizing invasiveness and increasing specificity by taking individual biological makeup into account, also known as "population-based personalized cancer screening." [ 2 ] While anyone can get cancer, [ 8 ] age is one of the biggest factors that increases the risk of cancer: 3 out of 4 cancers are found in people aged 55 or older. An average 35% of human cancer mortality is attributed to the diet of the individual. [ 9 ] Studies have linked excessive consumption of red or processed meat to an increased risk of breast cancer , colon cancer , and pancreatic cancer , a phenomenon which could be due to the presence of carcinogens in meats cooked at high temperatures. [ 10 ] [ 11 ] More specifically, a higher risk of breast cancer also has been shown to possibly be associated with a higher intake of red and processed meats, refined sugars, alcohol and saturated fats. [ 12 ] Researchers suggest that this association may be due to the inflammation processes and the increase of estrogen and testosterone from the foods in this diet. [ 12 ] In some cases, a high intake of eggs was also found to may be associated with a higher risk of breast cancer due to its high cholesterol contents. [ 12 ] Dietary recommendations for reducing cancer risk typically include an emphasis on vegetables , fruit , whole grains , and fish, and an avoidance of processed and red meat (beef, pork, lamb), animal fats, and refined carbohydrates . [ 13 ] [ 14 ] The World Cancer Research Fund recommends a diet rich in fruits and vegetables to reduce the risk of cancer. A diet rich in foods of plant origin, including non-starchy fruits and vegetables, non-starchy roots and tubers, and whole grains, may have protective effects against cancer. [ 15 ] Consumption of coffee is associated with a reduced risk of liver cancer and endometrial cancer . [ 16 ] [ 17 ] Additionally, a higher coffee intake was shown to be related to a lower risk of melanoma and oral/pharyngeal cancer. [ 17 ] However, a higher risk of childhood acute lymphocytic leukemia and bladder cancer actually is associated with higher coffee intake. [ 17 ] However, it's important to note that these claims are associations and there is not strong evidence that validates the effects of coffee consumption and cancer risk. [ 17 ] Substituting processed foods, such as biscuits, cakes or white bread – which are high in fat, sugars and refined starches – with a plant-based diet may reduce the risk of cancer. [ 15 ] In some cases, plant-based diets have shown to be inversely associated with overall cancer risk. [ 18 ] While many dietary recommendations have been proposed to reduce the risk of cancer, the evidence to support them is not definitive. [ 13 ] [ 14 ] The primary dietary factors that increase risk are obesity and alcohol consumption; with a diet low in fruits and vegetables and high in red meat being implicated but not confirmed. [ 19 ] [ 20 ] A 2014 meta-analysis did not find a relationship between consuming fruits and vegetables and reduced cancer risk. [ 21 ] Green tea comes from camellia sinensis and is made in a process that does not use fermentation. [ 22 ] Some studies have found that green tea could possibly have positive effects relating to cancer prevention. [ 22 ] Research shows that over half the studies (58%) they examined found that drinking green tea may prevent certain cancers, such as esophageal, stomach, pancreatic, liver and colorectal cancer. [ 22 ] But due to the various methodological problems that come with this type of research, the review concludes that the overall analysis of green tea consumption and cancer prevention is inconclusive. [ 22 ] Research shows that regular physical activity may help to reduce cancer up to 30%, [ 23 ] [ 24 ] [ 25 ] with up to 300 minutes per week of moderate to vigorous intensity of physical activity recommended. [ 26 ] [ 27 ] Possible mechanisms by which physical activity may reduce cancer risk include lowering levels of estrogen and insulin , reducing inflammation , and strengthening the immune system . [ 25 ] [ 28 ] In the general population, NSAIDs reduce the risk of colorectal cancer ; [ 29 ] however, due to the cardiovascular and gastrointestinal side effects, they cause overall harm when used to lower cancer risk. [ 30 ] Aspirin use after a cancer diagnosis is associated with about a 20% reduction in cancer mortality. [ 31 ] COX-2 inhibitors may decrease the rate of polyp formation in people with familial adenomatous polyposis however are associated with the same adverse effects as NSAIDs. [ 32 ] Daily use of tamoxifen or raloxifene has been demonstrated to reduce the risk of developing breast cancer in high-risk women. [ 33 ] The benefit verses harm for 5-alpha-reductase inhibitor such as finasteride is not clear. [ 34 ] Vitamins supplements have not been found to be effective at reducing overall cancer risk, [ 35 ] although observational studies consistently show that low blood levels of vitamin D are correlated with increased cancer risk. [ 36 ] [ 37 ] Whether this relationship is causal and vitamin D supplementation is protective is not determined. [ 38 ] Beta-carotene supplementation has been found to increase lung cancer rates in those who are at high risk. [ 39 ] Folic acid supplementation has not been found effective in preventing colon cancer and may increase colon polyps. [ 40 ] A 2018 systematic review concluded that selenium has no beneficial effect in reducing the risk of cancer based on high quality evidence. [ 41 ] The United States National Toxicology Program (NTP) has identified the chemical substances listed below as known human carcinogens in the NTP's 15th Report on Carcinogens. Simply because a substance has been designated as a carcinogen, however, does not mean that the substance will necessarily cause cancer. Many factors influence whether a person exposed to a carcinogen will develop cancer, including the amount and duration of the exposure and the individual's genetic background. [ 42 ] Recent Updates in Carcinogen Classification Updated evaluations by the International Agency for Research on Cancer ( IARC ) continue to confirm the carcinogenicity of long-recognized agents such as asbestos and benzene , which are included above in the NTP 15th report on carcinogens, while also guiding the assessment of emerging substances in consumer products. A meta-analysis published in 2023 found that exposure to certain endocrine-disrupting chemicals , including p,p′-DDT (and its metabolite p,p′-DDE ) and several polychlorinated biphenyl (PCB) variants, was associated with increased risk of breast cancer. [ 43 ] Genetic factors play a significant role in cancer risk, adding to the influence of modifiable environmental factors. Specific gene polymorphisms are associated with increased cancer risk. For instance, variations in the vitamin D receptor (VDR) gene are associated with elevated risks of both breast and ovarian cancers, suggesting that impaired vitamin D signaling may contribute to carcinogenesis . [ 44 ] [ 45 ] Similarly, inherited variations in the enzymes that contribute to the metabolism of carcinogens have been linked with an increased risk of colorectal cancer, demonstrating how genetic differences can affect the capacity of the body to break down cancer-causing substances. [ 46 ] In addition to these inherited factors, environmental exposures can also alter gene regulation through epigenetic modifications. A systematic review on epigenetics, microbiota , and breast cancer revealed that factors like maternal diet and stress may alter epigenetic markers and impact the development and progression of breast cancer. [ 47 ] Research on gene-environment interactions in colorectal cancer identified that lifestyle factors – such as the intake of processed meats, alcohol consumption, and the use of aspirin – affect cancer risk in individuals of specific genetic backgrounds, with aspirin’s protective effects varying according to genetic makeup. [ 48 ] Anti-cancer vaccines can be preventive or be used as therapeutic treatment . [ 2 ] All such vaccines incite adaptive immunity by enhancing cytotoxic T lymphocyte (CTL) recognition and activity against tumor-associated or tumor-specific antigens (TAA and TSAs). Vaccines have been developed that prevent infection by some carcinogenic viruses. [ 49 ] Human papillomavirus vaccine ( Gardasil and Cervarix ) decreases the risk of developing cervical cancer . [ 49 ] The hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer. [ 49 ] The administration of human papillomavirus and hepatitis B vaccinations is recommended when resources allow. [ 50 ] Some cancer vaccines are usually immunoglobulin -based and target antigens specific to cancer or abnormal human cells. [ 2 ] [ 51 ] These vaccines may be given to treat cancer during the progression of disease to boost the immune system's ability to recognize and attack cancer antigens as foreign entities. Antibodies for cancer cell vaccines may be taken from the patient's own body ( autologous vaccine) or from another patient ( allogeneic vaccine). [ 49 ] Several autologous vaccines, such as Oncophage for kidney cancer and Vitespen for a variety of cancers, have either been released or are undergoing clinical trial . FDA -approved vaccines, such as Sipuleucel-T for metastasizing prostate cancer or Nivolumab for melanoma and lung cancer can act either by targeting over-expressed or mutated proteins or by temporarily inhibiting immune checkpoints to boost immune activity. [ 2 ] [ 52 ] Screening procedures, commonly sought for more prevalent cancers, such as colon, breast, and cervical, have greatly improved in the past few decades from advances in biomarker identification and detection. [ 2 ] Early detection of pancreatic cancer biomarkers was accomplished using a SERS -based immunoassay approach. [ 53 ] A SERS-based multiplex protein biomarker detection platform in a microfluidic chip can be used to detect several protein biomarkers to predict the type of disease and critical biomarkers and increase the chance of diagnosis between diseases with similar biomarkers (e.g. pancreatic cancer , ovarian cancer , and pancreatitis ). [ 54 ] To improve the chances of detecting cancer early, all eligible people should take advantage of cancer screening services. However, overall uptake of cancer screening among the general population is not widespread, especially among disadvantaged groups (e.g. those with low income , mental illnesses , or are from different ethnic groups ) who face different barriers that lead to lower attendance rates. [ 55 ] Research indicates that these screening barriers are influenced by both individual circumstances and area-level factors. A systematic review of lung cancer screenings found that feelings of fear, anxiety, and negative attitudes toward the screening process can discourage individuals from participating. [ 56 ] Additionally, a review examining clinical and psychosocial aspects associated with breast, cervical, and colorectal cancer screening found that factors like personal beliefs, social support, and effective communication with healthcare providers are associated with screening attendance. [ 57 ] Beyond the personal and psychosocial factors, broader socioeconomic elements also impact screening participation rates. Women with lower income are 20% more likely to not participate in breast cancer screening, with lower education increasing the likelihood of skipping screening by 18%. Immigrant women have nearly triple the odds of non-participation, and individuals living further away from their assigned screening facility, as well as those with a male family doctor, are also less likely to participate in screening. [ 58 ] Rural communities often face significant transportation barriers, with long travel distances and limited access to public transportation further reducing access to screening services. In addition, in these rural areas, the uneven distribution of healthcare providers and limited availability of telehealth services can exacerbate these disparities, reducing access to specialized cancer screening. [ 59 ] The Role of Health Literacy in Cancer Prevention Health literacy – the ability to navigate and use health care information – is an important factor in cancer prevention. Studies show that individuals with better health literacy are more likely to follow through with cancer screening programs for breast, cervical, and colorectal cancers. [ 60 ] Some intervention programs aimed at improving health literacy are shown to not only boost understanding of health information but also address psychosocial aspects, such as patient communication and decision conflict. [ 61 ] These interventions include patient decision aids, multimedia educational tools, and clinician communication training, which are linked to improvements in patient knowledge, risk perception, and comfortability with screening processes. Enhancing health literacy by addressing patients' informational and emotional needs may help to reduce disparities in cancer prevention. Cervical cancer is usually screened through in vitro examination of the cells of the cervix (e.g. Pap smear ), colposcopy , or direct inspection of the cervix (after application of dilute acetic acid ), or testing for HPV , the oncogenic virus that is the necessary cause of cervical cancer. [ 49 ] Screening is recommended for women over 21 years, initially women between 21 and 29 years old are encouraged to receive Pap smear screens every three years, and those over 29 every five years. [ 2 ] For women older than the age of 65 and with no history of cervical cancer or abnormality, and with an appropriate precedence of negative Pap test results may cease regular screening. [ 62 ] Still, adherence to recommended screening plans depends on age and may be linked to " educational level , culture , psychosocial issues , and marital status ," further emphasizing the importance of addressing these challenges in regards to cancer screening. [ 2 ] Colorectal cancer is most often screened with the fecal occult blood test (FOBT). Variants of this test include guaiac-based FOBT (gFOBT), the fecal immunochemical test (FIT), and stool DNA testing (sDNA). [ 63 ] Further testing includes flexible sigmoidoscopy (FS), total colonoscopy (TC), or computed tomography (CT) scans if a total colonoscopy is non-ideal. The recommended age at which to begin and continue screening is 50–75 years. [ 2 ] [ 64 ] However, this is highly dependent on medical history and exposure to risk factors for colorectal cancer. [ 2 ] Effective screening has been shown to reduce the incidence of colorectal cancer by 33% and colorectal cancer mortality by 43%. [ 2 ] The estimated number of new breast cancer cases in the US in 2018 is predicted to be more than 1.7 million, with more than six hundred thousand deaths. [ 65 ] Factors such as breast size , reduced physical activity, obesity and overweight status , infertility and never having had children, hormone replacement therapy (HRT), and genetics are risk factors for breast cancer. [ 2 ] Mammograms are widely used to screen for breast cancer, and are recommended for women 50–74 years of age by the US Preventive Services Task Force (USPSTF). However, the USPSTF does not recommend mammograms for women 40–49 years old due to the possibility of overdiagnosis . [ 2 ] [ 66 ] Breast cancer is a leading cause of death for women worldwide, being the most common diagnosis for females in regards to cancer. [ 67 ] Current research outlines the possible ability for physical activity and diet to help breast cancer prevention. Researchers have found a link between physical activity and a reduced risk, recurrence and mortality in relation to breast cancer. [ 67 ] Physical activity has been shown to plays a crucial role in helping the immune system against cancer. [ 68 ] Physical activity and body mass index (BMI) are interrelated because of how an increase of physical activity possibly may decrease BMI, which has also shown to be a breast cancer prevention factor. [ 67 ] A recent meta-analysis examined 45,000 breast cancer patients and concluded that women who had higher levels of physical activity showed a possible lower risk for breast cancer recurrence and an overall lower risk of mortality from breast cancer. [ 69 ] Additionally, mammary tumor growth or volume was also shown to have possibly reduced due to physical activity. [ 67 ] When looking at metastasis , two studies found that physical activity may have reduced the metastasis of breast cancer that was present in the lungs, femur or abdominal area. [ 67 ] In one meta-analysis it was shown that for every 25 hours/week of nonoccupational activity breast cancer risk may be reduced by up to 2%, for every 10 hours/week of exercise breast cancer risk can be possibly be reduced by 3%, and for every 2 hours/week of moderate-to-vigorous recreational activity can possibly reduce breast cancer risk by 5%. [ 68 ] In some cases, physical activity has also been shown to lower the level of sex hormones , which in turn can possibly decrease breast cancer risk among women. [ 68 ] With the rise of new research, it's been suggested that the MedDiet may lower the risk of breast cancer. [ 68 ] Some research shows that following this diet could help with breast cancer risk, particularly among women who are postmenopausal . [ 70 ] However, other studies have not found an association between the MedDiet and breast cancer risk. [ 70 ] The MedDiet is known to be a healthy diet because it focuses on eating foods that are plant-based and high in carbohydrates and antioxidants , which has been shown to help reduce inflammation . [ 68 ] This diet includes foods such as various whole grains , nuts, beans, vegetables , fruits, herbs , spices , and olive oil as well as focusing on eating lean sources of meat such as fish and poultry instead of processed proteins. [ 68 ] [ 70 ] In some studies, there has been an inverse association between breast cancer risk and whole grain consumption. [ 68 ] [ 71 ] Research suggests certain aspects as to why whole grains can possibly help prevent breast cancer. Various bioactive phytochemicals including phenolic acids, alkylresorcinols , lignans , vitamin E , polysaccharides , carotenoids , phytosterols , and anthocyanins are present in whole grains. [ 68 ] These components are said to help prevent breast carcinogenesis . [ 68 ] However, other studies done have shown no association between breast cancer risk and whole grain intake. [ 71 ] Another food group, legumes , has been shown to possible lower breast cancer risk due to its high fiber contents. [ 68 ] An example of this food group that would be encouraged to eat is lentils , peas , beans and chickpeas . [ 68 ] One study found that women who ate >5.5 servings of fruit and vegetables per day had a 11% lower chance of getting breast cancer, compared to those who ate <2.5 servings per day. [ 68 ] Researchers suggested this was due to the antioxidants and micronutrients that have been shown to help reduce breast cancer risk. [ 68 ] However, other research shows that there is no association between pre- and postmenopausal breast cancer and eating foods with carotenoids or non-starchy vegetables . [ 70 ] As of 2017, tobacco use , diet and nutrition , physical activity , obesity/overweight status, infectious agents , and chemical and physical carcinogens have been reported to be the leading areas where cancer prevention can be practiced through enacting positive lifestyle changes, getting appropriate regular screening, and getting vaccinated. [ 72 ] The development of many common cancers are incited by such risk factors. For example, consumption of tobacco and alcohol, a medical history of genital warts and STDs , immunosuppression , unprotected sex , and early age of first sexual intercourse and pregnancy all may serve as risk factors for cervical cancer. Obesity, red meat or processed meat consumption, tobacco and alcohol , and a medical history of inflammatory bowel diseases are all risk factors for colorectal cancer (CRC). On the other hand, exercise and consumption of vegetables may help decrease the risk of CRC. [ 2 ] Several preventable causes of cancer were highlighted in Doll and Peto's landmark 1981 study, [ 5 ] estimating that 75 – 80% of cancers in the United States could be prevented by avoidance of 11 different factors. A more recent review of Doll and Peto's work confirmed that most of these estimates remain relevant today. [ 73 ] In addition, a 2013 review of more recent cancer prevention literature by Schottenfeld et al., [ 74 ] summarizing studies reported between 2000 and 2010, points to most of the same avoidable factors identified by Doll and Peto. However, Schottenfeld et al. considered fewer factors (e.g. non inclusion of diet) in their review than Doll and Peto, and indicated that avoidance of these fewer factors would result in prevention of 60% of cancer deaths. The table below indicates the proportions of cancer deaths attributed to different factors, summarizing the observations of Doll and Peto, Shottenfeld et al. and several other authors, and shows the influence of major lifestyle factors on the prevention of cancer, such as tobacco, an unhealthy diet, obesity and infections. * Included in diet †Carcinogenic infections include: for the uterine cervix ( human papillomavirus [HPV]), liver ( hepatitis B virus [HBV] and hepatitis C virus [HCV]), stomach ( Helicobacter pylori [ H pylori ]), lymphoid tissues ( Epstein-Barr virus [EBV]), nasopharynx (EBV), urinary bladder ( Schistosoma hematobium ), and biliary tract ( Opisthorchis viverrini , Clonorchis sinensis ) Cancer has been thought to be a preventable disease since the time of Roman physician Galen , who observed that an unhealthy diet was correlated with cancer incidence. In 1713, Italian physician Ramazzini hypothesized that abstinence caused lower rates of cervical cancer in nuns. Further observation in the 18th century led to the discovery that certain chemicals, such as tobacco, soot and tar (leading to scrotal cancer in chimney sweeps , as reported by Percivall Pott in 1775), could serve as carcinogens for humans. Although Pott suggested preventive measures for chimney sweeps (wearing clothes to prevent contact bodily contact with soot), his suggestions were only put into practice in Holland , resulting in decreasing rates of scrotal cancer in chimney sweeps. Later, the 19th century brought on the onset of the classification of chemical carcinogens. [ 83 ] In the early 20th century, physical and biological carcinogens, such as X-ray radiation or the Rous Sarcoma Virus discovered 1911, were identified. Despite observed correlation of environmental or chemical factors with cancer development, there was a deficit of formal prevention research and lifestyle changes for cancer prevention were not feasible during this time. [ 83 ] In Europe, in 1987 the European Commission launched the European Code Against Cancer to help educate the public about actions they can take to reduce their risk of getting cancer. [ 84 ] The first version of the code covered 10 recommendations covering tobacco, alcohol, diet, weight, sun exposure, exposure to known carcinogens, early detection and participation in organized breast and cervical cancer screening programs. [ 85 ] In the early 1990s, the European School of Oncology led a review of the code and added details about the scientific evidence behind each of the recommendations. [ 85 ] Later updates were coordinated by the International Agency for Research on Cancer . The fourth edition of the code, [1] , developed in 2012‒2013, also includes recommendations on participation in vaccination programs for hepatitis B (infants) and human papillomavirus (girls), breast feeding and hormone replacement therapy , and participation in organized colorectal cancer screening programs.	https://en.wikipedia.org/wiki/Cancer_prevention
A cancer registry is a systematic collection of data about cancer and tumor diseases. The data are collected by Cancer Registrars . Cancer Registrars capture a complete summary of patient history, diagnosis, treatment, and status for every cancer patient in the United States, and other countries. [ 1 ] The Surveillance, Epidemiology and End Results (SEER) program of the National Cancer Institute (NCI) was established in 1973 as a result of the National Cancer Act of 1971 . The National Program of Cancer Registries (NPCR) was established by Congress through the Cancer Registries Amendment Act in 1992, and administered by the Centers for Disease Control and Prevention (CDC). [ 2 ] NPCR and SEER together collect cancer data for the entire U.S. population. CDC and NCI, in collaboration with the North American Association of Central Cancer Registries , have been publishing annual federal cancer statistics in the United States Cancer Statistics: Incidence and Mortality report. Information maintained in the cancer registry includes: demographic information, medical history, diagnostic findings, cancer therapy and follow up details. [ 3 ] The data is used to evaluate patient outcome, quality of life, provide follow-up information, calculate survival rates, analyze referral pattern, allocate resources at regional or state level, report cancer incidence as required under state law, and evaluate efficacy of treatment modalities. [ 3 ] There exist population-based cancer registries, hospital cancer registries (also called hospital-based cancer registries), and special purpose registries. In 1926, Yale-New Haven Hospital became the first to set up a cancer registry. In 1956, the American College of Surgeons (ACoS) formally adopted a policy to encourage, through their Approvals Program, the development of hospital-based cancer registries. In 1973, the Surveillance, Epidemiology and End Results (SEER) Program of NCI established the first national cancer registry program. In 1992, U.S. Public Law 102-515 established the National Program of Cancer Registries (NPCR); it is administered by the US Centers for Disease Control and Prevention (CDC). [ 4 ] By 1993, most states considered cancer a reportable disease. Population-based cancer registries monitor the frequency of new cancer cases (so-called incident cases ) every year in well defined populations and over time by collecting case reports from different sources (treatment facilities, clinicians and pathologists , and death certificates). The frequency of these incident cases are expected per 100,000 of the mother population. If an unexpected accumulation can be observed, a hypothesis about possible causes is generated. This hypothesis is investigated in a second step by collecting more detailed data. The aim is to recognize and to reduce risks. Population-based registries can also monitor the effects of preventive measures. All population-based central registries in the United States and Canada are members of the North American Association of Central Cancer Registries . This organization acts as a voice for the registries when dealing with national standard-setting organizations, sets standards for digital cancer record transmission, and certifies the registries for the quality of their data, among other functions. Hospital cancer registries aim at the improvement of cancer therapy , improve quality of care, evaluate adherence to guidelines, etc. They also serve as a source for epidemiological studies. Therefore, they have to collect detailed data about diagnosis, therapy, dates of important milestones in treatment, etc. Improvements can be achieved by: Since the data needed by hospital cancer registries usually include those of population-based cancer registries and both use the same classifications , data can be sent from a hospital cancer registry to a population-based registry thus reducing documentation efforts. Important barriers and facilitators in this process include clear rules on data sharing, which in many countries may be problematic. [ 5 ] Some hospital and population-based cancer registries report their incidence data to national organizations that aggregate and publish the data, but in many countries the data are not centrally managed. The way in which these data are formatted to be submitted to these organizations are determined by standards released by standard-setting organizations. Edits are run on the data to check for inaccuracies and duplicate cases before being submitted electronically. Different organizations have different standards for data reliability and completeness, and some award certifications based on the adherence to these standards. [ 6 ] The Swedish Cancer Registry [ sv ] was established in 1958. Health care providers in Sweden are required to report newly detected cancer cases diagnosed at clinical, morphological, and laboratory examination (as well as those discovered during autopsy) to the registry. Every year, the regional registries send cancer data to the National Cancer Register. The information available in the registry include patient's personal information (PIN, sex, age and place of residence), medical records (date of diagnosis, site of the tumor, method used for diagnosis, and hospital where the patient is being treated), and follow-up data (date and cause of death or date of migration). [ 7 ] The UK's National Cancer Register is maintained by the National Cancer Registration and Analysis Service (NCRAS), which is one of the two disease registration services operating within the National Disease Registration Service (NDRS). The service is part of the NHS in England. [ 8 ] Individuals who do not want their personal information to be included in the register are able to opt out. [ 9 ] The Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute collects and publish data on cancer incidence and survival throughout the United States. The information from population-based cancer registries covers approximately 28 percent of the US population. This coverage includes 26 percent of African Americans, 41 percent of Hispanics, 43 percent of American Indians and Alaska Natives, 54 percent of Asians, and 71 percent of Hawaiian/Pacific Islanders. The SEER program population-based cancer registries include Arizona Indians, Cherokee Nation, Connecticut, Detroit, Georgia Center for Cancer Statistics (Atlanta, Great Georgia, and Rural Georgia), Greater Bay Area Cancer Registry (San Francisco-Oakland and San Jose-Monterey), Greater California, Hawaii, Iowa, Kentucky, Los Angeles, Louisiana, New Jersey, New Mexico, Seattle-Puget Sound, and Utah. Selection of the geographic areas is based on the ability to operate and maintain a high quality population-based cancer reporting system. [ 10 ] The National Program of Cancer Registries is a U.S.-based program with state-based cancer registries that collect, analyze, and report cancer cases and deaths to a central cancer registry. NPCR was established in 1992 and administered by the CDC. NPCR supports central cancer registries in 46 states, the District of Columbia, Puerto Rico, the U.S. Pacific Islands, and the U.S. Virgin Islands. This data covers approximately 97% of the U.S. population. State cancer registries monitor cancer trends, determine cancer patterns, direct planning and evaluation of cancer control programs, help set priorities for allocating health resources, promote research, and provide information on cancer incidence. The data collected helps public health professionals understand and address the cancer burden. The twelfth volume of Cancer Incidence in Five Continents, published by the International Agency for Research on Cancer , includes cancer incidence data from 32 NPCR-funded registries. NPCR's future direction is to expand the use of information technology designed to support, improve, and enhance the management and exchange of electronic data in cancer surveillance. ⁣ [ 11 ] Due to the lack of central and comprehensive sources of data, research on cancer rates amongst firefighters has been challenging. [ 12 ] [ 13 ] [ 14 ] [ 15 ] On July 7, 2018, Congress passed the Firefighter Cancer Registry Act of 2018 requiring the Centers for Disease Control and Prevention to create the National Firefighter Registry for Cancer designed to collect data on cancer rates among U.S. firefighters. [ 16 ] [ 17 ] [ 18 ] The Cali Cancer Registry ( Registro Poblacional de Cancer de Cali in Spanish) started in 1962 as a research program of the Department of Pathology of the University of Valle School of Medicine in Cali , Colombia . [ 19 ] Currently, Cali Cancer Registry is recognized by the International Agency for Research on Cancer (IARC), an entity of WHO. [ 20 ] Cali Cancer Registry uses quality assurance procedures based on IARC guidelines to validate the quality of cancer registration. [ 21 ] Due to advances in cancer control and the Cali Cancer Registry, Cali is the first city to implement the initiative C/Can 2025: Challenge of Cities Against Cancer, [ 22 ] a project of the Union for International Cancer Control (UICC) that seeks to increase the coverage and quality of oncological care in cities with more than one million inhabitants in low and middle income countries. [ 23 ]	https://en.wikipedia.org/wiki/Cancer_registry
BowelScreen , [ 1 ] BreastCheck [ 2 ] and CervicalCheck [ 3 ] are cancer screening programmes organised by the Health Service Executive (HSE) in Ireland . BowelScreen is the national bowel cancer screening programme. [ 1 ] It was launched in November 2012 by Minister for Health James Reilly , with the eventual aim of offering bi-annual scans to people ages 55 to 74. [ 4 ] It is offered every two years to residents of Ireland age 59 to 69. [ 5 ] The screening consists of an at-home stool test and, if a certain level of blood is found, a referral for a colonoscopy . [ 6 ] BreastCheck is the national breast cancer screening programme. [ 2 ] It was initially founded under Micheál Martin 's tenure as Minister for Health and Children in October 2000 as a pilot in a limited number of health boards . [ 7 ] [ 8 ] [ 9 ] Over 70% of the women invited to take part in the screening in the first year, accepted. [ 7 ] During the height of the COVID-19 pandemic in 2020, breast cancer and cervical cancer screenings were temporarily suspended and the number of breast cancer-related procedures and diagnoses were greatly reduced. [ 10 ] This has led to concerns over the lasting effects of the pandemic, including healthcare capacity issues and delayed diagnoses. [ 11 ] As of 2024 [update] , free breast cancer screening is offered every two years to all women aged 50 to 67. [ 12 ] Due to the pandemic, invitations for breast screening may be sent every three years instead of every two years. [ 13 ] CervicalCheck is the national cervical screening programme. [ 14 ] It was launched in September 2008 as the public name of the National Cancer Screening Service. [ 15 ] In May 2008, then chief executive officer Tony O'Brien dismissed claims that misdiagnoses would result from the use of US -based lab Quest Diagnostics . [ 15 ] In 2014, a woman presented with a confirmed diagnosis of cervical cancer after a CervicalCheck test showed no abnormalities. On 26 April 2018, the HSE confirmed that 206 women developed cervical cancer after having a screening test which was subsequently deemed to be potentially inaccurate, given the known limitations of screening using smear technology. [ 14 ] In May, HSE director-general Tony O'Brien took temporary leave of absence from the board of a US medical company amid renewed calls for him to stand aside from his position due to the ongoing controversy. [ 16 ] Tony O'Brien announced his resignation as director-general of the HSE with effect from close of business on 11 May. [ 17 ] This oncology article is a stub . You can help Wikipedia by expanding it . This article about an organisation in Ireland is a stub . You can help Wikipedia by expanding it . This article related to pathology is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cancer_screening_in_Ireland
Cancer staging is the process of determining the extent to which a cancer has grown and spread. A number from I to IV is assigned, with I being an isolated cancer and IV being a cancer that has metastasized and spread from its origin. The stage generally takes into account the size of a tumor , whether it has invaded adjacent organs , how many regional (nearby) lymph nodes it has spread to (if any), and whether it has appeared in more distant locations ( metastasized ). [ 1 ] Cancer staging can be divided into a clinical stage and a pathologic stage. In the TNM (Tumor, Node, Metastasis) system, clinical stage and pathologic stage are denoted by a small "c" or "p" before the stage (e.g., cT3N1M0 or pT2N0). This staging system is used for most forms of cancer, except brain tumors and hematological malignancies . Because they use different criteria, clinical stage and pathologic stage often differ. Pathologic staging is usually considered to be more accurate because it allows direct examination of the tumor in its entirety, contrasted with clinical staging which is limited by the fact that the information is obtained by making indirect observations of a tumor which is still in the body. However, clinical staging and pathologic staging often complement each other. Not every tumor is treated surgically, so pathologic staging is not always available. Also, sometimes surgery is preceded by other treatments such as chemotherapy and radiation therapy which shrink the tumor, so the pathologic stage may underestimate the true stage. Correct staging is critical because treatment (particularly the need for pre-operative therapy and/or for adjuvant treatment, the extent of surgery) is generally based on this parameter. Thus, incorrect staging would lead to improper treatment. For some common cancers the staging process is well-defined. For example, in the cases of breast cancer and prostate cancer, doctors routinely can identify that the cancer is early and that it has low risk of metastasis. [ 2 ] In such cases, medical specialty professional organizations recommend against the use of PET scans , CT scans , or bone scans because research shows that the risk of getting such procedures outweighs the possible benefits. [ 2 ] Some of the problems associated with overtesting include patients receiving invasive procedures, overutilizing medical services, getting unnecessary radiation exposure, and experiencing misdiagnosis. [ 2 ] Pathologic staging, where a pathologist examines sections of tissue , can be particularly problematic for two specific reasons: visual discretion and random sampling of tissue. "Visual discretion" means being able to identify single cancerous cells intermixed with healthy cells on a slide. Oversight of one cell can mean misstaging and lead to serious, unexpected spread of cancer. "Random sampling" refers to the fact that lymph nodes are cherry-picked from patients and random samples are examined. If cancerous cells present in the lymph node happen not to be present in the slices of tissue viewed, incorrect staging and improper treatment can result. New, highly sensitive methods of staging are in development. For example, the mRNA for GCC ( guanylyl cyclase c ), present only in the luminal aspect of intestinal epithelium , can be identified using molecular screening ( RT-PCR ) with a high degree of sensitivity and exactitude. Presence of GCC in any other tissue of the body represents colorectal metaplasia . Because of its high sensitivity, RT-PCR screening for GCC greatly reduces underestimation of disease stage. Researchers hope that staging with this level of precision will lead to more appropriate treatment and better prognosis . Furthermore, researchers hope that this same technique can be applied to other tissue-specific proteins . Staging systems are specific for each type of cancer (e.g., breast cancer and lung cancer ), but some cancers do not have a staging system. Although competing staging systems still exist for some types of cancer, the universally-accepted staging system is that of the UICC , which has the same definitions of individual categories as the AJCC . Systems of staging may differ between diseases or specific manifestations of a disease. For solid tumors, TNM is by far the most commonly used system, but it has been adapted for some conditions. Overall Stage Grouping is also referred to as Roman Numeral Staging. This system uses numerals I, II, III, and IV (plus the 0) to describe the progression of cancer. Within the TNM system, a cancer may also be designated as recurrent, meaning that it has appeared again after being in remission or after all visible tumor has been eliminated. Recurrence can either be local, meaning that it appears in the same location as the original, or distant, meaning that it appears in a different part of the body. Stage migration is a change in the distribution of stages in a particular cancer population, induced by either a change in the staging system itself or else a change in technology which allows more sensitive detection of tumor spread and therefore more sensitivity in detecting spread of disease (e.g., the use of MRI scans). Stage migration can lead to curious statistical phenomena (for example, the Will Rogers phenomenon ).	https://en.wikipedia.org/wiki/Cancer_staging
Cancer survival rates vary by the type of cancer , stage at diagnosis, treatment given and many other factors, including country. In general survival rates are improving, although more so for some cancers than others. Survival rate can be measured in several ways, median life expectancy having advantages over others in terms of meaning for people involved, rather than as an epidemiological measure. [ 1 ] [ 2 ] However, survival rates are currently often measured in terms of 5-year survival rates, which is the percentage of people who live at least five years after being diagnosed with cancer, and relative survival rates compare people with cancer to people in the overall population. [ 3 ] Several types of cancer are associated with high survival rates, including breast , prostate , testicular and colon cancer . Brain and pancreatic cancers have much lower median survival rates which have not improved as dramatically over the last forty years. [ 4 ] Indeed, pancreatic cancer has one of the worst survival rates of all cancers. Small cell lung cancer has a five-year survival rate of 4% according to Cancer Centers of America's Website. [ 5 ] The American Cancer Society reports 5-year relative survival rates of over 70% for women with stage 0-III breast cancer with a 5-year relative survival rate close to 100% for women with stage 0 or stage I breast cancer. The 5-year relative survival rate drops to 22% for women with stage IV ( metastatic ) breast cancer. [ 3 ] In cancer types with high survival rates, incidence is usually higher in the developed world , where longevity is also greater. Cancers with lower survival rates are more common in developing countries . [ 6 ] The highest cancer survival rates are in countries such as South Korea , Japan , Israel , Australia , and the United States . [ 7 ] In the United States there has been an increase in the 5-year relative survival rate between people diagnosed with cancer in 1975-1977 (48.9%) and people diagnosed with cancer in 2007-2013 (69.2%); these figures coincide with a 20% decrease in cancer mortality from 1950 to 2014. [ 8 ] Due to innovation in emerging treatments and cancer prevention strategies, the U.S.A cancer death rate has declined from 208.3 per 100,000 people in 1982 to 152.6 per 100,000 in 2017. [ 9 ] [ 10 ] [ 11 ] In males, researchers suggest that the overall reduction in cancer death rates is due in large part to a reduction in tobacco use over the last half century, estimating that the reduction in lung cancer caused by tobacco smoking accounts for about 40% of the overall reduction in cancer death rates in men and is responsible for preventing at least 146,000 lung cancer deaths in men during the time period 1991-2003. [ 12 ] The most common cancer among women in the United States is breast cancer (123.7 per 100,000), followed by lung cancer (51.5 per 100,000) and colorectal cancer (33.6 per 100,000), but lung cancer surpasses breast cancer as the leading cause of cancer death among women. [ 13 ] Researchers attribute the reduction in breast cancer mortality to improved treatment, including the increased use in adjuvant chemotherapy . [ 14 ] The National Institute of Health (NIH) attributes the increase in the 5-year relative survival of prostate cancer (from 69% in the 1970s to 100% in 2006) to screening and diagnosis and due to the fact that men that participate in screening tend to be healthier and live longer than the average man and testing techniques that are able to detect slow growing cancer before they become life-threatening. [ 15 ] The most common type of cancer among children and adolescents is leukemia , followed by brain and other central nervous system tumors. Survival rates for most childhood cancers have improved, with a notable improvement in acute lymphoblastic leukemia (the most common childhood cancer). Due to improved treatment, the 5-year survival rate for acute lymphoblastic leukemia has increased from less than 10% in the 1960s to about 90% during the time period 2003-2009. [ 16 ] The improvement in survival rates for many cancers in the last half century is due to improved understanding about the causes of cancer and the availability of new treatment options, which are continually evolving. Where surgery was previously the only option for treatment, cancer is now treated with radiation and chemotherapy , including combination chemotherapy that favors treatment with many drugs over just one. [ 17 ] Availability and access to clinical trials has also led to more targeted therapy and improved knowledge of treatment efficacy. There are currently over 60,000 clinical trials related to cancer registered on ClinicalTrials.gov, so novel approaches to cancer treatment are continuing to be developed. [ 18 ] The NCI lists over 100 targeted therapies that have been approved for the treatment of 26 different cancer types by the United States Food and Drug Administration. [ 19 ]	https://en.wikipedia.org/wiki/Cancer_survival_rates
A cancer survivor is a person with cancer of any type who is still living. Whether a person becomes a survivor at the time of diagnosis or after completing treatment , whether people who are actively dying are considered survivors, and whether healthy friends and family members of the cancer patient are also considered survivors, varies from group to group. Some people who have been diagnosed with cancer reject the term survivor or disagree with some definitions of it. How many people are cancer survivors depends on the definition used. Nearly 65% of adults diagnosed with cancer in the developed world are expected to live at least five years after the cancer is discovered. [ 1 ] In the U.S. for example, about 17 million Americans alive today—one in 20 people–are either currently undergoing treatment for cancer or have done so in the past [ 2 ] (up from 11 million, or one in thirty people, in 2009). [ 3 ] Globally, about 45 million people, mostly from wealthier countries, have survived cancer for at least five years. [ 2 ] For many people, surviving cancer can be highly traumatic and it is not uncommon for people to experience psychological distress such as post-traumatic stress-disorder or symptoms of post-traumatic-stress. [ 4 ] Some cancer survivors describe the process of living with and beating cancer as a life-changing experience [ 5 ] and some people who survive cancer may use the experience as opportunities for creative self-transformation into a "better person" or as motivation to meet goals of great personal importance, such as climbing a mountain or reconciling with an estranged family member . This process of post-traumatic growth is called benefit finding . [ 6 ] Cancer survivors often have specific medical and non-medical needs related to their cancer experience. Macmillan Cancer Support in the UK defines a cancer survivor as someone who is "living with or beyond cancer", namely someone who: The National Coalition for Cancer Survivorship (NCCS) pioneered the definition of survivor as being any person diagnosed with cancer, from the time of initial diagnosis until his or her death. This definition of survivor includes people who are dying from untreatable cancer. NCCS later expanded the definition of survivor even further to include family, friends and voluntary caregivers who are "impacted by the survivorship experience" in any way. [ 8 ] Part of the goal in promoting survivorship was to stop using the older, more discouraging label cancer victim . [ 2 ] The US National Cancer Institute 's Office of Cancer Survivorship uses a definition that focuses on identifying people with a medical history that includes any form of cancer, regardless of their self-identification with the word survivor . [ 9 ] The word survivor is a loaded term . [ 5 ] Within the breast cancer culture , survivorship is conferred upon women and men who are perceived as having had emotional or physical trauma , even if their breast cancer was a non-life-threatening pre-cancerous condition like LCIS or DCIS . The term tends to erase and degrade people who are dying of incurable cancer. This idea of survivorship emphasizes and values longevity of life after diagnosis, while overlooking issues of quality of life . [ 5 ] Some people reject the term survivor as being a narrow conceptualization of highly variable human experiences. Alternatives include alivers and thrivers , which put emphasis on living as well as possible, despite limitations and disability . [ 5 ] A third term, the diers , is used by some terminally ill patients who reject the claim that dying is part of survivorship or should be covered up with inappropriately optimistic language. [ 5 ] The term previvor has been used to describe unaffected carriers . Unaffected carriers, or previvors, are those who have not been diagnosed with cancer , but who know that they are likely to develop cancer due to certain genetic mutations that form a known cancer syndrome . They have sur vived the pre disposition, or higher risk, of cancer. [ 10 ] [ 11 ] As such, this is the first generation in human history who, armed with information about a predisposition to a cancer after opting into DNA testing, can make informed choices prior to cancer diagnosis. The typical previvor has tested positive for a BRCA mutation , learned that she is at high risk for developing breast cancer and ovarian cancer , or he is at high risk of developing prostate or male breast cancer, and is attempting to manage that risk through a combination of increased surveillance through mammograms, breast MRIs, pelvic ultrasounds , oophorectomy , bilateral mastectomy , PSA testing, MRI, and other medical procedures. There has been controversy over the term previvor , because the name compares these healthy women to people who have already been diagnosed with cancer. People who have finished cancer treatment often have psychological and physical medical challenges. [ 12 ] These effects can vary from person to person, change over time, and range in intensity from mild and intermittent to fully disabling . Different cancers and different treatments cause different long-term side effects. [ 2 ] Problems commonly include fatigue , [ 13 ] pain , [ 13 ] sleep problems , [ 14 ] physical side effects like lymphoedema , [ 15 ] weight gain, [ 16 ] anxiety and depression , [ 17 ] fear of cancer recurrence , [ 18 ] impacted sexual desire and or function, and impaired quality of life . [ 19 ] If the treatment is lengthy and disruptive, many patients experience some difficulty in returning to normal daily life . [ 20 ] The energy needed to cope with a rigorous treatment program may have caused them to disconnect from previous daily patterns, such as working , normal self-care , and housekeeping . Some survivors become dependent on the attention and sympathy that they received during their treatment and feel neglected when life returns to normal. [ 21 ] [ 22 ] There are tremendous implications that cancer has on the relationships that survivors have with their loved ones (particularly their partners) once their cancer has been treated, [ 23 ] and social support plays a critical role in their long-term emotional adjustment . [ 24 ] Cancer survivors tend to be more resilient than the general population. [ 25 ] Some survivors have to adjust to the idea that they will never be cured. Some survivors, even if the cancer has been permanently cured, struggle emotionally from the trauma of having experienced a life-threatening disease. [ 26 ] Cancer survivors experience more psychological distress than those who have never had cancer (5.6% compared to 3.0%). [ 27 ] Serious psychological distress was seen 40% more among cancer survivors of five years or more than in those who have never had cancer. [ 27 ] About 10% develop major depressive disorder ; others experience an adjustment disorder . [ 26 ] In young adult cancer survivors, one small study found that 20% of participants met the full clinical diagnosis of post-traumatic stress disorder (PTSD), and 45% to 95% displayed at least one symptom of PTSD. [ 28 ] The NCCN has developed a distress thermometer scale for measuring overall distress in cancer survivors. [ 2 ] Survivors of adult cancer are at an increased risk of suicidal ideation (having thoughts about suicide ), [ 29 ] while as many as 13% of childhood cancer survivors experience suicidal ideation. [ 30 ] Issues of pain and physical ailments have been hypothesized as major contributing factors in cancer survivors experiencing this suicidal ideation. People whose cancer is in remission may still have to cope with the uncertainty that at any time their cancer could return without warning. After the initial treatment has ended, anxiety is more common among cancer survivors than among other people. [ 31 ] This anxiety regarding the cancer's return is referred to as fear of cancer recurrence . [ 32 ] Many patients are anxious that any minor symptom indicates that the cancer has returned, with as many as 9 in 10 patients fearful that their cancer will recur or spread . [ 3 ] In addition to the appearance of any new aches and pains, common triggers for a fear that the cancer may return include hearing that someone else has been diagnosed with cancer, annual medical exams to determine whether the cancer recurred, and news stories about cancer. [ 33 ] This anxiety leads to more medical check ups, which can be measured even after a period of up to ten years. [ 34 ] This fear can have a significant effect on individuals' lives, resulting in difficulties in their daily life such as work and socialising , and difficulties planning for the future. [ 35 ] Overall, fear of cancer recurrence is related to a reduced quality of life in cancer survivors. [ 2 ] This fear is not unwarranted, as both pediatric and adult survivors have a higher than average risk of another cancer (a new cancer, sometimes called a second primary ), in addition to the possibility that the original cancer could recur. [ 2 ] These new cancers may have been caused by genetic predisposition, by the treatment for the first cancer, or by ordinary risk factors for cancer . [ 2 ] Some risk factors, such as smoking, drinking alcohol, overeating, and lack of physical activity, may be things the cancer survivor can modify, with a consequent reduction in the chance of a second cancer. [ 2 ] While fear of cancer recurrence can be adaptive at low levels (e.g., by prompting the person to get appropriate screening tests done), high levels of fear require psychological treatment. As of 2012 [update] , there are no psychometrically sound measures of this fear, which makes research into the effectiveness of treatment protocols difficult to interpret. [ 36 ] Treatments that are being investigated include: cognitive-behavioural therapy , [ 37 ] meta-cognitive therapy , [ 38 ] cognitive-existential group therapy, [ 39 ] mindfulness-based interventions , [ 40 ] and physical exercise . [ 41 ] Cancer survivors and their families have often incurred significant expenses or had to forego the opportunity to work regularly during treatment and recovery. [ 2 ] When treatment ends, they may be partially or fully disabled, either temporarily or permanently. They may have ongoing costs, such as expensive medications to prevent recurrence or address side effects. [ 2 ] As a result, they may experience financial distress. [ 2 ] Adult survivors of childhood cancer are twice as likely to be unemployed than healthy controls. The risk of unemployment depends on cancer diagnosis, with survivors of CNS and brain tumors being nearly 5 times more likely to be unemployed, whereas the risk for survivors of blood or bone cancer was found to be elevated but not significantly higher. [ 42 ] The cultural ideal of a survivor may add to individual patients' distress if the patient is unable or unwilling to live up to the ideal. [ 5 ] As described by Gayle Sulik in her book Pink Ribbon Blues: How Breast Cancer Culture Undermines Women's Health , the ideal survivor is bravely committed to mainstream medicine and optimistic or even certain of a physical cure. She [ Notes 1 ] is open about diagnosis and treatment and become an educated, empowered medical consumer . The ideal survivor, like a superwoman who simultaneously manages her home, family, and career, struggles valiantly to prevent cancer from affecting loved ones by appearing, behaving, and working as much as possible. Once the immediate crisis is past, the person may feel strongly pressured to donate time, money, and energy to cancer-related organizations . Above all, the ideal survivor does not die of cancer . People who publicly conform to this ideal are given social status and respect . [ 5 ] In terms of medical challenges, some survivors experience cancer-related fatigue , may have long-term side effects from cancer and its treatment, and may need extensive rehabilitation for mobility and function if aggressive surgery was required to remove the cancer. They may experience temporary or persistent post-chemotherapy cognitive impairment . Some young survivors lose their ability to have children . Cancer survivors frequently need medical monitoring, and some treatments for unrelated diseases in the future may be contraindicated. For example, a patient who has had a significant amount of radiation therapy may not be a good candidate for more radiation treatments in the future. To assist with these needs, survivor care plans have been promoted. [ 43 ] These are personalized documents that describe the person's diagnosis and treatment in detail, list common known side effects, and specifically outline the steps that the survivor should take in the future, ranging from maintaining a healthy weight to receiving specific medical tests on a stated schedule. However, these are not widely used, as they have been expensive and complicated to produce. [ 2 ] Medical tests to determine whether the cancer has returned commonly provoke fears. Informally, this is called scanxiety , a portmanteau of scan and anxiety . A desire to avoid feeling this fear can prompt survivors to postpone or refuse tests. [ 44 ] [ 45 ] This may be able to be helped by the follow-up of people who have had cancer post-treatment being undertaken via self-reported patient-related outcome measures rather than follow-up visits, but there is not enough controlled research looking into this. [ 46 ] Different health systems use different approaches to long-term medical monitoring. In the UK, the risk-stratified shared care model predominates. [ 2 ] This means that cancer survivors at low risk of future problems will be monitored mainly by the primary care provider, according to medical guidelines. Those at medium risk might be seen by the primary care provider one year, and then the oncologist the next year. Those at high risk are followed by the oncologist alone. Specialty centers may use a nurse-led model, in which survivors are followed by a nurse, often one who specializes in a particular type of cancer. [ 2 ] Large centers may have a multi-disciplinary model, in which a team made up of providers in different specialties work together to meet all of the cancer survivor's needs in the same clinic. [ 2 ] Another model, for cancer survivors with high health literacy , is self management , in which the cancer survivor knows what to do, which symptoms require medical advice, and how to obtain help when it is needed. [ 2 ] Survivors of childhood cancer have a life expectancy up to 28% shorter than people in the general population. [ 47 ] Therefore, there is a need to closely monitor these patients for much longer than usual. The Children's Oncology Group recommends that monitoring should include periodic follow-up and screening by a clinician familiar with these patients' risks. Improving these patients' longevity requires recognition and treatment of illnesses associated with late effects in the decades after therapy for childhood cancer. For example, survivors of childhood cancer may have more difficulty than typical with breastfeeding and require more support to undertake this health-promoting activity. [ 48 ] Childhood cancer survivors are also at risk for developing kidney diseases . [ 49 ] Others experience various forms of heart disease , particularly those exposed to anthracyclines or chest radiotherapy . [ 50 ] One challenge to achieving this goal is that childhood cancer survivors are both very adaptable and accustomed to denying difficulties ; as a result, they tend to minimize their symptoms . Therefore, internists may not give them all the attention they need and thus the actual help they may need. Symptom management, health promotion , specific attention to psychosocial needs, and surveillance for recurrence and specific late effects of treatment are helpful. [ 47 ] Health behaviour interventions may be able to reduce the impact of some of the chronic issues cancer survivors face by improving their dietary intake. [ 51 ] Likewise, physical exercise training interventions may have positive effects on physical fitness, including cardio-respiratory fitness , muscle strength and health-related quality of life. [ 52 ] Adolescent and young adult (AYA) survivors, often defined as being between the ages of 15 and 39, have seen advancements in technology and modern medicine causing a dramatic increase in the number of AYA survivors. Prior to 1970, childhood cancer was considered a universally fatal disease. From 1995 to 2000, however, the 5-year survival rate for children diagnosed with cancer was 80%. [ 53 ] Significant progress has been built in the last 25 years as there are now approximately 270,000 survivors of pediatric cancer in the U.S., which translates to approximately 1 in every 640 young adults being a survivor of childhood cancer. [ 54 ] [ 55 ] However, as studies have shown, as patient needs increase, the likelihood of having an unmet need also increases. [ 56 ] For the AYA population, 2 out of 3 childhood cancer survivors will develop a complication due to the therapy they received, and 1 out of 3 will develop serious or life-threatening complications, meaning they will need treatment and follow-up care. [ 57 ] In addition, AYAs may experience greater difficulties adhering to treatment , which may negatively impact future outcomes. [ 58 ] An AYA survivor faces a variety of issues as a result of their cancer diagnosis and treatment that are unique to their particular age group which differentiate their survivor population from the adult survivor population. For example, AYA survivors report that their education, employment, sexual functioning , [ 59 ] marriage, fertility , and other life values are impacted by their cancer. [ 60 ] [ 61 ] Compared to adult survivors, AYA survivors have a much greater risk of getting a second primary malignancy as a side effect of the treatment for their original diagnosis. It is believed that AYAs have a much higher relative risk of developing a second primary cancer because the intensity of the treatment for their original diagnosis, typically including any combination of chemotherapy , surgery, and radiation therapy, is much higher than the level of intensity given to patients over 40. [ 62 ] Furthermore, since AYA survivors are diagnosed and treated at such a young age, their length of time as a survivor is much longer than their adult counterparts, making it more likely they will face a second primary cancer in their lifetime. [ 62 ] Childhood cancer survivors, in particular, need comprehensive long-term follow-up care to thrive. One way this can be accomplished is through continuous follow-up care with a primary care physician who is trained to identify possible late effects from previous treatments and therapies. [ 63 ] The Children's Oncology Group (COG) has designed a set of survivorship guidelines that hope to aid both health care professionals and survivors themselves, in both the intricacies and basics of long-term follow-up care. The COG recommends that patients or their families put together their own treatment summary, so they can have their treatment history with them when they visit any health care provider. The COG suggests that all survivors include the following in their treatment summaries: With the treatment summary, experts hope that survivors will be better equipped to maintain quality follow-up care long after their original treatment. This is especially important for the AYA population, in particular, because they are typically facing major social changes regarding their relationship status , employment or education status, their insurance coverage, and even their place of residence, etc. Typically, most of these factors are stable for most older adults, and when they experience any changes, it would usually occur in one or two aspects of their life at a time. However, with people under the age of 40 is when most people undergo the most change. This reality underscores the importance of a smooth transition from child-centered to adult-focused health care services through which they are consistently managed. [ 65 ] The US Affordable Care Act (ACA) in 2010 makes it illegal for health insurance providers to deny coverage for a pre-existing condition , such as previously having survived cancer. [ 66 ] Young adults are required to have health insurance coverage and, with a few exceptions, will be able to be covered under their parent's coverage until the age of 26 as a dependent in their parent's plan. [ 66 ] Studies among endometrial cancer survivors show that satisfaction with information provided about the disease and treatment increases the quality of life, lowers depression and results in less anxiety. [ 67 ] People who receive information on paper, compared to oral , indicate that they receive more information and are more satisfied about the information provided. [ 68 ] The US Institute of Medicine and the Dutch Health Council recommend the use of a written "survivorship care plan", which is a summary of a patient's course of treatment, with recommendations for subsequent surveillance, management of late effects, and strategies for health promotion. [ 69 ] Cancer survivors are encouraged to meet the same guidelines for physical activity as the rest of the population. [ 70 ] [ 71 ] However, less than one-third of US cancer survivors met the Physical Activity Guideline for Americans . [ 72 ] Increased physical activity reduces both all-cause and cancer-specific mortality in breast [ 73 ] and colorectal cancer survivors [ 74 ] as well as all cancer survivors. [ 72 ] In addition, sedentary behaviors, particularly prolonged sitting, were associated with worse survival outcomes. [ 72 ] Physical activity improves quality of life among a range of cancer survivors [ 75 ] and may also assist with cancer-related fatigue and common co-morbidities. [ 76 ] [ 77 ] Diet can also impact long-term mortality, with evidence across various cancer types. [ 78 ] [ 79 ] However, adherence to diet and exercise recommendations among cancer survivors is often poor. [ 80 ] [ 81 ] Digital behaviour change interventions can be successful at increasing physical activity and may also help with diet in cancer survivors. [ 82 ] In breast cancer survivors, home-based multidimensional survivorship programmes have short-term beneficial impacts on quality of life and can reduce anxiety, fatigue and insomnia . [ 83 ] Mindfulness-based survivorship programs may be an effective way to improve the mental health of cancer survivors. [ 84 ] [ 85 ] Family members can be significantly affected by the cancer experience of their loved ones. [ 86 ] [ 87 ] They may need to be assessed and treated as a result of the emotional and mental strain. [ 2 ] For parents of children with cancer, finishing treatment can be a particularly vulnerable time. In the post-treatment period, some parents may experience increases in anxiety, depression and feelings of helplessness. [ 88 ] A sub-group of parents report post-traumatic stress symptoms up to years after treatment completion. [ 89 ] Evidence-based psychological interventions tailored to the needs of parents of childhood cancer survivors may assist parents in resuming their normal lives after their child has finished treatment. [ 90 ] Spouses of cancer survivors are more likely than other people to experience anxiety in the years after their partner's successful treatment. [ 31 ] Being married reduces the cancer survivor's risk of developing post-traumatic stress disorder or other psychological difficulties, but it increases the risk of the spouse developing mental health symptoms. [ 25 ] As of 2019, about 17 million people living in the US have previously been diagnosed with cancer. [ 2 ] By 2030 [update] , that number is expected to increase to 22 million. [ 2 ] Globally, about 45 million people have survived cancer for at least five years. [ 2 ] Most of these cancer survivors are from wealthier countries. [ 2 ] In the US, about 70% of people survive cancer for at least five years after diagnosis, and almost half will live for ten or more years. [ 2 ] About 20% of cancer survivors have lived 20 or more years past their diagnosis. [ 2 ] Because cancer is much more common in older adults, most cancer survivors are older adults. [ 2 ] Within the US, about 35% of cancer survivors are children, teenagers, or working-age adults. [ 2 ] About 45% of cancer survivors are between the ages of 65 and 80, and about 20% are older than that. [ 2 ] Cancer survivors are more likely to be women. [ 2 ] In the US, overall, there is survival difference of about six percentage points between white and Black cancer survivors, though this varies significantly according to the type of cancer. [ 2 ] The idea of cancer survivorship being part of cancer-related care can be traced back to two events. One was the gradual realization that survivors of childhood cancer had some specific, long-term care needs. [ 2 ] The other was a 1985 essay written by a physician who was diagnosed with cancer at the age of 32, [ 91 ] in which he described his experiences as belonging to three phases, which he called acute survival (active treatment), extended survival (recovering from cancer and its treatment), and eventually permanent survival (the long-term social, psychological, and physical effects on the cancer survivor and their loved ones). [ 2 ] The partnership that grew out of that publication became the National Coalition of Cancer Survivorship. [ 2 ] The National Cancer Institute's Office of Cancer Survivorship was created in 1995. [ 2 ]	https://en.wikipedia.org/wiki/Cancer_survivor
Cancerous micronuclei are a type of micronucleus that is associated with cancerous cells. Theodor Boveri originally observed the fact that abnormal nuclear morphologies commonly occur in cancer . Micronuclei are also referred to Howell-Jolly bodies ; discovered by hematologists William Henry Howell and Justin Marie Jolly in erythrocytes. Micronucleus induction by a chemical was first reported in Ehrlich ascites tumor cells treated with colchicine. The effect of environmental stressors on the expression of micronuclei was first analyzed in root tip cells under ionizing radiation . It can be inferred that nuclear abnormalities are a result of various molecular mechanisms. These events can ultimately lead to cell death . Micronuclei are characterized in the cells that have some sort of DNA damage. This includes damage caused by radiation , harmful chemicals , and random mutations that occur throughout the genome . Micronuclei are small bodies that can be seen budding off of a newly divided daughter cell. Micronuclei can contain a whole chromosome or part of a chromatid . The increased formation of micronuclei is usually an indication of increased DNA damage or mutation . It is characteristically found in cancer cells, or cells that have been exposed to increased risk factors. Micronuclei are small, extranuclear bodies that are formed during mitosis from lagging chromosomes . In anaphase , the microtubules are not attached properly to the chromosomes, which can cause pulling in a different direction. This results in parts of the chromatids or chromosomes being broken off and enveloped as an extra nucleus in one of the daughter cells. This is the main way that micronuclei are formed. Micronuclei can also be spontaneously formed as a byproduct of cellular defense. If the cell senses extra chromosomes , the cell can attempt to remove the extra chromosome in another cell membrane , separate from the other normal chromosome . Another mechanism to micronuclei formation is by a double-strand break in the DNA , creating a separate linear fragment. Furthermore, the breaking of an anaphase bridge could also lead to formation of a micronucleus. The formation of an abnormal nuclear structure called chromosome bridge also predisposes to micronucleation. Bridges arise from end-to-end chromosome fusions after DNA breakage or telomere crisis, incomplete DNA replication, or failed resolution of chromosome catenation. [ 1 ] Micronuclei are often overlooked in cancer diagnosis and treatment. If observed, they are viewable under a microscope and often located next to other larger nuclei . Based on the structure of a micronucleus, or the function of a cell, it seems to provide support in the central apparatus within the cell. Micronuclei are under investigation and research regarding whether or not they can be used to predict future cancer risks. It seems that they are easy to analyze compared to chromosome aberrations .	https://en.wikipedia.org/wiki/Cancerous_micronuclei
Cancers is a peer-reviewed , open access , medical journal published by MDPI covering all fields of oncology . [ 1 ] The editor-in-chief is Samuel C. Mok ( The University of Texas MD Anderson Cancer Center ). The Irish Association for Cancer Research (IACR) and the Signal Transduction Society (STS) are affiliated societies. The journal is abstracted and indexed in: According to the Journal Citation Reports , the journal has a 2020 impact factor of 6.639. [ 5 ] This article about an oncology journal is a stub . You can help Wikipedia by expanding it . See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .	https://en.wikipedia.org/wiki/Cancers_(journal)
Canine cancer detection is an approach to cancer screening that relies upon the claimed olfactory ability of dogs to detect, in urine or in breath, very low concentrations of the alkanes and aromatic compounds generated by malignant tumors . While some research has been promising, no verified studies by secondary research groups have substantiated the validity of positive, conclusive results. The proposal that dogs can detect cancer attracted widespread coverage in the general media. In 2015 the Huffington Post reported that studies have suggested that dogs may be able to detect lung cancer , melanoma , breast cancer and bladder cancer , and that dogs can be trained to detect cancer in 93% of cases. [ 1 ] In 2016, actress Shannen Doherty told Entertainment Tonight in an interview that her dog identified her breast cancer before doctors could diagnose it. [ 2 ] National Geographic said that "man's best friend can detect various cancers, including prostate cancer, colorectal cancer and melanoma." [ 3 ] On the other hand, a review by Australian Popular Science found that the more rigorous trials produced less positive results. [ 4 ] Another trial reported in Nature World News found disappointing results, but nevertheless "the researchers... believe that one day, dogs can still detect lung cancer." [ 5 ] NBC reported that Britain's National Health Service is behind the first clinical trial to test the ability of canines to detect cancer. [ 6 ] Although the first suggestion of this approach in a medical journal, The Lancet , dates back to 1989, [ 7 ] there were only occasional publications on the subject in the next decade. [ 8 ] However, two studies (one published in 2004 [ 9 ] [ 10 ] [ 11 ] and one in 2006), involving detection in urine, had promising results, with the 2006 report claiming a 99% accuracy in detecting lung cancer , [ 12 ] although both studies were preliminary and involved small numbers of patients. In a 2011 study, lung cancer was identified with a sensitivity of 71% and a specificity of 93%, using breath samples. [ 13 ] In a May 25, 2012 article, “What to make of Medical Dogs” published by Science-Based Medicine , Peter Lipson reported on his review of the scientific literature regarding these claims and found valid support for positive conclusions to be lacking: While anecdotes abound, there is scant literature to support this ability. One unimpressive pilot study looked at dogs’ potential ability to detect bladder cancers from urine samples. The idea behind cancer dogs is that there may be volatile compounds produced in cancer patients that dogs can detect by scent. In these studies, the compounds are not identified, not tested for, not named. There are many confounders , for example, in the few samples used, there may be other differences being detected by the dogs. [ 14 ] In the other study (I found very few) dogs were “trained” to detect lung and breast cancers in humans. The methodology of breath sampling is not validated as far as I can see, and once again, the putative compounds in breath are not identified. Statistically , the efficacy is marginal at best… I don’t doubt the social and emotional value of dogs as companions, and as active helpers in many circumstances. But beyond this, the evidence is wanting. [ 14 ]	https://en.wikipedia.org/wiki/Canine_cancer_detection
Cannon A waves , or cannon atrial waves , are waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias . When the atria and ventricles happen to contract simultaneously, the right atrium contracts against a closed tricuspid valve , resulting in back pressure into the venous system that can be seen in the jugular venous pulse as a high-amplitude "cannon wave". [ 1 ] [ 2 ] It is associated with heart block, in particular third-degree (complete) heart block . [ 3 ] It is also seen in pulmonary hypertension . [ 3 ] Cannon A waves may also be seen in ventricular tachycardia due to the inherent AV dissociation of the arrhythmia. [ citation needed ] This wave will cause pulsation in the neck and abdomen, headache , cough , and jaw pain. [ 2 ] This cardiovascular system article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cannon_A_waves
Capitalist Realism: Is There No Alternative? is a 2009 book by British philosopher Mark Fisher . It explores Fisher's concept of " capitalist realism ", which he describes as "the widespread sense that not only is capitalism the only viable political and economic system, but also that it is now impossible even to imagine a coherent alternative to it." [ 1 ] The book investigates what Fisher describes as the widespread effects of neoliberal ideology on popular culture, work, education, and mental health in contemporary society. The subtitle refers to British Prime Minister Margaret Thatcher 's pro-market slogan " There is no alternative ". Capitalist Realism was an unexpected success and has influenced a range of writers. [ 2 ] Widely regarded as Mark Fisher's most influential idea, capitalist realism is an ideological framework for viewing capitalism and its effects on politics, economics, and public thought. The name itself is a play on the term " socialist realism ". Fisher wrote extensively on the subject and frequently gave interviews with political bloggers and theorists on the subject, which expanded on his definition of the concept. [ 3 ] According to Fisher, the quotation "it is easier to imagine an end to the world than an end to capitalism", attributed to both Fredric Jameson and Slavoj Žižek , encompasses the essence of capitalist realism. Capitalist realism is loosely defined as the predominant conception that capitalism is the only viable economic system, and thus there can be no imaginable alternative. Fisher likens capitalist realism to a "pervasive atmosphere " that affects areas of cultural production, political-economic activity, and general thought. [ 4 ] Capitalist realism as I understand it cannot be confined to art or to the quasi-propagandistic way in which advertising functions. It is more like a pervasive atmosphere , conditioning not only the production of culture but also the regulation of work and education, and acting as a kind of invisible barrier constraining thought and action. [ 4 ] Capitalist realism propagates an idea of the post-political, in which the fall of the Soviet Union both solidified capitalism as the only effective political-economic system and removed the question of capitalism's dissolution from any political consideration. This has subverted the arena of political discussion from one in which capitalism is one of many potential means of operating an economy, to one in which political considerations operate solely within the confines of the capitalist system. Similarly, within the frame of capitalist realism, mainstream anti-capitalist movements shifted away from promoting alternative systems and toward mitigating capitalism's worst effects. Exponents of capitalist realism do not assert that capitalism is a perfect system, but instead that it is the only system that can operate in a means compatible with human nature and economic law. [ 5 ] By promoting the idea that innate human desire is only compatible with capitalism, any other system that is not based on the personal accumulation of wealth and capital is seen as counter to human nature and, by extension, impossible to implement under capitalist realism. [ 6 ] Fisher argues that the bank bailouts following the 2008 financial crisis were a quintessential example of capitalist realism in action, reasoning that the bailouts occurred largely because the idea of allowing the banking system to fail was unimaginable to both politicians and the general population. Due to the intrinsic value of banks to the capitalist system, Fisher proposes that the influence of capitalist realism meant that such a failure was never considered an option. As a consequence, Fisher observes, the neoliberal system survived and capitalist realism was further validated. [ 7 ] Fisher classifies the current state of capitalist realism in the neoliberal system in the following terms: The only powerful agents influencing politicians and managers in education are business interests. It's become far too easy to ignore workers and, partly because of this, workers feel increasingly helpless and impotent. The concerted attack on unions by neoliberal interest groups, together with the shift from a Fordist to a post-Fordist organisation of the economy – the move towards casualisation , just-in-time production , globalization – has eroded the power base of unions [and thus the labor force]. [ 7 ] Fisher regards capitalist realism as emerging from a purposeful push by the neoliberal right to transform the attitudes of both the general population and the left towards capitalism and specifically the post-Fordist form of capitalism that prevailed throughout the 1980s. The relative inability of the political left to come up with an alternative economic model in response to the rise of neoliberal capitalism and the concurrent Reaganomics era created a vacuum that facilitated the birth of a capitalist realist perspective. [ 3 ] The collapse of the Soviet Union, which Fisher believes represented the only real example of a working non-capitalist system, further cemented the place of capitalist realism both politically and in the general population, and was hailed as the decisive final victory of capitalism. According to Fisher, in a post-Soviet era, unchecked capitalism was able to reframe history into a capitalist narrative in which neoliberalism was the result of a natural progression of history and even embodied the culmination of human development. [ 8 ] Despite the fact that the emergence of capitalist realism is tied to the birth of neoliberalism, Fisher is clear to state that capitalist realism and neoliberalism are separate entities that simply reinforce each other. According to Fisher, capitalist realism has the potential to live past the demise of neoliberal capitalism, though Fisher posits that the opposite would not be true. [ 3 ] Capitalist realism is inherently anti-utopian, as it holds that no matter the flaws or externalities , capitalism is the only possible means of operation. Neoliberalism conversely glorifies capitalism by portraying it as providing the means necessary to pursue and achieve near-utopian socioeconomic conditions. In this way, capitalist realism pacifies opposition to neoliberalism's overly positive projections while neoliberalism counteracts the despair and disillusionment central to capitalist realism with its utopian claims. [ 6 ] According to Fisher, capitalist realism has so captured public thought that the idea of anti-capitalism no longer acts as the antithesis to capitalism. Instead, anti-capitalism is deployed as a means for reinforcing capitalism. This is done through modern media which aims to provide a safe means of entertaining anti-capitalist ideas without actually challenging the system. The lack of coherent alternatives, as presented through the lens of capitalist realism, leads many anti-capitalist movements to cease targeting the end of capitalism, but instead to mitigate its worst effects, often through individual consumption-based activities such as Product Red . [ 9 ] With regard to public views on capitalism, Fisher coined the term "reflexive impotence" which describes a phenomenon where people recognize the flawed nature of capitalism, but believe there are no means of effecting change. According to Fisher, this inaction leads to a self-fulfilling prophecy as well as a negative toll on their mental health. [ 10 ] Fisher identifies a widespread popular desire for a public sphere that operates outside of the state and free from the undesired "add-ons of capital". [ 11 ] However, he claims that it is the state alone that has been able to maintain public arenas against the capitalist push for mass privatization. Popular neoliberal thought supports the destruction of public spheres in favor of the privatization of public institutions such as education and health based on the assumption that the market best serves public needs. In this vein, Fisher also raises the idea of " business ontology ", which is the capitalist ideology in which purposes and objectives are understood exclusively in business terms. [ 12 ] He further postulates that in the case of uniformly business-oriented social conditions there is no place for the public and its only chance at survival is by means of extinguishing the business framework in public services, adding that "if businesses can't be run as businesses, why should public services?" [ 12 ] Thus, a frequent topic of Fisher's writing is the future of the public sphere in the face of neoliberal business ontology and what it might look like in absence of a centralized state-run industry. [ 11 ] [ 12 ] The "realism" aspect of capitalist realism and its inspiration—socialist realism—is based on Jacques Lacan 's distinction between the Real and "realities", such as capitalist realism, which are ideologically based understandings of the world that reject facts that lie outside of their interpretations. Fisher posits that an appeal to the Real which is suppressed by capitalist realism may begin to deconstruct the pervasiveness of the ideology. Fisher points to areas such as climate change, mental health, and bureaucracy that can be highlighted to show the weaknesses and gaps in capitalist realism. [ 13 ] The New Yorker noted that Capitalist Realism became a "cult favorite" due to Fisher's "relentless energy" and the book's "rousing call to arms". [ 14 ] In the wake of Fisher's work, other critical theorists in academia and the political blogosphere have employed the concept of capitalist realism as a theoretical framework. [ 15 ] [ 16 ]	https://en.wikipedia.org/wiki/Capitalist_Realism
Capnography is the monitoring of the concentration or partial pressure of carbon dioxide ( CO 2 ) in the respiratory gases. Its main development has been as a monitoring tool for use during anesthesia and intensive care . It is usually presented as a graph of CO 2 (measured in kilopascals, "kPa" or millimeters of mercury, "mmHg") plotted against time, or, less commonly, but more usefully, expired volume (known as volumetric capnography). The plot may also show the inspired CO 2 , which is of interest when rebreathing systems are being used. When the measurement is taken at the end of a breath (exhaling), it is called "end tidal" CO 2 (PETCO 2 ). [ 1 ] The capnogram is a direct monitor of the inhaled and exhaled concentration or partial pressure of CO 2 , and an indirect monitor of the CO 2 partial pressure in the arterial blood . In healthy individuals, the difference between arterial blood and expired gas CO 2 partial pressures is very small (normal difference 4-5 mmHg). In the presence of most forms of lung disease, and some forms of congenital heart disease (the cyanotic lesions) the difference between arterial blood and expired gas increases which can be an indication of new pathology or change in the cardiovascular-ventilation system. [ 2 ] [ 3 ] Oxygenation and capnography, although related, remain distinct elements in the physiology of respiration. Ventilation refers to the mechanical process of which the lungs expand and exchange volumes of gasses, however respiration further describes the exchange of gasses (mainly CO 2 and O 2 ) at the level of the alveoli. The process of respiration can be divided into two main functions: elimination of CO 2 waste and replenishing tissues with fresh O 2 . Oxygenation (typically measured via pulse oximetry ) measures the latter portion of this system. Capnography measures the elimination of CO 2 which may be of greater clinical usefulness than oxygenation status. [ 4 ] During the normal cycle of respiration , a single breath can be divided into two phases: inspiration and expiration. At the beginning of inspiration, the lungs expand and CO 2 free gasses fill the lungs. As the alveoli are filled with this new gas, the concentration of CO 2 that fills the alveoli is dependent on the ventilation of the alveoli and the perfusion (blood flow) that is delivering the CO 2 for exchange. Once expiration begins to occur, the lung volume decreases as air is forced out the respiratory tract. The volume of CO 2 that is exhaled at the end of exhalation is generated as a by product of metabolism from tissue throughout the body. The delivery of CO 2 to the alveoli for exhalation is dependent on an intact cardiovascular system to ensure adequate blood flow from the tissue to the alveoli. If cardiac output (the amount of blood that is pumped out of the heart) is decreased, the ability to transport CO 2 is also decreased which is reflected in a decreased expired amount of CO 2 . The relationship of cardiac output and end tidal CO 2 is linear, such that as cardiac output increases or decreases, the amount of CO 2 is also adjusted in the same manner. Therefore the monitoring of end tidal CO 2 can provide vital information on the integrity of the cardiovascular system, specifically how well the heart is able to pump blood. [ 5 ] The amount of CO 2 that is measured during each breath requires an intact cardiovascular system to delivery the CO 2 to the alveoli which is the functional unit of the lungs. During phase I of expiration, the CO 2 transported to the lungs gas occupies a given space that is not involved in gas exchange, called dead space. Phase II of expiration is when the CO 2 within the lungs is forced up the respiratory tract on its way to leave the body, which causes mixing of the air from the dead space with the air in the functional alveoli responsible for gas exchange. Phase III is the final portion of expiration which reflects CO 2 only from the alveoli and not the dead space. These three phases are important to understand in clinical scenarios since a change in the shape and absolute values can indicate respiratory and/or cardiovascular compromise. [ 6 ] During anesthesia, there is interplay between two components: the patient and the anesthesia administration device (which is usually a breathing circuit and a ventilator ). The critical connection between the two components is either an endotracheal tube or a mask, and CO 2 is typically monitored at this junction. Capnography directly reflects the elimination of CO 2 by the lungs to the anesthesia device. Indirectly, it reflects the production of CO 2 by tissues and the circulatory transport of CO 2 to the lungs. [ 7 ] When expired CO 2 is related to expired volume rather than time, the area beneath the curve represents the volume of CO 2 in the breath, and thus over the course of a minute, this method can yield the CO 2 per minute elimination, an important measure of metabolism. Sudden changes in CO 2 elimination during lung or heart surgery usually imply important changes in cardiorespiratory function. [ 8 ] Capnography has been shown to be more effective than clinical judgement alone in the early detection of adverse respiratory events such as hypoventilation , esophageal intubation and circuit disconnection; thus allowing patient injury to be prevented. During procedures done under sedation, capnography provides more useful information, e.g. on the frequency and regularity of ventilation, than pulse oximetry . [ 9 ] [ 10 ] Capnography provides a rapid and reliable method to detect life-threatening conditions (malposition of tracheal tubes , unsuspected ventilatory failure, circulatory failure and defective breathing circuits) and to circumvent potentially irreversible patient injury. Capnography and pulse oximetry together could have helped in the prevention of 93% of avoidable anesthesia mishaps according to an ASA ( American Society of Anesthesiologists ) closed claim study. [ 11 ] Capnography is increasingly being used by EMS personnel to aid in their assessment and treatment of patients in the prehospital environment. These uses include verifying and monitoring the position of an endotracheal tube or a blind insertion airway device . A properly positioned tube in the trachea guards the patient's airway and enables the paramedic to breathe for the patient. A misplaced tube in the esophagus can lead to the patient's death if it goes undetected. [ 12 ] A study in the March 2005 Annals of Emergency Medicine, comparing field intubations that used continuous capnography to confirm intubations versus non-use showed zero unrecognized misplaced intubations in the monitoring group versus 23% misplaced tubes in the unmonitored group. [ 13 ] The American Heart Association (AHA) affirmed the importance of using capnography to verify tube placement in their 2005 CPR and Emergency Cardiovascular Care Guidelines. [ 14 ] The AHA also notes in their new guidelines that capnography, which indirectly measures cardiac output, can also be used to monitor the effectiveness of CPR and as an early indication of return of spontaneous circulation (ROSC). Studies have shown that when a person doing CPR tires, the patient's end-tidal CO 2 ( PETCO2 , the level of carbon dioxide released at the end of expiration) falls, and then rises when a fresh rescuer takes over. Other studies have shown when a patient experiences return of spontaneous circulation, the first indication is often a sudden rise in the PETCO2 as the rush of circulation washes untransported CO 2 from the tissues. Likewise, a sudden drop in PETCO2 may indicate the patient has lost pulses and CPR may need to be initiated. [ 15 ] Paramedics are also now beginning to monitor the PETCO2 status of nonintubated patients by using a special nasal cannula that collects the carbon dioxide. A high PETCO2 reading in a patient with altered mental status or severe difficulty breathing may indicate hypoventilation and a possible need for the patient to be intubated . Low PETCO2 readings on patients may indicate hyperventilation . [ 16 ] Capnography, because it provides a breath by breath measurement of a patient's ventilation, can quickly reveal a worsening trend in a patient's condition by providing paramedics with an early warning system into a patient's respiratory status. When compared to oxygenation which is measured by pulse oximetry, there are several disadvantages that capnography can help address to provide a more accurate reflection of cardiovascular integrity. One shortcoming of measuring pulse oximetry alone is that administration of supplemental oxygen (ie. via nasal cannula) can delay desaturation in a patient if they stopped breathing, therefore delaying medical intervention. Capnography provides a rapid way to directly assess ventilation status and indirectly assess cardiac function. Clinical studies are expected to uncover further uses of capnography in asthma , congestive heart failure , diabetes , circulatory shock, pulmonary embolus , acidosis , and other conditions, with potential implications for the prehospital use of capnography. [ 17 ] Registered nurses , but more so RRTs (respiratory therapists), in critical care settings may use capnography to determine if a nasogastric tube , which is used for feeding, has been placed in the trachea as opposed to the esophagus. [ 18 ] Usually a patient will cough or gag if the tube is misplaced, but most patients in critical care settings are sedated or comatose. If a nasogastric tube is accidentally placed in the trachea instead of the esophagus, the tube feedings will go into the lungs, which is a life-threatening situation. If the monitor displays typical CO 2 waveforms then placement should be confirmed. [ 19 ] Capnography provides information about CO 2 production, pulmonary (lung) perfusion, alveolar ventilation, respiratory patterns , and elimination of CO 2 from the anesthesia breathing circuit and ventilator. The shape of the curve is affected by some forms of lung disease; in general there are obstructive conditions such as bronchitis , emphysema and asthma , in which the mixing of gases within the lung is affected. [ 20 ] Conditions such as pulmonary embolism and congenital heart disease, which affect perfusion of the lung, do not, in themselves, affect the shape of the curve, but greatly affect the relationship between expired CO 2 and arterial blood CO 2 . Capnography can also be used to measure carbon dioxide production, a measure of metabolism . Increased CO 2 production is seen during fever and shivering. Reduced production is seen during anesthesia and hypothermia . [ 21 ] Capnographs work on the principle that CO 2 is a polyatomic gas and therefore absorbs infrared radiation . A beam of infrared light is passed across the gas sample to fall on a sensor. The presence of CO 2 in the gas leads to a reduction in the amount of light falling on the sensor, which changes the voltage in a circuit. The analysis is rapid and accurate, but the presence of nitrous oxide in the gas mix changes the infrared absorption via the phenomenon of collision broadening. [ 22 ] This must be corrected for measuring the CO 2 in human breath by measuring its infrared absorptive power. This was established as a reliable technique by John Tyndall in 1864, though 19th and early 20th century devices were too cumbersome for everyday clinical use. [ 23 ] Today, technologies have since improved and are able to measure the values of CO 2 near instantaneously and has become a standard practice in medical settings. There are currently two main types of CO 2 sensors that are used in clinical practice: main-stream sensors and side-stream sensors. Both effectively serve the same function to quantify the amount of CO 2 that is being exhaled in each breath. The capnogram waveform provides information about various respiratory and cardiac parameters. The capnogram double-exponential model attempts to quantitatively explain the relationship between respiratory parameters and the exhalatory segment of a capnogram waveform. [ 24 ] According to the model, each exhalatory segment of capnogram waveform follows the analytical expression: where In particular, this model explains the rounded "shark-fin" shape of the capnogram observed in patients with obstructive lung disease .	https://en.wikipedia.org/wiki/Capnography
Capsular contracture is a response of the immune system to foreign materials in the human body. Medically, it occurs mostly in context of the complications from breast implants and artificial joint prosthetics. The occurrence of capsular contraction follows the formation of capsules of tightly woven collagen fibers, created by the immune response to the presence of foreign objects surgically installed to the human body, e.g. breast implants, artificial pacemakers , orthopedic prostheses ; biological protection by isolation and toleration. Capsular contracture occurs when the collagen-fiber capsule shrinks, tightens and compresses the breast implant, much like the collapse of a bubble gum bubble. [ 1 ] It is a medical complication that can be painful and discomforting, and might distort the aesthetics of the breast implant and the breast. Although the cause of capsular contracture is unknown, factors common to its incidence include bacterial contamination, rupture of the breast-implant shell, leakage of the silicone-gel filling, and hematoma . Moreover, because capsular contracture is a consequence of the immune system defending the patient's bodily integrity and health, it might recur, even after the requisite corrective surgery for the initial incidence. The degree of an incidence of capsular contracture is graded using the four-grade Baker scale: The surgical implantation methods that have reduced capsular contracture include submuscular breast implant placement, using either textured or polyurethane-coated implants, [ 2 ] [ 3 ] [ 4 ] limited handling of the implants, minimal contact with the chest wall skin before their insertions, and irrigating the surgical sites with triple-antibiotic solutions. [ 5 ] [ 6 ] The use of macrotextured implants and polyurethene-coated implants may increase the risk of BIA-ALCL , a rare form of lymphoma associated to the presence of breast implants. [ 7 ] [ 8 ] The correction of capsular contracture might require the surgical removal (release) of the capsule, or the removal, and possible replacement, of the breast implant, itself. Closed capsulotomy (disrupting the capsule via external manipulation), a once-common maneuver for treating hard capsules, was discontinued because it might rupture the breast implant. Non-surgical methods of treating capsules include massage, external ultrasound , [ 9 ] treatment with leukotriene pathway inhibitors (e.g. Accolate , Singulair ), [ 10 ] [ 11 ] specific dietary supplements [ 12 ] and pulsed electromagnetic field therapy. [ 13 ] The Mentor Worldwide LLC corporation, one of the three, U.S. FDA-approved breast-implant device manufacturers, conducted a study of the medical complications suffered by breast implantation surgery patients. In March 2000, at a Food and Drug Administration presentation, the Mentor report indicated that 43 per cent of patients with saline breast implants reported medical complications occurring within three years of the surgery; moreover, 10 per cent of that percentage group complained of capsular contracture. [ citation needed ]	https://en.wikipedia.org/wiki/Capsular_contracture
Captain of the ship doctrine is the legal doctrine which holds that, during an operation in an operating room , a surgeon of record is liable for all actions conducted in the course of the operation. [ 1 ] The doctrine is a form of the "borrowed servant doctrine", in which a party usually liable for his, her, its, or their actions is absolved of responsibility when that "borrowed servant" is asked to do something that is outside of the bounds of policy. [ 2 ] The doctrine was coined in McConnel v. Williams , 361 Pa. 355, 65 A.2d 243, 246 (1949), in which the Supreme Court of Pennsylvania ruled that, "it can readily be understood that in the course of an operation in the operating room of a hospital, and until the surgeon leaves that room at the conclusion of the operation... he is in the same complete charge of those who are present and assisting him as in the captain of a ship over all on board, and that such supreme control is indeed essential in view of the high degree of protection to which an anesthetized, unconscious patient is entitled...". [ 3 ] The doctrine emerged in 1949 and was popular in the 1950s, but the application of this doctrine declined as patients who suffered a tort sued under the charitable immunity doctrine. [ 4 ] In the 21st century, consistent with the Supreme Courts of multiple states, the Supreme Court of Wisconsin declined to adopt the doctrine. [ 4 ] Although the doctrine has been deemed "anachronistic", a "prostrate doctrine" and "indiscriminate repetition", among other things, the phrase remains in current usage. [ 4 ]	https://en.wikipedia.org/wiki/Captain_of_the_ship_doctrine
Carcinoembryonic antigen ( CEA ) describes a set of highly-related glycoproteins involved in cell adhesion . CEA is normally produced in gastrointestinal tissue during fetal development, but the production stops before birth. Consequently, CEA is usually present at very low levels in the blood of healthy adults (about 2–4 ng/mL). [ 2 ] However, the serum levels are raised in some types of cancer, which means that it can be used as a tumor marker in clinical tests. Serum levels can also be elevated in heavy smokers . [ 3 ] CEA are glycosyl phosphatidyl inositol (GPI) cell-surface-anchored glycoproteins whose specialized sialo fucosylated glycoforms serve as functional colon carcinoma L-selectin and E-selectin ligands, which may be critical to the metastatic dissemination of colon carcinoma cells. [ 4 ] [ 5 ] [ 6 ] Immunologically they are characterized as members of the CD66 cluster of differentiation . The proteins include CD66a , CD66b , CD66c , CD66d , CD66e , CD66f . CEA was first identified in 1965 by Phil Gold , a Canadian physician, scientist and professor and Samuel O. Freedman who is also a Canadian professor of immunology in human colon cancer tissue extracts. [ 7 ] The CEA blood test is not reliable for diagnosing cancer or as a screening test for early detection of cancer. [ 8 ] Most types of cancer do not result in a high CEA level. [ 9 ] Serum from individuals with colorectal carcinoma often has higher levels of CEA than healthy individuals (above approximately 2.5ng/mL). [ 10 ] CEA measurement is mainly used as a tumor marker to monitor colorectal carcinoma treatment, to identify recurrences after surgical resection, for staging or to localize cancer spread through measurement of biological fluids. [ 11 ] CEA levels may also be raised in gastric carcinoma , pancreatic carcinoma , lung carcinoma , breast carcinoma , and medullary thyroid carcinoma , as well as some non-neoplastic conditions like ulcerative colitis , pancreatitis , cirrhosis , [ 12 ] COPD , Crohn's disease , hypothyroidism [ 13 ] as well as in smokers . [ 14 ] Elevated CEA levels should return to normal after successful surgical removal of the tumor and can be used in follow up, especially of colorectal cancers. [ 15 ] CEA elevation is known to be affected by multiple factors. It varies inversely with tumor grade; well-differentiated tumors secrete more CEA. CEA is elevated more in tumors with lymph node and distant metastasis than in organ-confined tumors and, thus, varies directly with tumor stage. Left-sided tumors generally tend to have higher CEA levels than right-sided tumors. [ 16 ] Tumors causing bowel obstruction produce higher CEA levels. [ 16 ] Aneuploid tumors produce more CEA than diploid tumors. [ 17 ] Liver dysfunction increases CEA levels as the liver is the primary site of CEA metabolism. [ 3 ] An anti-CEA antibody is an antibody against CEA. Such antibodies to CEA are commonly used in immunohistochemistry to identify cells expressing the glycoprotein in tissue samples. In adults, CEA is primarily expressed in cells of tumors (some malignant, some benign) [ 19 ] but they are particularly associated with the adenocarcinomas , such as those arising in the colon, lung, breast, stomach, or pancreas. It can therefore be used to distinguish between these and other similar cancers. For example, it can help to distinguish between adenocarcinoma of the lung and mesothelioma , a different type of lung cancer which is not normally CEA positive. Because even monoclonal antibodies to CEA tend to have some degree of cross-reactivity, occasionally giving false positive results, it is commonly employed in combination with other immunohistochemistry tests, such as those for BerEp4 , WT1 , and calretinin . [ 20 ] For cancers that highly express CEA, targeting CEA through radioimmunotherapy is one of the therapy approaches. [ 21 ] Engineered antibodies such as single-chain Fv antibodies (sFvs) or bispecific antibodies have been used for targeting and therapy of CEA expressing tumors both in vitro and in vivo with promising results [ 22 ] [ 23 ] Regions of high CEA levels in the body can be detected with the monoclonal antibody arcitumomab . [ 24 ] CEA and related genes make up the CEA family belonging to the immunoglobulin superfamily. In humans, the carcinoembryonic antigen family consists of 29 genes, 18 of which are normally expressed. [ 25 ] The following is a list of human genes which encode carcinoembryonic antigen-related cell adhesion proteins: CEACAM1 , CEACAM3 , CEACAM4 , CEACAM5 , CEACAM6 , CEACAM7 , CEACAM8 , CEACAM16 , CEACAM18 , CEACAM19 , CEACAM20 , CEACAM21 CEA is expressed in many different types of cancer like lung, gastric , pancreatic and colorectal cancer. Many clinical trials have been performed . [ citation needed ] CEA is used as tumor biomarker that can be used for Targeted Radionuclide Therapy . The cT84.66 is a chimeric antibody of murine origin that has been tested in phase I clinical trials with 111-In and 90-Yttrium. [ 26 ] [ 27 ] 111-In and 90-Y are β- emitters that are used in clinics for imaging and therapy respectively. The results were promising but a number of patients demostrated immune responses and they had to withdraw from participating in the clinical trial. [ 28 ] The cT84.66 antibody was huminized and in 2020, a phase I clinical trial was performed during which 18 cancer patients received an injection of 90Y-DOTA-M5A. [ 29 ] The results of this trial demonstrated a stable disease for 10/18 patients ( 56%) and had no immunogenic response. [ citation needed ] M5A-DOTA was coupled with 225-Ac , which is an alpa emitter, and an in vivo study was performed where cytokine therapy was combined with a-therapy. [ 30 ] The result of the study revealed the benefit of combining these two treamtents. Based on the results of this study, an ongoing clinical phase I study is currently underway (NCT05204147). The goal of this study is to establish the safety level and THE possible benefit of administrating M5A-DOTA-225-Ac. [ citation needed ]	https://en.wikipedia.org/wiki/Carcinoembryonic_antigen
Carcinogenesis is a peer-reviewed medical journal in the field of cancer biology . It was established in 1980 and is published monthly by Oxford University Press . As of 2010 [update] , the editor-in-chief is Curtis C. Harris ( National Cancer Institute ). [ 1 ] Carcinogenesis publishes articles in four sections: cancer biology covers the cell and molecular biology of cancer, as well as mutation and DNA repair ; molecular epidemiology includes genetic predisposition to cancer ; cancer prevention covers chemoprophylaxis as well as dietary factors; and carcinogenesis covers all forms of carcinogens , including their metabolism and detection in the environment. [ 2 ] Authors can pay to have their articles released freely online as part of a hybrid open access scheme. [ 3 ] Free or reduced-rate online access is available to educational institutions in low-income countries. [ 4 ] [ 5 ] The journal was established in 1980 by R. Colin Garner ( University of York ) and Anthony Dipple ( National Cancer Institute ). [ 4 ] [ 6 ] The original scope of Carcinogenesis was defined in the first issue as research relating to "the prevention of cancer in man", and the journal was conceived from the outset as a multidisciplinary journal, with the intention of encouraging the "cross-fertilization of ideas" across the "very broad spectrum of scientific endeavour" of cancer research. [ 7 ] In 2008, the journal added the subtitle " Integrative Cancer Research " to reflect its multidisciplinary scope. [ 8 ] The journal was originally published by IRL Press , [ 6 ] [ 9 ] [ 10 ] which merged with Oxford University Press in 1989. [ 4 ] [ 11 ] Carcinogenesis is abstracted and indexed in Biological Abstracts , BIOSIS Previews , CAB Abstracts , Chemical Abstracts , Current Contents /Life Sciences, BIOBASE – Current Awareness in Biological Sciences, EMBASE , Excerpta Medica , Global Health , MEDLINE , ProQuest , and the Science Citation Index . [ 2 ] According to the Journal Citation Reports , the journal has a 2020 impact factor of 4.944. [ 12 ]	https://en.wikipedia.org/wiki/Carcinogenesis_(journal)
Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to neuroendocrine tumors (formerly known as carcinoid tumors ). [ 1 ] The syndrome is caused by neuroendocrine tumors most often found in the gut releasing biologically active substances into the blood causing symptoms such as flushing and diarrhea , and less frequently, heart failure , vomiting and bronchoconstriction . [ 2 ] [ 1 ] The carcinoid syndrome occurs in approximately 10% of all neuroendocrine tumors [ 1 ] or about 30–40% of more advanced/well developed neuroendocrine tumors. [ 2 ] The biologically active substances that are released by the tumors cause the symptoms of the carcinoid syndrome. [ 4 ] [ 2 ] [ 1 ] These substances act on the vessels to produce the symptoms of the carcinoid syndrome. [ 2 ] [ 1 ] Less common symptoms include malabsorption (leading to pellagra ), fatigue, muscle loss, and cognitive impairment. [ 1 ] Late complications may include mesenteric and retroperitoneal fibroses as well. [ 2 ] The carcinoid syndrome occurs secondary to neuroendocrine tumors . [ 1 ] [ 2 ] These tumors occur mostly in the gut and less commonly in the lungs, but may also occur in other places in the body such as the pancreas, kidneys, and other organs. [ 1 ] [ 2 ] [ 5 ] [ 6 ] [ 7 ] Neuroendocrine tumors produce several biologically active substances, mainly amines and peptides. [ 1 ] There are over 40 substances known to be secreted by these tumors but the exact effect of each and their contribution to the carcinoid syndrome is unknown. [ 6 ] The most common substances found to be released and contribute to the syndrome include serotonin, histamine, tachykinins, kallikrein, and prostaglandins with the greatest contribution appearing to be from serotonin. [ 6 ] [ 2 ] [ 1 ] The symptoms of the carcinoid syndrome result from the action of these substances largely on the blood vessels. [ 1 ] These biologic substances are often metabolized and inactivated by the liver in a process known as first pass metabolism . This is why carcinoid syndrome most often occurs in patients whom the neuroendocrine tumor has metastasized to the liver, which allows the substances to bypass the first pass metabolism. [ 1 ] [ 6 ] [ 7 ] Neuroendocrine tumors arising in the bronchi may be associated with manifestations of carcinoid syndrome without liver metastases because their biologically active products reach the systemic circulation before passing through the liver and being metabolized . Tryptophan metabolism is altered in the carcinoid syndrome. With neuroendocrine tumors, there is a shift in conversion of tryptophan to serotonin from the normal 1% to as high as 70%. [ 1 ] [ 8 ] Increased amounts of serotonin lead to increased gut motility causing the diarrhea seen in carcinoid syndrome. [ 1 ] [ 6 ] [ 8 ] Increased amounts of serotonin can also cause the flushing seen as the main symptom of carcinoid syndrome. [ 2 ] Tryptophan is also needed for niacin synthesis which can be a cause for pellagra associated with carcinoid syndrome. [ 1 ] In the pulmonary neuroendocrine tumors or metastases, histamine release and kallikrein metabolism are the vasoactive mediators of flushing and the other symptoms of carcinoid syndrome. [ 2 ] [ 1 ] Carcinoid crisis is an extreme exacerbation of the carcinoid syndrome. This results from excessive release of amines by the neuroendocrine tumors. It is largely a result of stressful procedures such as anesthesia, surgery, or radiation treatment. Symptoms of carcinoid crisis include flushing, hypotension, arrhythmia and bronchospasm. [ 2 ] [ 9 ] Carcinoid heart disease is the result of valvular damage related to the vasoactive substances released by the neuroendocrine tumor reaching the right side of the heart. [ 5 ] This mainly affects the right side of the heart unless there is anomalous circulation (i.e. patent foramen ovale) because the lungs will metabolize the substances released by the tumor similar to how the liver will. [ 5 ] After initial tissue injury around the valves, plaque will develop and fibrosis will occur, possibly mediated by excess serotonin. [ 5 ] With a certain degree of clinical suspicion, the most useful initial test is the 24-hour urine levels of 5-HIAA (5-hydroxyindoleacetic acid), the end product of serotonin metabolism. [ 10 ] Chromogramin A, a glycoprotein released by neuroendocrine tumors, can be used to detect non-secreting tumors. [ 1 ] [ 11 ] Imaging studies should be largely focused on the abdomen and pelvis because the neuroendocrine tumors causing the carcinoid syndrome largely arise in the gut. [ 11 ] Nuclear medicine gamma camera imaging that utilizes radioactive somatostatin analogues such as indium-111 pentetreotide are used to localize the tumor. [ 11 ] PET scan can also be used to find the primary tumor site. [ 7 ] Bronchoscopy with biopsy can performed if there is evidence of a pulmonary tumor. [ 1 ] For patients with serotonin elevated 5x the upper limit of normal or more, an echocardiogram is recommended for evaluation of carcinoid heart disease. [ 1 ] Other conditions similar to the carcinoid syndrome that should be considered include: [ 1 ] Treatment of the carcinoid syndrome is focused on controlling the proliferation of the primary tumor and symptomatic control of the symptoms with somatostatin analogues octreotide or lanreotide. [ 2 ] [ 1 ] [ 12 ] These analogues can help control the growth of the tumor itself and the associated symptoms of the carcinoid syndrome. [ 12 ] In patients whose symptoms are refractory to initial doses, increasing the dose or switching to another analogue pasireotide may be effective. [ 12 ] In patients who continue to be refractory, mTOR inhibitors such as everolimus. [ 12 ] The TPH inhibitor telotristat ethyl may be useful in controlling diarrhea associated with the carcinoid syndrome. [ 12 ] Peptide directed radiotherapy (PRRT) is another alternative treatment for patients who failed somatostain analogue therapy. [ 12 ] This method uses radioactive somatostatin analogues such as 177 Lu-Dotatate or 90 Y-Edotreotide to target tumors directly. [ 12 ] These therapies are effective for metastatic disease but studies have been limited to about 6-month time periods. [ 12 ] Cytoreductive surgery performed chemically with 131 metaiodobenzylguanidine ( 131 I-MIBG) may also control symptoms starting around 6–15 months post procedure and lasting as long as 39 months. [ 12 ] There are also procedures that target the liver directly such as radiofrequency ablation or radioembolization that deliver targeted therapy directly to the liver through special catheters. [ 12 ] This is especially useful for patients with liver metastases. [ 12 ] [ 2 ] [ 7 ] The most important aspect of treating carcinoid heart disease is detecting its presence with echocardiography, likely with color doppler. [ 12 ] Treatment consists of the same treatment as patients with heart failure with definitive treatment being surgical valve repair or replacement. [ 12 ] Disease progression is difficult to ascertain because the disease can metastasize anywhere in the body and can be too small to identify with any current technology. Markers of the condition such as chromogranin-A are imperfect indicators of disease progression. [ 13 ] The incidence of neuroendocrine tumors in the US lies somewhere from 2.7 to 4.3 per 100,000 people and appears to be increasing over time. [ 1 ] [ 9 ] The incidence of the carcinoid syndrome is about 0.27 per 100,000 people in the US, [ 9 ] about 10% of all people with neuroendocrine tumors. [ 1 ] There does not appear to be any variance by gender however patients of African American ethnicity appear to be affected by the carcinoid syndrome more often. [ 1 ] [ 9 ] The carcinoid syndrome can affect other animals similarly to humans. [ 14 ] Similarly to humans, the carcinoid syndrome is due to neuroendocrine tumors that arise mainly from the bowel but also from other organs. [ 14 ] Common signs in animals include vomiting, diarrhea, and weight loss but other symptoms that are more common in humans such as flushing, hypotension and diarrhea can also occur. [ 14 ] Similar to humans, the cause of the carcinoid syndrome is the release of bioactive substances such as serotonin and histamine. [ 14 ]	https://en.wikipedia.org/wiki/Carcinoid_syndrome
Carcinoma is a malignancy that develops from epithelial cells . [ 1 ] Specifically, a carcinoma is a cancer that begins in a tissue that lines the inner or outer surfaces of the body, and that arises from cells originating in the endodermal , mesodermal [ 2 ] or ectodermal germ layer during embryogenesis . [ 3 ] Carcinomas occur when the DNA of a cell is damaged or altered and the cell begins to grow uncontrollably and becomes malignant . It is from the Greek : καρκίνωμα , romanized : karkinoma , lit. 'sore, ulcer, cancer' (itself derived from karkinos meaning crab ). [ 4 ] As of 2004, no simple and comprehensive classification system has been devised and accepted within the scientific community. [ 5 ] Traditionally, however, malignancies have generally been classified into various types using a combination of criteria, including: [ 6 ] The cell type from which they start; specifically: Other criteria that play a role include: There are a large number of rare subtypes of anaplastic, undifferentiated carcinoma. Some of the more well known include the lesions containing pseudo- sarcomatous components: spindle cell carcinoma (containing elongated cells resembling connective tissue cancers), giant cell carcinoma (containing huge, bizarre, multinucleated cells), and sarcomatoid carcinoma (mixtures of spindle and giant cell carcinoma). Pleomorphic carcinoma contains spindle cell and/or giant cell components, plus at least a 10% component of cells characteristic of more highly differentiated types (i.e. adenocarcinoma and/or squamous cell carcinoma). Very rarely, tumors may contain individual components resembling both carcinoma and true sarcoma , including carcinosarcoma and pulmonary blastoma . [ 8 ] A history of cigarette smoking is the most common cause of large cell carcinoma. The term carcinoma has also come to encompass malignant tumors composed of transformed cells whose origin or developmental lineage is unknown (see cancer of unknown primary origin ; CUP), but that possess certain specific molecular, cellular, and histological characteristics typical of epithelial cells. This may include the production of one or more forms of cytokeratin or other intermediate filaments , intercellular bridge structures, keratin pearls, and/or tissue architectural motifs such as stratification or pseudo-stratification. [ 5 ] [ 6 ] The term carcinoma in situ (or CIS) is a term for cells that are significantly abnormal but not cancer. [ 10 ] They are thus not typically carcinomas. [ 11 ] Cancer occurs when a single progenitor cell accumulates mutations and other changes in the DNA , histones , and other biochemical compounds that make up the cell's genome . The cell genome controls the structure of the cell's biochemical components, the biochemical reactions that occur within the cell, and the biological interactions of that cell with other cells. Certain combinations of mutations in the given progenitor cell ultimately result in that cell (also called a cancer stem cell) displaying a number of abnormal, malignant cellular properties that, when taken together, are considered characteristic of cancer, including: If this process of continuous growth, local invasion, and regional and distant metastasis is not halted via a combination of stimulation of immunological defenses and medical treatment interventions, the result is that the host has a continuously increasing burden of tumor cells throughout the body. Eventually, the tumor burden increasingly interferes with normal biochemical functions carried out by the host's organs , and death ultimately ensues. Carcinoma is but one form of cancer—one composed of cells that have developed the cytological appearance, histological architecture, or molecular characteristics of epithelial cells. [ 5 ] [ 6 ] A progenitor carcinoma stem cell can be formed from any of a number of oncogenic combinations of mutations in a totipotent cell, [ 13 ] a multipotent cell, [ 13 ] or a mature differentiated cell. [ 14 ] Metastatic carcinoma is cancer that is able to grow at sites distant from the primary site of origin; thus, dissemination to the skin may occur with any malignant neoplasm , and these infiltrates may result from direct invasion of the skin from underlying tumors, may extend by lymphatic or hematogenous spread, or may be introduced by therapeutic procedures. [ 15 ] : 628–9 Whole genome sequencing has established the mutation frequency for whole human genomes. The mutation frequency in the whole genome between generations for humans (parent to child) is about 70 new mutations per generation. [ 16 ] Carcinomas, however, have much higher mutation frequencies. The particular frequency depends on tissue type, whether a mis-match DNA repair deficiency is present, and exposure to DNA damaging agents such as components of tobacco smoke. Tuna and Amos have summarized the mutation frequencies per megabase (Mb) in some carcinomas, [ 17 ] as shown in the table (along with the indicated frequencies of mutations per genome). The likely major underlying cause of mutations in carcinomas is DNA damage. [ citation needed ] For example, in the case of lung cancer, DNA damage is caused by agents in exogenous genotoxic tobacco smoke (e.g. acrolein , formaldehyde , acrylonitrile , 1,3-butadiene , acetaldehyde , ethylene oxide and isoprene ). [ 18 ] Endogenous (metabolically caused) DNA damage is also very frequent, occurring on average more than 60,000 times a day in the genomes of human cells. [ citation needed ] Externally and endogenously caused damages may be converted into mutations by inaccurate translesion synthesis or inaccurate DNA repair (e.g. by non-homologous end joining ). The high frequency of mutations in the total genome within carcinomas suggests that, often, an early carcinogenic alteration may be a deficiency in DNA repair. For instance, mutation rates substantially increase (sometimes by 100-fold) in cells defective in DNA mismatch repair . [ 19 ] A deficiency in DNA repair, itself, can allow DNA damages to accumulate, and error-prone translesion synthesis past some of those damages may give rise to mutations. In addition, faulty repair of these accumulated DNA damages may give rise to epigenetic alterations or epimutations . While a mutation or epimutation in a DNA repair gene, itself, would not confer a selective advantage, such a repair defect may be carried along as a passenger in a cell when the cell acquires an additional mutation/epimutation that does provide a proliferative advantage. Such cells, with both proliferative advantages and one or more DNA repair defects (causing a very high mutation rate), likely give rise to the high frequency of total genome mutations seen in carcinomas. In somatic cells, deficiencies in DNA repair sometimes arise by mutations in DNA repair genes, but much more often are due to epigenetic reductions in expression of DNA repair genes. Thus, in a sequence of 113 colorectal carcinomas, only four had somatic missense mutations in the DNA repair gene MGMT , while the majority of these cancers had reduced MGMT protein expression due to methylation of the MGMT promoter region. [ 20 ] Carcinomas can be definitively diagnosed through biopsy , including fine-needle aspiration (FNA), core biopsy , or subtotal removal of single node,. [ 21 ] Microscopic examination by a pathologist is then necessary to identify molecular, cellular, or tissue architectural characteristics of epithelial cells. Some carcinomas are named for their or the putative cell of origin, (e.g. hepatocellular carcinoma , renal cell carcinoma ). Staging of carcinoma refers to the process of combining physical/clinical examination, pathological review of cells and tissues, surgical techniques, laboratory tests, and imaging studies in a logical fashion to obtain information about the size of the neoplasm and the extent of its invasion and metastasis . Carcinoma stage is the variable that has been most consistently and tightly linked to the prognosis of the malignancy. Carcinomas are usually staged with Roman numerals. In most classifications, Stage I and Stage II carcinomas are confirmed when the tumor has been found to be small and/or to have spread to local structures only. Stage III carcinomas typically have been found to have spread to regional lymph nodes, tissues, and/or organ structures, while Stage IV tumors have already metastasized through the blood to distant sites, tissues, or organs. In some types of carcinomas, Stage 0 carcinoma has been used to describe carcinoma in situ , and occult carcinomas detectable only via examination of sputum for malignant cells (in lung carcinomas ). In more recent staging systems, substages (a, b, c) are becoming more commonly used to better define groups of patients with similar prognosis or treatment options. The criteria for staging can differ dramatically based upon the organ system in which the tumor arises. For example, the colon [ 23 ] and bladder cancer [ 24 ] staging system relies on depth of invasion, staging of breast carcinoma is more dependent on the size of the tumor, and in renal carcinoma, staging is based on both the size of the tumor and the depth of the tumor invasion into the renal sinus. Carcinoma of the lung has a more complicated staging system, taking into account a number of size and anatomic variables. [ 25 ] The UICC/AJCC TNM systems are most often used. [ clarification needed ] [ 26 ] For some common tumors, however, classical staging methods (such as the Dukes classification for colon cancer ) are still used. Grading of carcinomas refers to the employment of criteria intended to semi-quantify the degree of cellular and tissue maturity seen in the transformed cells relative to the appearance of the normal parent epithelial tissue from which the carcinoma derives. Grading of carcinoma is most often done after a treating physician and/or surgeon obtains a sample of suspected tumor tissue using surgical resection , needle or surgical biopsy , direct washing or brushing of tumor tissue, sputum cytopathology , etc. A pathologist then examines the tumor and its stroma , perhaps utilizing staining , immunohistochemistry , flow cytometry , or other methods. Finally, the pathologist classifies the tumor semi-quantitatively into one of three or four grades, including: Although there is definite and convincing statistical correlation between carcinoma grade and tumor prognosis for some tumor types and sites of origin, the strength of this association can be highly variable. It may be stated generally, however, that the higher the grade of the lesion, the worse is its prognosis. [ 27 ] [ 28 ] While cancer is generally considered a disease of old age, children can also develop cancer. [ 29 ] In contrast to adults, carcinomas are exceptionally rare in children. Less than 1% of carcinoma diagnoses are in children. [ 30 ] The two biggest risk factors for ovarian carcinoma are age and family history. [ 31 ]	https://en.wikipedia.org/wiki/Carcinoma
Carcinosis , or carcinomatosis , is disseminated cancer , forms of metastasis , whether used generally or in specific patterns of spread. Carcinomatosis is often restricted to tumors of epithelial origin, adenocarcinomas , while sarcomatosis describes the dissemination of tumors of mesenchymal origin, sarcomas . [ 1 ] When most tumors metastasize to the lung, they form distinct nodules, but about 7% spread through the lymph vessels of the lung. [ 2 ] They may impair breathing in several ways; the lung becomes stiffer; blood vessels traveling alongside the distended lymph vessels become compressed. [ 3 ] A pattern of multiple small nodular metastases has been described as miliary carcinosis which has a radiographic appearance similar to miliary tuberculosis. [ 4 ] Any potential space may be seeded with tumor cells that grow along surfaces, but which may not invade below the surfaces. In rare cases, the joint spaces are affected. [ 5 ] The lining of the abdominal cavity is a common site for surface dissemination. Ovarian carcinomas are common. Fluid produced by the cells can produce ascites which is typical in carcinomatosis, but less common in peritoneal sarcomatosis. [ 1 ] Fluid can be serous as seen in primary peritoneal carcinoma or mucinous such as found in pseudomyxoma peritonei which is typically a tumor derived from the appendix . [ 6 ] Pleural carcinosis is associated with malignant pleural effusion and poor prognosis. [ 7 ] The meningeal covering of the central nervous system may be the site of tumor growth. Breast cancer , lung cancer and melanoma are the most common tumors. [ 8 ] Colorectal cancer patients with peritoneal involvement can be treated with oxaliplatin - or irinotecan -based chemotherapy. Such treatment is not expected to be curative, but can extend the lives of patients. [ 9 ] Some patients may be cured through hyperthermic intraperitoneal chemotherapy , but the procedure entails a high degree of risk for morbidity or death.	https://en.wikipedia.org/wiki/Carcinosis
Carctol is an ineffective cancer treatment made by mixing eight Indian herbs. [ 1 ] First promoted in 1968 by Nandlal Tiwari, [ 1 ] it gained widespread popularity in United Kingdom. [ 2 ] Carctol has been aggressively marketed as being able to treat cancer and reduce the side-effects of chemotherapy . However, there is no medical evidence that it has any benefits whatsoever for people with cancer. [ 1 ] Carctol is a herbal dietary supplement marketed with claims it is based on traditional ayurvedic medicine . [ 1 ] It is made from Hemidesmus indicus , Tribulus terrestris , Piper cubeba , Ammani vesicatoria , Lepidium sativum , Blepharis edulis , Smilax china , and Rheum australe ( syn. R. emodi ). [ 1 ] It was In 2009, Edzard Ernst wrote that it was still promoted in the United Kingdom ; public relations companies hired by its sellers had garnered it wide coverage on the web and, [ 2 ] according to the British Medical Journal , in the media generally. [ 3 ] Edzard Ernst has noted a complete absence of any form of scientific evidence to assert that carctol is any beneficial to cancer patients. [ 2 ] A few studies about the chemical composition of carctol along with inconclusive surveys of patients who used it were noted to be published in non-peer reviewed journals. [ 2 ] Cancer Research UK say of carctol, "available scientific evidence does not support its use for the treatment of cancer in humans". [ 1 ] Harriet A. Hall includes carctol among the biologically-based remedies promoted by naturopaths . Hall laments that frauds and quacks persistently try to take advantage of the vulnerability of cancer patients. [ 4 ] This article about alternative medicine is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Carctol
The Cardiac Arrest Registry to Enhance Survival or CARES was initiated in 2004 as an agreement between the Centers for Disease Control and Prevention and the Department of Emergency Medicine at Emory University . It is a simple but powerful database that allows cities to collect a small set of performance measures from 9-1-1 , first responders , fire departments , and Emergency Medical Services , and link it with outcome data from hospitals . [ 1 ] This data enables cities to perform internal benchmarking and improve their response to cardiac arrest by strengthening the chain of survival in their community. [ 2 ] [ 3 ] Because most EMS systems don't measure their response effectively, they are unable to implement change in an effective manner. [ 4 ] Since the program's inception, survival from cardiac arrest in the city of Atlanta has increased from 3% to 15%. [ 5 ] For the last half of 2007, survival in Atlanta increased to 31.2%. [ 6 ] According to the CDC , the specific objectives of the project are: [ 7 ] New Castle County, Delaware	https://en.wikipedia.org/wiki/Cardiac_Arrest_Registry_to_Enhance_Survival
The Cardiac Arrhythmia Suppression Trial ( CAST ) was a double-blind, randomized, controlled study designed to test the hypothesis that suppression of premature ventricular complexes (PVC) with class I antiarrhythmic agents after a myocardial infarction (MI) would reduce mortality . It was conducted between 1986 and 1989 and included over 1700 patients in 27 centres. [ 1 ] The study found that the tested drugs increased mortality instead of lowering it as was expected. [ 2 ] The publication of these results in 1991/92, in combination with large follow-up studies for drugs that had not been tested in CAST, led to a paradigm shift in the treatment of MI patients. Class I and III antiarrhythmics are now only used with extreme caution after MI, or they are contraindicated completely. [ 3 ] The second Cardiac Arrhythmia Suppression Trial (CAST II) modified the enrollment criteria to include patients at higher risk for serious arrhythmia. [ 4 ] This included 1) patients enrolled within 4 to 90 days of a previous MI, 2) a left ventricular ejection fraction lower than 40%, 3) prior to enrollment, suppression of PVCs had occurred with the drugs (vs. placebo) using a double-blinded design, and 4) patients having more serious arrhythmias would also be included. [ citation needed ] The drugs used ( encainide , flecainide, and moracizine) successfully reduced the amount of PVCs, but led to more arrhythmia-related deaths. Total mortality was significantly higher with both encainide and flecainide at a mean follow-up period of 10 months. Within about two years after enrollment, encainide and flecainide were discontinued because of increased mortality and sudden cardiac death. CAST II compared moracizine to placebo, but was also stopped because of early (within two weeks) cardiac death in the moracizine group, and long-term survival seemed highly unlikely. The excess mortality was attributed to proarrhythmic effects of the agents. Class I antiarrhythmics are proarrhythmic during heart ischemia in animals. [ 5 ]	https://en.wikipedia.org/wiki/Cardiac_Arrhythmia_Suppression_Trial
The Cardiac Electrophysiology Society ( CES ) is an international society of basic and clinical scientists and physicians interested in cardiac electrophysiology and arrhythmias . [ 1 ] The Cardiac Electrophysiology Society's founder was George Burch in 1949 and its current president is Jonathan C. Makielski, M.D. This article about a medical organization or association is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cardiac_Electrophysiology_Society
Cardiac Pacemakers, Inc. ( CPI ), doing business as Guidant Cardiac Rhythm Management , manufactured implantable cardiac rhythm management devices, such as pacemakers and defibrillators . It sold microprocessor-controlled insulin pumps and equipment to regulate heart rhythm. It developed therapies to treat irregular heartbeat. The company was founded in 1971 and is based in Saint Paul, Minnesota , and is presently a subsidiary of Boston Scientific . [ 1 ] CPI was founded in February 1972 in Saint Paul, Minnesota . The first $50,000 capitalization for CPI was raised from a phone booth on the Minneapolis skyway system. [ 2 ] They began designing and testing their implantable cardiac pacemaker powered with a new longer-life lithium battery in 1971. The first heart patient to receive a CPI pacemaker emerged from surgery in June 1973. Within two years, the upstart company that challenged Medtronic had sold approximately 8,500 pacemakers. [ 3 ] Medtronic at the time had 65% of the artificial pacemaker market. CPI was the first spin-off from Medtronic. It competition using the world's first lithium-powered pacemaker. Medtronic's market share plummeted to 35%. [ 4 ] [ 5 ] Founding partners Anthony Adducci , Manny Villafaña , Jim Baustert, and Art Schwalm, were former Medtronic employees. Lawsuits ensued, all of which were settled out of court. [ 6 ] The company sold 8,500 pacemakers, increasing sales from zero in 1972 to over $47 million. In early 1978, CPI was concerned about a friendly takeover attempt. Despite impressive sales, the company's stock price had fluctuated wildly the year before, dropping from $33 to $11 per share. Some speculated that the stock was being sold short, while others attributed the price to the natural volatility of high-tech stock. As a one-product company, CPI was susceptible to changing market conditions, and its founders knew they needed to diversify. They considered two options: acquiring other medical device companies or being acquired themselves. They chose the latter. Several companies expressed interest in acquiring CPI, including 3M , American Hospital Supply, Pfizer , and Johnson & Johnson . However, Eli Lilly and Company , one of the premier pharmaceutical companies in the United States, was the most enthusiastic suitor. "Lilly had the research expertise, highly compatible interests, and similar values," Anthony Adducci recalls. "At CPI, we haven't been able to dedicate the dollars and time necessary to develop new products beyond our staple lithium-powered pacemaker. Lilly was a $2 billion company. We knew they had tremendous resources, especially in research and development." [ 6 ] Additionally, Eli Lilly and CPI were already interested in developing insulin pumps, and Lilly was working with cardiovascular drugs, a natural link to CPI's heart pacemaker business. Before the final negotiations in late 1978, there were numerous flights between Minneapolis and Indianapolis for CPI principals and representatives of Piper, Jaffray & Hopwood's corporate finance department. Lilly, a pharmaceutical giant, and CPI, the upstart pacemaker company, sat down at a bargaining table at a motel in suburban Bloomington, Minnesota . CPI's negotiation team included Anthony Adducci, Art Schwalm, Tom King, and Hunt Greene. In December 1978, the company was acquired by Eli Lilly and Company for $127 million. [ 7 ] CPI designed and manufactured the world's first pacemaker with a lithium anode and a lithium-iodide electrolyte solid-state battery. The pacemaker structure is enclosed in a hermetically sealed metallic enclosure, allowing electrode leads to pass in a sealed relationship. The surface of the casing is polished metal, with a zone through which the external electrode leads pass. [ 8 ] The Lithium-iodide or lithium anode cells revolutionized the medical industry by increasing the pacemaker life from 1 year up to 11 years. It became the standard for pacemaker designs.	https://en.wikipedia.org/wiki/Cardiac_Pacemakers,_Inc.
Cardiac Risk in the Young ( CRY ) is a humanitarian charitable organisation helping to raise awareness of young sudden cardiac death (YSCD, SCD), including sudden arrhythmic death syndrome (SADS, SDS). CRY was established in May 1995 by Alison Cox MBE and is based in the United Kingdom . The charity supports the families of victims of YSCD, facilitates the heart screening of young people through cardiac testing programmes and contributes to medical research . The CRY General Election Manifesto 2015 states: “Through awareness, support and screening many deaths can be prevented, and research into these conditions will be the key to providing the knowledge crucial to saving these young lives.” [ 1 ] CRY offers support to those who have suffered tragedies through a network of trained volunteer bereavement supporters, [ 2 ] counselling groups and medical information. [ 3 ] The charity also offers support and regular meetings to young people diagnosed with a cardiac condition through their myheart Network. [ 4 ] CRY holds regular subsidised ECG screening clinics for those aged 14 to 35 across the UK, [ 5 ] with the majority of events funded by bereaved families and free to the public. The charity funds an expert centre for fast-track cardiac pathology in the UK, the CRY Centre for Cardiac Pathology [ 6 ] (CRY CCP) at St George's Hospital , London. The centre is directed by Professor Mary Sheppard. Pathology is free of charge when the cause of death is unascertained and the deceased was aged 35 or under. CRY also funds the CRY Centre for Inherited Cardiovascular Disease and Sports Cardiology at St George’s Hospital. Professor Sanjay Sharma, medical director of the London Marathon , is CRY’s consultant cardiologist and leads their research programme. [ 7 ] On 15 July 2004 CRY launched its National Postcard Campaign [ 8 ] to highlight the deaths of eight young people per week from undiagnosed heart problems by featuring their pictures. The campaign was launched at a Parliamentary Reception in Westminster . From August 2004 the Postcard has been re-launched as region specific including South West, North East, South, North West, Scotland and Wales versions. In February 2009 the postcard campaign was updated to "12 a week" [ 9 ] and continues to draw attention the number of young people with undetected heart conditions.	https://en.wikipedia.org/wiki/Cardiac_Risk_in_the_Young
Cardiac aberrancy is a type of disruption in the shape of the electrocardiogram signal, representing abnormal activation of the ventricular heart muscle via the electrical conduction system of the heart . Normal activation utilizes the bundle of His and Purkinje fibers to produce a narrow (QRS) electrical signal. Aberration occurs when the electrical activation of the heart, which is caused by a series of action potentials , is conducting improperly which can result in temporary changes in the morphology that looks like: This is in contrast to a permanent dysfunction of the electrical pathways that produces wide QRS complexes in one of the above patterns or combinations of patterns (ie, bifascicular block ). In the context of atrial fibrillation , the Ashman phenomenon is a form of aberrancy. Aberrancy is due to prematurity in which part of the conduction system is still refractory and cannot conduct the premature depolarization. This effect can sometimes be seen in the setting of a faster heart rate ( tachycardia ) and so is termed "rate-related aberrancy." After the first aberrant complex, subsequent complexes may be wide due to concealed conduction rather than aberrancy. This cardiovascular system article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cardiac_aberrancy
Unlike the action potential in skeletal muscle cells , the cardiac action potential is not initiated by nervous activity. Instead, it arises from a group of specialized cells known as pacemaker cells , that have automatic action potential generation capability. In healthy hearts, these cells form the cardiac pacemaker and are found in the sinoatrial node in the right atrium . They produce roughly 60–100 action potentials every minute. The action potential passes along the cell membrane causing the cell to contract, therefore the activity of the sinoatrial node results in a resting heart rate of roughly 60–100 beats per minute. All cardiac muscle cells are electrically linked to one another, by intercalated discs which allow the action potential to pass from one cell to the next. [ 1 ] [ 2 ] This means that all atrial cells can contract together, and then all ventricular cells. Rate dependence of the action potential is a fundamental property of cardiac cells and alterations can lead to severe cardiac diseases including cardiac arrhythmia and sometimes sudden death. [ 3 ] Action potential activity within the heart can be recorded to produce an electrocardiogram (ECG). This is a series of upward and downward spikes (labelled P, Q, R, S and T) that represent the depolarization (voltage becoming more positive) and repolarization (voltage becoming more negative) of the action potential in the atria and ventricles . [ 4 ] Similar to skeletal muscle, the resting membrane potential (voltage when the cell is not electrically excited) of ventricular cells is around −90 millivolts (mV; 1 mV = 0.001 V), i.e. the inside of the membrane is more negative than the outside. The main ions found outside the cell at rest are sodium (Na + ), and chloride (Cl − ), whereas inside the cell it is mainly potassium (K + ). [ 6 ] The action potential begins with the voltage becoming more positive; this is known as depolarization and is mainly due to the opening of sodium channels that allow Na + to flow into the cell. After a delay (known as the absolute refractory period ), the action potential terminates as potassium channels open, allowing K + to leave the cell and causing the membrane potential to return to negative, this is known as repolarization . Another important ion is calcium (Ca 2+ ) , which can be found inside the cell in the sarcoplasmic reticulum (SR) where calcium is stored, and is also found outside of the cell. Release of Ca 2+ from the SR, via a process called calcium-induced calcium release , is vital for the plateau phase of the action potential (see phase 2, below) and is a fundamental step in cardiac excitation-contraction coupling . [ 7 ] There are important physiological differences between the pacemaker cells of the sinoatrial node , that spontaneously generate the cardiac action potential and those non-pacemaker cells that simply conduct it, such as ventricular myocytes ). The specific differences in the types of ion channels expressed and mechanisms by which they are activated results in differences in the configuration of the action potential waveform, as shown in figure 2. Cardiac automaticity also known as autorhythmicity , is the property of the specialized conductive muscle cells of the heart to generate spontaneous cardiac action potentials. [ 8 ] [ 9 ] Automaticity can be normal or abnormal, caused by temporary ion channel characteristic changes such as certain medication usage, or in the case of abnormal automaticity the changes are in electrotonic environment , caused, for example, by myocardial infarction . [ 10 ] The standard model used to understand the cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of the ventricular myocyte action potential, with reference also to the SAN action potential. In the ventricular myocyte, phase 4 occurs when the cell is at rest, in a period known as diastole . In the standard non-pacemaker cell the voltage during this phase is more or less constant, at roughly -90 mV. [ 11 ] The resting membrane potential results from the flux of ions having flowed into the cell (e.g. sodium and calcium), the flux of ions having flowed out of the cell (e.g. potassium, chloride and bicarbonate), as well as the flux of ions generated by the different membrane pumps, being perfectly balanced. [ citation needed ] The activity of these pumps serve two purposes. The first is to maintain the existence of the resting membrane potential by countering the depolarisation due to the leakage of ions not at the electrochemical equilibrium (e.g. sodium and calcium). These ions not being at the equilibrium is the reason for the existence of an electrical gradient, for they represent a net displacement of charges across the membrane, which are unable to immediately re-enter the cell to restore the electrical equilibrium. Therefore, their slow re-entrance in the cell needs to be counterbalanced or the cell would slowly lose its membrane potential. [ citation needed ] The second purpose, intricately linked to the first, is to keep the intracellular concentration more or less constant, and in this case to re-establish the original chemical gradients, that is to force the sodium and calcium which previously flowed into the cell out of it, and the potassium which previously flowed out of the cell back into it (though as the potassium is mostly at the electrochemical equilibrium, its chemical gradient will naturally reequilibrate itself opposite to the electrical gradient, without the need for an active transport mechanism). [ citation needed ] For example, the sodium (Na + ) and potassium (K + ) ions are maintained by the sodium-potassium pump which uses energy (in the form of adenosine triphosphate (ATP) ) to move three Na + out of the cell and two K + into the cell. Another example is the sodium-calcium exchanger which removes one Ca 2+ from the cell for three Na + into the cell. [ 12 ] During this phase the membrane is most permeable to K + , which can travel into or out of cell through leak channels, including the inwardly rectifying potassium channel. [ 13 ] Therefore, the resting membrane potential is mostly equal to K + equilibrium potential and can be calculated using the Goldman-Hodgkin-Katz voltage equation . [ citation needed ] However, pacemaker cells are never at rest. In these cells, phase 4 is also known as the pacemaker potential . During this phase, the membrane potential slowly becomes more positive, until it reaches a set value (around -40 mV; known as the threshold potential) or until it is depolarized by another action potential, coming from a neighboring cell. [ citation needed ] The pacemaker potential is thought to be due to a group of channels, referred to as HCN channels (Hyperpolarization-activated cyclic nucleotide-gated) . These channels open at very negative voltages (i.e. immediately after phase 3 of the previous action potential; see below) and allow the passage of both K + and Na + into the cell. Due to their unusual property of being activated by very negative membrane potentials, the movement of ions through the HCN channels is referred to as the funny current (see below). [ 14 ] Another hypothesis regarding the pacemaker potential is the 'calcium clock'. Calcium is released from the sarcoplasmic reticulum within the cell. This calcium then increases activation of the sodium-calcium exchanger resulting in the increase in membrane potential (as a +3 charge is being brought into the cell (by the 3Na + ) but only a +2 charge is leaving the cell (by the Ca 2+ ) therefore there is a net charge of +1 entering the cell). This calcium is then pumped back into the cell and back into the SR via calcium pumps (including the SERCA ). [ 15 ] This phase consists of a rapid, positive change in voltage across the cell membrane ( depolarization ) lasting less than 2 ms in ventricular cells and 10–20 ms in SAN cells. [ 16 ] This occurs due to a net flow of positive charge into the cell. [ citation needed ] In non-pacemaker cells (i.e. ventricular cells), this is produced predominantly by the activation of Na + channels , which increases the membrane conductance (flow) of Na + (g Na ). These channels are activated when an action potential arrives from a neighbouring cell, through gap junctions . When this happens, the voltage within the cell increases slightly. If this increased voltage reaches the threshold potential (approximately −70 mV) it causes the Na + channels to open. This produces a larger influx of sodium into the cell, rapidly increasing the voltage further to around +50 mV, [ 6 ] i.e. towards the Na + equilibrium potential. However, if the initial stimulus is not strong enough, and the threshold potential is not reached, the rapid sodium channels will not be activated and an action potential will not be produced; this is known as the all-or-none law . [ 17 ] [ 18 ] The influx of calcium ions (Ca 2+ ) through L-type calcium channels also constitutes a minor part of the depolarisation effect. [ 19 ] The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change of the cardiac action potential and is known as dV/dt max . In pacemaker cells (e.g. sinoatrial node cells ), however, the increase in membrane voltage is mainly due to activation of L-type calcium channels. These channels are also activated by an increase in voltage, however this time it is either due to the pacemaker potential (phase 4) or an oncoming action potential. The L-type calcium channels are activated more slowly than the sodium channels, therefore, the depolarization slope in the pacemaker action potential waveform is less steep than that in the non-pacemaker action potential waveform. [ 11 ] [ 20 ] This phase begins with the rapid inactivation of the Na + channels by the inner gate (inactivation gate), reducing the movement of sodium into the cell. At the same time potassium channels (called I to1 ) open and close rapidly, allowing for a brief flow of potassium ions out of the cell, making the membrane potential slightly more negative. This is referred to as a 'notch' on the action potential waveform. [ 11 ] There is no obvious phase 1 present in pacemaker cells. This phase is also known as the "plateau" phase due to the membrane potential remaining almost constant, as the membrane slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase delayed rectifier potassium channels (I ks ) allow potassium to leave the cell while L-type calcium channels (activated by the influx of sodium during phase 0) allow the movement of calcium ions into the cell. These calcium ions bind to and open more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. These calcium ions are responsible for the contraction of the heart. [ citation needed ] Calcium also activates chloride channels called I to2 , which allow Cl − to enter the cell. Increased calcium concentration in the cell also increases activity of the sodium-calcium exchangers, while increased sodium concentration (from the depolarisation of phase 0) increases activity of the sodium-potassium pumps. The movement of all these ions results in the membrane potential remaining relatively constant, with K + outflux, Cl − influx as well as Na + /K + pumps contributing to repolarisation and Ca 2+ influx as well as Na + /Ca 2+ exchangers contributing to depolarisation. [ 21 ] [ 11 ] This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia). There is no plateau phase present in pacemaker action potentials. During phase 3 (the "rapid repolarization" phase) of the action potential, the L-type Ca 2+ channels close, while the slow delayed rectifier (I Ks ) K + channels remain open as more potassium leak channels open. This ensures a net outward positive current, corresponding to negative change in membrane potential , thus allowing more types of K + channels to open. These are primarily the rapid delayed rectifier K + channels (I Kr ) and the inwardly rectifying K + current, I K1 . This net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize. The delayed rectifier K + channels close when the membrane potential is restored to about -85 to -90 mV, while I K1 remains conducting throughout phase 4, which helps to set the resting membrane potential [ 22 ] Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost, the contraction stops and the heart muscles relax. [ citation needed ] In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca 2+ and the opening of the rapid delayed rectifier potassium channels (I Kr ). [ 23 ] Cardiac cells have two refractory periods , the first from the beginning of phase 0 until part way through phase 3; this is known as the absolute refractory period during which it is impossible for the cell to produce another action potential. This is immediately followed, until the end of phase 3, by a relative refractory period, during which a stronger-than-usual stimulus is required to produce another action potential. [ 24 ] [ 25 ] These two refractory periods are caused by changes in the states of sodium and potassium channels . The rapid depolarization of the cell, during phase 0, causes the membrane potential to approach sodium's equilibrium potential (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state. During this state the channels cannot be opened regardless of the strength of the excitatory stimulus—this gives rise to the absolute refractory period. The relative refractory period is due to the leaking of potassium ions, which makes the membrane potential more negative (i.e. it is hyperpolarised), this resets the sodium channels; opening the inactivation gate, but still leaving the channel closed. Because some of the voltage-gated sodium ion channels have recovered and the voltage-gated potassium ion channels remain open, it is possible to initiate another action potential if the stimulus is stronger than a stimulus which can fire an action potential when the membrane is at rest. [ 26 ] Gap junctions allow the action potential to be transferred from one cell to the next (they are said to electrically couple neighbouring cardiac cells ). They are made from the connexin family of proteins, that form a pore through which ions (including Na + , Ca 2+ and K + ) can pass. As potassium is highest within the cell, it is mainly potassium that passes through. This increased potassium in the neighbour cell causes the membrane potential to increase slightly, activating the sodium channels and initiating an action potential in this cell. (A brief chemical gradient driven efflux of Na+ through the connexon at peak depolarization causes the conduction of cell to cell depolarization, not potassium.) [ 27 ] These connections allow for the rapid conduction of the action potential throughout the heart and are responsible for allowing all of the cells in the atria to contract together as well as all of the cells in the ventricles. [ 28 ] Uncoordinated contraction of heart muscles is the basis for arrhythmia and heart failure. [ 29 ] Ion channels are proteins that change shape in response to different stimuli to either allow or prevent the movement of specific ions across a membrane. They are said to be selectively permeable. Stimuli, which can either come from outside the cell or from within the cell, can include the binding of a specific molecule to a receptor on the channel (also known as ligand-gated ion channels ) or a change in membrane potential around the channel, detected by a sensor (also known as voltage-gated ion channels ) and can act to open or close the channel. The pore formed by an ion channel is aqueous (water-filled) and allows the ion to rapidly travel across the membrane. [ 33 ] Ion channels can be selective for specific ions, so there are Na + , K + , Ca 2+ , and Cl − specific channels. They can also be specific for a certain charge of ions (i.e. positive or negative). [ 34 ] Each channel is coded by a set of DNA instructions that tell the cell how to make it. These instructions are known as a gene . Figure 3 shows the important ion channels involved in the cardiac action potential, the current (ions) that flows through the channels, their main protein subunits (building blocks of the channel), some of their controlling genes that code for their structure, and the phases that are active during the cardiac action potential. Some of the most important ion channels involved in the cardiac action potential are described briefly below. Hyperpolarization-activated cyclic nucleotide-gated channels (HCN channels) are located mainly in pacemaker cells, these channels become active at very negative membrane potentials and allow for the passage of both Na + and K + into the cell (which is a movement known as a funny current, I f ). These poorly selective, cation (positively charged ions) channels conduct more current as the membrane potential becomes more negative (hyperpolarised). The activity of these channels in the SAN cells causes the membrane potential to depolarise slowly and so they are thought to be responsible for the pacemaker potential. Sympathetic nerves directly affect these channels, resulting in an increased heart rate (see below). [ 35 ] [ 14 ] These sodium channels are voltage-dependent, opening rapidly due to depolarization of the membrane, which usually occurs from neighboring cells, through gap junctions. They allow for a rapid flow of sodium into the cell, depolarizing the membrane completely and initiating an action potential. As the membrane potential increases, these channels then close and lock (become inactive). Due to the rapid influx sodium ions (steep phase 0 in action potential waveform) activation and inactivation of these channels happens almost at exactly the same time. During the inactivation state, Na + cannot pass through (absolute refractory period). However they begin to recover from inactivation as the membrane potential becomes more negative (relative refractory period). [ citation needed ] The two main types of potassium channels in cardiac cells are inward rectifiers and voltage-gated potassium channels. [ citation needed ] Inwardly rectifying potassium channels (K ir) favour the flow of K + into the cell. This influx of potassium, however, is larger when the membrane potential is more negative than the equilibrium potential for K + (~-90 mV). As the membrane potential becomes more positive (i.e. during cell stimulation from a neighbouring cell), the flow of potassium into the cell via the K ir decreases. Therefore, K ir is responsible for maintaining the resting membrane potential and initiating the depolarization phase. However, as the membrane potential continues to become more positive, the channel begins to allow the passage of K + out of the cell. This outward flow of potassium ions at the more positive membrane potentials means that the K ir can also aid the final stages of repolarisation. [ 36 ] [ 37 ] The voltage-gated potassium channels (K v ) are activated by depolarization. The currents produced by these channels include the transient out potassium current I to1 . This current has two components. Both components activate rapidly, but I to,fast inactivates more rapidly than I to, slow . These currents contribute to the early repolarization phase (phase 1) of the action potential. [ citation needed ] Another form of voltage-gated potassium channels are the delayed rectifier potassium channels. These channels carry potassium currents which are responsible for the plateau phase of the action potential, and are named based on the speed at which they activate: slowly activating I Ks , rapidly activating I Kr and ultra-rapidly activating I Kur . [ 38 ] There are two voltage-gated calcium channels within cardiac muscle: L-type calcium channels ('L' for Long-lasting) and T-type calcium channels ('T' for Transient, i.e. short). L-type channels are more common and are most densely populated within the T-tubule membrane of ventricular cells, whereas the T-type channels are found mainly within atrial and pacemaker cells , but still to a lesser degree than L-type channels. [ citation needed ] These channels respond to voltage changes across the membrane differently: L-type channels are activated by more positive membrane potentials, take longer to open and remain open longer than T-type channels. This means that the T-type channels contribute more to depolarization (phase 0) whereas L-type channels contribute to the plateau (phase 2). [ 39 ] In the heart's conduction system electrical activity that originates from the sinoatrial node (SAN) is propagated via the His - Purkinje network, the fastest conduction pathway within the heart. The electrical signal travels from the sinoatrial node, which stimulates the atria to contract, to the atrioventricular node (AVN) , which slows down conduction of the action potential from the atria to the ventricles . This delay allows the ventricles to fully fill with blood before contraction. The signal then passes down through a bundle of fibres called the bundle of His , located between the ventricles, and then to the Purkinje fibers at the bottom (apex) of the heart, causing ventricular contraction. [ citation needed ] In addition to the SAN, the AVN and Purkinje fibres also have pacemaker activity and can therefore spontaneously generate an action potential. However, these cells usually do not depolarize spontaneously, simply because action potential production in the SAN is faster. This means that before the AVN or Purkinje fibres reach the threshold potential for an action potential, they are depolarized by the oncoming impulse from the SAN [ 40 ] This is called "overdrive suppression". [ 41 ] Pacemaker activity of these cells is vital, as it means that if the SAN were to fail, then the heart could continue to beat, albeit at a lower rate (AVN= 40-60 beats per minute, Purkinje fibres = 20-40 beats per minute). These pacemakers will keep a patient alive until the emergency team arrives. [ citation needed ] An example of premature ventricular contraction is the classic athletic heart syndrome . Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to atrioventricular block , where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death. [ 42 ] The speed of action potential production in pacemaker cells is affected, but not controlled by the autonomic nervous system . The sympathetic nervous system (nerves dominant during the body's fight-or-flight response ) increase heart rate (positive chronotropy ), by decreasing the time to produce an action potential in the SAN. Nerves from the spinal cord release a molecule called noradrenaline , which binds to and activates receptors on the pacemaker cell membrane called β1 adrenoceptors . This activates a protein, called a G s -protein (s for stimulatory). Activation of this G-protein leads to increased levels of cAMP in the cell (via the cAMP pathway ). cAMP binds to the HCN channels (see above), increasing the funny current and therefore increasing the rate of depolarization, during the pacemaker potential. The increased cAMP also increases the opening time of L -type calcium channels, increasing the Ca 2+ current through the channel, speeding up phase 0. [ 43 ] The parasympathetic nervous system ( nerves dominant while the body is resting and digesting) decreases heart rate (negative chronotropy ), by increasing the time taken to produce an action potential in the SAN. A nerve called the vagus nerve , that begins in the brain and travels to the sinoatrial node, releases a molecule called acetylcholine (ACh) which binds to a receptor located on the outside of the pacemaker cell, called an M2 muscarinic receptor . This activates a G i -protein (I for inhibitory), which is made up of 3 subunits (α, β and γ) which, when activated, separate from the receptor. The β and γ subunits activate a special set of potassium channels, increasing potassium flow out of the cell and decreasing membrane potential, meaning that the pacemaker cells take longer to reach their threshold value. [ 44 ] The G i -protein also inhibits the cAMP pathway therefore reducing the sympathetic effects caused by the spinal nerves. [ 45 ] Antiarrhythmic drugs are used to regulate heart rhythms that are too fast. Other drugs used to influence the cardiac action potential include sodium channel blockers , beta blockers , potassium channel blockers , and calcium channel blockers . [ citation needed ]	https://en.wikipedia.org/wiki/Cardiac_action_potential
Cardiac allograft vasculopathy (CAV) is a progressive type of coronary artery disease in people who have had a heart transplant . [ 1 ] As the donor heart has lost its nerve supply there is typically no chest pain, and CAV is usually detected on routine testing. [ 2 ] It may present with symptoms such as tiredness and breathlessness. [ 2 ] It arises when the blood vessels supplying the transplanted heart change in structure. [ 3 ] They gradually narrow and restrict its blood flow , subsequently leading to impairment of the heart muscle or sudden death. [ 4 ] In addition to the same risk factors for coronary artery disease due to the build up of plaque , CAV is more likely to occur if the donor was older or died from explosive brain death , and if there is cytomegalovirus infection . [ 2 ] Its mechanism involves immunological ( innate and adaptive ) and nonimmunological factors, with distinct features on histological samples of coronary arteries . [ 2 ] Other major causes of death following heart transplantation include graft failure, organ rejection and infection. [ 5 ] Diagnosis is by regular follow-up and monitoring of the transplanted heart for early signs of disease. [ 2 ] Tests include coronary angiography , intravascular ultrasound , dobutamine stress echocardiography , positron emission tomography , computed tomographic angiography (CT angiography) and several biomarkers . [ 2 ] Statins and aspirin are commenced early after transplantation and on detection of CAV. [ 2 ] Medications including sirolimus and everolimus can slow disease progression. [ 2 ] A repeat heart transplantation may be required. [ 6 ] CAV affects around half of heart transplant recipients within 10 years. [ 2 ] It contributes to the death of 11-13% one year from heart transplantation. [ 1 ] Cardiac allograft vasculopathy is an accelerated type of coronary artery disease in people who have had a heart transplantation. [ 7 ] Unlike the chest tightness of angina in those who have not had a heart transplant, people with CAV typically do not experience chest pain because the donor heart has lost its nerve supply . [ 2 ] A few regain nerves some years later and may develop unusual chest pain. [ 8 ] People with CAV may present with a broad spectrum of symptoms including tiredness, nausea, or abdominal discomfort or may have no symptoms at all. [ 2 ] Shortness of breath and arrhythmias may also occur. [ 8 ] Similar to coronary artery disease in those who have not had a heart transplant, risk factors to CAV include high blood pressure , high cholesterol , and diabetes mellitus . [ 2 ] Other risk factors exclusive to CAV include older donors , cytomegalovirus infection and circulating antibodies after heart transplantation. [ 2 ] The mechanism of donor brain death, [ 8 ] particularly explosive brain death in the donor has been shown to be a significant factor. It is probably the combination of injuries to the allograft that determine the risk of developing CAV. [ 2 ] Immunological ( innate and adaptive ) and nonimmunological factors contribute to the complex pathogenesis of CAV. [ 2 ] In those nontransplanted people who develop coronary artery disease due to atherosclerosis, progression of disease is slow, histological changes are confined mainly to the main coronary arteries and arterial dilatation is observed as a form of compensatory remodelling. [ 8 ] However, in CAV, histology specimens typically show concentric thickening of the intimal layer of the main coronary arteries on the surface of the heart and in intramyocardial arteries which can become obliterated within a few years. [ 2 ] [ 8 ] There is smooth muscle cell migration, foamy macrophages and lymphocytic infiltrates. This can be seen to affect the whole length of the coronary arteries and often the smaller arteries. [ 2 ] Calcification does not always occur in CAV and if it does appear, it happens late. [ 8 ] The compensatory arterial dilation does not occur in CAV. [ 8 ] Unlike in nontransplanted people with coronary artery disease due to atherosclerosis , in CAV occlusion with thrombus of the vessel lumen is rare. [ 2 ] Inflammation and endothelial injury can be triggered by the donor arrest , organ procurement , and allograft ischaemia and reperfusion . [ 2 ] As symptoms are so variable and often absent, diagnosis has been a challenge. Hence, regular follow-up and monitoring of the allograft for early signs of disease is advocated. [ 2 ] Surveillance is performed by regularly repeating coronary angiography in the cardiac catheterization laboratory , the diagnostic test of choice. [ 2 ] This is typically performed annually for the first five years after transplantation. [ 8 ] Angiography in CAV characteristically demonstrates diffuse stenoses in large coronary arteries and a reduced number of smaller coronary arteries, also known as "peripheral pruning". [ 2 ] [ 6 ] However, because CAV frequently affects the entire length of the coronary artery, CAV may not be apparent by angiography alone. [ 2 ] Intravascular ultrasound (IVUS) is more sensitive at reliably detecting subtle changes in the thickness of the intimal layer of the artery walls and provide measurements of artery lumen. Following transplantation, serial measurements are compared to the baseline. A greater than 0.5 mm increase in intimal thickness one year after transplantation is predictive of CAV changes on angiography within five years. The paradoxical reduction in the number of blood vessels, can also be detected by intravascular ultrasound. [ 2 ] [ 8 ] IVUS, however, tends to be used for research due to its drawbacks of being invasive, requiring the use of contrast material and cost. [ 8 ] Alternatively, dobutamine stress echocardiography (DSE) is commonly performed and has an 85% sensitivity for the presence of CAV. A negative DSE correlates with a good prognosis. [ 8 ] Other noninvasive diagnostics include positron emission tomography and computed tomographic angiography (CT angiography). [ 2 ] In addition, ECGs may show atypical features of ischaemia. [ 8 ] Biomarkers for increased risk of CAV include C-reactive protein , serum brain natriuretic peptide and troponin I have been suggested. [ 2 ] The degree of CAV after heart transplantation has been obtained from a variety of sources including The Cardiac Transplant Research Database, the ISHLT registry and The United Network for Organ Sharing registry. [ 8 ] The International Society for Heart and Lung Transplantation (ISHLT) have formulated and standardized a terminology, based on diagnostic findings, to define the presence and severity of CAV, which in turn reflects prognosis. [ 8 ] [ 10 ] The severity of CAV is defined by the degree of narrowing of the coronary arteries and the presence of restrictive heart disease. [ 8 ] Prevention of CAV progression is important as once developed, CAV existing treatments are often ineffective. [ 2 ] Commencing the statins pravastatin and simvastatin early after transplantation reduces the incidence and severity of CAV. [ 2 ] [ 8 ] When combined with immunosuppressants, the progression of CAV could possibly be slowed by vitamins C and E . [ 8 ] Since the role of aspirin is already established in coronary artery disease in those who have not had a heart transplant, it is usually given after heart transplantation too. [ 2 ] On detection of CAV, medications including mTOR inhibitors sirolimus and everolimus have been shown to slow disease progression. [ 2 ] Clinically significant CAV may require percutaneous coronary interventions for focal disease, but the likelihood of restenosis is high. [ 2 ] A repeat heart transplantation may be considered. [ 2 ] Once there is reduced left ventricular ejection fraction and symptoms of heart failure , the outcome is typically poor. [ 2 ] The risk of major adverse cardiovascular events is increased by 3.4 fold if CAV is present on angiography. [ 8 ] The frequency of CAV after heart transplantation has been obtained from a variety of sources including The Cardiac Transplant Research Database, the ISHLT registry and The United Network for Organ Sharing registry. [ 8 ] In comparison to between 1994 and 2001, there has been a decline in incidence of CAV between 2001 and 2007. [ 8 ] ISHLT figures show an incidence of CAV of around 50% at 10 years after heart transplantation. [ 8 ] CAV is a leading cause of late mortality following heart transplantation. [ 2 ] Most are not severe but it contributes to the death of 11-13% one year from heart transplantation. [ 1 ] Unlike rejection and infection, CAV in the transplanted heart was not initially a predicted outcome. [ 12 ] Early survivors of heart transplants soon developed this form of vasculopathy of their coronary arteries, initially identified at post-mortems. [ 12 ] There were early suggestions that preventing cytomegalovirus (CMV) infection could decrease the prevalence of CAV. [ 12 ] The impact of CAV has changed over time, with early recipients being younger, having more rejection and cardiovascular risk factors and less use of statins. [ 12 ] Later recipients used statins routinely and were introduced to the immunosuppressive agent mycophenolate mofetil (MMF) and CMV prophylaxis. [ 12 ] In addition, the later recipients were monitored for antibody-mediated cardiac allograft rejection (AMR). [ 12 ] Before 2010 there was no uniform international standards for the nomenclature of CAV. [ 4 ] A consensus statement on a standard language for CAV was first published in 2010 by the ISHLT. [ 4 ] This was devised in a similar way to the earlier acute rejection grading system by endomyocardial biopsy . [ 10 ] [ 13 ] Antibody-mediated cardiac allograft rejection (AMR) is a significant factor leading to the rapid progression of CAV. [ 12 ] Future research directions in this area may include prospective databases that correlate clinical factors with surveillance of the incidence and severity of AMR, the frequency of CMV infection, and the use of immunosuppressants. The role of inducing immune tolerance has yet to be established. [ 12 ]	https://en.wikipedia.org/wiki/Cardiac_allograft_vasculopathy
Cardiac amyloidosis is a subcategory of amyloidosis where there is depositing of the protein amyloid in the cardiac muscle and surrounding tissues. Amyloid, a misfolded and insoluble protein, can become a deposit in the heart's atria, valves, or ventricles . These deposits can cause thickening of different sections of the heart, leading to decreased cardiac function . [ 1 ] The overall decrease in cardiac function leads to a plethora of symptoms. [ 2 ] This multisystem disease was often misdiagnosed, with a corrected analysis only during autopsy. Advancements of technologies have increased earlier accuracy of diagnosis. Cardiac amyloidosis has multiple sub-types including light chain , familial , and senile . [ 3 ] One of the most studied types is light chain cardiac amyloidosis. [ 2 ] Prognosis depends on the extent of the deposits in the body and the type of amyloidosis. [ 4 ] New treatment methods are actively being researched in regards to the treatment of heart failure and specific cardiac amyloidosis problems. [ 5 ] [ 6 ] The multiple subtypes of cardiac amyloidosis have varying epidemiological, diagnostic, and prognostic characteristics. [ 4 ] This relatively rare form of cardiac amyloidosis occurs in an estimated six to ten cases per 1,000,000 people. [ 4 ] This sub- type usually affects males over the age of 60 [ 4 ] and is rapidly progressive. Pathogenesis of this form is due to the aggregation of immunoglobulin lambda light chains . [ 3 ] These chains are created by an abnormal expansion of plasma cells . [ 3 ] Over time, these light chains deposit into the interstitial tissue within the myocardium. [ 4 ] Diagnostic tests includes serum and urine electrophoresis , [ 4 ] laboratory testing for the determination of elevated levels of troponin and BNP , and ECGs showing low QRS voltages. [ 2 ] This type is caused by mutations of proteins involved in amyloid formation, including transthyretin (TTR), fibrinogen , apolipoprotein A1 , or apolipoprotein A2 . Due to the multiple number of potential genetic causes the incidence of this form is variable. The vast majority of familial cardiac amyloidosis still present after the age of 60. [ 4 ] A common mutation is the TTR gene mutation Val122Ile. [ 2 ] It is estimated that 3.5–4% of African Americans in The United States have the Val 122lle mutation. [ 4 ] This type of amyloidosis can be identified by genetic testing for protein mutation. [ 4 ] For the diagnosis of familial cardiac amyloidosis to be made a biopsy with histological evaluation must be obtained. [ 7 ] In this histological evaluation special stains are utilized to visualize the amyloid deposits . [ 7 ] One such stain is Congo Red , which binds specifically to the amyloid deposit and can be characterized by various lighting methods. [ 7 ] Under polarized light, the amyloid deposits while show pathognomonic apple green birefringence, and under plain light the deposits will appear a light salmon pink color. [ 7 ] Familial amyloidosis symptoms are centered around neuropathological and cardiac problems. [ 3 ] Cardiac manifestations of the TTR mutation present more often in The United States. [ 4 ] This type is considered the wild-type mutation which leads to the development of TTR deposits . [ 2 ] It usually affects males over 70 years with the manifestation of carpal tunnel syndrome . [ 4 ] Similar to the other subtypes of cardiac amyloidosis, a biopsy is required for diagnosis. [ 4 ] However, formal diagnosis of Senile cardiac amyloidosis is a diagnosis of exclusion. [ 4 ] Biopsy with histological evaluation can rule out Light chain and Familial subtypes, leaving the diagnosis of Senile. [ 4 ] This type is often misdiagnosed. However, greater use of cardiac magnetic resonance has increased the rate of diagnosis [ 2 ] The severity of the disease tends to be less than the Light chain and Familial variants. [ 4 ] This is due to the amount of time that it takes to accumulate the amyloid depositions being longer in the Senile variant. [ 4 ] Symptoms of cardiac amyloidosis are a combination of heart failure and amyloid deposition in various other organs. [ 2 ] Amyloid deposition in the heart causes restrictive diastolic heart failure that progresses to systolic heart failure. [ 8 ] Cardiac manifestations include: For patients with light-chain amyloidosis, there can be depositions of amyloid into numerous different organs. [ 2 ] Deposition of amyloid into other organs makes the diagnosis of cardiac amyloidosis difficult as these extracardiac manifestations mask the diagnosis. [ 2 ] Extracardiac manifestations include: The general cause of cardiac amyloidosis is the misfolding of a specific protein precursor depending on the amyloidosis type. Protein precursors include immunoglobulin-derived light chains and transthyretin mutations. [ 3 ] The misfolding of the protein causes it to have insoluble beta-pleated sheets, [ 2 ] creating an amyloid. Amyloid, the aggregation, or clumping, of proteins, is resistant to degradation by the body. Amyloids are mostly fibrils , while also containing a P component, apolipoprotein , collagen , fibronectin , and laminin . [ 2 ] The P component, a pentameric protein , stabilizes the fibrils of the amyloid, which reduces their clearance from the body. [ 1 ] Deposits of the amyloids can occur throughout the body, including the heart, liver, kidneys, spleen, adrenal glands, and bones. Deposits in the extracellular cardiac space can stiffen the heart, resulting in restriction of the ventricles. [ 3 ] This restriction in ventricular motion results in a decreased ability for the heart to pump efficiently, leading to the various symptoms associated with cardiac amyloidosis. [ 4 ] Echocardiography is a safe and non-invasive method that can be used to assess the structural and functional disease of the heart. [ 4 ] Amyloidosis presents with ventricle and valvular thickening, biatrial enlargement, [ 4 ] restrictive filling pattern, with normal to mildly reduced systolic function [ 8 ] and decreased diastolic filling . [ 4 ] An echo can be used to evaluate for prognosis of the disease, measuring the different strains within the heart. [ 4 ] Cardiac amyloidosis produces specific alterations to the functionality of the heart. Echocardiography can be utilized to detect this specific pattern (relative preservation of the apical myocardium with decreased longitudinal strain in the mid and basal sections), which is 90–95% sensitive and 80–85% specific for cardiac amyloidosis. [ 4 ] Echocardiography can be used to help physicians with diagnosis, however, it can only be used for the suggestion of the disease, not the confirmation, unless it is late stage amyloidosis. [ 1 ] ECGs of patients with cardiac amyloidosis usually show a low voltage in the limb leads, with an unusual extreme right axis. There is usually a normal P-wave , however, it can be slightly prolonged. For patients with light-chain amyloidosis, the QRS complex pattern is skewed, [ 1 ] with poor R-waves of the chest leads. [ 2 ] Holter ECGs can be used to identify asymptomatic arrhythmias . [ 2 ] EKG changes may be present, showing low voltage and conduction abnormalities like atrioventricular block or sinus node dysfunction. [ 8 ] Atrial fibrillation (AF) is observed in up to 70% of patients at the time of diagnosis, and patients typically have controlled ventricular rates caused by concomitant conduction system disease. [ 11 ] Laboratory tests including urea and creatinine levels , liver enzymes , glucose, thyroid function , full blood count , and clotting tests. The analysis of serum and urine for presence of monoclonal immunoglobulin is also done through immunofixation for detection of the monoclonal band. Presence of the monoclonal band would be consistent with light chain amyloidosis. For light chain amyloidosis, serum immunoglobulin free light chain assay can be used for diagnosis and following of the amyloidosis. [ 1 ] In light-chain amyloidosis, a low paraprotein level can be present. [ 3 ] There are two main cardiac biomarkers used in the assessment of cardiac amyloidosis, troponin and N-terminal proBNP. [ 12 ] As expected, with cardiac damage and dysfunction, there can be an elevation of these markers in patients with cardiac amyloidosis. These markers have been incorporated into the various staging/scoring systems used by physicians to determine severity of the disease and prognosis. [ 12 ] Extracardiac biopsies of tissues of the kidney, liver, peripheral nerve, or abdominal fat can be used to confirm the presence of amyloid deposits. Amyloid deposits in biopsy samples are confirmed through the use of Congo red dye , which produces a green birefringence when viewed under polarized light. Sirius red staining or electron microscopy examination can also be done. The determination of the type of amyloid can be done by immunohisto-labeling techniques as well as immunofluorescence staining. [ 1 ] For light-chain amyloidosis patients, bone marrow biopsies could be conducted to determine the baseline percentage of plasma cells and to rule out multiple myeloma . [ 3 ] Right heart catheterization is the test used to test for elevated diastolic ventricular pressures . This test is more invasive and would be performed after inconclusive endomyocardial biopsy samples. [ 1 ] Cardiac magnetic resonance (CMR) is capable of measuring the thickness of different areas of the heart. This can be used for quantification of the deposits in the heart. [ 1 ] CMR also shows the characterization of myocardial tissue through patterns of gadolinium enhancements. [ 2 ] However, none of the CMR technique is able to differentiate ATTR-CM and AL-CM definitely. [ 13 ] For AL-CM, 68% of them have symmetrical and concentric left ventricular hypertrophy . On the other hand, for ATTR-CM, 79% of them have asymmetrical left ventricular hypertrophy and 18% of them have symmetrical and concentric left ventricular hypertrophy. [ 13 ] In T1-weighted imaging , edema in the heart can be detected with a high T1 signal. Meanwhile, enlargement of heart cells will reduce the T1 signal. Using T1 signal, Extracellular volume (ECV) is useful to determine the degree of amyloid deposition around the heart cells and detect the regression of amyloid deposits after treatment. ECV is higher in ATTR-CM than in AL-CM. [ 13 ] In T2-weighted imaging, the T2 signal is increased in acute myocarditis (inflammation of heart muscles), and myocardial infarction (heart attack). T2 signal is also increased in AL-CM and ATTR-CM but the signal is greater in AL-CM before starting chemotherapy. [ 13 ] Late gadolinum enhancement (LGE) can determine the severity of deposition of amyloid in heart tissue. The higher the LGE signal, the more severe the heart involvement. It can be divided into three stages: no LGE, sub endocardial LGE, and full-thickness (transmural) LGE. [ 13 ] Scintigraphy can be used to measure the extent and distribution of the amyloid throughout the body, including the liver, kidney, spleen, and heart. [ 2 ] A radiolabelled serum amyloid P component can be administered to a patient intravenously and the P component pools to the amyloid deposit proportional to the size of the deposit. The labeling of the P component can then be pictured by a gamma camera . [ 1 ] Technetium radionuclide scans can now reliably diagnosis cardiac amyloidosis, with certain scanning methods having greater than 99% sensitivity (but only 91% specific for amyloidosis). [ 14 ] In this method of imaging, radiolabeled technetium is injected into the body where it binds to cardiac amyloid deposits. [ 14 ] A subsequent scan is taken to determine where the tracer stays, therefore highlighting the amyloid deposition in the heart. [ 14 ] This method allows for a noninvasive definitive diagnosis of cardiac amyloidosis (as in the past an endomyocardial biopsy was required) [ 14 ] Mass spectrometry can be used to determine whether the protein is light-chain or familial amyloidosis by identifying the protein subunit . [ 9 ] Treatments differ according to the type of amyloidosis present. [ 1 ] The majority of treatment is aimed at preserving heart function and treating heart failure symptoms. [ 3 ] Light chain (AL-CM) Treatment: Since the cause of this subtype of cardiac amyloidosis is the excessive production of free light chains, the major goal of treatment is the reduction in concentration of light chains. [ 5 ] For light-chain amyloidosis, the use of FLC assays and NT-proBNP levels can be used to monitor the progression of amyloidosis and any response to treatments. [ 1 ] One of the major routes to decrease the production of these excess light chains is to kill the abnormal cells that are producing them. [ 5 ] Chemotherapeutic agents such as melphalan or bortezomib can be used to kill off the abnormal cell line that is producing the free light chains. [ 5 ] Following chemotherapy, a bone marrow transplant can be utilized to restore the normal cell lines. [ 5 ] There are newer medications ( ixazomib , carfilzomib , daratumumab , elotuzumab ) under research for the treatment of multiple myeloma that can help to decrease the production of free light chains. [ 5 ] New data suggests that orthotopic heart transplant followed by melphalan and stem cell transplant produces results similar to non cardiac amyloidosis indicated heart transplant. [ 5 ] To treat complications, medications can be prescribed including midodrine for autonomic neuropathy , amiodarone for patients with atrial fibrillation to prevent arrhythmias , and warfarin used after a cardioembolic episode. [ 1 ] Familial (ATTR m -CM) Treatment: In recent years there have been developments in the treatment of Familial/Transthyretin cardiac amyloidosis including methods to suppress transthyretin production, stabilize amyloid fibrils, and medications that can destroy already existing fibrils. [ 6 ] For familial amyloidosis, ACE-inhibitors and beta-blockers can be prescribed if there is no autonomic neuropathy. [ 1 ] The use of pacemakers (both right ventricular pacing and biventricular pacing) or implantable cardioverter defibrillators remains questionable in cardiac amyloidosis. [ 17 ] In 2012, Craig Lewis, a 55 year old Texan, presented at the Texas Heart Institute with a severe case of amyloidosis. He was given an experimental continuous-flow artificial heart transplant which saved his life. Lewis died 5 weeks later of liver failure after slipping into a coma due to the amyloidosis. [ 18 ] Overall prognosis is dependent on the extent of cardiac dysfunction . Worse outcomes have been seen when echocardiography shows left ventricular wall thickness, poor systolic function and severe diastolic dysfunction. [ 1 ] Light chain (AL-CM) Prognosis: For light-chain amyloidosis early detection leads to best possibility of therapies prolonging the period of remission. [ 3 ] Well treated light chain cardiac amyloidosis has a 4-year survival rate of around 90%. [ 5 ] In patients that undergo stem cell transplant the average survival time increases to 10 years. [ 5 ] Staging systems have been developed to stratify severity of the disease, including the Mayo Biomarker Stage, which utilizes various biomarkers such as troponin I , troponin T , BNP , and NT-proBNP , and Free light chain concentrations. [ 5 ] Familial (ATTR m -CM) Prognosis: Due to the extensive number of variables involved in this subtype, prognosis varies depending on the specific type of familial cardiac amyloidosis. [ 5 ] Variables involve mutant vs wild type transthyretin mutation and age of onset of symptoms. [ 5 ] In comparison to light chain amyloidosis, the familial subtype is slower to progress and has a more favorable prognosis. [ 5 ] However, the Val 122lle mutation (most common cause of familial cardiac amyloidosis) has a 4-year survival rate of 16% with an average length of 26 months. [ 5 ] A delay in recognition plays a major factor in this reduced survival rate. [ 5 ]	https://en.wikipedia.org/wiki/Cardiac_amyloidosis
Cardiac asthma is the medical condition of intermittent wheezing , coughing, and shortness of breath that is associated with underlying congestive heart failure (CHF). [ 1 ] Symptoms of cardiac asthma are related to the heart's inability to effectively and efficiently pump blood in a CHF patient. [ 2 ] This can lead to accumulation of fluid in and around the lungs ( pulmonary congestion ), disrupting the lung's ability to oxygenate blood. Cardiac asthma carries similar symptoms to bronchial asthma , but is differentiated by lacking inflammatory origin. [ 1 ] [ 3 ] Because of the similarity in symptoms, diagnosis of cardiac versus bronchial asthma relies on full cardiac workup and pulmonary function testing . [ 2 ] [ 4 ] Treatment is centered on improving cardiac function , maintaining blood oxygen saturation levels, and stabilizing total body water volume and distribution. [ 1 ] [ 4 ] The most common findings of cardiac asthma are the presence of wheeze, cough, or shortness of breath (predominantly occurring at night or when lying down ) in a patient that possesses signs of congestive heart failure . [ 4 ] [ 5 ] [ 6 ] [ 7 ] Additional findings consist of production of frothy or watery sputum and presence of water in the lungs that can be heard via stethoscope. [ 8 ] In severe cases, a patient can experience multiple night time episodes of breathlessness, changes in skin coloration , and episodes of bloody sputum. [ 1 ] The underlying causes for cardiac asthma stem from the eventual back up of fluid into the pulmonary vasculature as a result of the heart's, particularly left sided, inability to effectively and efficiently pump blood. [ 2 ] The accumulation of fluid in the heart creates a higher than normal pressure system that places increasing pressure demands on the pulmonary venous system in order for appropriate oxygenation of blood to occur. [ 4 ] This results in what is called pulmonary venous hypertension (PVH), and results in distention and recruitment of pulmonary capillaries to help distribute the increased pressure gradient. [ 2 ] [ 4 ] At the capillary, there is a microvascular barrier that helps regulate fluid status via molecular pressure forces such as forces that push outward from vessels and pressures that pull or attract into vessels . [ 2 ] With increasing PVH, pressure outward overcomes pressure inward, and fluid is distributed to the lung interstitium , preserving oxygen exchange at the capillary. [ 2 ] Fluid is transported to the hilum and pleural space , and removed via the lymphatic system . [ 2 ] [ 7 ] At first, the body is capable of handling excess water. Later, the capillary vasculature is overwhelmed by increased pressure and fluid backs up into the alveolar sac , resulting in pulmonary edema and decreased oxygenation capability. [ 2 ] Additionally, increased pressure demands on capillary vasculature result in increases in vascular tone to include remodeling of pre-capillary vessels such as medial wall hypertrophic changes . [ 2 ] Over time, the remodeling efforts of the vessels can progress to hyperplastic changes of the vessels' wall construction, and results in increased pulmonary vascular resistance . [ 2 ] There is ongoing interest into establishing connections of cardiac asthma to abnormalities in bronchiole anatomy. [ 1 ] [ 4 ] Current evaluation has proposed multiple mechanisms for increased airway resistance, and focus is on four alternate explanations: The diagnosis of cardiac asthma is accomplished through workup of congestive heart failure, complete with: As well as evaluation of lung function via: Treatment of asthma symptoms in CHF patients is directed towards optimizing the patient's cardiovascular status and correcting potential oxygen deficit. [ 4 ] Current recommendations in acute asthma symptoms are utilization of diuretics such as furosemide , venodilators such as nitroglycerin , and morphine . [ 1 ] The initial strategy should focus on decreasing patient fluid retention with diuretic therapy, thereby decreasing cardiac preload and overall fluid load in pulmonary circuit ( pulmonary congestion ). [ 1 ] Next, if aggressive diuresis is not adequately correcting symptoms, venodilators can be used to distribute blood and fluid to the venous system, thereby decreasing cardiac preload and left heart pressures contributing to pulmonary congestion. [ 1 ] Lastly, morphine can be utilized for assistance in improving ease of breathing through a presumed mechanism similar to venodilation, as well as reducing patient anxiety. [ 1 ] Additionally, applications of supplemental oxygen and repositioning to upright or standing positions in events of low blood oxygen saturation and difficulty breathing can be utilized as needed. [ 1 ] Chronic management of cardiac asthma is directed at optimizing therapy of heart failure. Current recommendations can be found at its respective page ( congestive heart failure ). [ 1 ] There is importance of distinguishing whether asthma is of bronchial or cardiac origin because management of bronchial asthma is primarily centered on utilization of inhalers, such as bronchodilators and corticosteroids. At this point in time, there has been limited evidence of improvement of cardiac asthma symptoms with utilization of inhalers. [ 1 ] [ 4 ] [ 5 ]	https://en.wikipedia.org/wiki/Cardiac_asthma
Cardiac catheterization ( heart cath ) is the insertion of a catheter into a chamber or vessel of the heart . This is done both for diagnostic and interventional purposes. A common example of cardiac catheterization is coronary catheterization that involves catheterization of the coronary arteries for coronary artery disease and myocardial infarctions ("heart attacks"). Catheterization is most often performed in special laboratories with fluoroscopy and highly maneuverable tables. These "cath labs" are often equipped with cabinets of catheters, stents , balloons , etc. of various sizes to increase efficiency. Monitors show the fluoroscopy imaging, electrocardiogram (ECG), pressure waves, and more. Coronary angiography is a diagnostic procedure that allows visualization of the coronary vessels. Fluoroscopy is used to visualize the lumens of the arteries as a 2-D projection. Should these arteries show narrowing or blockage, then techniques exist to open these arteries. Percutaneous coronary intervention is a blanket term that involves the use of mechanical stents, balloons, etc. to increase blood flow to previously blocked (or occluded) vessels. [ citation needed ] Measuring pressures in the heart is also an important aspect of catheterization. The catheters are fluid filled conduits that can transmit pressures to outside the body to pressure transducers . This allows measuring pressure in any part of the heart that a catheter can be maneuvered into. [ citation needed ] Measuring blood flow is also possible through several methods. Most commonly, flows are estimated using the Fick principle and thermodilution. These methods have drawbacks, but give invasive estimations of the cardiac output, which can be used to make clinical decisions (e.g., cardiogenic shock , heart failure ) to improve the person's condition. [ citation needed ] Cardiac catheterization can be used as part of a therapeutic regimen to improve outcomes for survivors of out-of-hospital cardiac arrest. [ 1 ] Cardiac catheterization often requires the use of fluoroscopy to visualize the path of the catheter as it enters the heart or as it enters the coronary arteries. The coronary arteries are known as "epicardial vessels" as they are located in the epicardium, the outermost layer of the heart. [ 2 ] The use of fluoroscopy requires radiopaque contrast, which in rare cases can lead to contrast-induced kidney injury (see Contrast-induced nephropathy ). People are constantly exposed to low doses of ionizing radiation during procedures. [ 3 ] Ideal table positioning between the x-ray source and receiver, and radiation monitoring via thermoluminescent dosimetry , are two main ways of reducing a person's exposure to radiation. [ 3 ] People with certain comorbidities (people who have more than one condition at the same time) have a higher risk of adverse events during the cardiac catheterization procedure. [ 3 ] These comorbidity conditions include aortic aneurysm , aortic stenosis , extensive three-vessel coronary artery disease , diabetes , uncontrolled hypertension , obesity , chronic kidney disease , and unstable angina . [ 4 ] Left heart catheterization (LHC) is an ambiguous term and sometime clarification is required: [ citation needed ] technique is also used to assess the amount of occlusion (or blockage) in a coronary artery, often described as a percentage of occlusion. A thin, flexible wire is inserted into either the femoral artery or the radial artery and threaded toward the heart until it is in the ascending aorta . Radial access is not associated with an increased risk of stroke over femoral access. [ 5 ] At this point, a catheter is guided over the wire into the ascending aorta, where it can be maneuvered into the coronary arteries through the coronary ostia. [ 4 ] In this position, the interventional cardiologist can inject contrast and visualize the flow through the vessel. If necessary, the physician can utilize percutaneous coronary intervention techniques, including the use of a stent (either bare-metal or drug-eluting ) to open the blocked vessel and restore appropriate blood flow. In general, occlusions greater than 70% of the width of the vessel lumen are thought to require intervention. However, in cases where multiple vessels are blocked (so-called "three-vessel disease"), the interventional cardiologist may opt instead to refer the patient to a cardiothoracic surgeon for coronary artery bypass graft (CABG; see Coronary artery bypass surgery ) surgery. [ citation needed ] Right heart catheterization (RHC) allows the physician to determine the pressures within the heart (intracardiac pressures). The heart is most often accessed via the internal jugular or femoral vein; arteries are not used. Values are commonly obtained for the right atrium, right ventricle, pulmonary artery, and pulmonary capillary "wedge" pressures. Right heart catheterizations also allow the physician to estimate the cardiac output, the amount of blood that flows from the heart each minute, and the cardiac index, a hemodynamic parameter that relates the cardiac output to a patient's body size. Determination of cardiac output can be done by releasing a small amount of saline solution (either chilled or at room temperature) in one area of the heart and measuring the change in blood temperature over time in another area of the heart. [ citation needed ] Right heart catheterization is often done for pulmonary hypertension , heart failure , and cardiogenic shock . The pulmonary artery catheter can be placed, used, and removed, or it can be placed and left in place for continuous monitoring. The latter can be done an intensive care unit (ICU) to permit frequent measurement of the hemodynamic parameters in response to interventions. [ citation needed ] Parameters obtainable from a right heart catheterization: [ citation needed ] Coronary catheterization is an invasive process and comes with risks that include stroke, heart attack, and death. Like any procedure, the benefits should outweigh the risks and so this procedure is reserved for those with symptoms of serious heart diseases and is never used for screening purposes. Other, non-invasive tests are better used when the diagnosis or certainty of the diagnosis is not as clear. [ citation needed ] Indications for cardiac catheterization include the following: [ 6 ] Right heart catheterization, along with pulmonary function testing and other testing should be done to confirm pulmonary hypertension prior to having vasoactive pharmacologic treatments approved and initiated. [ 7 ] Placement of internal pacemakers and defibrillators are done through catheterization as well. An exception to this is placement of electrodes on the outer surface of the heart (called epicardial electrodes). Otherwise, electrodes are placed through the venous system into the heart and left there permanently. Typically, these devices are placed in the left upper chest and enter the left subclavian vein and electrodes are placed in the right atrium, right ventricle, and coronary sinus (for the left ventricle stimulation). [ citation needed ] Echocardiography is a non-invasive method to evaluate the heart valves. However, sometimes the valve pressure gradients need to be measured directly because echo is equivocal for the severity of valve disease. Invasive assessment of the valve can be done with catheterization by placing a catheter across the valve and measuring the pressures simultaneously on each side of the valve to obtain the pressure gradient. [ 8 ] In conjunction with a right heart catheterization, the valve area can be estimated. For example, in aortic valve area calculation the Gorlin equation can be used to calculate the area if the cardiac output, pressure gradient, systolic period, and heart rate are known. [ citation needed ] Evaluation of the blood flow to the lungs can be done invasively through catheterization. Contrast is injected into the pulmonary trunk, left or right pulmonary artery, or segment of the pulmonary artery. [ citation needed ] Cardiac shunts can be evaluated through catheterization. Using oxygen as a marker, the oxygen saturation of blood can be sampled at various locations in and around the heart. For example, a left-to-right atrial septal defect will show a marked increase in oxygen saturation in the right atrium, ventricle, and pulmonary artery as compared to the mixed venous oxygen saturation from the oxygenated blood from the lungs mixing into the venous return to the heart. Utilizing the Fick principle , the ratio of blood flow in the lungs (Qp) and system circulations (Qs) can calculate the Qp:Qs ratio. Elevation of the Qp:Qs ratio above 1.5 to 2.0 suggests that there is a hemodynamically significant left-to-right shunt (such that the blood flow through the lungs is 1.5 to 2.0 times more than the systemic circulation). This ratio can be evaluated non-invasively with echocardiography too, however. [ citation needed ] A "shunt run" is often done when evaluating for a shunt by taking blood samples from superior vena cava (SVC), inferior vena cava (IVC), right atrium , right ventricle , pulmonary artery , and system arterial. Abrupt increases in oxygen saturation support a left-to-right shunt and lower than normal systemic arterial oxygen saturation supports a right-to-left shunt. Samples from the SVC & IVC are used to calculate mixed venous oxygen saturation . [ citation needed ] By injecting contrast into the left ventricle, the outline of the ventricle can be measured in both systole and diastole to estimate the ejection fraction (a marker of heart function). Due to the high contrast volumes and injection pressures, this is often not performed unless other, non-invasive methods are not acceptable, not possible, or conflicting. [ citation needed ] Advancements in cardiac catheterization have permitted replacement of heart valves by means of blood vessels. This method allows valve replacement without open heart surgery and can be performed on people who are high-risk for such a surgery. [ citation needed ] Catheterization can also be used to perform balloon septostomy , which is the widening of a foramen ovale , patent foramen ovale ( PFO ), or atrial septal defect ( ASD ) using a balloon catheter . This can be done in certain congenital heart diseases in which the mechanical shunting is required to sustain life such as in transposition of the great vessels . [ citation needed ] Hypertrophic cardiomyopathy is a disease in which the myocardium is thickened and can cause blood flow obstruction. If hemodynamically significant, this excess muscle can be removed to improve blood flow. Surgically, this can be done with septal myectomy . However, it can be done through catheterization and by injecting ethanol to destroy the tissue in an alcohol septal ablation . This is done by selected an appropriate septal artery supplying the intended area and, essentially, causing a localized, controlled myocardial infarction of the area with ethanol. [ citation needed ] Complications of cardiac catheterization and tools used during catheterization include, but not limited to: [ citation needed ] The likelihood of these risks depends on many factors that include the procedure being performed, the overall health state of the patient, situational (elective vs emergent), medications (e.g., anticoagulation ), and more. [ citation needed ] "Cardiac catheterization" is a general term for a group of procedures. Access to the heart is obtained through a peripheral artery or vein. Commonly, this includes the radial artery , internal jugular vein , and femoral artery / vein . Each blood vessel has its advantages and disadvantages. Once access is obtained, plastic catheters (tiny hollow tubes) and flexible wires are used to navigate to and around the heart. Catheters come in numerous shapes, lengths, diameters, number of lumens, and other special features such as electrodes and balloons. Once in place, they are used to measure or intervene. Imaging is an important aspect to catheterization and commonly includes fluoroscopy but can also include forms of echocardiography ( TTE , TEE , ICE ) and ultrasound ( IVUS ). [ citation needed ] Obtaining access uses the Seldinger technique by puncturing the vessel with a needle, placing a wire through the needle into the lumen of the vessel, and then exchanging the needle for a larger plastic sheath. Finding the vessel with a needle can be challenging and both ultrasound and fluoroscopy can be used to aid in finding and confirming access. Sheaths typically have a side port that can be used to withdraw blood or inject fluids/medications, and they also have an end hole that permits introducing the catheters, wires, etc. coaxially into the blood vessel. [ citation needed ] Once access is obtained, what is introduced into the vessel depends on the procedure being performed. Some catheters are formed to a particular shape and can really only be manipulated by inserting/withdrawing the catheter in the sheath and rotating the catheter. Others may include internal structures that permit internal manipulation (e.g., intracardiac echocardiography ). [ citation needed ] Finally, when the procedure is completed, the catheters are removed and the sheath is removed. With time, the hole made in the blood vessel will heal. Vascular closure devices can be used to speed along hemostasis. Much equipment is required for a facility to perform the numerous possible procedures for cardiac catheterization. General: [ citation needed ] Percutaneous coronary intervention: [ citation needed ] Electrophysiology: [ citation needed ] The history of cardiac catheterization dates back to Stephen Hales (1677-1761) and Claude Bernard (1813-1878), who both used it on animal models. Clinical application of cardiac catheterization begins with Dr. Werner Forssmann in 1929, who inserted a catheter into the vein of his own forearm, guided it fluoroscopically into his right atrium, and took an X-ray picture of it. [ 9 ] However, even after this achievement, hospital administrators removed Forssmann from his position owing to his unorthodox methods. [ 9 ] During World War II , André Frédéric Cournand , a physician at NewYork-Presbyterian/Columbia , then Columbia-Bellevue, opened the first catheterization lab. In 1956, Forssmann and Cournand were co-recipients of the Nobel Prize in Physiology or Medicine for the development of cardiac catheterization. Dr. Eugene A. Stead performed research in the 1940s, which paved the way for cardiac catheterization in the USA. [ citation needed ]	https://en.wikipedia.org/wiki/Cardiac_catheterization
The cardiac conduction system ( CCS , also called the electrical conduction system of the heart ) [ 1 ] transmits the signals generated by the sinoatrial node – the heart 's pacemaker , to cause the heart muscle to contract , and pump blood through the body's circulatory system . The pacemaking signal travels through the right atrium to the atrioventricular node , along the bundle of His , and through the bundle branches to Purkinje fibers in the walls of the ventricles . The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles. [ 2 ] The conduction system consists of specialized heart muscle cells , situated within the myocardium . [ 3 ] There is a skeleton of fibrous tissue that surrounds the conduction system which can be seen on an ECG . Dysfunction of the conduction system can cause irregular heart rhythms including rhythms that are too fast or too slow . Electrical signals arising in the SA node (located in the right atrium ) stimulate the atria to contract. Then the signals travel to the atrioventricular node (AV node), which is located in the interatrial septum . After a short delay that gives the ventricles time to fill with blood, the electrical signal diverges and is conducted through the left and right bundle branches of His to the respective Purkinje fibers for each side of the heart, as well as to the endocardium at the apex of the heart, then finally to the ventricular epicardium; causing the ventricles to contract. [ 2 ] These signals are generated rhythmically, which results in the coordinated rhythmic contraction and relaxation of the heart. On the microscopic level, the wave of depolarization propagates to adjacent cells via gap junctions located on the intercalated disc . The heart is a functional syncytium as opposed to a skeletal muscle syncytium . In a functional syncytium, electrical impulses propagate freely between cells in every direction, so that the myocardium functions as a single contractile unit. This property allows rapid, synchronous depolarization of the myocardium. While advantageous under normal circumstances, this property can be detrimental, as it has potential to allow the propagation of incorrect electrical signals. These gap junctions can close to isolate damaged or dying tissue, as in a myocardial infarction (heart attack). Embryologic evidence of generation of the cardiac conduction system illuminates the respective roles of this specialized set of cells. Innervation of the heart begins with a brain only centered parasympathetic cholinergic first order. It is then followed by rapid growth of a second order sympathetic adrenergic system arising from the formation of the thoracic spinal ganglia . The third order of electrical influence of the heart is derived from the vagus nerve as the other peripheral organs form. [ 4 ] Cardiac muscle has some similarities to neurons and skeletal muscle, as well as important unique properties. Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels and a flood of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and release of Ca 2+ from the t-tubules . This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum , and free Ca 2+ causes muscle contraction . After a delay, potassium channels reopen, and the resulting flow of K + out of the cell causes repolarization to the resting state. [ 5 ] [ 6 ] There are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most importantly the spontaneous depolarizations necessary for the SA node's pacemaker activity. In order to maximize efficiency of contractions and cardiac output , the conduction system of the heart has: An electrocardiogram is a recording of the electrical activity of the heart. Under normal conditions, electrical activity is spontaneously generated by the SA node , the cardiac pacemaker. This electrical impulse is propagated throughout the right atrium , and through Bachmann's bundle to the left atrium , stimulating the myocardium of the atria to contract. The conduction of the electrical impulses throughout the atria is seen on the ECG as the P wave . [ 5 ] [ 7 ] As the electrical activity is spreading throughout the atria, it travels via specialized pathways, known as internodal tracts , from the SA node to the AV node . The AV node functions as a critical delay in the conduction system. Without this delay, the atria and ventricles would contract at the same time, and blood wouldn't flow effectively from the atria to the ventricles. The delay in the AV node forms much of the PR segment on the ECG, and part of atrial repolarization can be represented by the PR segment. The distal portion of the AV node is known as the bundle of His . [ 8 ] The bundle of His splits into two branches in the interventricular septum: the left bundle branch and the right bundle branch. The left bundle branch activates the left ventricle , while the right bundle branch activates the right ventricle . The left bundle branch is short, splitting into the left anterior fascicle and the left posterior fascicle. The left posterior fascicle is relatively short and broad, with dual blood supply, making it particularly resistant to ischemic damage. The left posterior fascicle transmits impulses to the papillary muscles, leading to mitral valve closure. As the left posterior fascicle is shorter and broader than the right, impulses reach the papillary muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-tensioning of the chordae tendinae, increasing the resistance to flow through the mitral valve during left ventricular contraction. [ 5 ] This mechanism works in the same manner as pre-tensioning of car seatbelts. The two bundle branches taper out to produce numerous Purkinje fibers , which stimulate individual groups of myocardial cells to contract. [ 5 ] The spread of electrical activity through the ventricular myocardium produces the QRS complex on the ECG. Atrial repolarization occurs and is masked during the QRS complex by ventricular depolarization on the ECG. The last event of the cycle is the repolarization of the ventricles . It is the restoring of the resting state. In the ECG, repolarization includes the J point, ST segment, and T and U waves. [ 9 ] The transthoracically measured PQRS portion of an electrocardiogram is chiefly influenced by the sympathetic nervous system . The T (and occasionally U) waves are chiefly influenced by the parasympathetic nervous system guided by integrated brainstem control from the vagus nerve and the thoracic spinal accessory ganglia . An impulse ( action potential ) that originates from the SA node at a relative rate of 60–100 bpm is known as a normal sinus rhythm . If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known as sinus bradycardia . If SA nodal impulses occur at a rate exceeding 100 bpm, the consequent rapid heart rate is sinus tachycardia . These conditions are not necessarily bad symptoms, however. Trained athletes, for example, usually show heart rates slower than 60 bpm when not exercising. If the SA node fails to initialize, the AV junction can take over as the main pacemaker of the heart. The AV junction consists of the AV node, the bundle of His, and the surrounding area; it has a regular rate of 40 to 60 bpm. These "junctional" rhythms are characterized by a missing or inverted P wave. If both the SA node and the AV junction fail to initialize the electrical impulse, the ventricles can fire the electrical impulses themselves at a rate of 20 to 40 bpm and will have a QRS complex of greater than 120 ms. This is necessary for the heart to be in good function. An arrhythmia is an abnormal rhythm or speed of rhythm of the heartbeat. A slow heart rate of 60 or less beats per minute is defined as bradycardia . A fast heart rate of more than 100 beats per minute is defined as tachycardia . An arrhythmia is defined as one that is not physiological such as the lowered heart rate that a trained athlete may naturally have developed; the resting heart rates may be less than 60 bpm. When an arrhythmia cannot be treated by medication (or other standard cardioversion measures), an artificial pacemaker may be implanted to control the conduction system.	https://en.wikipedia.org/wiki/Cardiac_conduction_system
Cardiac contractility modulation is a therapy which is intended for the treatment of patients with moderate to severe heart failure ( NYHA class II–IV ) with symptoms despite optimal medical therapy who can benefit from an improvement in cardiac output. The short- and long-term use of this therapy enhances the strength of ventricular contraction and therefore the heart's pumping capacity by modulating (adjusting) the myocardial contractility . This is provided by a pacemaker -like device that applies non-excitatory electrical signals adjusted to and synchronized with the electrical action in the cardiac cycle . [ 1 ] [ 2 ] [ 3 ] In cardiac contractility modulation therapy, electrical stimulation is applied to the cardiac muscle during the absolute refractory period . In this phase of the cardiac cycle, electrical signals cannot trigger new cardiac muscle contractions, hence this type of stimulation is known as a non-excitatory stimulation. However, the electrical signals increase the influx of calcium ions into the cardiac muscle cells ( cardiomyocytes ). [ 4 ] [ 5 ] In contrast to other electrical stimulation treatments for heart failure, such as pacemaker therapy or implantable cardioverter defibrillators (ICD), cardiac contractility modulation does not directly affect cardiac rhythm. Rather, the aim is to enhance the heart's natural contraction (the native cardiac contractility) sustainably over long periods of time. Furthermore, unlike most interventions that increase cardiac contractility, cardiac contractility modulation is not associated with an unfavorable increase in oxygen demand by the heart (measured in terms of Myocardial Oxygen Consumption or MVO 2 ). This may be explained by the beneficial effect the therapy has in improving cardiac efficiency. [ 6 ] [ 7 ] [ 8 ] A meta-analysis in 2014 [ 2 ] and an overview of device-based treatment options in heart failure in 2013 [ 9 ] concluded that cardiac contractility modulation treatment is safe, [ 1 ] [ 9 ] that it is generally beneficial to patients [ 1 ] [ 9 ] and that the treatment increases the exercise tolerance (ET) and quality of life (QoL) of patients. [ 2 ] Furthermore, preliminary long-term survival data shows that cardiac contractility modulation is associated with lower long-term mortality in heart failure patients when compared with expected rates among similar patients not treated with cardiac contractility modulation. [ 10 ] Based on the results of the pivotal FIX-HF-5C trial, [ 11 ] the FDA approved cardiac contractility modulation therapy for use in the United States on March 21, 2019. [ 12 ] The FDA approved the OPTIMIZER Smart System, which delivers cardiac contractility modulation therapy, as indicated to improve 6-minute hall walk distance, quality of life, and functional status of NYHA Class III heart failure patients who remain symptomatic despite guideline directed medical therapy, who are in normal sinus rhythm, are not indicated for cardiac resynchronization therapy, and have a left ventricular ejection fraction ranging from 25% to 45%. [ citation needed ] Based on the results of clinical trials, [ 3 ] [ 13 ] cardiac contractility modulation devices are approved and available for clinical use in all European Union countries and in Australia , Turkey , India and Hong Kong , as well as in other countries that recognize CE marking for medical devices . [ citation needed ] Based on the approval of cardiac contractility modulation devices, the therapy is a treatment option for patients that are at least 18 years old who suffer from heart failure symptoms due to left ventricular systolic dysfunction (LVSD) despite adequate medical treatment. Further clinical research are under way to identify which patient group within the scope of the device approval benefits most from cardiac contractility modulation treatment. [ 1 ] [ 2 ] [ 3 ] [ 14 ] Criteria for the classification of patients with left ventricular systolic heart failure include the severity of the disease based on functional parameters (NYHA classification), the average percentage of blood volume ejected by the left ventricle with each heart beat (left ventricular ejection fraction or LVEF) and the duration of the QRS complex seen in the electrocardiogram (ECG). Most clinical studies on cardiac contractility modulation therapy have involved heart failure patients who were classified initially as NYHA Class II, III or IV and had a normal QRS duration (QRS duration ≤ 120 ms). The efficacy of cardiac contractility modulation on patients in an earlier stage of heart failure has not yet been studied. [ 2 ] [ 15 ] A subsequent evaluation study (subgroup analysis) has already suggested a particular patient group that responds exceptionally well to cardiac contractility modulation therapy. The patients were characterized by a disease severity of NYHA class III and a left ventricular ejection fraction of ≥ 25%. [ 1 ] [ 16 ] Although studies on cardiac contractility modulation therapy have focused on patients with a normal QRS duration (i.e. ≤ 120 ms), it is possible to use the therapy in patients who meet the treatment indication but who do not have a normal QRS duration. [ 3 ] [ 17 ] [ 18 ] A preliminary study has previously shown that cardiac contractility modulation may be safe and effective in such patients who have not responded to cardiac resynchronization therapy (CRT). [ 19 ] Cardiac resynchronization therapy (CRT; also known as biventricular pacing) has proven to be an effective treatment in heart failure. [ 20 ] However, CRT is generally recommended exclusively for patients with a preserved sinus rhythm and a prolonged QRS complex (≥ 120 ms) who also suffer from left bundle branch block (LBBB), or for patients without left bundle branch block but who have a preserved sinus rhythm and a QRS complex with a width of ≥ 150 ms. [ 20 ] However, only 30-40% of all heart failure patients show such a prolonged QRS complex, and therefore the 60-70% of patients who have a normal QRS complex cannot be treated with CRT. In addition, around 30% of the patients eligible for CRT treatment do not respond to CRT. [ 2 ] [ 15 ] [ 17 ] Until recently, the only other available device-based treatment was the left ventricular assist device (LVAD). LVAD therapy is indicated in patients with severe illness and is associated with several hours of surgery (involving a cardiopulmonary bypass ). It is usually considered as a therapy providing a "bridge to transplant" for heart failure patients classified as NYHA class IV, and is intended to support heart function until a heart transplant is received. [ 2 ] [ 15 ] [ 17 ] Current research results suggest that the therapeutic gap described above could now be closed by the cardiac contractility modulation therapy. [ 2 ] [ 15 ] [ 17 ] Additionally, a long-term study showed that the cardiac contractility modulation was able to stop the common and prognostically unfavorable long-term prolongation of QRS duration in heart failure patients. This result was interpreted as signaling the safety of the treatment and as an indicator that patients could benefit from cardiac contractility modulation therapy in the long term. If the QRS-stabilizing effect were to be confirmed in further studies, the cardiac contractility modulation would become the first device-based treatment for heart failure with the potential to halt QRS prolongation, a factor associated with a poor prognosis. [ 21 ] The guidelines issued by the European Society of Cardiology (ESC) in 2016, mention cardiac contractility modulation therapy as a therapy option to be considered in selected group of patients with HF. Mostly these guidelines are endorsed by national cardiac societies in individual countries within the European Union. [ 20 ] [ 22 ] Cardiac contractility modulation has proven to be effective and safe in randomized controlled trials involving several hundred patients. [ 23 ] [ 24 ] [ 25 ] The nature and extent of the effect of cardiac contractility modulation have been the subject of numerous investigations. Although various individual publications, as well as one of two meta-analyses, have presented the efficacy and significant potential of cardiac contractility modulation in the treatment of heart failure, medical evaluation of the therapy efficacy is not yet complete. Scientists point out, however, that this was also the case for CRT therapy when it was first introduced, advocating the provision of cardiac contractility modulation to suitable patients before further studies are completed. [ 3 ] [ 17 ] To date (February 2015), there are at least two meta-analyses studying the efficacy of cardiac contractility modulation therapy on heart failure, [ 2 ] [ 26 ] a large number of review articles (e.g. [ 3 ] [ 17 ] [ 18 ] [ 27 ] [ 28 ] ) and at least two survey articles on device-based treatments of advanced heart failure [ 1 ] [ 15 ] which address cardiac contractility modulation. Furthermore, there are more than 70 individual publications focusing specifically on cardiac contractility modulation therapy. [ 29 ] Further randomized controlled trials studying the effect of cardiac contractility modulation on the progression of heart failure have been initiated and are currently (as of February 2015) recruiting patients. [ 3 ] [ 14 ] [ 17 ] Giallauria et al. evaluated the three randomized controlled trials (RCTs) currently available on cardiac contractility modulation as a treatment for heart failure patients. [ 2 ] [ 23 ] [ 24 ] The three trials included a total of 641 patients and assessed the effect of cardiac contractility modulation either in comparison to a sham treatment [ 23 ] [ 24 ] or in comparison to the best medical treatment. [ 25 ] In contrast to an earlier meta-analysis by Kwong et al. [ 26 ] the study did not evaluate the data based on summarized results alone, but on the basis of the individual data sets of the 641 enrolled patients. The study concluded that cardiac contractility modulation significantly improved important markers of cardiac performance. These included the maximal oxygen uptake (peak VO2 or pVO2 – measured by ventilatory parameters during a cardiopulmonary exercise test), which is indicative of improved survival, [ 30 ] and the 6-minute walk test . The quality of life of participating patients, measured by the Minnesota Living with Heart Failure Questionnaire (MLWHFQ), also improved significantly. However, both meta-analyses demanded additional and larger randomized controlled trials in order to evaluate the effect of the therapy more precisely. [ citation needed ] Giallauria et al. describe the success of cardiac contractility modulation and the further potential of the therapy. Particular emphasis is given to the possibility that cardiac contractility modulation therapy may close the therapeutic gap in heart failure treatment if previous study outcomes are confirmed. [ citation needed ] As of February 2015, the effect of cardiac contractility modulation therapy on the long-term mortality rates of heart failure patients has not been studied in a randomized controlled trial. Some preliminary single-center studies have been reported though. [ 10 ] Kuschyk et al. evaluated the long-term efficacy and survival of patients with cardiac contractility modulation. [ 10 ] Their analysis included 81 patients with a disease severity of NYHA class II, III or IV and a mean follow-up of around 3 years. The analysis compared the observed mortality rate with the prediction of the Meta-analysis Global Group in Chronic Heart Failure (MAGGIC) model [ 31 ] [ 32 ] which is based on the records of over 39,000 heart failure patients. Unlike a previous long-term outcome study of cardiac contractility modulation, [ 33 ] this study was not limited by a widely heterogeneous group of patients. Following long-term observation, the study concluded that cardiac contractility modulation improved quality of life, exercise tolerance, NYHA class, left ventricular ejection fraction (LVEF) and brain natriuretic peptide (BNP) levels. Mortality rates were significantly lower than predicted at year 1, and lower than predicted but not statistically significant at year 3. [ citation needed ] Heart failure is a chronic disease that usually progresses gradually. [ 20 ] The rate of progression and the degree of symptoms of the disease varies between different patients. Cardiac contractility modulation therapy aims to treat heart failure through a medium- to long-term treatment, over the course of weeks and months. [ citation needed ] According to large implanting clinics, after the implantation wound is healed, the lifestyle of a patient is not restricted by the implanted device. [ 34 ] Leisure, travel (by car, train, ship or plane), hobbies and sex life will not be restricted. The patient may perceive an improved capacity for these activities and overall enhanced performance and exercise capacity in response to the actual therapy. [ citation needed ] In the past, the most important contraindication in cardiac contractility modulation treatment was permanent and long-standing persistent atrial fibrillation . The signal application in current cardiac contractility modulation devices was timed and triggered according to the electrical activity of the atrium . In atrial fibrillation, electrical activity in the atrium is severely disturbed and is therefore not a reliable basis for the triggering of cardiac contractility modulation signals. This also applies to other diseases involving severe disturbance in electrical atrial sensing. [ 35 ] Requests have been raised in scientific literature for an improved cardiac contractility modulation algorithm which would allow the therapy to be delivered independently from any atrial signal. A pioneering study had shown that an improved cardiac contractility modulation algorithm could make the therapy an effective treatment for patients with persistent atrial fibrillation. [ 35 ] Following these study results the new generation was developed and can now offer cardiac contractility modulation therapy also for patients with atrial fibrillation. [ citation needed ] Other irregular rhythms, including frequent premature ventricular contractions (ventricular extra systoles) or a distinct signal transduction disorder in the heart (untreated AV block of more than 300 ms), may represent contraindications. CRT treatment should be considered in lieu of cardiac contractility modulation in patients with left bundle branch block (LBBB) and a QRS duration of over 120 ms, or when the QRS duration is greater than 150 ms and independent of LBBB. [ 9 ] [ 20 ] As with conventional pacemaker therapy, the cardiac contractility modulation device cannot be implanted if the leads cannot be positioned appropriately in the heart. In cases where there is an artificial heart valve between the right atrium and ventricle (a mechanical prosthetic tricuspid valve), the valve function could be greatly affected by the ventricular leads. In some instances it may be impossible to guide the leads through the main veins in the upper half of the body to the heart due to venous thrombosis , for example VVI pacemakers , in the case of 100% stimulation, are also contraindicated. [ 9 ] The most frequently encountered adverse events related to cardiac contractility modulation therapy are lead fracture or lead dislodgement. [ 25 ] Other reported complications include: These side effects are similar to those that occur with other electrical stimulation therapies, such as pacemakers, CRT devices or ICD devices. [ 30 ] Furthermore, recorded complications did not differ between patients with activated or deactivated cardiac contractility modulation devices. [ 17 ] Overall, cardiac contractility modulation treatment was demonstrated to have no negative impact on health markers. [ 17 ] Similarly to patients with other electrical stimulation devices, patients with a cardiac contractility modulation device must follow certain precautions arising from the device implantation and its function. The mechanism of action of cardiac contractility modulation has been subject to continuous research since its initial discovery. Based on animal testing and experiments on human myocardial tissue obtained by biopsies , essential parts of the mechanism of action have been identified. [ 4 ] [ 39 ] According to current understanding (as of February 2015), the mechanism of action of cardiac contractility modulation may be summarized in the following manner: The signals applied during the electrical non-excitatory state of the cardiac muscle cells (the absolute refractory period) cause an increase in myocyte calcium in the cytosol during systole. This increases the muscle contraction strength. Additionally, within minutes, cell metabolism and gene expression , which are typically abnormal in heart failure, improve towards their normal state. [ 39 ] This beneficial effect occurs initially only in the area adjacent to the electrodes, but with time also spreads to remote areas of the cardiac muscle. [ 39 ] Cardiac contractility modulation therefore restores the structure and function of damaged cells back towards their normal state. In some cases, disease-related changes in the ventricular heart structure can be partially reversed by cardiac contractility modulation through a process known as reverse remodeling of the heart. [ 3 ] [ 4 ] [ 5 ] [ 18 ] [ 40 ] [ 41 ] Development of cardiac contractility modulation began in the late 1990s. [ 42 ] [ 43 ] Studies on individual cardiac muscle cells using a patch-clamp technique had already shown, in 1969, that a voltage applied during the absolute refractory period through leads between the interior of the cell and its outside environment increased the calcium influx through the cell membrane and improved the contraction of cardiac muscle cells. [ 44 ] [ 45 ] In 2001, scientists observed that a similar effect occurs even if the voltage is applied exclusively outside the cardiac muscle cells. [ 46 ] Additionally, it was observed that therapeutically useful effects on the cardiac muscle were achieved if the electrical signals were applied not only to single cells but to large areas using larger leads, as used in conventional cardiac pacemakers. The contractility of both a healthy heart and a damaged heart could be increased through application of appropriate signals during the absolute refractory period of the cardiac muscle cells. [ 47 ] [ 48 ] An implantable cardiac contractility modulation device was received by a patient for the first time in 2001. [ 49 ] [ 50 ] The first study on the therapeutic effects of in humans was presented in 2004. [ 51 ] To date, more than 3,000 heart failure patients have been treated with cardiac contractility modulation worldwide, [ 13 ] including 641 patients under the study conditions recommended by the Cochrane Collaboration as being necessary for inclusion in a meta-analysis. [ 2 ] Cardiac contractility modulation device implantation was first successfully done in India in Royal Hospital, Trivandrum, Kerala, under the leadership of Dr. C. Bharath Chandran. Advocate Harishankar was the first person in India to get the cardiac contractility modulation device implanted.	https://en.wikipedia.org/wiki/Cardiac_contractility_modulation
Cardiac electrophysiology is a branch of cardiology and basic science focusing on the electrical activities of the heart . The term is usually used in clinical context, to describe studies of such phenomena by invasive (intracardiac) catheter recording of spontaneous activity as well as of cardiac responses to programmed electrical stimulation - clinical cardiac electrophysiology . However, cardiac electrophysiology also encompasses basic research and translational research components. Specialists studying cardiac electrophysiology, either clinically or solely through research, are known as cardiac electrophysiologists. Electrophysiological (EP) studies are performed to assess complex arrhythmias , elucidate symptoms, evaluate abnormal electrocardiograms , assess risk of developing arrhythmias in the future, and design treatment. These procedures include therapeutic methods (typically radiofrequency ablation , or cryoablation ) in addition to diagnostic and prognostic procedures. Other therapeutic modalities used in this field include antiarrhythmic drug therapy and implantation of pacemakers , implantable cardioverter-defibrillators and cardiac resynchronisation therapy devices. [ 1 ] [ 2 ] The cardiac electrophysiology (EP) study typically measures the response of myocardium to programmed electrical stimulation (PES) on specific pharmacological regimens in order to assess the likelihood that the regimen will successfully prevent potentially fatal sustained ventricular tachycardia (VT) or ventricular fibrillation VF (VF) in the future. Sometimes a series of EP study drug trials must be conducted to enable the cardiologist to select the one regimen for long-term treatment that best prevents or slows the development of VT or VF following PES. Such studies may also be conducted in the presence of a newly implanted or newly replaced cardiac pacemaker or ICD. [ 1 ] A specialist in cardiac electrophysiology is known as an electrophysiologist, or "heart electrician" in layman' terms. Cardiac electrophysiology is a subspecialty of cardiology in most countries and usually requires two or more years of EP fellowship training after a general cardiology residency. In early 2011, the Centers for Medicare and Medicaid Services promoted cardiac electrophysiology to its own specialty category in the United States. Cardiac electrophysiologists are trained to perform interventional cardiac electrophysiology studies and cardiac rhythm management device implantations. [ 1 ] Cardiac electrophysiologists specialize in a sub-area of electrophysiology , which in turn is a sub-area of physiology . This specialization usually requires education at the doctoral (PhD, DSc, or MD/DO) level to become a principal investigator for research projects. The area of research is often multi-disciplinary involving chemistry, bioelectrics, biology, and biomedical engineering. The flagship tools used by cardiac electrophysiologists overlap with the toolbox of the neuroscientist including patch clamp and optical mapping . [ 3 ] Mapping specialists (EP techs, EP physiologists) are typically educated up to the Bachelor's or Master's level and are employed by either a cardiac electrophysiology company or department. Often international certification such as Certified Electrophysiology Specialist (CEPS) by the International Board of Heart Rhythm Examiners (IBHRE) or EHRA Certified Electrophysiology Specialist (ECES) or equivalent is required. Cardiac electrophysiology is a relatively young subdiscipline of cardiology and internal medicine. It was developed during the mid-1970s by Hein J. J. Wellens , professor of medicine at the University of Maastricht in the Netherlands and attending cardiologist at the Academic Hospital in Maastricht . In 1980 the first microprocessor based stimulator was developed there. The author of the definitive textbook in the field is by the late Mark E. Josephson , former Robinette Professor of Medicine and chief of cardiology at the University of Pennsylvania School of Medicine in Philadelphia, Pennsylvania , professor of medicine at Harvard Medical School , and attending cardiologist at Beth Israel Deaconess Medical Center in Boston, Massachusetts . [ 4 ] The most recent published edition of Clinical Cardiac Electrophysiology: Techniques and Interpretations is the 6th edition in 2020. [ 5 ] The Heart Rhythm Society , founded in 1979, promotes education and advocacy for cardiac arrhythmia professionals (including cardiac electrophysiologists) and patients. European Heart Rhythm Association, a part of European Society of Cardiology , is active in Europe. [ 6 ] Founded in 1985 as NASPExAM, the International Board of Heart Rhythm Examiners (IBHRE) offers knowledge based board exams for physicians and allied health professionals working in the field of cardiac electrophysiology and cardiac rhythm device management. [ 7 ] European Heart Rhythm Association (EHRA) provides knowledge and practical competency based certification to physicians and allied health professionals [ 8 ] as well as accreditation of cardiac electrophysiology training centres [ 9 ] in Europe and neighbouring countries. Electroanatomic mapping uses electric and magnetic fields to create three dimensional models of heart structures using specialized catheters.	https://en.wikipedia.org/wiki/Cardiac_electrophysiology
In medicine , the cardiac examination , also precordial exam , is performed as part of a physical examination , or when a patient presents with chest pain suggestive of a cardiovascular pathology . It would typically be modified depending on the indication and integrated with other examinations especially the respiratory examination . [ 1 ] Like all medical examinations, the cardiac examination follows the standard structure of inspection, palpation and auscultation. The patient is positioned in the supine position tilted up at 45 degrees if the patient can tolerate this. The head should rest on a pillow and the arms by their sides. The level of the jugular venous pressure (JVP) should only be commented on in this position as flatter or steeper angles lead to artificially elevated or reduced level respectively. Also, left ventricular failure leads to pulmonary edema which increases and may impede breathing if the patient is laid flat. Lighting should be adjusted so that it is not obscured by the examiner who will approach from the right hand side of the patient as is medical custom. The torso and neck should be fully exposed and access should be available to the legs. General Inspection: Inspect the hands for: Inspect the head for: Then inspect the precordium for: The pulses should be palpated, first the radial pulse commenting on rate and rhythm then the brachial pulse commenting on character and finally the carotid pulse again for character. The pulses may be: The valve areas are palpated for abnormal pulsations (palpable heart murmurs known as thrills ) and precordial movements (known as heaves ). Heaves are best felt with the heel of the hand at the sternal border. The apex beat is found approximately in the fifth left intercostal space in the mid-clavicular line . It can be impalpable for a variety of reasons including obesity , emphysema , effusion and rarely dextrocardia . The apex beat is assessed for size, amplitude, location, impulse and duration. There are specific terms to describe the sensation such as tapping, heaving and thrusting. Often the apex beat is felt diffusely over a large area, in this case the most inferior and lateral position it can be felt in should be described as well as the location of the largest amplitude. Finally the sacrum and ankles are checked for pitting edema which is caused by right ventricular failure in isolation or as part of congestive cardiac failure . One should comment on To complete the exam blood pressure should be checked, an ECG recorded, funduscopy performed to assess for Roth spots or papilledema . A full peripheral circulation exam should be performed.	https://en.wikipedia.org/wiki/Cardiac_examination
Cardiac excitation-contraction coupling ( Cardiac EC coupling ) describes the series of events, from the production of an electrical impulse (action potential) to the contraction of muscles in the heart . [ 1 ] This process is of vital importance as it allows for the heart to beat in a controlled manner, without the need for conscious input. EC coupling results in the sequential contraction of the heart muscles that allows blood to be pumped, first to the lungs ( pulmonary circulation ) and then around the rest of the body ( systemic circulation ) at a rate between 60 and 100 beats every minute, when the body is at rest. [ 2 ] This rate can be altered, however, by nerves that work to either increase heart rate ( sympathetic nerves ) or decrease it ( parasympathetic nerves ), as the body's oxygen demands change. Ultimately, muscle contraction revolves around a charged atom (ion) , calcium (Ca 2+ ) , [ 3 ] which is responsible for converting the electrical energy of the action potential into mechanical energy (contraction) of the muscle. This is achieved in a region of the muscle cell, called the transverse tubule during a process known as calcium induced calcium release . [ 4 ] Located in the wall of the right atrium is a group of specialised cells, called the Sinoatrial node (SAN) . These cells, unlike most other cells within the heart , can spontaneously produce action potentials . [ 5 ] These action potentials travel along the cell membrane (sarcolemma) , as impulses, passing from one cell to the next through channels, in structures known as gap junctions . [ 6 ] Certain regions of the sarcolemma penetrate deep into the cell . These are known as transverse-tubules (t-tubules) , which are also found in skeletal muscle cells and allow for the action potential to travel into the centre of the cell. [ 7 ] Special proteins called L-type calcium channels (also known as dihydropyridine receptors (DHPR)) are located on the t-tubule membrane and are activated by the action potential. Activated DHPRs open, forming a channel that allows Ca 2+ to pass into the cell. This increase in Ca 2+ then binds to and activates another receptor , called a type 2 ryanodine receptor (RyR2) , located on the membrane of a structure known as the sarcoplasmic reticulum (SR) . The sarcoplasmic reticulum is a Ca 2+ storehouse within the cell and is located very close to the T-tubule. Activation of RyR2 causes it to open, releasing even more Ca 2+ into the cell . This release of calcium is called a calcium spark . The initial flow of Ca 2+ into the cell causes a larger release of Ca 2+ within the cell , so therefore the process is called calcium induced calcium release (CICR) . [ 8 ] The increase in Ca 2+ , produced by CICR, now does two things. Firstly, it binds to the intracellular side of the DHPR, signalling the channels to close and preventing further influx of Ca 2+ into the cell. Secondly Ca 2+ indirectly activates proteins , called myofilaments , resulting in muscle contraction . The two main myofilaments in cardiac (and skeletal ) muscle are actin and myosin . Ca 2+ binds to a protein called troponin , which is bound to the actin filament. This binding causes a shape change in the troponin which exposes areas on the actin , to which the head of the myosin filament binds. The binding of the myosin head to actin is known as a cross-bridge. A molecule , called adenosine triphosphate (ATP) which is produced by an intracellular structure called a mitochondrion , is then used, as a source of energy, to help move the myosin head, carrying the actin. As a result, the actin slides across the myosin filament shortening the muscle. This is called a power stroke. Myosin then detaches from the actin and resets itself back to its original position, binding to another part of the actin and producing another power stroke, shortening the muscle further. This process continues, with the myosin head moving in a motion similar to that of an oar rowing a boat, until the Ca 2+ level within the cell decreases (see figure 1). [ 9 ] Contraction ends when the Ca 2+ is removed from the cell. When this happens, the troponin changes back to its original shape, blocking the binding sites on actin and preventing the formation of crossbridges. This decrease in Ca 2+ within the cell is brought about by a variety of proteins , known collectively as ion transporters . The main pumps involved are: the sarcoplasmic reticulum Ca 2+ -ATPase , which pumps Ca 2+ back into the SR, the Sarcolemmal sodium-calcium exchanger , which pumps one Ca 2+ out of the cell, in exchange for 3 sodium ions being pumped into the cell, the Sarcolemmal Ca 2+ -ATPase , which uses ATP to pump Ca 2+ directly out of the cell and the Mitochondrial Ca 2+ Uniport system , which pumps Ca 2+ into the mitochondria. [ 10 ] Sympathetic nerves work by releasing a protein ( neurotransmitter ) called noradrenaline which binds to a specific receptor ( beta 1 adrenoceptor ) located in the sarcolemma and the t-tubule membrane of cardiac cells . This activates a protein, called a G-protein and results in a series of reactions (known as a cyclic AMP pathway ) that leads to the production of a molecule called cAMP ( cyclic adenosine monophosphate ). In the SAN cAMP binds to an ion channel involved in action potential initiation, speeding up the production of the action potential (see sinoatrial node for more detail). cAMP also, activates a protein called protein kinase A ( PKA ). PKA affects both the L-type calcium channels (also known as dihydropyridine receptors (DHPR)) and RyR , increasing the rise in Ca 2+ within the contractile cells and therefore increasing rate of muscle contraction . PKA also affects the myofilaments as well as a protein called phospholamban (PLB; see sarcoplasmic reticulum for more details), speeding up the rate of Ca 2+ decline in the cell and so speeding up muscle relaxation . [ 2 ] Parasympathetic nerves work by releasing a neurotransmitter called acetylcholine (ACh) which binds to specific receptor ( M2 muscarinic receptor ) on the sarcolemma of both SAN cells and ventricular cells. This again activates a G-protein . However this G-protein works by inhibiting, the cAMP pathway, therefore, preventing the sympathetic nervous system from increasing heart rate. As well as this, in the SAN, the G-protein activates specific potassium channel, that opposes action potential initiation (see SAN for more details), thus slowing heart rate. [ 2 ]	https://en.wikipedia.org/wiki/Cardiac_excitation-contraction_coupling
Cardiac magnetic resonance imaging perfusion ( cardiac MRI perfusion , CMRI perfusion ), also known as stress CMR perfusion , [ 1 ] is a clinical magnetic resonance imaging test performed on patients with known or suspected coronary artery disease to determine if there are perfusion defects in the myocardium of the left ventricle that are caused by narrowing of one or more of the coronary arteries . CMR perfusion is increasingly used in cardiac imaging to test for inducible myocardial ischaemia and has been well validated against other imaging modalities such as invasive angiography [ 2 ] [ 3 ] or FFR. Several recent large-scale studies have shown non-inferiority or superiority to SPECT imaging. It is becoming increasingly established as a marker of prognosis in patients with coronary artery disease. [ 4 ] [ 5 ] There are two main reasons for doing this test: [ citation needed ] In contrast to the nuclear imaging modalities ( PET and SPECT ), CMR perfusion does not involve the use of ionising radiation and can therefore be used multiple times without the risk to the patient of exposure to radiation. [ citation needed ] It is a non-invasive test, is generally regarded as a safe (see below) procedure and is well tolerated by patients (apart from people with claustrophobia) [ citation needed ] The majority of scans are performed using a stress/rest protocol using adenosine as the stressor which acts to induce ischaemia in the myocardium by the coronary 'steal' phenomenon. Some centers use inotrope dobutamine to stress the heart and the images are interpreted in a similar fashion to dobutamine stress echocardiogram . This article concentrates on adenosine stress scans. [ citation needed ] An intravenous infusion of adenosine is given at 140 μg/Kg/min for 3 minutes with continuous heart rate and blood pressure recording to induce hyperaemia (normally seen as a drop in systolic blood pressure of 10mmHg or a rise in heart rate of 10bpm). Following this, an intravenous bolus of 0.05 mmol/kg of a gadolinium chelate (such as gadodoteric acid) is administered via an antecubital fossa vein on the contralateral arm to the adenosine. [ citation needed ] Typically, 3 short axis slices, each of 10mm thickness, are acquired per cardiac cycle, at the basal, mid papillary and apical levels of the left ventricle. A single shot prospectively gated, balanced TFE sequence is used with a typical resolution of 2.5 x 2.5mm. The patient is then allowed to rest until the haemodynamic effects of the adenosine have stopped (typically 5 minutes). The same scan protocol is then performed at rest. [ citation needed ] The images are stored as video files and are analysed on a dedicated workstation. The majority of clinical scans are analysed qualitatively by visually comparing the stress and rest scans in parallel. In a normal scan, the wash in (1st pass) of gadolinium into the myocardium can be seen as the myocardium turning from black to mid grey uniformly throughout the whole of the left ventricle in both the stress and rest scans. In an abnormal scan an area of the myocardium will turn grey slower than the surrounding tissue as the blood (and hence gadolinium) enters more slowly due to a narrowing of the coronary artery supplying it. This is called a perfusion defect and usually represents myocardial ischaemia. It may be seen on both the rest and stress scans in which case it is called a matched perfusion defect and is probably due to an area or scar from a previous myocardial infarction. If it is only seen on the stress scan it is called an area of inducible perfusion defect (ischaemia). The position in the left ventricle of the perfusion defects are described using the AHA 17 segment model. [ 6 ] Stress CMR cannot be performed on all patients due to the relative or absolute contraindications listed below, this is a problem, especially in patients who either have a pacemaker or severe renal failure. [ citation needed ] The acquisition of the images is very sensitive to the rhythm of the heart and scans of patients with atrial fibrillation, bigeminy or trigeminy will sometimes be of low quality and may not be interpretable. [ citation needed ] Due to the high contrast between the blood pool and the myocardium it is common to get what looks like a thin subendocardial area of ischaemia called the Gibbs artifact , this however, is less common with newer technology allowing higher resolution imaging. [ citation needed ] In patients who have had a previous myocardial infarction or previous coronary artery bypass surgery, the images may be very difficult to interpret and in such cases, the analysis of the scans is performed with the complement of another imaging modality (such as coronary angiography). [ citation needed ] It is a non-invasive test as is generally regarded as safe however, there are some patients for whom this is contraindicated and there are a number of potential complications: [ citation needed ] Contraindications are as follows: [ citation needed ] It is common for the patient to get a number of mild symptoms when they are given the Adenosine infusion, such as feeling hot and sweaty, short of breath, nauseous and noticing that their heart is beating faster. These, if they occur, resolve rapidly (normally within 60 seconds) after the Adensoine infusion has stopped. [ citation needed ] There are a number of more serious and much less common side effects, including transient heart block, bronchoconstriction and a 1 in 10,000 risk of anaphylaxis caused by the gadolinium contrast agent. These can invariably be successfully treated with no long term side effects. [ citation needed ] Adenosine infusion is associated with some very rare but very serious side effects, including acute pulmonary oedema and cardiac arrest (occurring in ≈1 in 1000 patients). [ citation needed ]	https://en.wikipedia.org/wiki/Cardiac_magnetic_resonance_imaging_perfusion
Cardiac monitoring generally refers to continuous or intermittent monitoring of heart activity to assess a patient's condition relative to their cardiac rhythm . Cardiac monitoring is usually carried out using electrocardiography , which is a noninvasive process that records the heart's electrical activity and displays it in an electrocardiogram. [ 1 ] It is different from hemodynamic monitoring, which monitors the pressure and flow of blood within the cardiovascular system . The two may be performed simultaneously on critical heart patients. Cardiac monitoring for ambulatory patients (those well enough to walk around) is known as ambulatory electrocardiography and uses a small, wearable device, such as a Holter monitor , wireless ambulatory ECG , or an implantable loop recorder . Data from a cardiac monitor can be transmitted to a distant monitoring station in a process known as telemetry or biotelemetry . Cardiac monitoring in an emergency department setting focuses primarily on the monitoring of arrhythmia , myocardial infarction , and QT interval monitoring. [ 2 ] It is categorized into one of three classes using a rating system developed by the American College of Cardiology Emergency Cardiac Care Committee: In the setting of out-of-hospital acute medical care , ambulance services and other emergency medical services providers utilize heart monitors to assess the patient's cardiac rhythm. Providers licensed or certified at the Paramedic level are qualified to interpret ECGs. Information obtained from ECGs can then be used to direct the patient's treatment at a care facility, particularly in catheterization labs. [ 4 ] In the emergency department , cardiac monitoring is a part of the monitoring of vital signs in emergency medicine , and generally includes electrocardiography . [ 2 ] Some digital patient monitors, especially those used by EMS services, often incorporate a defibrillator into the patient monitor itself. These monitor/defibrillators usually have the normal capabilities of an ICU monitor, but have manual (and usually semi-automatic AED) defibrillation capabilities. This is particularly good for EMS services, who need a compact, easy to use monitor and defibrillator, as well as for patient transport. Most monitor defibrillators also have transcutaneous pacing capability via large AED like adhesive pads (which often can be used for monitoring, defibrillation and pacing) that are applied to the patient in an anterior-posterior configuration. The monitor defibrillator units often have specialized monitoring parameters such as waveform capnography, invasive BP, and, in some monitors, Masimo Rainbow SET pulse oximetry, which can also monitor carbon monoxide and methemoglobin levels. Most modern monitors also allow for transmission of an ECG sample to an emergency department for interpretation; this process may be used to speed up patient care in certain situations, such as bypassing the ED and proceeding to a cath lab . Examples of monitor defibrillators are the Lifepak 12, 15 and 20 made by Physio-Control , the Philips Heartstart MRx, and the E, R, and X Series by ZOLL Medical. There are two broad classifications for cardiac event monitors: manual (or dumb) and automatic. Automatic ECG event monitors have the ability to monitor the patient's ECG and make recordings of abnormal events without requiring patient intervention. Manual ECG event recorders require the patient to be symptomatic and to activate the device to record an event; this makes these devices useless whilst, for example, the patient is sleeping. A third classification, the implantable loop recorder , provides both automatic and manual abilities. An example of automatic monitoring is the transtelephonic cardiac event monitor. This monitor contacts ECG technicians, via telephone, on a regular basis, transmitting ECG rhythms for ongoing monitoring. The transtelephonic cardiac event monitor can normally store approximately five "cardiac events" usually lasting 30–60 seconds. Monitoring of the heart rate can be performed as part of electrocardiography , but it can also be measured conveniently with specific heart rate monitors . Such heart rate monitors are largely used by performers of various types of physical exercise . A generic cardiac monitor has the following functions: There are many different types of cardiac monitors. In personal use, the Holter monitor is an external monitor which uses wires with patches that attach to the skin to continuously measure and record heart activity for 1–2 days. [ 5 ] An Event Recorder can be worn on the body for up to 30 days. [ 6 ] A Mobile Cardiac Telemetry unit is a wearable monitor that detects, records, and transmits heart rhythms for up to 30 days. For long term use, an Insertable Cardiac Monitor is placed under the skin and automatically detects and records abnormal heart rhythms for up to 5 years. [ 7 ] Monitoring the fetal heart rate is becoming increasingly prevalent in the standard care of antepartum pregnant patients. [ 8 ] As of 2002, 85% of pregnancies in the United States were monitored using electronic fetal monitoring. Electronic fetal monitoring generally uses Doppler ultrasound technology to provide real-time feedback on the fetus's cardiac activity during both gestation and labor, [ 9 ] however other technologies such as analyzing the voltage generated by the contracting uterine muscle measured at the skin surface or recording both the fetal ECG and mother's ECG and filtering out the mother's ECG are emerging. [ 10 ] The new wearable heart rate monitors indirectly measure the heart rate with reflectance photoplethysmography. The monitor illuminates the skin tissue with light emitting diode (LED) and detects the intensity of light reflected with the photodetector. [ 11 ] Wearable optical heart rate monitors are less reliable than electrode-based heart rate monitors. The accuracy of the wearable optical heart rate monitors varies with the type of exercise. Skin tone and motion artifacts contributes to this error. [ 11 ] [ 12 ]	https://en.wikipedia.org/wiki/Cardiac_monitoring
Cardiac muscle (also called heart muscle or myocardium ) is one of three types of vertebrate muscle tissues , the others being skeletal muscle and smooth muscle . It is an involuntary, striated muscle that constitutes the main tissue of the wall of the heart . The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall (the pericardium ) and the inner layer (the endocardium ), with blood supplied via the coronary circulation . It is composed of individual cardiac muscle cells joined by intercalated discs , and encased by collagen fibers and other substances that form the extracellular matrix . Cardiac muscle contracts in a similar manner to skeletal muscle , although with some important differences. Electrical stimulation in the form of a cardiac action potential triggers the release of calcium from the cell's internal calcium store, the sarcoplasmic reticulum . The rise in calcium causes the cell's myofilaments to slide past each other in a process called excitation-contraction coupling . Diseases of the heart muscle known as cardiomyopathies are of major importance. These include ischemic conditions caused by a restricted blood supply to the muscle such as angina , and myocardial infarction . Cardiac muscle tissue or myocardium forms the bulk of the heart. The heart wall is a three-layered structure with a thick layer of myocardium sandwiched between the inner endocardium and the outer epicardium (also known as the visceral pericardium). The inner endocardium lines the cardiac chambers, covers the cardiac valves , and joins with the endothelium that lines the blood vessels that connect to the heart. On the outer aspect of the myocardium is the epicardium which forms part of the pericardial sac that surrounds, protects, and lubricates the heart. [ 1 ] Within the myocardium, there are several sheets of cardiac muscle cells or cardiomyocytes. The sheets of muscle that wrap around the left ventricle closest to the endocardium are oriented perpendicularly to those closest to the epicardium. When these sheets contract in a coordinated manner they allow the ventricle to squeeze in several directions simultaneously – longitudinally (becoming shorter from apex to base), radially (becoming narrower from side to side), and with a twisting motion (similar to wringing out a damp cloth) to squeeze the maximum possible amount of blood out of the heart with each heartbeat. [ 2 ] Contracting heart muscle uses a lot of energy, and therefore requires a constant flow of blood to provide oxygen and nutrients. Blood is brought to the myocardium by the coronary arteries . These originate from the aortic root and lie on the outer or epicardial surface of the heart. Blood is then drained away by the coronary veins into the right atrium . [ 1 ] Cardiac muscle cells (also called cardiomyocytes) are the contractile myocytes of the cardiac muscle. The cells are surrounded by an extracellular matrix produced by supporting fibroblast cells . Specialised modified cardiomyocytes known as pacemaker cells , set the rhythm of the heart contractions. The pacemaker cells are only weakly contractile without sarcomeres, and are connected to neighboring contractile cells via gap junctions . [ 3 ] They are located in the sinoatrial node (the primary pacemaker) positioned on the wall of the right atrium , near the entrance of the superior vena cava . [ 4 ] Other pacemaker cells are found in the atrioventricular node (secondary pacemaker). Pacemaker cells carry the impulses that are responsible for the beating of the heart. They are distributed throughout the heart and are responsible for several functions. First, they are responsible for being able to spontaneously generate and send out electrical impulses . They also must be able to receive and respond to electrical impulses from the brain. Lastly, they must be able to transfer electrical impulses from cell to cell. [ 5 ] Pacemaker cells in the sinoatrial node, and atrioventricular node are smaller and conduct at a relatively slow rate between the cells. Specialized conductive cells in the bundle of His , and the Purkinje fibers are larger in diameter and conduct signals at a fast rate. [ 6 ] The Purkinje fibers rapidly conduct electrical signals; coronary arteries to bring nutrients to the muscle cells, and veins and a capillary network to take away waste products. [ 7 ] Cardiac muscle cells are the contracting cells that allow the heart to pump. Each cardiomyocyte needs to contract in coordination with its neighboring cells - known as a functional syncytium - working to efficiently pump blood from the heart, and if this coordination breaks down then – despite individual cells contracting – the heart may not pump at all, such as may occur during abnormal heart rhythms such as ventricular fibrillation . [ 8 ] Viewed through a microscope, cardiac muscle cells are roughly rectangular, measuring 100–150μm by 30–40μm. [ 9 ] Individual cardiac muscle cells are joined at their ends by intercalated discs to form long fibers. Each cell contains myofibrils , specialized protein contractile fibers of actin and myosin that slide past each other. These are organized into sarcomeres , the fundamental contractile units of muscle cells. The regular organization of myofibrils into sarcomeres gives cardiac muscle cells a striped or striated appearance when looked at through a microscope, similar to skeletal muscle. These striations are caused by lighter I bands composed mainly of actin, and darker A bands composed mainly of myosin. [ 7 ] Cardiomyocytes contain T-tubules , pouches of cell membrane that run from the cell surface to the cell's interior which help to improve the efficiency of contraction. The majority of these cells contain only one nucleus (some may have two central nuclei), unlike skeletal muscle cells which contain many nuclei . Cardiac muscle cells contain many mitochondria which provide the energy needed for the cell in the form of adenosine triphosphate (ATP), making them highly resistant to fatigue. [ 9 ] [ 7 ] T-tubules are microscopic tubes that run from the cell surface to deep within the cell. They are continuous with the cell membrane, are composed of the same phospholipid bilayer , and are open at the cell surface to the extracellular fluid that surrounds the cell. T-tubules in cardiac muscle are bigger and wider than those in skeletal muscle , but fewer in number. [ 9 ] In the centre of the cell they join, running into and along the cell as a transverse-axial network. Inside the cell they lie close to the cell's internal calcium store, the sarcoplasmic reticulum . Here, a single tubule pairs with part of the sarcoplasmic reticulum, called a terminal cisterna, in a combination known as a diad . [ 10 ] The functions of T-tubules include rapidly transmitting electrical impulses known as action potentials from the cell surface to the cell's core, and helping to regulate the concentration of calcium within the cell in a process known as excitation-contraction coupling . [ 9 ] They are also involved in mechano-electric feedback, [ 11 ] as evident from cell contraction induced T-tubular content exchange (advection-assisted diffusion), [ 12 ] which was confirmed by confocal and 3D electron tomography observations. [ 13 ] The cardiac syncytium is a network of cardiomyocytes connected by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an atrial syncytium and a ventricular syncytium that are connected by cardiac connection fibres. [ 14 ] Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncytium obeys the all or none law . [ 15 ] Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during embryonic development ). The discs are responsible mainly for force transmission during muscle contraction. Intercalated discs consist of three different types of cell-cell junctions: the actin filament anchoring fascia adherens junctions , the intermediate filament anchoring desmosomes , and gap junctions . [ 16 ] They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. The three types of junction act together as a single area composita . [ 16 ] [ 17 ] [ 18 ] [ 19 ] Under light microscopy , intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section. [ 20 ] Cardiac fibroblasts are vital supporting cells within cardiac muscle. They are unable to provide forceful contractions like cardiomyocytes , but instead are largely responsible for creating and maintaining the extracellular matrix which surrounds the cardiomyocytes. [ 7 ] Fibroblasts play a crucial role in responding to injury, such as a myocardial infarction . Following injury, fibroblasts can become activated and turn into myofibroblasts – cells which exhibit behaviour somewhere between a fibroblast (generating extracellular matrix) and a smooth muscle cell (ability to contract). In this capacity, fibroblasts can repair an injury by creating collagen while gently contracting to pull the edges of the injured area together. [ 21 ] Fibroblasts are smaller but more numerous than cardiomyocytes, and several fibroblasts can be attached to a cardiomyocyte at once. When attached to a cardiomyocyte they can influence the electrical currents passing across the muscle cell's surface membrane, and in the context are referred to as being electrically coupled, [ 22 ] as originally shown in vitro in the 1960s, [ 23 ] and ultimately confirmed in native cardiac tissue with the help of optogenetic techniques. [ 24 ] Other potential roles for fibroblasts include electrical insulation of the cardiac conduction system , and the ability to transform into other cell types including cardiomyocytes and adipocytes . [ 21 ] The extracellular matrix (ECM) surrounds the cardiomyocyte and fibroblasts. The ECM is composed of proteins including collagen and elastin along with polysaccharides (sugar chains) known as glycosaminoglycans . [ 7 ] Together, these substances give support and strength to the muscle cells, create elasticity in cardiac muscle, and keep the muscle cells hydrated by binding water molecules. [ citation needed ] The matrix in immediate contact with the muscle cells is referred to as the basement membrane , mainly composed of type IV collagen and laminin . Cardiomyocytes are linked to the basement membrane via specialised glycoproteins called integrins . [ 25 ] Humans are born with a set number of heart muscle cells, or cardiomyocytes, which increase in size as the heart grows larger during childhood development. Evidence suggests that cardiomyocytes are slowly turned over during aging, but less than 50% of the cardiomyocytes present at birth are replaced during a normal life span. [ 26 ] The growth of individual cardiomyocytes not only occurs during normal heart development, it also occurs in response to extensive exercise ( athletic heart syndrome ), heart disease, or heart muscle injury such as after a myocardial infarction. A healthy adult cardiomyocyte has a cylindrical shape that is approximately 100μm long and 10–25μm in diameter. Cardiomyocyte hypertrophy occurs through sarcomerogenesis, the creation of new sarcomere units in the cell. During heart volume overload, cardiomyocytes grow through eccentric hypertrophy. [ 27 ] The cardiomyocytes extend lengthwise but have the same diameter, resulting in ventricular dilation. During heart pressure overload, cardiomyocytes grow through concentric hypertrophy. [ 27 ] The cardiomyocytes grow larger in diameter but have the same length, resulting in heart wall thickening. The physiology of cardiac muscle shares many similarities with that of skeletal muscle . The primary function of both muscle types is to contract, and in both cases, a contraction begins with a characteristic flow of ions across the cell membrane known as an action potential . The cardiac action potential subsequently triggers muscle contraction by increasing the concentration of calcium within the cytosol. The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole , following a period of robust contraction and pumping of blood, dubbed systole . After emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. A normally performing heart must be fully expanded before it can efficiently pump again. The rest phase is considered polarized. The resting potential during this phase of the beat separates the ions such as sodium, potassium, and calcium. Myocardial cells possess the property of automaticity or spontaneous depolarization . This is the direct result of a membrane which allows sodium ions to slowly enter the cell until the threshold is reached for depolarization. Calcium ions follow and extend the depolarization even further. Once calcium stops moving inward, potassium ions move out slowly to produce repolarization. The very slow repolarization of the CMC membrane is responsible for the long refractory period. [ 28 ] [ 29 ] However, the mechanism by which calcium concentrations within the cytosol rise differ between skeletal and cardiac muscle. In cardiac muscle, the action potential comprises an inward flow of both sodium and calcium ions. The flow of sodium ions is rapid but very short-lived, while the flow of calcium is sustained and gives the plateau phase characteristic of cardiac muscle action potentials. The comparatively small flow of calcium through the L-type calcium channels triggers a much larger release of calcium from the sarcoplasmic reticulum in a phenomenon known as calcium-induced calcium release . In contrast, in skeletal muscle, minimal calcium flows into the cell during action potential and instead the sarcoplasmic reticulum in these cells is directly coupled to the surface membrane. This difference can be illustrated by the observation that cardiac muscle fibers require calcium to be present in the solution surrounding the cell to contract, while skeletal muscle fibers will contract without extracellular calcium. During contraction of a cardiac muscle cell, the long protein myofilaments oriented along the length of the cell slide over each other in what is known as the sliding filament theory . There are two kinds of myofilaments, thick filaments composed of the protein myosin , and thin filaments composed of the proteins actin , troponin and tropomyosin . As the thick and thin filaments slide past each other the cell becomes shorter and fatter. In a mechanism known as cross-bridge cycling , calcium ions bind to the protein troponin, which along with tropomyosin then uncover key binding sites on actin. Myosin, in the thick filament, can then bind to actin, pulling the thick filaments along the thin filaments. When the concentration of calcium within the cell falls, troponin and tropomyosin once again cover the binding sites on actin, causing the cell to relax. It was commonly believed that cardiac muscle cells could not be regenerated. However, this was contradicted by a report published in 2009. [ 30 ] Olaf Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. By using DNA samples from many hearts, the researchers estimated that a 4-year-old renews about 20% of heart muscle cells per year, and about 69% of the heart muscle cells of a 50-year-old were generated after they were born. [ 30 ] One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process. [ 31 ] In the 2000s, the discovery of adult endogenous cardiac stem cells was reported, and studies were published that claimed that various stem cell lineages, including bone marrow stem cells were able to differentiate into cardiomyocytes, and could be used to treat heart failure . [ 32 ] [ 33 ] However, other teams were unable to replicate these findings, and many of the original studies were later retracted for scientific fraud. [ 34 ] [ 35 ] Cardiac muscle forms both the atria and the ventricles of the heart. Although this muscle tissue is very similar between cardiac chambers, some differences exist. The myocardium found in the ventricles is thick to allow forceful contractions, while the myocardium in the atria is much thinner. The individual myocytes that make up the myocardium also differ between cardiac chambers. Ventricular cardiomyocytes are longer and wider, with a denser T-tubule network. Although the fundamental mechanisms of calcium handling are similar between ventricular and atrial cardiomyocytes, the calcium transient is smaller and decays more rapidly in atrial myocytes, with a corresponding increase in calcium buffering capacity. [ 36 ] The complement of ion channels differs between chambers, leading to longer action potential durations and effective refractory periods in the ventricles. Certain ion currents such as I K(UR) are highly specific to atrial cardiomyocytes, making them a potential target for treatments for atrial fibrillation . [ 37 ] Diseases affecting cardiac muscle, known as cardiomyopathies , are the leading cause of death in developed countries . [ 38 ] The most common condition is coronary artery disease , in which the blood supply to the heart is reduced . The coronary arteries become narrowed by the formation of atherosclerotic plaques . [ 39 ] If these narrowings become severe enough to partially restrict blood flow, the syndrome of angina pectoris may occur. [ 39 ] This typically causes chest pain during exertion that is relieved by rest. If a coronary artery suddenly becomes very narrowed or completely blocked, interrupting or severely reducing blood flow through the vessel, a myocardial infarction or heart attack occurs. [ 40 ] If the blockage is not relieved promptly by medication , percutaneous coronary intervention , or surgery , then a heart muscle region may become permanently scarred and damaged. [ 41 ] Specific cardiomyopathies include: increased left ventricular mass ( hypertrophic cardiomyopathy ), [ 42 ] abnormally large ( dilated cardiomyopathy ), [ 43 ] or abnormally stiff ( restrictive cardiomyopathy ). [ 44 ] Some of these conditions are caused by genetic mutations and can be inherited. [ 45 ] Heart muscle can also become damaged despite a normal blood supply. The heart muscle may become inflamed in a condition called myocarditis , [ 46 ] most commonly caused by a viral infection [ 47 ] but sometimes caused by the body's own immune system . [ 48 ] Heart muscle can also be damaged by drugs such as alcohol, long standing high blood pressure or hypertension , or persistent abnormal heart racing . [ 49 ] Many of these conditions, if severe enough, can damage the heart so much that the pumping function of the heart is reduced. If the heart is no longer able to pump enough blood to meet the body's needs, this is described as heart failure . [ 49 ] Significant damage to cardiac muscle cells is referred to as myocytolysis which is considered a type of cellular necrosis defined as either coagulative or colliquative. [ 50 ] [ 51 ]	https://en.wikipedia.org/wiki/Cardiac_muscle
The cardiac nerves are autonomic nerves which supply the heart . [ 1 ] They include: The nerves go down to the root of the neck with these following association: Posterior: "prevertebral fascia overlying anterolateral surface of vertebral bodies" Superior: "common carotid artery" Inferior: "subclavian artery" Laterally: "sympathetic trunk" [ 2 ] This neuroanatomy article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cardiac_nerve
The cardiac pacemaker is the heart 's natural rhythm generator. It employs pacemaker cells that produce electrical impulses, known as cardiac action potentials , which control the rate of contraction of the cardiac muscle , that is, the heart rate . In most humans, these cells are concentrated in the sinoatrial (SA) node , the primary pacemaker, which regulates the heart’s sinus rhythm . Sometimes a secondary pacemaker sets the pace, if the SA node is damaged or if the electrical conduction system of the heart has problems. Cardiac arrhythmias can cause heart block , in which the contractions lose their rhythm. In humans, and sometimes in other animals, a mechanical device called an artificial pacemaker (or simply "pacemaker") may be used after damage to the body's intrinsic conduction system to produce these impulses synthetically. The sinoatrial node (SA node) is the primary pacemaker of the heart. It is a region of cardiac muscle on the wall of the upper right atrium near to the superior vena cava entrance. The cells that make up the SA node are specialized cardiomyocytes known as pacemaker cells that can spontaneously generate cardiac action potentials . These signals are propagated through the heart's electrical conduction system . [ 1 ] [ 2 ] Only one percent of the heart muscle cells are conductive, the rest of the cardiomyocytes are contractile . The SA node controls the rate of contraction for the entire heart muscle because its cells have the quickest rate of spontaneous depolarization, thus they initiate action potentials the quickest. The action potential generated by the SA node passes down the electrical conduction system of the heart , and depolarizes the other potential pacemaker cells at the AV node to initiate action potentials before these other cells have had a chance to generate their own spontaneous action potential, thus they contract and propagate electrical impulses to the pace set by the cells of the SA node. This is the normal conduction of electrical activity in the heart. The pacemaker cells are connected to neighboring contractile cells via gap junctions , which enable them to locally depolarize adjacent cells. Gap junctions allow the passage of positive cations from the depolarization of the pacemaker cell to adjacent contractile cells. This starts the depolarization and eventual action potential in contractile cells. Having cardiomyocytes connected via gap junctions allow all contractile cells of the heart to act in a coordinated fashion and contract as a unit. All the while being in sync with the pacemaker cells; this is the property that allows the pacemaker cells to control contraction in all other cardiomyocytes. Cells in the SA node spontaneously depolarize , ultimately resulting in contraction, approximately 100 times per minute. This native rate is constantly modified by the activity of sympathetic and parasympathetic nerve fibers via the autonomic nervous system , so that the average resting heart rate in adult humans is about 70 beats per minute. Impulses from the sinus node reach the atrioventricular node which acts as the secondary pacemaker. The cells of the AV node normally discharge at about 40–60 beats per minute. The atrioventricular node and the Bundle of His , a little further down, are located in the region separating the atria from the ventricles known as the atrioventricular junction. The Bundle of His transmits signals to the bundle branches , which send them on to the Purkinje fibers . These will also produce a spontaneous cardiac action potential at a rate of 30–40 beats per minute, so if the SA and AV node both fail to function, these cells can also become pacemakers but with a much lower rate of conduction than either the primary or secondary pacemakers. There are three main stages in the generation of an action potential in a pacemaker cell. Since the stages are analogous to contraction of cardiac muscle cells , they have the same naming system. This can lead to some confusion as phases one and two are absent, leaving only phases zero, three, and four. The key to the rhythmic firing of pacemaker cells is that, unlike neurons , these cardiomyocytes will slowly depolarize by themselves and do not need any outside innervation from the autonomic nervous system to fire action potentials. In all other cells, the resting potential (-60mV to -70mV) is caused by a continuous outflow or "leak" of potassium ions through ion channel proteins in the membrane that surrounds the cells. However, in pacemaker cells, this potassium permeability (efflux) decreases as time goes on, causing a slow depolarization. In addition, there is a slow, continuous inward flow of sodium , called the funny current, or pacemaker current . These two relative ion concentration changes slowly depolarize (make more positive) the inside membrane potential (voltage) of the cell, giving these cells their pacemaker potential. When the membrane potential gets depolarized to about -40mV it has reached threshold (cells enter phase 0), allowing an action potential to be generated. Though much faster than the depolarization of phase 4, the upstroke in a pacemaker cell is slow compared to that in an axon . The SA and AV node do not have fast sodium channels like neurons, and the depolarization is mainly caused by a slow influx of calcium ions. (The funny current also increases). Calcium enters the cell via voltage-sensitive calcium channels that open when the threshold is reached. This calcium influx produces the rising phase of the action potential, which results in the reversal of membrane potential to a peak of about +10mV. It is important to note that intracellular calcium causes muscular contraction in contractile cells, and is the effector ion. In heart pacemaker cells, phase 0 depends on the activation of L-type calcium channels instead of the activation of voltage-gated fast sodium channels, which are responsible for initiating action potentials in contractile (non-pacemaker) cells. For this reason, the pacemaker action potential rising phase slope is more gradual than that of the contractile cell (image 2). The reversal of membrane potential triggers the opening of potassium leak channels, resulting in the rapid loss of potassium ions from the inside of the cell, causing repolarization (V m gets more negative). The calcium channels are also inactivated soon after they open. In addition, as sodium channels become inactivated, sodium permeability into the cell is decreased. These ion concentration changes slowly repolarize the cell to resting membrane potential (-60mV). Another important note at this phase is that ionic pumps restore ion concentrations to pre-action potential status. The sodium-calcium exchanger ionic pump works to pump calcium out of the intracellular space , thus effectively relaxing the cell. The sodium/potassium pump restores ion concentrations of sodium and potassium ions by pumping sodium out of the cell and pumping (exchanging) potassium into the cell. Restoring these ion concentrations is vital because it enables the cell to reset itself and enables it to repeat the process of spontaneous depolarization leading to activation of an action potential. If the SA node does not function, or the impulse generated in the SA node is blocked before it travels down the electrical conduction system, a group of cells further down the heart will become its pacemaker. [ 3 ] This center is typically represented by cells inside the atrioventricular node (AV node), which is an area between the atria and ventricles , within the atrial septum . If the AV node also fails, Purkinje fibers are occasionally capable of acting as the default or "escape" pacemaker. An ectopic pacemaker also known as an ectopic focus or ectopic foci, is a group of excitable cells that causes a premature heart beat outside the normally functioning SA node of the heart. It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat. If chronic this can result in arhythmias such as tachycardia , bradycardia , or ventricular fibrillation . An artificial pacemaker may be used to counter this. A pacemaker is an artificial cardiac pacemaker, that is an implanted medical device that generates electrical impulses delivered by electrodes to the chambers of the heart either the upper atria, or lower ventricles to cause the targeted chambers to contract and pump blood. By doing so, the artificial pacemaker takes over from the primary SA node pacemaker to regulate the function of the heart's electrical conduction system.	https://en.wikipedia.org/wiki/Cardiac_pacemaker
Cardiac psychology is a specialization of health psychology that focuses on the primary and secondary prevention of heart disease by incorporating strategies to address the emotional and behavioral barriers to lifestyle changes (e.g. smoking cessation ), and that seeks to enhance recovery in cardiac patients by means of providing patients tools (e.g. stress management and psychotherapy) to cope with life and physical changes associated with their disease. Cardiac psychologists can help cardiac patients across the lifespan: prevention, pre-surgery, post-surgery, and rehabilitation of cardiac disease with a particular emphasis on achieving optimal quality of life outcomes. Cardiac psychology includes both research and clinical practice aspects. The earliest published mention of cardiac psychology in Western medicine literature was in 1628 when William Harvey wrote that "a mental disturbance provoking pain, excessive joy, hope or anxiety extends to the heart, where it affects temper." [ 1 ] Research labs have been founded at Tilburg University , Tilburg Netherlands [ 2 ] led by Susanne Pedersen , [ 3 ] and at East Carolina University , Greenville, North Carolina [ 4 ] led by Samuel Sears , [ 5 ] that focus on psychological aspects of cardiac disease. Cardiac psychology as a term was first used by Robert Allan, PhD, and Stephen Schiedt, MD, as a title of their 1996 book, Heart and Mind: The Practice of Cardiac Psychology and launched increased attention to the clinical practice of cardiac psychology. More recently, additional texts, such as Psychotherapy with Cardiac Patients , (2008) by Ellen Dornelas, [ 6 ] have attempted to update the literature related to clinical techniques used in the care of cardiac patients. Significant research reviews have also been published spanning psychological factors in cardiac care, [ 7 ] [ 8 ] implantable electronic medical devices ( pacemaker , implantable cardioverter-defibrillator , etc.) [ 9 ] [ 10 ] and congestive heart failure . [ 11 ]	https://en.wikipedia.org/wiki/Cardiac_psychology
Cardiac resynchronisation therapy ( CRT or CRT-P ) is the insertion of electrodes in the left and right ventricles of the heart, as well as on occasion the right atrium , to treat heart failure by coordinating the function of the left and right ventricles via a pacemaker , a small device inserted into the anterior chest wall. [ 1 ] CRT is indicated in patients with a low ejection fraction (typically <35%) indicating heart failure , where electrical activity has been compromised, with prolonged QRS duration to >120 ms . [ 2 ] The insertion of electrodes into the ventricles is done under local anesthetic , with access to the ventricles most commonly via the subclavian vein , although access may be conferred from the axillary or cephalic veins . Right ventricular access is direct, while left ventricular access is conferred via the coronary sinus (CS). CRT defibrillators ( CRT-D ) also incorporate the additional function of an implantable cardioverter-defibrillator (ICD), to quickly terminate an abnormally fast, life-threatening heart rhythm. CRT and CRT-D have become increasingly important therapeutic options for patients with moderate and severe heart failure. [ 3 ] CRT with pacemaker only is often termed "CRT-P" to help distinguish it from CRT with defibrillator (CRT-D). The key indication for CRT is left bundle branch block (LBBB) of the heart, a cardiac abnormality leading to delayed left ventricular contraction. LBBB causes a QRS prolongation of ≥120 ms on the electrocardiogram , contributing to poor left ventricular coordination and reduced systolic function, thereby reduced ejection fraction (<35%). This reduction in ejection fraction is considered heart failure. [ 2 ] Heart failure patients are generally considered if in New York Heart Association (NYHA) class II or III heart failure. Current National Institute for Health and Care Excellence (NICE) guidelines state that CRT-D device placement is inappropriate for class IV heart failure, but placement of CRT-P devices may be appropriate in certain circumstances. [ 4 ] [ 5 ] [ 6 ] CRT requires the placement of an electrical device for biventricular pacing, along with placement of (at least) two pacing leads, to facilitate stable left ventricular and right ventricular pacing. For all elements, the first stage of the process is local anaesthetic followed by incision to allow for approach from the appropriate vein. From here, the leads and device can be inserted. [ 1 ] A venipuncture is made, and a guide wire inserted into the vein, where it is guided, with use of real time X-ray imaging , through to the right ventricle. The guide wire is then used to assist in the placement of the electrode lead, which travels through the venous system into the right ventricle where the electrode is embedded. [ 1 ] This is generally performed subsequent to RV lead placement, with the RV lead providing a backup in case of accidental damage to the electric fibers of the heart , causing an asystolic event . As with the RV lead, a guide wire is first inserted, allowing for the insertion of a multi-delivery catheter . The catheter is subsequently maneuvered to the opening of the coronary sinus in the right atrium. From here a contrast media is injected, allowing the surgical team to obtain a coronary sinus phlebogram to direct the placement of the lead into the most suitable coronary vein . [ 1 ] Once the phlebogram has been obtained, the multi-delivery catheter is used to guide in the lead, from the chosen vein of entry, into the right atrium, through the coronary sinus and into the relevant cardiac vein. [ 1 ] Left ventricular lead placement is the most complicated and potentially hazardous element of the operation, due to the significant variability of coronary venous structure. Alterations in heart structure, fatty deposits, valves and natural variations all cause additional complications in the process of cannulation. [ 1 ] However, this risk can be reduced using AI-based [ 8 ] preoperative visualization of LV venous anatomy using computer tomography (CT) imaging. The device is inserted in a subcutaneous pocket created by the surgeon, the choice of left or right side of the chest wall is determined mainly by the patient's preference or location of preexisting device. The device, similar to that of a traditional pacemaker , is generally no larger than a pocket watch and has inserts for the electrode leads. [ 1 ] Several studies have also shown that CRT can decrease mortality, reverse left ventricular remodeling , and improve quality of life, walking distance, and peak oxygen uptake ( VO 2 max ). [ 9 ] A 2013 study showed that CRT improved the left ventricular ejection fraction (LVEF) by an average of 10.6% 12 months after placement. [ 10 ] Key complications include: [ 2 ] Several research papers [ 12 ] [ 13 ] have proposed software platforms for planning and guiding the implantation of CRT devices. This research proposes using pre-operative images to characterize tissue and left ventricle activation to identify potential target regions for deploying the CRT leads.	https://en.wikipedia.org/wiki/Cardiac_resynchronization_therapy
Cardiac rhythmicity is the spontaneous depolarization and repolarization event that occurs in a repetitive and stable manner within the cardiac muscle. Rhythmicity is often abnormal or lost in cases of cardiac dysfunction or cardiac failure . It is the ability of the heart to maintain a relatively stable relation between its systole and diastole . Not increasing one on the expense of the other. However, external factors may lead to the disruption of the heart's rhythmicity. This cardiovascular system article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cardiac_rhythmicity
In cardiology , a cardiac shunt is a pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system . It may be described as right-left , left-right or bidirectional, or as systemic-to-pulmonary or pulmonary-to-systemic . The direction may be controlled by left and/or right heart pressure , a biological or artificial heart valve or both. The presence of a shunt may also affect left and/or right heart pressure either beneficially or detrimentally. The left and right sides of the heart are named from a dorsal view, i.e., looking at the heart from the back or from the perspective of the person whose heart it is. There are four chambers in a heart: an atrium (upper) and a ventricle (lower) on both the left and right sides. [ 1 ] In mammals and birds , blood from the body goes to the right side of the heart first. [ 2 ] Blood enters the upper right atrium , is pumped down to the right ventricle and from there to the lungs via the pulmonary artery. [ 3 ] Blood going to the lungs is called the pulmonary circulation . [ 4 ] When the blood returns to the heart from the lungs via the pulmonary vein, it goes to the left side of the heart , entering the upper left atrium . Blood is then pumped to the lower left ventricle and from there out of the heart to the body via the aorta. This is called the systemic circulation . A cardiac shunt is when blood follows a pattern that deviates from the systemic circulation, i.e., from the body to the right atrium, down to the right ventricle, to the lungs, from the lungs to the left atrium, down to the left ventricle and then out of the heart back to the systemic circulation. A left-to-right shunt is when blood from the left side of the heart goes to the right side of the heart. This can occur either through a hole in the ventricular or atrial septum that divides the left and the right heart or through a hole in the walls of the arteries leaving the heart, called great vessels . Left-to-right shunts occur when the systolic blood pressure in the left heart is higher than the right heart, which is the normal condition in birds and mammals. The most common congenital heart defects ( CHD s) which cause shunting are atrial septal defects ( ASD ), patent foramen ovale ( PFO ), ventricular septal defects ( VSD ), and patent ductus arteriosi ( PDA ). In isolation, these defects may be asymptomatic , or they may produce symptoms which can range from mild to severe, and which can either have an acute or a delayed onset. However, these shunts are often present in combination with other defects; in these cases, they may still be asymptomatic, mild or severe, acute or delayed, but they may also work to counteract the negative symptoms caused by another defect (as with d-Transposition of the great arteries ). Some acquired shunts are modifications of congenital ones: a balloon septostomy can enlarge a foramen ovale (if performed on a newborn ), PFO or ASD; or prostaglandin can be administered to a newborn to prevent the ductus arteriosus from closing. Biological tissues may also be used to construct artificial passages. Evaluation can be done during a cardiac catheterization with a "shunt run" by taking blood samples from superior vena cava (SVC), inferior vena cava (IVC), right atrium , right ventricle , pulmonary artery , and system arterial. Abrupt increases in oxygen saturation support a left-to-right shunt and lower than normal systemic arterial oxygen saturation supports a right-to-left shunt. Samples from the SVC & IVC are used to calculate mixed venous oxygen saturation using the Flamm formula and Qp:Qs ratio where P V {\displaystyle P_{V}} is the pulmonary vein, P A {\displaystyle P_{A}} is the pulmonary artery, S A {\displaystyle S_{A}} is the systemic arterial, and S V {\displaystyle S_{V}} is the mixed-venous The Qp:Qs ratio is based upon the Fick principle and it is reduced to the above equation and eliminates the need to know cardiac output and hemoglobin concentration. Mechanical shunts such as the Blalock-Taussig shunt are used in some cases of CHD to control blood flow or blood pressure. All reptiles have the capacity for cardiac shunts. [ 5 ]	https://en.wikipedia.org/wiki/Cardiac_shunt
Cardiac tamponade , also known as pericardial tamponade ( / ˌ t æ m . p ə ˈ n eɪ d / [ 4 ] ), is a compression of the heart due to pericardial effusion (the build-up of pericardial fluid in the sac around the heart ). [ 2 ] Onset may be rapid or gradual. [ 2 ] Symptoms typically include those of obstructive shock including shortness of breath , weakness, lightheadedness , and cough. [ 1 ] Other symptoms may relate to the underlying cause. [ 1 ] Common causes of cardiac tamponade include cancer , kidney failure , chest trauma , myocardial infarction , and pericarditis . [ 2 ] [ 5 ] Other causes include connective tissues diseases , hypothyroidism , aortic rupture , autoimmune disease , and complications of cardiac surgery . [ 2 ] [ 6 ] In Africa, tuberculosis is a relatively common cause. [ 1 ] Diagnosis may be suspected based on low blood pressure , jugular venous distension , or quiet heart sounds (together known as Beck's triad ). [ 2 ] [ 1 ] [ 7 ] A pericardial rub may be present in cases due to inflammation. [ 2 ] The diagnosis may be further supported by specific electrocardiogram (ECG) changes, chest X-ray , or an ultrasound of the heart . [ 2 ] If fluid increases slowly the pericardial sac can expand to contain more than 2 liters; however, if the increase is rapid, as little as 200 mL can result in tamponade. [ 2 ] Tamponade is a medical emergency. [ 5 ] When it results in symptoms, drainage is necessary. [ 8 ] This can be done by pericardiocentesis , surgery to create a pericardial window , or a pericardiectomy . [ 2 ] Drainage may also be necessary to rule out infection or cancer. [ 8 ] Other treatments may include the use of dobutamine or in those with low blood volume , intravenous fluids . [ 1 ] Those with few symptoms and no worrisome features can often be closely followed. [ 2 ] The frequency of tamponade is unclear. [ 9 ] One estimate from the United States places it at 2 per 10,000 per year. [ 3 ] Onset may be rapid (acute) or more gradual (subacute). [ 10 ] [ 2 ] Signs of cardiac tamponade typically include those of cardiogenic shock including shortness of breath , weakness, lightheadedness , cough [ 1 ] and those of Beck's triad e.g. jugular vein distention, quiet heart sounds and hypotension . Other symptoms may relate to the underlying cause. [ 1 ] Other general signs of shock (such as fast heart rate , shortness of breath and decreasing level of consciousness ) may also occur. However, some of these signs may not be present in certain cases. A fast heart rate, although expected, may be absent in people with uremia and hypothyroidism . [ 1 ] According to Reddy and co-authors, cardiac tamponade and its progression can be described in 3 different phases. [ 11 ] In phase I, the required filling pressure increases due to the high stiffness of the ventricles. This is because of the accumulation of pericardial fluid in the pericardial cavity. During phase II, the pericardial pressure exceeds the ventricular filling pressure caused by the further accumulation of pericardial fluid. This results in a decrease in cardiac input and output. A further decrease of cardiac input and output is typical in phase III of the progression of cardiac tamponade. This is caused by the equilibration of left ventricular filling and pericardial pressure, leading to “severe deterioration of end-organ perfusion.” [ 11 ] Some of the symptoms, as a consequence, include abdominal pain due to liver engorgement. Cardiac tamponade is caused by a large or uncontrolled pericardial effusion , i.e. the buildup of fluid inside the pericardium. [ 12 ] This commonly occurs as a result of chest trauma (both blunt and penetrating), [ 13 ] but can also be caused by myocardial infarction , myocardial rupture , cancer (most often Hodgkin lymphoma ), uremia , pericarditis , or cardiac surgery, [ 12 ] and rarely occurs during retrograde aortic dissection , [ 14 ] or while the person is taking anticoagulant therapy. [ 15 ] The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood , but pus is also found in some circumstances. [ 12 ] One of the most common settings for cardiac tamponade is in the first 7 days after heart surgery. [ 16 ] After heart surgery, chest tubes are placed to drain blood. These chest tubes, however, are prone to clot formation. When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade. [ 17 ] The pericardium, the double-walled sac surrounding the heart, consists of a fibrous pericardium layer on the outside and a double-layered serous pericardium on the inside. [ 18 ] Between the two layers of the serous pericardium is the pericardial space, which is filled with lubricating serous fluid that prevents friction as the heart contracts. [ 19 ] The outer layer of the heart is made of fibrous tissue [ 20 ] which does not easily stretch, so once excess fluid begins to enter the pericardial space, pressure starts to increase. [ 12 ] Consequently, the heart becomes compressed due to its inability to fully relax. [ 21 ] If fluid continues to accumulate, each successive diastolic period leads to less blood entering the ventricles. Eventually, increasing pressure on the heart forces the septum to bend in towards the left ventricle , leading to a decrease in stroke volume . [ 12 ] This causes the development of obstructive shock , which if left untreated may lead to cardiac arrest (often presenting as pulseless electrical activity ). [ 22 ] The decrease in stroke volume can also ultimately lead to a decrease in cardiac output, which could be signaled by tachycardia and hypotension. [ 21 ] The three classic signs, known as Beck's triad , are low blood pressure , jugular-venous distension, and muffled heart sounds . [ 24 ] Other signs may include pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration), [ 12 ] and ST segment changes on the electrocardiogram , [ 24 ] which may also show low voltage QRS complexes . [ 15 ] Tamponade can often be diagnosed radiographically. Echocardiography , which is the diagnostic test of choice, often demonstrates an enlarged pericardium or collapsed ventricles. A large cardiac tamponade will show as an enlarged globular-shaped heart on chest x-ray. During inspiration, the negative pressure in the thoracic cavity will cause increased pressure into the right ventricle. This increased pressure in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. At the same time, right ventricle volume is markedly diminished and sometimes it can collapse. [ 15 ] Initial diagnosis of cardiac tamponade can be challenging, as there is a broad differential diagnosis . [ 10 ] The differential includes possible diagnoses based on symptoms, time course, mechanism of injury, patient history. Rapid onset cardiac tamponade may also appear similar to pleural effusions, obstructive shock , shock, pulmonary embolism, and tension pneumothorax . [ 13 ] [ 10 ] If symptoms appeared more gradually, the differential diagnosis includes acute heart failure . [ 25 ] In a person with trauma presenting with pulseless electrical activity in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade. [ 26 ] In addition to the diagnostic complications afforded by the wide-ranging differential diagnosis for chest pain, diagnosis can be additionally complicated by the fact that people will often be weak or faint at presentation. For instance, a fast rate of breathing and difficulty breathing on exertion that progresses to air hunger at rest can be a key diagnostic symptom, but it may not be possible to obtain such information from people who are unconscious or who have convulsions at presentation. [ 1 ] Initial treatment given will usually be supportive in nature, for example administration of oxygen , and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. Some teams have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury. [ citation needed ] Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis , which can be life-saving. If the person has already suffered a cardiac arrest , pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action. [ citation needed ] Initial management in hospital is by pericardiocentesis . [ 13 ] This involves the insertion of a needle through the skin and into the pericardium and aspirating fluid under ultrasound guidance preferably. This can be done laterally through the intercostal spaces, usually the fifth, or as a subxiphoid approach. [ 27 ] [ 28 ] A left parasternal approach begins 3 to 5 cm left of the sternum to avoid the left internal mammary artery, in the 5th intercostal space . [ 29 ] Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead, [ 13 ] during which the pericardium is cut open to allow fluid to drain. Following stabilization of the person, surgery is provided to seal the source of the bleed and mend the pericardium. [ citation needed ] Following heart surgery, the amount of chest tube drainage is monitored. If the drainage volume drops off, and the blood pressure goes down, this can suggest a tamponade due to chest tube clogging. In that case, the person is taken back to the operating room for an emergency reoperation. [ citation needed ] If aggressive treatment is offered immediately and no complications arise (shock, AMI or arrhythmia, heart failure, aneurysm, carditis, embolism, or rupture), or they are dealt with quickly and fully contained, then adequate survival is still a distinct possibility. [ citation needed ] The frequency of tamponade is unclear. [ 9 ] One estimate from the United States places it at 2 per 10,000 per year. [ 3 ] It is estimated to occur in 2% of those with stab or gunshot wounds to the chest. [ 30 ]	https://en.wikipedia.org/wiki/Cardiac_tamponade
The cardiac transient outward potassium current (referred to as I to1 or I to [ 1 ] ) is one of the ion currents across the cell membrane of heart muscle cells . It is responsible for the (brief) repolarizing phase 1 of the cardiac action potential (which suceeds depolarisation, and precedes the plateau phase). [ 2 ] The I to is produced by movement of positively charged potassium (K + ) ions from the intracellular into the extracellular space . It exhibits rapid activation and inactivation. [ 3 ] I to1 is complemented with I to2 resulting from Cl − ions to form the transient outward current I to . [ citation needed ] The I to1 is generated by voltage-gated K+ channels Kv1.4 , Kv4.2 , and (especially) Kv4.3 ; these channels undergo ball-and-chain inactivation to terminate the current. [ 3 ] It occurs in atrial, ventricular, and conduction system cells. In ventricular myocardium, it is more potent in the epicardium than the endocardium; this transmural I to1 gradient underlies the J wave ECG finding. [ 3 ]	https://en.wikipedia.org/wiki/Cardiac_transient_outward_potassium_current
According to the cardiocentric hypothesis , the heart is the primary location of human emotions, cognition, and awareness. [ 1 ] This notion may be traced back to ancient civilizations such as Egypt and Greece , where the heart was regarded not only as a physical organ but also as a repository of emotions and wisdom. [ 2 ] Aristotle , a well-known Greek philosopher in this field, contributed to the notion by thinking the heart to be the centre of both emotions and intellect. He believed that the heart was the center of the psycho-physiological system and that it was responsible for controlling sensation, thought, and body movement. He also observed that the heart was the origin of the veins in the body and that the existence of pneuma in the heart was to function as a messenger, traveling through blood vessels to produce sensation. [ 3 ] This point of view remained throughout history, spanning the Middle Ages and Renaissance , influencing medical and intellectual debate. [ 2 ] An opposing theory called "cephalocentrism", which proposed that the brain played the dominant role in controlling the body, was first introduced by Pythagoras in 550 BC, who argued that the soul resides in the brain and is immortal. [ 4 ] His statements were supported by Plato , Hippocrates , and Galen of Pergamon . Plato believed that the body is a "prison" of the mind and soul and that in death the mind and soul become separated from the body, meaning that neither one of them could die. [ 5 ] In ancient Egypt , people believed that the heart is the seat of the soul and the origin of the channels to all other parts of the body, including arteries , veins , nerves , and tendons . The heart was also depicted as determining the fate of ancient Egyptians after they died. It was believed that Anubis , the god of mummification , would weigh the deceased person's heart against a feather. If the heart was too heavy, it would be considered guilty and consumed by the Ammit , a mythological creature. If it was lighter than the feather, the spirit of the deceased would be allowed to go to heaven . Therefore, the heart was kept in the mummy while other organs were generally removed. [ 6 ] In the ancient Near East , the heart ( libbu ) was considered the seat of consciousness, moral agency, cognition, wisdom, understanding, and of the emotions subject to the will (desire, love, friendship, etc). Emotional expressions in Mesopotamian texts link a positive relationship between the heart and the occurrence of feelings of pride, desire, love, and notions of sexual arousal and shame. Idioms like "his heart is awake" were used to describe an individual regaining their consciousness, and "as it pleases the heart" could be used to describe the sensation of pleasure that one experiences. The heart is the source of both the good and evil in a person, as well as the center of the human capacity of religiosity. [ 7 ] [ 8 ] However, the ancient Greeks , Aristotle promoted the cardiocentric hypothesis based on his experience with animal dissection. [ 9 ] He found that certain primitive animals could move and feel without the brain, and so deduced that the brain was not responsible for movement or feeling. Apart from that, he pointed out that the brain was at the top of the body, far from the centre of the body, and felt cold. He also performed anatomical examinations after strangling the specimen, which would cause vasoconstriction of the arterioles in the lungs . This likely had the effect of forcing blood to engorge the veins and make them more visible in the following dissection. Aristotle observed that the heart was the origin of the veins in the body, and concluded that the heart was the centre of the psycho-physiological system. He also stated that the existence of pneuma in the heart was to function as a messenger, traveling through blood vessels to produce sensation. Movement of body parts was thought to be controlled by the heart as well. From Aristotle's perspective, the heart was composed of sinews which allowed the body to move. [ 10 ] In the fourth century BC, Diocles of Carystus reasserted that the heart was the physiological centre of sensation and thought. He also recognised that the heart had two cardiac ears. Although Diocles also proposed that the left brain was responsible for intelligence and the right one was for sensation, he believed that the heart was dominant over the brain for listening and understanding. [ 11 ] Praxagoras of Cos was a follower of Aristotle's cardiocentric theory and was the first one to distinguish arteries and veins. He conjectured that arteries carry pneuma while transporting blood. [ clarification needed ] He also proved that a pulse can be detected from the arteries and explained that the arteries' ends narrowed into nerves. [ 12 ] Lucretius stated around 55 BCE, "The dominant force in the whole body is that guiding principle which we term mind or intellect. This is firmly lodged in the midregion of the breast. Here is the place where fear and alarm pulsate. Here is felt the caressing touch of joy. Here, then, is the seat of the intellect and the mind." [ 13 ] [ 14 ] According to the Mystic Treatises of Isaac the Syrian , "the heart is the central organ of the inward senses; this means the sense of senses, because it is the root. And if the root is holy, so also are all the branches." [ 15 ] Cardiocentrism is accepted in the Quran . [ 16 ] The Islamic philosopher and physician Avicenna followed Galen of Pergamon , believing that one's spirit was confined in three chambers of the brain and accepted that nerves originate from the brain and spinal cord , which control body movement and sensation. However, he maintained the earlier cardiocentric hypothesis. He stated that activation for voluntary movement began in the heart and was then transported to the brain. Similarly, messages were delivered from a peripheral environment to the brain and then via the vagus nerve to the heart. [ citation needed ] In the Middle Ages, the German Catholic friar Albertus Magnus made contributions to physiology and biology. His treatise was based on Galen's cephalocentric theory and was profoundly affected by Avicenna's preeminent Canon, which itself had been influenced by Aristotle. He combined these ideas in a new way which suggested that nerves branched off from the brain but that the origin was the heart. He concluded that philosophically, all matters originated from the heart, and in the corporeal explanation, all nerves started from the brain. [ citation needed ] William Harvey , an early modern English physiologist, also agreed with Aristotle's cardiocentric view. He was the first to describe the basic operation of the circulatory system, by which blood was pumped by the heart to the rest of the body, in detail. He explained that the heart was the centre of the body and the source of life in his treatise De Motu Cordis et Sanguinis in Animalibus . Hippocrates of Kos was the first to suggest that the brain was the seat of the soul and intelligence. From his treatise De morbo sacro , he pointed out that the brain controls the rest of the body and is responsible for sensation and understanding. Apart from that, he believed that all feelings originated from the brain. Galen of Pergamon was a biologist and physician. His approach to the investigation of the brain was due to his rigorous anatomical methodology. He pointed out that only correct dissection will support the incontrovertible statement. He reached the conclusion that the brain was responsible for sensation and thought, and that nerves originated at the spinal cord and brain. [ 17 ] The "little brain in the heart" is an intricate system of nerve cells that control and regulate the heart's activity. It is also called the intrinsic cardiac nervous system (ICNS). [ 18 ] It consists of about 40,000 neurons that form clusters or ganglia around the heart, especially near the top where the blood vessels enter and exit. These neurons communicate with each other and with the brain through chemical and electrical signals. [ 19 ] The intrinsic cardiac nervous system has several functions, such as:	https://en.wikipedia.org/wiki/Cardiocentric_hypothesis
Cardiogenic shock is a medical emergency resulting from inadequate blood flow to the body's organs due to the dysfunction of the heart . Signs of inadequate blood flow include low urine production (<30 mL/hour), cool arms and legs, and decreased level of consciousness. People may also have a severely low blood pressure and heart rate. Causes of cardiogenic shock include cardiomyopathic , arrhythmic, and mechanical. Cardiogenic shock is most commonly precipitated by a heart attack . [ 4 ] Treatment of cardiogenic shock depends on the cause with the initial goals to improve blood flow to the body. If cardiogenic shock is due to a heart attack, attempts to open the heart's arteries may help. Certain medications, such as dobutamine and milrinone, improve the heart's ability to contract and can also be used. When these measures fail, more advanced options such as mechanical support devices or heart transplantation can be pursued. Cardiogenic shock is a condition that is difficult to fully reverse even with an early diagnosis. [ 4 ] However, early initiation of treatment may improve outcomes. Care should also be directed to any other organs that are affected by this lack of blood flow (e.g., dialysis for the kidneys, mechanical ventilation for lung dysfunction). Mortality rates for cardiogenic shock are high but have been decreasing in the United States. This is likely due to its rapid identification and treatment in recent decades. Some studies have suggested that this is possibly related to new treatment advances. Nonetheless, the mortality rates remain high and multi-organ failure in addition to cardiogenic shock is associated with higher rates of mortality. [ 5 ] The presentation is the following: [ citation needed ] Cardiogenic shock is caused by the failure of the heart to pump effectively. It is due to damage to the heart muscle , most often from a heart attack or myocardial contusion . [ 6 ] Other causes include abnormal heart rhythms , cardiomyopathy , heart valve problems, ventricular outflow obstruction (i.e. systolic anterior motion in hypertrophic cardiomyopathy ), or ventriculoseptal defects. It can also be caused by a sudden decompressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream ( Henry's law ), causing heart failure . [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ 13 ] [ 14 ] [ 15 ] An electrocardiogram helps to establish the exact diagnosis and guides treatment, it may reveal: Echocardiography may show poor ventricular function, signs of PED, [ clarification needed ] rupture of the interventricular septum , an obstructed outflow tract or cardiomyopathy. [ citation needed ] The Swan–Ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics . [ citation needed ] When cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis . [ citation needed ] If the cardiac index falls acutely below 2.2 L/min/m 2 , the person may be in cardiogenic shock. [ citation needed ] Initial management of cardiogenic shock involves medications to augment the heart's function. Certain medications, such as dobutamine or milrinone , enhance the heart's pumping function and are often used first-line to improve the low blood pressure and delivery of blood to the rest of the body. [ 4 ] Patients who have cardiogenic shock unresponsive to medication therapy may be candidates for more advanced options such as a mechanical circulatory support device. There are several types of mechanical circulatory support devices, the most common being intra-aortic balloon pumps, left ventricular assist devices, and venous-arterial extra-corporeal membrane oxygenation. It is important to note, however, that none of these devices are permanent solutions but rather are a bridge to a more definitive therapy such as a heart transplantion . An intra-aortic balloon pump is a device placed by a cardiac surgeon into the descending aorta . It consists of a small balloon filled with helium that helps the heart to pump blood by inflating during diastole (the resting phase of the cardiac cycle) and deflating during systole (the contracting phase of the cardiac cycle). [ 16 ] Intra-aortic balloon pumps do not directly increase cardiac output, but importantly, they decrease the amount of pressure that the heart has to pump against, thereby allowing for more blood flow and oxygen to be delivered to the heart muscles. [ 17 ] Intra-aortic balloon pumps have been around for several decades and are most commonly used first-line of the mechanical circulatory support devices. [ 4 ] However, it is not without its potential complications. Potential complications include injury upon insertion of the device to arteries supplying the spinal cord as well as risks with any procedure such as bleeding and infection. [ 17 ] Contraindications to intra-aortic balloon pumps include aortic dissection, an abdominal aortic aneurysm, and irregularly fast heart beats. [ 16 ] There are several types of left ventricular assist devices, with the Impella devices being some of the most common. This device is placed by a cardiac surgeon into the left ventricle of the heart and essentially acts as a pump, drawing blood from the left ventricle and pushing it out into the aorta so that it could be delivered to the rest of the body. [ 4 ] Unlike intra-aortic balloon pumps, the Impella acts independently from the cardiac cycle. [ 17 ] It can be adjusted to pump at faster rates to take blood out of the left ventricle and into the aorta more quickly, thereby decreasing the amount of work that the left ventricle has to do. [ 4 ] While the Impella is commonly used in settings of cardiogenic shock, some evidence suggests that it placing an Impella device in an acute cardiogenic shock setting, where the heart fails to pump suddenly, may not necessarily guarantee increased survival. [ 18 ] Potential complications specific to an Impella device include hemolysis (shearing of the blood cells) as well as the formation of lesions on the heart valve, namely the mitral or aortic valves . [ 17 ] Contraindications to an Impella device insertion include aortic dissection, the presence of a mechanical aortic valve, and the presence of a blood clot in the left ventricle. [ 16 ] Venous-arterial extra-corporeal membrane oxygenation is a circuit support system that is meant to replace the function of the heart as it heals or awaits a more definitive treatment. [ 17 ] It consists of a circuit that essentially drains blood from a patient's venous system, runs that blood through a circulator which adds oxygen and removes carbon dioxide, and ultimately returns blood back into the patient's arterial system where the newly oxygenated blood can be delivered to the person's organs. Some evidence suggests that the combination of both an Impella device and Venous-arterial extra-corporeal membrane oxygenation may decrease the heart's pulmonary capillary wedge pressure , thereby decreasing the amount of stress on the cardiac muscles. [ 19 ] Because Venous-arterial extra-corporeal membrane oxygenation is a very invasive procedure, it is not usually the first-line chosen device for patients in cardiogenic shock and is often reserved only for patients who have not only cardiogenic shock but also respiratory failure and/or concomitant cardiac arrest . [ 17 ] Complications of venous-arterial extra-corporeal membrane oxygenation include an air embolism , pulmonary edema , and blood clotting in the circuit machine. [ 17 ]	https://en.wikipedia.org/wiki/Cardiogenic_shock
Cardiogeriatrics , or geriatric cardiology , is the branch of cardiology and geriatric medicine that deals with the cardiovascular disorders in elderly people . Cardiac disorders such as coronary heart disease , including myocardial infarction , heart failure , cardiomyopathy , and arrhythmias such as atrial fibrillation , are common and are a major cause of mortality in elderly people. [ 1 ] [ 2 ] [ 3 ] Vascular disorders such as atherosclerosis and peripheral arterial disease cause significant morbidity and mortality in aged people. [ 1 ] [ 2 ] [ 3 ] Guidelines of the Cardiogeriatrics Department of the Brazilian Cardiology Society were published in English. [ 3 ] The American Journal of Geriatric Cardiology [ 4 ] is the official journal of the Society of Geriatric Cardiology . [ 5 ]	https://en.wikipedia.org/wiki/Cardiogeriatrics
Cardiology (from Ancient Greek καρδίᾱ (kardiā) ' heart ' and - λογία ( -logia ) ' study ' ) is the study of the heart. Cardiology is a branch of medicine that deals with disorders of the heart and the cardiovascular system . The field includes medical diagnosis and treatment of congenital heart defects , coronary artery disease , heart failure , valvular heart disease , and electrophysiology . Physicians who specialize in this field of medicine are called cardiologists , a sub-specialty of internal medicine . Pediatric cardiologists are pediatricians who specialize in cardiology. Physicians who specialize in cardiac surgery are called cardiothoracic surgeons or cardiac surgeons , a specialty of general surgery . [ 1 ] All cardiologists in the branch of medicine study the disorders of the heart, but the study of adult and child heart disorders each require different training pathways. Therefore, an adult cardiologist (often simply called "cardiologist") is inadequately trained to take care of children, and pediatric cardiologists are not trained to treat adult heart disease. Surgical aspects outside of cardiac rhythm device implant are not included in cardiology and are in the domain of cardiothoracic surgery . For example, coronary artery bypass surgery (CABG), cardiopulmonary bypass and valve replacement are surgical procedures performed by surgeons, not cardiologists. Typically a cardiologist would first identify who is in need of cardiac surgery and refer them to a cardiac surgeon for the procedure. However, some invasive procedures such as cardiac catheterization and pacemaker implantation are performed by cardiologists. Cardiology is a specialty of internal medicine . To become a cardiologist in the United States , a three-year residency in internal medicine is followed by a three-year fellowship in cardiology. It is possible to specialize further in a sub-specialty. Recognized sub-specialties in the U.S. by the Accreditation Council for Graduate Medical Education are clinical cardiac electrophysiology , interventional cardiology , adult congenital heart disease, and advanced heart failure and transplant cardiology. Cardiologists may further become certified in echocardiography by the National Board of Echocardiography, [ 2 ] in nuclear cardiology by the Certification Board of Nuclear Cardiology, in cardiovascular computed tomography by the Certification Board of Cardiovascular Computed Tomography in cardiovascular MRI by the Certification Board of Cardiovascular Magnetic Resonance. [ 3 ] Recognized subspecialties in the U.S. by the American Osteopathic Association Bureau of Osteopathic Specialists include clinical cardiac electrophysiology and interventional cardiology . [ 4 ] In India, a three-year residency in General Medicine or Pediatrics after M.B.B.S. and then three years of residency in cardiology are needed to be a D.M. (holder of a Doctorate of Medicine [D.M.])/ Diplomate of National Board (DNB) in Cardiology. [ citation needed ] Per Doximity , adult cardiologists earn an average of $436,849 per year in the U.S. [ 5 ] Cardiac electrophysiology is the science of elucidating, diagnosing, and treating the electrical activities of the heart. The term is usually used to describe studies of such phenomena by invasive (intracardiac) catheter recording of spontaneous activity as well as of cardiac responses to programmed electrical stimulation (PES). These studies are performed to assess complex arrhythmias , elucidate symptoms, evaluate abnormal electrocardiograms , assess risk of developing arrhythmias in the future, and design treatment. These procedures increasingly include therapeutic methods (typically radiofrequency ablation , or cryoablation ) in addition to diagnostic and prognostic procedures. Other therapeutic modalities employed in this field include antiarrhythmic drug therapy and implantation of pacemakers and automatic implantable cardioverter-defibrillators (AICD). [ 6 ] [ 7 ] The cardiac electrophysiology study typically measures the response of the injured or cardiomyopathic myocardium to PES on specific pharmacological regimens in order to assess the likelihood that the regimen will successfully prevent potentially fatal sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) in the future. Sometimes a series of electrophysiology-study drug trials must be conducted to enable the cardiologist to select the one regimen for long-term treatment that best prevents or slows the development of VT or VF following PES. Such studies may also be conducted in the presence of a newly implanted or newly replaced cardiac pacemaker or AICD. [ 6 ] Clinical cardiac electrophysiology is a branch of the medical specialty of cardiology and is concerned with the study and treatment of rhythm disorders of the heart. Cardiologists with expertise in this area are usually referred to as electrophysiologists. Electrophysiologists are trained in the mechanism, function, and performance of the electrical activities of the heart. Electrophysiologists work closely with other cardiologists and cardiac surgeons to assist or guide therapy for heart rhythm disturbances (arrhythmias). They are trained to perform interventional and surgical procedures to treat cardiac arrhythmia. [ 8 ] The training required to become an electrophysiologist is long and requires eight years after medical school (within the U.S.). Three years of internal medicine residency, three years of cardiology fellowship, and two years of clinical cardiac electrophysiology. [ 9 ] Cardiogeriatrics, or geriatric cardiology, is the branch of cardiology and geriatric medicine that deals with the cardiovascular disorders in elderly people. Cardiac disorders such as coronary heart disease , including myocardial infarction , heart failure , cardiomyopathy , and arrhythmias such as atrial fibrillation , are common and are a major cause of mortality in elderly people. [ 10 ] [ 11 ] Vascular disorders such as atherosclerosis and peripheral arterial disease cause significant morbidity and mortality in aged people. [ 12 ] [ 13 ] Cardiac imaging includes echocardiography (echo), cardiac magnetic resonance imaging (CMR), and computed tomography of the heart. Those who specialize in cardiac imaging may undergo more training in all imaging modes or focus on a single imaging modality. Echocardiography (or "echo") uses standard two-dimensional, three-dimensional, and Doppler ultrasound to create images of the heart. It is used to evaluate and quantify cardiac size and function, valvular function, and can assist with diagnosis and treatment of conditions including heart failure, heart attack, valvular heart disease, congenital heart defects, pericardial disease, and aortic disease. Those who specialize in echo may spend a significant amount of their clinical time reading echos and performing transesophageal echo, in particular using the latter during procedures such as insertion of a left atrial appendage occlusion device. Transesophageal echo provides higher spatial resolution than trans thoracic echocardiography and because the probe is located in the esophagus, it is not limited by attenuation due to anterior chest structures such as the ribs, chest wall, breasts, lungs that can hinder the quality of trans thoracic echocardiography. It is generally indicated for a variety of indications including: when the standard transthoracic echocardiogram is non diagnostic, for detailed evaluation of abnormalities that are typically in the far field, such as the aorta, left atrial appendage, evaluation of native or prosthetic heart valves, evaluation of cardiac masses, evaluation of endocarditis, valvular abscesses, or for the evaluation of cardiac source of embolus. It is frequently used in the setting of atrial fibrillation or atrial flutter to facilitate the clinical decision with regard to anticoagulation, cardioversion and/or radio frequency ablation. [ 14 ] Cardiac MRI utilizes special protocols to image heart structure and function with specific sequences for certain diseases such as hemochromatosis and amyloidosis . Cardiac CT utilizes special protocols to image heart structure and function with particular emphasis on coronary arteries. Interventional cardiology is a branch of cardiology that deals specifically with the catheter based treatment of structural heart diseases. [ 15 ] A large number of procedures can be performed on the heart by catheterization, including angiogram, angioplasty, atherectomy, and stent implantation. These procedures all involve insertion of a sheath into the femoral artery or radial artery (but, in practice, any large peripheral artery or vein) and cannulating the heart under X-ray visualization (most commonly fluoroscopy ). This cannulation allows indirect access to the heart, bypassing the trauma caused by surgical opening of the chest. The main advantages of using the interventional cardiology or radiology approach are the avoidance of the scars and pain, and long post-operative recovery. Additionally, interventional cardiology procedure of primary angioplasty is now the gold standard of care for an acute myocardial infarction. This procedure can also be done proactively, when areas of the vascular system become occluded from atherosclerosis . The Cardiologist will thread this sheath through the vascular system to access the heart. This sheath has a balloon and a tiny wire mesh tube wrapped around it, and if the cardiologist finds a blockage or stenosis , they can inflate the balloon at the occlusion site in the vascular system to flatten or compress the plaque against the vascular wall. Once that is complete a stent is placed as a type of scaffold to hold the vasculature open permanently. A relatively newer specialization of cardiology is in the field of heart failure and heart transplant. Cardiomyopathy is a disease of the heart muscle that make it larger or stiffer, sometimes making the heart worse at pumping blood. [ 16 ] Specialization of general cardiology to just that of the cardiomyopathies leads to also specializing in heart transplant and pulmonary hypertension . A recent specialization of cardiology is that of cardiooncology. This area specializes in the cardiac management in those with cancer and in particular those with plans for chemotherapy or those who have experienced cardiac complications of chemotherapy. In recent times, the focus is gradually shifting to preventive cardiology due to increased cardiovascular disease burden at an early age. According to the WHO, 37% of all premature deaths are due to cardiovascular diseases and out of this, 82% are in low and middle income countries. [ 17 ] Clinical cardiology is the sub specialty of cardiology which looks after preventive cardiology and cardiac rehabilitation. Preventive cardiology also deals with routine preventive checkup though noninvasive tests, specifically electrocardiography, fasegraphy , stress tests, lipid profile and general physical examination to detect any cardiovascular diseases at an early age, while cardiac rehabilitation is the upcoming branch of cardiology which helps a person regain their overall strength and live a normal life after a cardiovascular event. A subspecialty of preventive cardiology is sports cardiology . Because heart disease is the leading cause of death in the world including United States (cdc.gov), national health campaigns and randomized control research has developed to improve heart health. Helen B. Taussig is known as the founder of pediatric cardiology. She became famous through her work with Tetralogy congenital heart defect in which oxygenated and deoxygenated blood enters the circulatory system resulting from a ventricular septal defect (VSD) right beneath the aorta. This condition causes newborns to have a bluish-tint, cyanosis , and have a deficiency of oxygen to their tissues, hypoxemia . She worked with Alfred Blalock and Vivien Thomas at the Johns Hopkins Hospital where they experimented with dogs to look at how they would attempt to surgically cure these "blue babies". They eventually figured out how to do just that by the anastomosis of the systemic artery to the pulmonary artery and called this the Blalock-Taussig Shunt . [ 18 ] Tetralogy of Fallot , pulmonary atresia , double outlet right ventricle , transposition of the great arteries , persistent truncus arteriosus , and Ebstein's anomaly are various congenital cyanotic heart diseases, in which the blood of the newborn is not oxygenated efficiently, due to the heart defect. As more children with congenital heart disease are surviving into adulthood, a hybrid of adult and pediatric cardiology has emerged called adult congenital heart disease (ACHD). This field can be entered as either adult or pediatric cardiology. ACHD specializes in congenital diseases in the setting of adult diseases (e.g., coronary artery disease, COPD, diabetes) that is, otherwise, atypical for adult or pediatric cardiology. As the center focus of cardiology, the heart has numerous anatomical features (e.g., atria , ventricles , heart valves ) and numerous physiological features (e.g., systole , heart sounds , afterload ) that have been encyclopedically documented for many centuries. The heart is located in the middle of the abdomen with its tip slightly towards the left side of the abdomen. Disorders of the heart lead to heart disease and cardiovascular disease and can lead to a significant number of deaths: cardiovascular disease is the leading cause of death in the U.S. and caused 24.95% of total deaths in 2008. [ 19 ] The primary responsibility of the heart is to pump blood throughout the body. It pumps blood from the body — called the systemic circulation — through the lungs — called the pulmonary circulation — and then back out to the body. This means that the heart is connected to and affects the entirety of the body. Simplified, the heart is a circuit of the circulation . [ 20 ] While plenty is known about the healthy heart, the bulk of study in cardiology is in disorders of the heart and restoration, and where possible, of function. The heart is a muscle that squeezes blood and functions like a pump. The heart's systems can be classified as either electrical or mechanical, and both of these systems are susceptible to failure or dysfunction. The electrical system of the heart is centered on the periodic contraction (squeezing) of the muscle cells that is caused by the cardiac pacemaker located in the sinoatrial node . The study of the electrical aspects is a sub-field of electrophysiology called cardiac electrophysiology and is epitomized with the electrocardiogram (ECG/EKG). The action potentials generated in the pacemaker propagate throughout the heart in a specific pattern. The system that carries this potential is called the electrical conduction system . Dysfunction of the electrical system manifests in many ways and may include Wolff–Parkinson–White syndrome , ventricular fibrillation , and heart block . [ 21 ] The mechanical system of the heart is centered on the fluidic movement of blood and the functionality of the heart as a pump . The mechanical part is ultimately the purpose of the heart and many of the disorders of the heart disrupt the ability to move blood. Heart failure is one condition in which the mechanical properties of the heart have failed or are failing, which means insufficient blood is being circulated. Failure to move a sufficient amount of blood through the body can cause damage or failure of other organs and may result in death if severe. [ 22 ] Coronary circulation is the circulation of blood in the blood vessels of the heart muscle (the myocardium). The vessels that deliver oxygen-rich blood to the myocardium are known as coronary arteries. The vessels that remove the deoxygenated blood from the heart muscle are known as cardiac veins. These include the great cardiac vein , the middle cardiac vein , the small cardiac vein and the anterior cardiac veins . As the left and right coronary arteries run on the surface of the heart, they can be called epicardial coronary arteries. These arteries, when healthy, are capable of autoregulation to maintain coronary blood flow at levels appropriate to the needs of the heart muscle. These relatively narrow vessels are commonly affected by atherosclerosis and can become blocked, causing angina or myocardial infarction (a.k.a., a heart attack). The coronary arteries that run deep within the myocardium are referred to as subendocardial. The coronary arteries are classified as "end circulation", since they represent the only source of blood supply to the myocardium; there is very little redundant blood supply, which is why blockage of these vessels can be so critical. The cardiac examination (also called the "precordial exam"), is performed as part of a physical examination , or when a patient presents with chest pain suggestive of a cardiovascular pathology . It would typically be modified depending on the indication and integrated with other examinations especially the respiratory examination . [ 23 ] Like all medical examinations, the cardiac examination follows the standard structure of inspection, palpation and auscultation. [ 24 ] [ 25 ] Cardiology is concerned with the normal functionality of the heart and the deviation from a healthy heart. Many disorders involve the heart itself, but some are outside of the heart and in the vascular system. Collectively, the two are jointly termed the cardiovascular system, and diseases of one part tend to affect the other. Coronary artery disease, also known as "ischemic heart disease", [ 26 ] is a group of diseases that includes: stable angina , unstable angina , myocardial infarction, and is one of the causes of sudden cardiac death . [ 27 ] It is within the group of cardiovascular diseases of which it is the most common type. [ 28 ] A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. [ 29 ] Occasionally it may feel like heartburn . Usually symptoms occur with exercise or emotional stress , last less than a few minutes, and get better with rest. [ 29 ] Shortness of breath may also occur and sometimes no symptoms are present. [ 29 ] The first sign is occasionally a heart attack. [ 30 ] Other complications include heart failure or an irregular heartbeat . [ 30 ] Risk factors include: high blood pressure , smoking , diabetes , lack of exercise, obesity , high blood cholesterol , poor diet, and excessive alcohol , among others. [ 31 ] [ 32 ] Other risks include depression . [ 33 ] The underlying mechanism involves atherosclerosis of the arteries of the heart . A number of tests may help with diagnoses including: electrocardiogram, cardiac stress testing , coronary computed tomographic angiography , and coronary angiogram , among others. [ 34 ] Prevention is by eating a healthy diet, regular exercise, maintaining a healthy weight and not smoking. [ 35 ] Sometimes medication for diabetes, high cholesterol, or high blood pressure are also used. [ 35 ] There is limited evidence for screening people who are at low risk and do not have symptoms. [ 36 ] Treatment involves the same measures as prevention. [ 37 ] [ 38 ] Additional medications such as antiplatelets including aspirin , beta blockers , or nitroglycerin may be recommended. [ 38 ] Procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG) may be used in severe disease. [ 38 ] [ 39 ] In those with stable CAD it is unclear if PCI or CABG in addition to the other treatments improve life expectancy or decreases heart attack risk. [ 40 ] In 2013 CAD was the most common cause of death globally, resulting in 8.14 million deaths (16.8%) up from 5.74 million deaths (12%) in 1990. [ 28 ] The risk of death from CAD for a given age has decreased between 1980 and 2010 especially in developed countries . [ 41 ] The number of cases of CAD for a given age has also decreased between 1990 and 2010. [ 42 ] In the U.S. in 2010 about 20% of those over 65 had CAD, while it was present in 7% of those 45 to 64, and 1.3% of those 18 to 45. [ 43 ] Rates are higher among men than women of a given age. [ 43 ] Heart failure, or formally cardiomyopathy, is the impaired function of the heart, and there are numerous causes and forms of heart failure. The causes of cardiomyopathy can be genetic , viral, or lifestyle-related. Key symptoms of cardiomyopathy include shortness of breath, fatigue, and irregular heartbeats. Understanding the specific function of cardiac muscle is crucial, as the heart muscle's main role is to pump blood throughout the body efficiently. [ 44 ] Cardiac arrhythmia, also known as "cardiac dysrhythmia" or "irregular heartbeat", is a group of conditions in which the heartbeat is too fast, too slow, or irregular in its rhythm. A heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia . A heart rate that is too slow – below 60 beats per minute – is called bradycardia . [ 45 ] Many types of arrhythmia present no symptoms. When symptoms are present, they may include palpitations , or feeling a pause between heartbeats. More serious symptoms may include lightheadedness , passing out , shortness of breath , or chest pain . [ 46 ] While most types of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure . [ 45 ] [ 47 ] Others may result in cardiac arrest . [ 47 ] There are four main types of arrhythmia: extra beats , supraventricular tachycardias , ventricular arrhythmias , and bradyarrhythmias . Extra beats include premature atrial contractions , premature ventricular contractions , and premature junctional contractions . Supraventricular tachycardias include atrial fibrillation , atrial flutter , and paroxysmal supraventricular tachycardia . Ventricular arrhythmias include ventricular fibrillation and ventricular tachycardia . [ 47 ] [ 48 ] Arrhythmias are due to problems with the electrical conduction system of the heart . [ 45 ] Arrhythmias may occur in children; however, the normal range for the heart rate is different and depends on age. [ 47 ] A number of tests can help diagnose arrhythmia, including an electrocardiogram and Holter monitor . [ 49 ] Most arrhythmias can be effectively treated. [ 45 ] Treatments may include medications, medical procedures such as a pacemaker , and surgery. Medications for a fast heart rate may include beta blockers or agents that attempt to restore a normal heart rhythm such as procainamide . This later group may have more significant side effects especially if taken for a long period of time. Pacemakers are often used for slow heart rates. Those with an irregular heartbeat are often treated with blood thinners to reduce the risk of complications. Those who have severe symptoms from an arrhythmia may receive urgent treatment with a jolt of electricity in the form of cardioversion or defibrillation . [ 50 ] Arrhythmia affects millions of people. [ 51 ] In Europe and North America, as of 2014, atrial fibrillation affects about 2% to 3% of the population. [ 52 ] Atrial fibrillation and atrial flutter resulted in 112,000 deaths in 2013, up from 29,000 in 1990. [ 28 ] Sudden cardiac death is the cause of about half of deaths due to cardiovascular disease or about 15% of all deaths globally. [ 53 ] About 80% of sudden cardiac death is the result of ventricular arrhythmias. [ 53 ] Arrhythmias may occur at any age but are more common among older people. [ 51 ] Cardiac arrest is a sudden stop in effective blood flow due to the failure of the heart to contract effectively. [ 54 ] Symptoms include loss of consciousness and abnormal or absent breathing . [ 55 ] [ 56 ] Some people may have chest pain , shortness of breath , or nausea before this occurs. [ 56 ] If not treated within minutes, death usually occurs. [ 54 ] The most common cause of cardiac arrest is coronary artery disease . Less common causes include major blood loss , lack of oxygen, very low potassium , heart failure , and intense physical exercise. A number of inherited disorders may also increase the risk including long QT syndrome . The initial heart rhythm is most often ventricular fibrillation . [ 57 ] The diagnosis is confirmed by finding no pulse. [ 55 ] While a cardiac arrest may be caused by heart attack or heart failure these are not the same. [ 54 ] Prevention includes not smoking, physical activity, and maintaining a healthy weight. [ 58 ] Treatment for cardiac arrest is immediate cardiopulmonary resuscitation (CPR) and, if a shockable rhythm is present, defibrillation . [ 59 ] Among those who survive targeted temperature management may improve outcomes. [ 60 ] An implantable cardiac defibrillator may be placed to reduce the chance of death from recurrence. [ 58 ] In the United States , cardiac arrest outside of hospital occurs in about 13 per 10,000 people per year (326,000 cases). In hospital cardiac arrest occurs in an additional 209,000 [ 61 ] Cardiac arrest becomes more common with age. It affects males more often than females. [ 62 ] The percentage of people who survive with treatment is about 8%. Many who survive have significant disability . Many U.S. television shows, however, have portrayed unrealistically high survival rates of 67%. [ 63 ] Hypertension , also known as "high blood pressure", is a long term medical condition in which the blood pressure in the arteries is persistently elevated. [ 64 ] High blood pressure usually does not cause symptoms. [ 65 ] Long term high blood pressure, however, is a major risk factor for coronary artery disease , stroke , heart failure , peripheral vascular disease , vision loss , and chronic kidney disease . [ 66 ] [ 67 ] Lifestyle factors can increase the risk of hypertension. These include excess salt in the diet, excess body weight , smoking , and alcohol consumption. [ 65 ] [ 68 ] Hypertension can also be caused by other diseases, or occur as a side-effect of drugs. [ 69 ] Blood pressure is expressed by two measurements, the systolic and diastolic pressures, which are the maximum and minimum pressures, respectively. [ 65 ] Normal blood pressure when at rest is within the range of 100–140 millimeters mercury (mmHg) systolic and 60–90 mmHg diastolic. [ 70 ] High blood pressure is present if the resting blood pressure is persistently at or above 140/90 mmHg for most adults. [ 68 ] Different numbers apply to children. [ 71 ] When diagnosing high blood pressure, ambulatory blood pressure monitoring over a 24-hour period appears to be more accurate than "in-office" blood pressure measurement at a physician's office or other blood pressure screening location. [ 64 ] [ 68 ] [ 72 ] Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications. [ 73 ] Lifestyle changes include weight loss, decreased salt intake, physical exercise, and a healthy diet. [ 68 ] If changes in lifestyle are insufficient, blood pressure medications may be used. [ 73 ] A regimen of up to three medications effectively controls blood pressure in 90% of people. [ 68 ] The treatment of moderate to severe high arterial blood pressure (defined as >160/100 mmHg) with medication is associated with an improved life expectancy and reduced morbidity . [ 74 ] The effect of treatment for blood pressure between 140/90 mmHg and 160/100 mmHg is less clear, with some studies finding benefits [ 75 ] [ 76 ] while others do not. [ 77 ] High blood pressure affects between 16% and 37% of the population globally. [ 68 ] In 2010, hypertension was believed to have been a factor in 18% (9.4 million) deaths. [ 78 ] Essential hypertension is the form of hypertension that by definition has no identifiable cause. It is the most common type of hypertension, affecting 95% of hypertensive patients, [ 79 ] [ 80 ] [ 81 ] [ 82 ] it tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age , and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension. Hypertension can increase the risk of cerebral , cardiac , and renal events. [ 83 ] Secondary hypertension is a type of hypertension which is caused by an identifiable underlying secondary cause. It is much less common than essential hypertension, affecting only 5% of hypertensive patients. It has many different causes including endocrine diseases , kidney diseases , and tumors . It also can be a side effect of many medications . [ 84 ] Complications of hypertension are clinical outcomes that result from persistent elevation of blood pressure. [ 85 ] Hypertension is a risk factor for all clinical manifestations of atherosclerosis since it is a risk factor for atherosclerosis itself. [ 86 ] [ 87 ] [ 88 ] [ 89 ] [ 90 ] It is an independent predisposing factor for heart failure , [ 91 ] [ 92 ] coronary artery disease , [ 93 ] [ 94 ] stroke , [ 85 ] renal disease , [ 95 ] [ 96 ] [ 97 ] and peripheral arterial disease . [ 98 ] [ 99 ] It is the most important risk factor for cardiovascular morbidity and mortality , in industrialized countries . [ 100 ] A congenital heart defect, also known as a "congenital heart anomaly" or "congenital heart disease", is a problem in the structure of the heart that is present at birth . [ 101 ] Signs and symptoms depend on the specific type of problem. [ 102 ] Symptoms can vary from none to life-threatening. [ 101 ] When present they may include rapid breathing, bluish skin , poor weight gain, and feeling tired. [ 103 ] It does not cause chest pain. [ 103 ] Most congenital heart problems do not occur with other diseases. [ 102 ] Complications that can result from heart defects include heart failure . [ 103 ] The cause of a congenital heart defect is often unknown. [ 104 ] Certain cases may be due to infections during pregnancy such as rubella , use of certain medications or drugs such as alcohol or tobacco , parents being closely related, or poor nutritional status or obesity in the mother. [ 102 ] [ 105 ] Having a parent with a congenital heart defect is also a risk factor. [ 106 ] A number of genetic conditions are associated with heart defects including Down syndrome , Turner syndrome , and Marfan syndrome . [ 102 ] Congenital heart defects are divided into two main groups: cyanotic heart defects and non-cyanotic heart defects , depending on whether the child has the potential to turn bluish in color. [ 102 ] The problems may involve the interior walls of the heart, the heart valves , or the large blood vessels that lead to and from the heart. [ 101 ] Congenital heart defects are partly preventable through rubella vaccination , the adding of iodine to salt, and the adding of folic acid to certain food products. [ 102 ] Some defects do not need treatment. [ 101 ] Other may be effectively treated with catheter based procedures or heart surgery . [ 107 ] Occasionally a number of operations may be needed. [ 107 ] Occasionally heart transplantation is required. [ 107 ] With appropriate treatment outcomes, even with complex problems, are generally good. [ 101 ] Heart defects are the most common birth defect . [ 102 ] [ 108 ] In 2013 they were present in 34.3 million people globally. [ 108 ] They affect between 4 and 75 per 1,000 live births depending upon how they are diagnosed. [ 102 ] [ 106 ] About 6 to 19 per 1,000 cause a moderate to severe degree of problems. [ 106 ] Congenital heart defects are the leading cause of birth defect-related deaths. [ 102 ] In 2013 they resulted in 323,000 deaths down from 366,000 deaths in 1990. [ 28 ] Tetralogy of Fallot is the most common congenital heart disease arising in 1–3 cases per 1,000 births. The cause of this defect is a ventricular septal defect (VSD) and an overriding aorta . These two defects combined causes deoxygenated blood to bypass the lungs and going right back into the circulatory system. The modified Blalock-Taussig shunt is usually used to fix the circulation. This procedure is done by placing a graft between the subclavian artery and the ipsilateral pulmonary artery to restore the correct blood flow. Pulmonary atresia happens in 7–8 per 100,000 births and is characterized by the aorta branching out of the right ventricle. This causes the deoxygenated blood to bypass the lungs and enter the circulatory system. Surgeries can fix this by redirecting the aorta and fixing the right ventricle and pulmonary artery connection. There are two types of pulmonary atresia, classified by whether or not the baby also has a ventricular septal defect . [ 109 ] [ 110 ] Double outlet right ventricle (DORV) is when both great arteries, the pulmonary artery and the aorta, are connected to the right ventricle. There is usually a VSD in different particular places depending on the variations of DORV, typically 50% are subaortic and 30%. The surgeries that can be done to fix this defect can vary due to the different physiology and blood flow in the defected heart. One way it can be cured is by a VSD closure and placing conduits to restart the blood flow between the left ventricle and the aorta and between the right ventricle and the pulmonary artery. Another way is systemic-to-pulmonary artery shunt in cases associated with pulmonary stenosis . Also, a balloon atrial septostomy can be done to relieve hypoxemia caused by DORV with the Taussig-Bing anomaly while surgical correction is awaited. [ 111 ] There are two different types of transposition of the great arteries , Dextro-transposition of the great arteries and Levo-transposition of the great arteries , depending on where the chambers and vessels connect. Dextro-transposition happens in about 1 in 4,000 newborns and is when the right ventricle pumps blood into the aorta and deoxygenated blood enters the bloodstream. The temporary procedure is to create an atrial septal defect . A permanent fix is more complicated and involves redirecting the pulmonary return to the right atrium and the systemic return to the left atrium, which is known as the Senning procedure . The Rastelli procedure can also be done by rerouting the left ventricular outflow, dividing the pulmonary trunk, and placing a conduit in between the right ventricle and pulmonary trunk. Levo-transposition happens in about 1 in 13,000 newborns and is characterized by the left ventricle pumping blood into the lungs and the right ventricle pumping the blood into the aorta. This may not produce problems at the beginning, but will eventually due to the different pressures each ventricle uses to pump blood. Switching the left ventricle to be the systemic ventricle and the right ventricle to pump blood into the pulmonary artery can repair levo-transposition. [ citation needed ] Persistent truncus arteriosus is when the truncus arteriosus fails to split into the aorta and pulmonary trunk. This occurs in about 1 in 11,000 live births and allows both oxygenated and deoxygenated blood into the body. The repair consists of a VSD closure and the Rastelli procedure. [ 112 ] [ 113 ] Ebstein's anomaly is characterized by a right atrium that is significantly enlarged and a heart that is shaped like a box. This is very rare and happens in less than 1% of congenital heart disease cases. The surgical repair varies depending on the severity of the disease. [ 114 ] Pediatric cardiology is a sub-specialty of pediatrics . To become a pediatric cardiologist in the U.S., one must complete a three-year residency in pediatrics, followed by a three-year fellowship in pediatric cardiology. Per doximity , pediatric cardiologists make an average of $303,917 in the U.S. [ 5 ] Diagnostic tests in cardiology are the methods of identifying heart conditions associated with healthy vs. unhealthy, pathologic heart function. The starting point is obtaining a medical history , followed by Auscultation . Then blood tests , electrophysiological procedures , and cardiac imaging can be ordered for further analysis. Electrophysiological procedures include electrocardiogram, cardiac monitoring , cardiac stress testing , and the electrophysiology study . [ citation needed ] Cardiology is known for randomized controlled trials that guide clinical treatment of cardiac diseases. While dozens are published every year, there are landmark trials that shift treatment significantly. Trials often have an acronym of the trial name, and this acronym is used to reference the trial and its results. Some of these landmark trials include:	https://en.wikipedia.org/wiki/Cardiology
Cardiomyoplasty is a surgical procedure in which healthy muscle from another part of the body is wrapped around the heart to provide support for the failing heart. [ 1 ] Most often the latissimus dorsi muscle is used for this purpose. A special pacemaker is implanted to make the skeletal muscle contract. If cardiomyoplasty is successful and increased cardiac output is achieved, it usually acts as a bridging therapy, giving time for damaged myocardium to be treated in other ways, such as remodeling by cellular therapies. [ 2 ] [ 3 ] Cellular cardiomyoplasty is a method which augments myocardial function and cardiac output by directly growing new muscle cells in the damaged myocardium (heart muscle). Tissue engineering, which is now being categorized as a form of regenerative medicine, can be defined as biomedical engineering to reconstruct, repair, and improve biological tissues. Research efforts in tissue engineering have been ongoing and it is emerging as one of the key areas of medical research. Furthermore, there are vast developments in tissue engineering, which involve leveraging of technologies from biomaterials, molecular medicine, biochemistry, nanotechnology, genetic and biomedical engineering for regeneration and cell expansion targets to restructure and/or repair human organs. Injection of cardiomyogenic and/or angiogenic stem cells have been proposed as alternatives to existing treatments. For cardiovascular application, skeletal myoblasts are of great interest as they can be easily isolated and are associated with high proliferation rate. These cells have also been demonstrated to be hypoxia -resistant. Bone marrow contains different cell populations, which exhibit excellent plasticity toward cardiogenic and endothelial cells. These cell populations are endothelial progenitor cells, hematopoietic stem cells and mesenchymal stem cells. Adipose tissue host progenitor cells with reported interesting cardiomyogenic and vasculogenic potential in the sense that they improve heart functions and reduce infarction size in rodent animal models. Subcutaneous adipose tissue is also a source of mesenchymal stem cells and have demonstrated positive outcomes in terms of cardiovascular tissue remodeling. Mammal hearts also host naturally occurring cardiac stem cells which may be capable of differentiating themselves into cardiomyocytes, endothelial cells and cardiac fibroblasts. [ 4 ] This self-regeneration capacity gives rise to alternatives to classical cellular therapies whereby administration of growth factors such as Thymosin β4 for cell activation and migration are solely necessary. Largely democratized in terms of population information, embryonic stem cells are known for their strong capacity for expansion and differentiation into cardiomyocytes, endothelial cells and cardiac fibroblasts. However, if non autologous, immunosuppression therapy is associated with such treatment. Hence, research has been focused on induced pluripotent stem cells (iPSCs) from somatic human tissue. Further to cell and necessary relevant growth factor selection, cell delivery is an important issue. Indeed, the intracoronary route is the most straightforward cell delivery route as associated with intramyocardial cellular retention; retention rates are however low, i.e. exceed 10%. Washed off cells reach other organs or die, which can be an issue at the time of prepare ICH module 8. Other alternative injection routes have been studied, namely injection via sternotomy, endomyocardial and intracoronary routes. Nevertheless, all methods aforementioned have been associated with limited cardiac function improvements and limited cell survival once implanted in the fibrous myocardium. To resume, stem cells and delivery routes aforementioned are suitable for cardiomyoplasty as demonstrated safe with some degree of benefit for the patient. However, cardiac remodelling remains limited due to limited cell residency, impact of mechanical forces onto cell survival and tissue hypoxia. Furthermore, lack of cellular electrochemical coupling can lead to arrhythmias. Another point of consideration concerns the use of embryonic stem cells, whereby indifferentiation yields uncontrolled proliferation and possible consequent formation of teratomas. Also iPSCs have been associated with viral infection and eventual oncogenicity. Cardiac tissue engineering is a new technology based on the use of combinations of cells with regenerative capacity, biological and/or synthetic materials, cell signaling agents to induce the regeneration of an organ or damaged tissue. In an ideal scenario, regenerated tissue would reproduce sophisticated asymmetric helicodoidal architecture of the myocardium with the production of specialized extracellular matrix to stimulate vascularization in the implanted tissue. From a cellular perspective, [ 5 ] available techniques are monolayer cell construct onto temperature-sensitive polymer, where their detachment is driven by behavior of the mechanical properties of the synthetic support without the need of any enzymatic digestion such as trypsin. Cardiomyocites sheets have also been successfully implanted with an observed contractile function as a result of inter-cellular communication between the host and graft. However, from a practical point of view, such approach lacks of translational character as all studies share the lack of reproducibility, i.e. a construct of similar characteristics of the native tissue does not guarantee the same results. Another approach resides in the use of hydrogels. Natural hydrogels such as Matrigel, [ 6 ] collagen and fibrin have been used as entrapment matrices, wherein the cells to be injected are embedded. However the associated high pressure of injection is associated with a high mortality rate for the cells thereby negatively impacting the benefit ratio of this approach. Furthermore, from a technical point of view, due to the polydispersity of these natural hydrogels, purification is a requisite but very difficult step. Synthetic hydrogels, such as polyethylene glycol , polylactic acid, polylactic acid-co-glycolic acid, polycaprolactone, polyacrylamide and polyurethane have been proposed. Metalloproteinase-sensitive polyethylene is of particular interest. Indeed, this polymer modulates its mechanical and biophysical properties accordingly to enzymatic activities associated with cardiomyogenic differentiation of implanted cells. To date, no hydrogel matrix is FDA-approved for stem cell therapy use despite a large number of biomaterials currently commercially available. A general comment on hydrogel based technologies: Natural hydrogel are well tolerated by the host and cells due to their mimicking the natural ECM in terms of backbone and microstructure. However they suffer from batch to batch variation (a drawback for current Good Manufacturing Practices (cGMPs) required for clinical application), high degradation rates, and poor tenability. Synthetic hydrogels are reproducible, tunable and amenable regulatory and manufacturing protocols. [ 7 ] [ 8 ] [ 9 ] Their chemical modification permits the integration of cellular attachment sites and a certain control over degradation rates. Semi-synthetic hydrogels share characteristics of both classes. Indeed, they permit either the modification of the purified natural biopolymers or by coupling the synthetic component with integrin and/or growth factor binding sites.	https://en.wikipedia.org/wiki/Cardiomyoplasty
A frequent type of syncope, termed vasovagal syncope is originated by intense cardioinhibition, mediated by a sudden vagal reflex, that causes transitory cardiac arrest by asystole and/or transient total atrioventricular block . [ 1 ] [ 2 ] It is known as “Vaso-vagal Syncope”, “Neurocardiogenic Syncope” or “Neurally-mediated Reflex Syncope”. [ 3 ] Although many different therapies have been tried in this condition, severe and refractory cases have been treated with pacemaker implantation despite great controversies about its benefit. [ 4 ] [ 5 ] The “ Cardioneuroablation ” is a technique created in the nineties and patented in USA , aiming to eliminate the cardiac branch of vagal reflex in order to treat the neurocardiogenic syncope without pacemaker implantation. [ 6 ] [ 7 ] It is performed without surgery , by using radiofrequency catheter ablation with one-day hospital. [ citation needed ] The results up to 100 months follow-up are showing better outcome than clinical measures or pacemaker implantation with changing the tilt-test on to normal and by absence of syncope in more than 90% of patients without medications. [ 8 ] [ 9 ]	https://en.wikipedia.org/wiki/Cardioneuroablation
Cardiooncology , cardio-oncology or cardiovascular oncology is an interdisciplinary field of medicine which study the molecular and clinical alterations in cardiovascular system during the different methods of treatment of cancer , especially chemotherapy and targeted therapy . [ 1 ] Since 2018 the European Society of Cardiology has had a council of cardio-oncology. [ 2 ] This cardiovascular system article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cardiooncology
Cardiorenal syndrome ( CRS ) refers to the spectrum of disorders in which acute or chronic dysfunction of the heart or kidneys leads to acute or chronic dysfunction of the other. [ 1 ] The condition is classified into five subtypes based on the primary organ dysfunction and whether the disease process is acute or chronic. The heart and the kidneys maintain hemodynamic stability and organ perfusion through an intricate network. CRS results from a complex interplay of hemodynamic alterations, neurohormonal activation, inflammatory mediators , and endothelial dysfunction , all contributing to progressive organ injury. [ 2 ] Cardiorenal syndrome is commonly associated with conditions such as heart failure , chronic kidney disease (CKD) , acute kidney injury (AKI) , and systemic hypertension . [ 3 ] Management of CRS primarily focuses on addressing the underlying cause while mitigating the complications associated with the syndrome. Since volume overload is a predominant feature in most patients, treatment typically involves fluid removal, primarily through loop diuretics , with thiazides as adjuncts for diuretic resistant cases. [ 4 ] Ultrafiltration is reserved for refractory cases. [ 4 ] Depending on the case, additional therapies such as ACE inhibitors , angiotensin II receptor blockers , mineralocorticoid receptor antagonists , and inotropes may be utilized. [ 5 ] Despite available treatments, CRS remains associated with high morbidity and mortality. Cardiorenal syndrome (CRS) encompasses a spectrum of disorders in which acute or chronic dysfunction in the heart or kidneys leads to dysfunction in the other organ. Therefore, the clinical signs and symptoms are consistent with congestive heart failure and chronic kidney disease . The clinical presentation of most patients typically involves fluid overload , reduced cardiac output , and worsening renal function. Patients with acute cardiorenal syndrome often present with clinical features of pulmonary or systemic congestion and acute kidney injury . [ 4 ] Symptoms of peripheral edema and shortness of breath are common both in patients with CHF and CKD or a combination thereof. Patients will frequently exhibit signs of acute decompensated heart failure , such as volume overload characterized by peripheral edema, pulmonary congestion , jugular venous distension , and shortness of breath. [ 3 ] Prolonged effects of heart failure, such as fatigue and exercise intolerance, may also be present. Symptoms of acute cardiorenal syndrome also often present with classic indicators of renal dysfunction. Increased serum levels of creatinine and BUN , as well as reduced urine production may indicate worsening renal function. [ 6 ] The primary risk factors for the development of cardiorenal syndrome are pre-existing cardiac or renal disease. The following risk factors have been associated with increased incidence of CRS. [ 7 ] Clinical: Heart: Kidney: Cardiorenal syndrome (CRS) pathophysiology involves a complex bidirectional interaction between the heart and kidneys. [ citation needed ] The underlying mechanisms are broadly categorized into hemodynamic and non-hemodynamic factors. Hemodynamic factors primarily include changes in blood flow, such as reduced cardiac output and elevated central venous or intra-abdominal pressures. Non-hemodynamic factors include neurohormonal activation, oxidative stress , and systemic inflammation . These mechanisms often act synergistically, contributing to the progressive dysfunction of both organs. [ 2 ] Reduced cardiac output , commonly due to heart failure or other cardiovascular conditions, leads to decreased renal perfusion. [ 8 ] Historically, this reduction in perfusion was considered the primary driver of kidney dysfunction in heart failure. However, recent studies suggest that venous congestion may play an even more critical role. Heart failure increases central venous and intra-abdominal pressures, which are important regulators of renal blood flow. [ 9 ] Elevated venous pressures reduce the net glomerular filtration pressure, promoting renal injury. [ 10 ] These changes contribute to worsening volume overload and further deterioration of cardiac and renal function. The renin-angiotensin-aldosterone system (RAAS) is activated in response to reduced renal perfusion. Although RAAS normally helps maintain blood pressure and organ perfusion, chronic over-activation leads to inappropriate sodium and water retention. This exacerbates volume overload and perpetuates a cycle of worsening heart and kidney function. [ 11 ] [ 12 ] In addition to hemodynamic changes, several non-hemodynamic mechanisms contribute to the progression of CRS. These include neurohormonal activation, oxidative stress, and systemic inflammation, all of which are associated with structural and functional deterioration in both the heart and kidneys. [ 13 ] Neurohormonal systems, primarily the RAAS and sympathetic nervous system (SNS), are activated in response to reduced renal perfusion. [ 13 ] In heart failure, these systems become over-activated, causing peripheral vasoconstriction and extracellular fluid retention. [ 12 ] Beyond hemodynamic effects, RAAS and SNS activation stimulate oxidative and inflammatory pathways and contribute to cardiac remodeling and progressive dysfunction. [ 13 ] Oxidative stress and inflammation also play critical roles. Elevated levels of reactive oxygen species (ROS), endothelin , and arginine vasopressin contribute to endothelial dysfunction, myocardial hypertrophy, and fibrosis, as well as to renal tubular injury and glomerular dysfunction. [ 14 ] An imbalance between nitric oxide and ROS exacerbates endothelial dysfunction and impairs organ perfusion. There is a close interaction within these cardio-renal connectors as well as between these factors and the hemodynamic factors which makes the study of CRS pathophysiology complicated. [ 2 ] Diagnosing cardiorenal syndrome (CRS) is challenging due to the complex and interconnected nature of cardiac and renal dysfunction. [ citation needed ] It is critical to diagnose CRS at an early stage in order to achieve optimal therapeutic efficacy. There is no specific test to diagnose cardiorenal syndrome. Instead, diagnosis relies on clinical evaluation, laboratory data, and imaging, often in the context of known heart failure, kidney disease, or both. [ 1 ] The diagnosis of heart failure requires the presence of clinical signs and symptoms supported by evidence of a structural or functional cardiac abnormality. This diagnostic requirement for cardiorenal syndrome includes similar evidence for both the heart and kidneys. [ 5 ] Cardiac biomarkers can help to identify cardiac dysfunction in the evaluation for Cardiorenal syndrome. [ citation needed ] Brain-naturetic peptide (BNP) is a peptide that is elevated in the presence of cardiac stress and volume overload. [ citation needed ] Cardiac troponin is a biomarker that can be useful to indicate ongoing myocardial damage and stress. The use of BNP and troponin can be confounded by decreased renal clearance in patients with chronic kidney function. Despite the limitations, these biomarkers can help to identify cardiac dysfunction crucial to the diagnosis of CRS. Though less frequently used in clinical practice, Galectin-3 and ST2 (suppressor of tumorigenicity 2), markers of fibrosis and myocardial stress, can add prognostic value. [ 5 ] Unlike markers of heart damage or stress such as troponin , creatine kinase, natriuretic peptides, reliable markers for acute kidney injury are lacking. [ citation needed ] Recently, research has found several biomarkers that can be used for early detection of acute kidney injury before serious loss of organ function may occur. Several of these biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-B-D-glucosaminidase (NAG), Cystatin C, and kidney injury molecule-1 (KIM-1) which have been shown to be involved in tubular damage. [ 9 ] Other biomarkers that have been shown to be useful include BNP, IL-18, and fatty acid binding protein (FABP). [ 9 ] However, there is great variability in the measurement of these biomarkers and their use in diagnosing CRS must be assessed. [ 15 ] The diagnosis of Cardiorenal syndrome utilizes imaging to provide key insights into structural and functional changes in the heart and kidneys. Echocardiography is the primary tool to assess heart function and can provide data on heart chamber performance, valvular abnormalities, and estimates of filling pressures. Lung ultrasound has recently emerged as a commonly used bedside tool to identify pulmonary edema. Imaging of the kidneys is commonly performed using ultrasound to assess size, structural changes, and perfusion. [ 5 ] Ronco et al. first proposed a five-part classification system for CRS in 2008 which was also accepted at ADQI consensus conference in 2010. [ 1 ] These include: Acute cardiorenal syndrome occurs in patients who experience an abrupt decrease in cardiac function, causing an acute kidney injury and/or dysfunction. The sudden reduction in kidney function is frequently caused by acute decompensated heart failure , acute coronary syndrome , cardiogenic shock , and/or low flow syndrome following cardiac surgery. [ 3 ] The extent of renal injury can vary, often causing acute kidney injury (AKI) , but it can also result in acute renal failure. Type 1 CRS carries the risk of advancing to more severe stages of chronic kidney disease and end-stage renal disease (ESRD) . [ 16 ] Type 2 CRS refers to the specific situation in which chronic heart dysfunction results in progressive kidney dysfunction. Cardiac conditions such as heart failure with reduced or preserved ejection fraction, atrial fibrillation, ischemic cardiomyopathy, and congenital heart disease can result in adaptive changes in renal perfusion and neurohormonal activation over time. [ 1 ] [ 13 ] These conditions cause a time-dependent and progressive decline in renal function. The distinction between CRS type 2 and CRS type 4 is based on the assumption that, also in advanced and chronic disease, two different pathophysiological mechanisms can be distinguished, whereas both CKD and HF often develop due to a common pathophysiological background, most notably hypertension and diabetes mellitus . Furthermore, the feasibility of the distinction between CRS type 2 and 4 in terms of diagnosis can be questioned. [ 17 ] Type 3 CRS involves a abrupt decrease in renal function resulting in an acute cardiac disorder. An example of type 3 CRS would be the development of acute heart failure , acute coronary syndrome or arrhythmia following the onset of an AKI, or intrinsic kidney disease. [ 1 ] Drug-induced renal disease, rhabdomyolysis , and acute nephritic syndromes have been associated with Type 3 CRS. [ 3 ] Type 4 cardiorenal syndrome is the development of chronic heart dysfunction as a result of chronic kidney disease. Many studies have found increased rates of cardiovascular disease in patients with CKD, that occur in a dose-dependent relationship, with the greatest reductions in GFR resulting in the greatest risk for CVD development. [ 16 ] The data from scientific literature indicates that CKD increases the risk for developing heart disease. [ 1 ] This subtype of CRS refers to a separate condition resulting in simultaneous cardiac and renal systems dysfunction. These cases often involve a systemic illness such as sepsis , multiple traumas, amyloidosis , sarcoidosis , diabetes mellitus , hepatitis b , hepatitis c , systemic lupus erythematosus (SLE) , and significant burns, causing an abrupt decrease in both cardiac and renal function.[1] Type 5 CRS can also be the result of the administration of chemotherapy medications and the use of illicit substances such as heroin and cocaine . [ 16 ] [ 3 ] Braam et al. argue that classifying the CRS based on the order in which the organs are affected and the timeframe (acute vs chronic) is too simplistic and without a mechanistic classification it is difficult to study CRS. [ 2 ] They view the cardiorenal syndrome in a more holistic, integrative manner. [ 2 ] [ 18 ] They defined the cardiorenal syndrome as a pathophysiological condition in which combined heart and kidney dysfunction amplifies progression of failure of the individual organ, by inducing similar pathophysiological mechanisms. Therefore, regardless of which organ fails first, the same neurohormonal systems are activated causing accelerated cardiovascular disease, and progression of damage and failure of both organs. These systems are broken down into two broad categories of "hemodynamic factors" and non-hemodynamic factors or "cardiorenal connectors". [ 2 ] Medical management of patients with CRS is often challenging as the treatment of one organ system may adversely affect the other. Many of the medications used to treat heart failure may worsen kidney function. Chronic kidney disease has been shown to have an adverse effect on morbidity and mortality in patients with heart failure. [ 19 ] Many of the most impactful clinical trials regarding heart failure management have excluded patients with significant renal impairment, limiting the understanding of treatment in cardiorenal syndrome. [ 20 ] [ 21 ] The management of cardiorenal syndrome will vary depending on the subtype, as well as individual patient considerations. Patients with kidney failure are less likely to get all guideline-based therapies. Patients who have moderate to severe CKD was seen to have similar care when compared to those patients who had normal kidney function. This helps show how healthcare workers can do more to increase the outcome of those suffering. [ 22 ] Diuretics play a crucial role in managing fluid overload in patients with acute heart failure, with or without CRS. Although not supported by data from large clinical trials like other heart failure treatments, the clinical best practices regarding diuretics remain uncertain. Diuretics are widely considered a standard of care to reduce volume overload caused by acute heart failure based on expert opinion alone. [ 5 ] Guidelines recommend using diuretics cautiously by using minimal required dosing and close monitoring in patients with kidney disease, as they may potentially cause dehydration and worsening renal function. [ 20 ] Loop diuretics are the primary agents used in heart failure. Diuretic resistance is frequently a challenge for physicians to overcome which they may tackle by changing the dosage, frequency, or adding a second drug. [ 23 ] The use of ACE inhibitors have long term protective effect on kidney and heart tissue. Angiotensin inhibition with an ACE inhibitor or angiotensin II receptor blocker (ARB) is a standard part of treatment for heart failure. The use of Ace inhibitors and ARBs in heart failure has been shown to improve survival and reduce kidney dysfunction.However, they should be used with caution in patients with CRS and kidney failure. Although patients with kidney failure may experience slight deterioration of kidney function in the short term, the use of ACE inhibitors is shown to have prognostic benefit over the long term. [ 23 ] Two studies have suggested that the use of ACEI alongside statins might be an effective regimen to prevent a substantial number of CRS cases in high risk patients and improve survival and quality of life in these people. There are data suggesting combined use of statin and an ACEI improves clinical outcome more than a statin alone and considerably more than ACE inhibitor alone. [ 24 ] Recently, a new class of drugs for the treatment of chronic heart failure, angiotensin receptor neprilysin inhibitors (ARNI), has emerged as an alternative to ACE inhibitors and ARBs. This drug class has the effects of an ARB, blocking the effects of angiotensin II, combined with the inhibition of the enzyme neprilysin, which prevents the breakdown of natriuretic peptides. [ 25 ] Clinical studies have shown the clinical benefits of ARNIs in patients with heart failure and chronic kidney disease, supporting their use. [ 5 ] The guidelines regarding the clinical use of ARNIs in cardiorenal syndrome are still evolving. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are medications commonly used in regimens for treating heart failure and preserving renal function. SGLT2 inhibitors function to block glucose reabsorption in the kidney. These agents have demonstrated cardiovascular and renal protective benefits, such as reducing volume overload and preventing kidney damage caused by inflammation and oxidative stress. [ 26 ] Treatment with an ACE inhibitor or ARB may not sufficiently suppress the RAAS system in the long term. Mineralocorticoid receptor antagonists may be added to the regimen to provide additional RAAS suppression, resulting in more significant long-erm cardiorenal benefits. [ 5 ] [ 11 ] Beta-blockers are commonly used in guideline-directer heart failure medication regimens and may also be used in the treatment of cardiorenal syndrome. By blocking the effects of epinephrine , beta-blockers reduce blood pressure and significantly improve mortality and hospitalization rates in patients with heart failure and chronic kidney disease. [ 13 ] Ultrafiltration involves the removal of fluid from the venous system via filtration, in a process similar to dialysis . Ultrafiltration is generally reserved for patients in acute decompensated heart failure that have volume overload resistant to diuretics. [ 5 ] Many case reports have shown improved kidney function with ultrafiltration, however the clinical value has yet to be established. [ 9 ] [ 5 ] Inotropes are a class of drugs that enhance the contractile force produced by the heart and the overall cardiac output. [ 27 ] Due to their mechanism, they have the potential to treat cardiorenal syndrome by improving heart function and reducing venous congestion. However, the efficacy of inotropes as a long-term therapy has yet to be proven. They may be used in patients with cardiorenal syndrome in the instance of cardiogenic shock . [ 11 ] [ 5 ] CRT , a form of cardiac pacing , helps to improve heart function by electrically activating the ventricles to synchronize their contractions. [ 5 ] CRT has been shown to improve renal response in patients with chronic kidney disease and congestive heart failure. [ 11 ] Kidney failure is very common in patients with congestive heart failure . It was shown that kidney failure complicates one-third of all admissions for heart failure, which is the leading cause of hospitalization in the United States among adults over 65 years old. [ 9 ] Not only is this the leading cause of hospitalization, it also increases the stays in the ICU. [ 28 ] These complications led to longer hospital stay, higher mortality, and greater chance for readmission. The inpatient mortality was seen to be much higher for patients with much more sever renal dysfunction. [ 22 ] The increase of hospital and ICU stays also increases the cost of care in the hospital. Not only are there patients suffering from their disease, they are also suffering financially due to the cost of the hospital stays. [ 28 ] Another study found that 39% of patients in NYHA class 4 and 31% of patients in NYHA class 3 had severely impaired kidney function. [ 29 ] Similarly, kidney failure can have deleterious effects on cardiovascular function. It was estimated that about 44% of deaths in patients with end-stage kidney failure (ESKF) are due to cardiovascular disease. [ 30 ]	https://en.wikipedia.org/wiki/Cardiorenal_syndrome
Cardiothoracic surgery is the field of medicine involved in surgical treatment of organs inside the thoracic cavity — generally treatment of conditions of the heart ( heart disease ), lungs ( lung disease ), and other pleural or mediastinal structures. In most countries, cardiothoracic surgery is further subspecialized into cardiac surgery (involving the heart and the great vessels ) and thoracic surgery (involving the lungs, esophagus , thymus , etc.); the exceptions are the United States , Australia , New Zealand , the United Kingdom , India and some European Union countries such as Portugal . [ 1 ] A cardiac surgery residency typically comprises anywhere from four to six years (or longer) of training to become a fully qualified surgeon. [ 2 ] Cardiac surgery training may be combined with thoracic surgery and/or vascular surgery and called cardiovascular (CV) / cardiothoracic (CT) / cardiovascular thoracic (CVT) surgery. Cardiac surgeons may enter a cardiac surgery residency directly from medical school , or first complete a general surgery residency followed by a fellowship . Cardiac surgeons may further sub-specialize cardiac surgery by doing a fellowship in a variety of topics including pediatric cardiac surgery, cardiac transplantation , adult-acquired heart disease, weak heart issues, and many more problems in the heart. [ citation needed ] The highly competitive Surgical Education and Training (SET) program in Cardiothoracic Surgery is six years in duration, usually commencing several years after completing medical school. Training is administered and supervised via a bi-national (Australia and New Zealand) training program. Multiple examinations take place throughout the course of training, culminating in a final fellowship exam in the final year of training. Upon completion of training, surgeons are awarded a Fellowship of the Royal Australasian College of Surgeons (FRACS), denoting that they are qualified specialists. Trainees having completed a training program in General Surgery and have obtained their FRACS will have the option to complete fellowship training in Cardiothoracic Surgery of four years in duration, subject to college approval. It takes around eight to ten years minimum of post-graduate (post-medical school) training to qualify as a cardiothoracic surgeon. Competition for training places and for public (teaching) hospital places is very high currently, leading to concerns regarding workforce planning in Australia. [ citation needed ] Historically, cardiac surgeons in Canada completed general surgery followed by a fellowship in CV / CT / CVT. During the 1990s, the Canadian cardiac surgery training programs changed to six-year "direct-entry" programs following medical school. The direct-entry format provides residents with experience related to cardiac surgery they would not receive in a general surgery program (e.g. echocardiography , coronary care unit , cardiac catheterization etc.). Residents in this program will also spend time training in thoracic and vascular surgery . Typically, this is followed by a fellowship in either Adult Cardiac Surgery, Heart Failure/Transplant, Minimally Invasive Cardiac Surgery, Aortic Surgery, Thoracic Surgery, Pediatric Cardiac Surgery or Cardiac ICU. Contemporary Canadian candidates completing general surgery and wishing to pursue cardiac surgery often complete a cardiothoracic surgery fellowship in the United States. The Royal College of Physicians and Surgeons of Canada also provides a three-year cardiac surgery fellowship for qualified general surgeons that is offered at several training sites including the University of Alberta , the University of British Columbia and the University of Toronto . [ citation needed ] Thoracic surgery is its own separate 2–3 year fellowship of general or cardiac surgery in Canada. Cardiac surgery programs in Canada: [ citation needed ] Cardiac surgery training in the United States is combined with general thoracic surgery and called cardiothoracic surgery or thoracic surgery. A cardiothoracic surgeon in the U.S. is a physician who first completes a general surgery residency (typically 5–7 years), followed by a cardiothoracic surgery fellowship (typically 2–3 years). The cardiothoracic surgery fellowship typically spans two or three years, but certification is based on the number of surgeries performed as the operating surgeon, not the time spent in the program, in addition to passing rigorous board certification tests. Two other pathways to shorten the duration of training have been developed: (1) a combined general-thoracic surgery residency consisting of four years of general surgery training and three years of cardiothoracic training at the same institution and (2) an integrated six-year cardiothoracic residency (in place of the general surgery residency plus cardiothoracic residency), which have each been established at many programs (over 20). [ 3 ] Applicants match into the integrated six-year (I-6) programs directly out of medical school, and the application process has been extremely competitive for these positions as there were approximately 160 applicants for 10 spots in the U.S. in 2010. As of May 2013, there are 20 approved programs, which include the following: Integrated six-year Cardiothoracic Surgery programs in the United States: [ citation needed ] The American Board of Thoracic Surgery offers a special pathway certificate in congenital cardiac surgery which typically requires an additional year of fellowship. This formal certificate is unique because congenital cardiac surgeons in other countries do not have formal evaluation and recognition of pediatric training by a licensing body. The earliest operations on the pericardium (the sac that surrounds the heart) took place in the 19th century and were performed by Francisco Romero (1801) [ 4 ] Dominique Jean Larrey , Henry Dalton , and Daniel Hale Williams . [ 5 ] The first surgery on the heart itself was performed by Norwegian surgeon Axel Cappelen on 4 September 1895 at Rikshospitalet in Kristiania, now Oslo . He ligated a bleeding coronary artery in a 24-year-old man who had been stabbed in the left axilla and was in deep shock upon arrival. Access was through a left thoracotomy . The patient awoke and seemed fine for 24 hours, but became ill with increasing temperature and he ultimately died from what the post mortem proved to be mediastinitis on the third postoperative day. [ 6 ] [ 7 ] The first successful surgery of the heart, performed without any complications, was by Ludwig Rehn of Frankfurt , Germany , who repaired a stab wound to the right ventricle on September 7, 1896. [ 8 ] [ 9 ] Surgery in great vessels ( aortic coarctation repair, Blalock-Taussig shunt creation, closure of patent ductus arteriosus ) became common after the turn of the century and falls in the domain of cardiac surgery, but technically cannot be considered heart surgery. One of the more commonly known cardiac surgery procedures is the coronary artery bypass graft (CABG) , also known as "bypass surgery." In 1925 operations on the heart valves were unknown. Henry Souttar operated successfully on a young woman with mitral stenosis . He made an opening in the appendage of the left atrium and inserted a finger into this chamber in order to palpate and explore the damaged mitral valve. The patient survived for several years [ 10 ] but Souttar's physician colleagues at that time decided the procedure was not justified and he could not continue. [ 11 ] [ 12 ] Cardiac surgery changed significantly after World War II . In 1948 four surgeons carried out successful operations for mitral stenosis resulting from rheumatic fever . Horace Smithy (1914–1948) revived an operation due to Dr Dwight Harken of the Peter Bent Brigham Hospital using a punch to remove a portion of the mitral valve . Charles Bailey (1910–1993) at the Hahnemann Hospital , Philadelphia , Dwight Harken in Boston and Russell Brock at Guy's Hospital all adopted Souttar's method. All these men started work independently of each other, within a few months. This time Souttar's technique was widely adopted although there were modifications. [ 11 ] [ 12 ] In 1947 Thomas Holmes Sellors (1902–1987) of the Middlesex Hospital operated on a Fallot's Tetralogy patient with pulmonary stenosis and successfully divided the stenosed pulmonary valve . In 1948, Russell Brock , probably unaware of Sellor's work, used a specially designed dilator in three cases of pulmonary stenosis . Later in 1948 he designed a punch to resect the infundibular muscle stenosis which is often associated with Fallot's Tetralogy . Many thousands of these "blind" operations were performed until the introduction of heart bypass made direct surgery on valves possible. [ 11 ] Open heart surgery is a procedure in which the patient's heart is opened and surgery is performed on the internal structures of the heart. It was discovered by Wilfred G. Bigelow of the University of Toronto that the repair of intracardiac pathologies was better done with a bloodless and motionless environment, which means that the heart should be stopped and drained of blood. The first successful intracardiac correction of a congenital heart defect using hypothermia was performed by C. Walton Lillehei and F. John Lewis at the University of Minnesota on September 2, 1952. The following year, Soviet surgeon Aleksandr Aleksandrovich Vishnevskiy conducted the first cardiac surgery under local anesthesia . [ citation needed ] Surgeons realized the limitations of hypothermia – complex intracardiac repairs take more time and the patient needs blood flow to the body, particularly to the brain . The patient needs the function of the heart and lungs provided by an artificial method, hence the term cardiopulmonary bypass . John Heysham Gibbon at Jefferson Medical School in Philadelphia reported in 1953 the first successful use of extracorporeal circulation by means of an oxygenator , but he abandoned the method, disappointed by subsequent failures. In 1954 Lillehei realized a successful series of operations with the controlled cross-circulation technique in which the patient's mother or father was used as a ' heart-lung machine '. John W. Kirklin at the Mayo Clinic in Rochester, Minnesota started using a Gibbon type pump-oxygenator in a series of successful operations, and was soon followed by surgeons in various parts of the world. [ citation needed ] Nazih Zuhdi performed the first total intentional hemodilution open heart surgery on Terry Gene Nix, age 7, on February 25, 1960, at Mercy Hospital, Oklahoma City, OK. The operation was a success; however, Nix died three years later in 1963. [ 13 ] In March, 1961, Zuhdi, Carey, and Greer, performed open heart surgery on a child, age 3 + 1 ⁄ 2 , using the total intentional hemodilution machine. In 1985 Zuhdi performed Oklahoma's first successful heart transplant on Nancy Rogers at Baptist Hospital. The transplant was successful, but Rogers, who had cancer , died from an infection 54 days after surgery. [ 14 ] Since the 1990s, surgeons have begun to perform " off-pump bypass surgery " – coronary artery bypass surgery without the aforementioned cardiopulmonary bypass . In these operations, the heart is beating during surgery, but is stabilized to provide an almost still work area in which to connect the conduit vessel that bypasses the blockage; in the U.S., most conduit vessels are harvested endoscopically, using a technique known as endoscopic vessel harvesting (EVH). [ citation needed ] Some researchers believe that the off-pump approach results in fewer post-operative complications, such as postperfusion syndrome , and better overall results. Study results are controversial as of 2007, the surgeon's preference and hospital results still play a major role. [ citation needed ] A new form of heart surgery that has grown in popularity is robot-assisted heart surgery . This is where a machine is used to perform surgery while being controlled by the heart surgeon. The main advantage to this is the size of the incision made in the patient. Instead of an incision being at least big enough for the surgeon to put his hands inside, it does not have to be bigger than "pencil-sized" holes for the robot's much smaller "hands" to enter a surgical patient's body. [ 15 ] In September 2024, the first successful fully robotic heart transplant took place at King Faisal Specialist Hospital and Research Centre in Riyadh , led by surgeon Feras Khaliel, head of the hospital's cardiac surgery and director of its Robotics and Minimally Invasive Surgery Program. [ 16 ] In December 2024, the first robotic surgery for a combined robotic aortic valve replacement (AVR) and coronary artery bypass grafting (CABG) was successfully performed through one small incision at West Virginia University , led by surgeon Vinay Badhwar, who is the executive chair of the WVU Heart and Vascular Institute and a vice president of the Society of Thoracic Surgeons . [ 17 ] [ 18 ] Pediatric cardiovascular surgery is surgery of the heart of children. The first operations to repair cardio-vascular [ 19 ] defects in children were performed by Clarence Crafoord in Sweden when he repaired coarctation of the aorta in a 12-year-old boy. [ 20 ] The first attempts to palliate congenital heart disease were performed by Alfred Blalock with the assistance of William Longmire, Denton Cooley, and Blalock's experienced technician, Vivien Thomas in 1944 at Johns Hopkins Hospital. [ 21 ] Techniques for repair of congenital heart defects without the use of a bypass machine were developed in the late 1940s and early 1950s. Among them was an open repair of an atrial septal defect using hypothermia, inflow occlusion and direct vision in a 5-year-old child performed in 1952 by Lewis and Lillihei. Lillihei used cross-circulation between a boy and his father to maintain perfusion while performing a direct repair of a ventricular septal defect in a 4-year-old child in 1954. [ 22 ] He continued to use cross-circulation and performed the first corrections of tetralogy of Fallot and presented those results in 1955 at the American Surgical Association. In the long-run, pediatric cardiovascular surgery would rely on the cardiopulmonary bypass machine developed by Gibbon and Lillehei as noted above. [ citation needed ] The development of cardiac surgery and cardiopulmonary bypass techniques has reduced the mortality rates of these surgeries to relatively low ranks. For instance, repairs of congenital heart defects are currently estimated to have 4–6% mortality rates. [ 23 ] [ 24 ] A major concern with cardiac surgery is the incidence of neurological damage. Stroke occurs in 5% of all people undergoing cardiac surgery, and is higher in patients at risk for stroke. [ 25 ] A more subtle constellation of neurocognitive deficits attributed to cardiopulmonary bypass is known as postperfusion syndrome , sometimes called "pumphead". The symptoms of postperfusion syndrome were initially felt to be permanent, [ 26 ] but were shown to be transient with no permanent neurological impairment. [ 27 ] To assess the performance of surgical units and individual surgeons, a popular risk model has been created called the EuroSCORE . This takes a number of health factors from a patient and using precalculated logistic regression coefficients attempts to give a percentage chance of survival to discharge. Within the UK this EuroSCORE was used to give a breakdown of all the centres for cardiothoracic surgery and to give some indication of whether the units and their individual surgeons performed within an acceptable range. The results are available on the CQC website. [ 28 ] The precise methodology used has however not been published to date nor has the raw data on which the results are based. [ citation needed ] Infection represents the primary non-cardiac complication from cardiothoracic surgery. Infections include mediastinitis, infectious myo- or pericarditis, endocarditis, cardiac device infection, pneumonia, empyema, and bloodstream infections. Clostridioides difficile colitis can develop when prophylactic or post-operative antibiotics are used. Post-operative patients of cardiothoracic surgery are at risk of nausea, vomiting, dysphagia, and aspiration pneumonia. [ 29 ] A pleurectomy is a surgical procedure in which part of the pleura is removed. It is sometimes used in the treatment of pneumothorax and mesothelioma . [ 30 ] In case of pneumothorax, only the apical and the diaphragmatic portions of the parietal pleura are removed. [ citation needed ] Lung volume reduction surgery, or LVRS, can improve the quality of life for certain patients with COPD of emphysematous type, when other treatment options are not enough. Parts of the lung that are particularly damaged by emphysema are removed, allowing the remaining, relatively good lung to expand and work more efficiently. The beneficial effects are correlated with the achieved reduction in residual volume. [ 31 ] Conventional LVRS involves resection of the most severely affected areas of emphysematous, non- bullous lung (aim is for 20–30%). This is a surgical option involving a mini-thoracotomy for patients in end stage COPD due to underlying emphysema, and can improve lung elastic recoil as well as diaphragmatic function . [ citation needed ] The National Emphysema Treatment Trial (NETT) was a large multicentre study (N = 1218) comparing LVRS with non-surgical treatment. Results suggested that there was no overall survival advantage in the LVRS group, except for mainly upper-lobe emphysema + poor exercise capacity, and significant improvements were seen in exercise capacity in the LVRS group. [ 32 ] Later studies have shown a wider scope of treatment with better outcomes. [ 33 ] Possible complications of LVRS include prolonged air leak (mean duration post surgery until all chest tubes removed is 10.9 ± 8.0 days. [ 34 ] In people who have a predominantly upper lobe emphysema, lung volume reduction surgery could result in better health status and lung function, though it also increases the risk of early mortality and adverse events. [ 35 ] LVRS is used widely in Europe, though its application in the United States is mostly experimental. [ 36 ] A less invasive treatment is available as a bronchoscopic lung volume reduction procedure. [ 37 ] Not all lung cancers are suitable for surgery. The stage , location and cell type are important limiting factors. In addition, people who are very ill with a poor performance status or who have inadequate pulmonary reserve would be unlikely to survive. Even with careful selection, the overall operative death rate is about 4.4%. [ 38 ] In non-small cell lung cancer staging , stages IA, IB, IIA, and IIB are suitable for surgical resection. [ 39 ] Pulmonary reserve is measured by spirometry . If there is no evidence of undue shortness of breath or diffuse parenchymal lung disease , and the FEV 1 exceeds 2 litres or 80% of predicted, the person is fit for pneumonectomy . If the FEV 1 exceeds 1.5 litres, the patient is fit for lobectomy. [ 40 ] There is weak evidence to indicate that participation in exercise programs before lung cancer surgery may reduce the risk of complications after surgery. [ 41 ] A prolonged air leak (PAL) can occur in 8–25% of people following lung cancer surgery. [ 42 ] [ 43 ] This complication delays chest tube removal and is associated with an increased length of hospital stay following a lung resection (lung cancer surgery). [ 44 ] [ 45 ] The use of surgical sealants may reduce the incidence of prolonged air leaks, however, this intervention alone has not been shown to results in a decreased length of hospital stay following lung cancer surgery. [ 46 ] There is no strong evidence to support using non-invasive positive pressure ventilation following lung cancer surgery to reduce pulmonary complications. [ 47 ]	https://en.wikipedia.org/wiki/Cardiothoracic_surgery
Cardiotoxicity is the occurrence of heart dysfunction as electric or muscle damage , resulting in heart toxicity. [ 1 ] This can cause heart failure, arrhythmia, myocarditis, and cardiomyopathy in patients. [ 2 ] Some effects are reversible, while in others, permanent damage requiring further treatment may arise. The heart becomes weaker and is not as efficient in pumping blood. Cardiotoxicity may be caused by chemotherapy (a usual example is the class of anthracyclines ) [ 3 ] [ 4 ] treatment and/or radiotherapy; [ 5 ] complications from anorexia nervosa ; adverse effects of heavy metals intake; [ 6 ] the long-term abuse of or ingestion at high doses of certain strong stimulants such as cocaine ; [ 7 ] or an incorrectly administered drug such as bupivacaine . [ 8 ] Many mechanisms have been used to explain cardiotoxicity. While many times, differing etiologies share the same mechanism, it generally depends on the agent inducing cardiac damage. For example, the primary mechanism is thought to be oxidative stress on cardiac myocytes. [ 8 ] It is thought that reactive oxygen species (ROS) overwhelm the antioxidant defenses of cardiac cells, causing direct cellular damage. This oxidative damage can disrupt mitochondrial function, therefore disrupting energy production in the heart muscle itself, leading to energy depletion via depleted ATP and promoting cell death through apoptosis or necrosis. [ 9 ] Other mechanisms of cardiotoxicity include inflammatory, [ 10 ] DNA damaging, and disrupted cell signaling. DNA damage and disrupted cellular signaling are the proposed mechanism for many cardiotoxic chemotherapeutics. [ 11 ] Regardless of the mechanism, clinical manifestations include heart failure, arrhythmia, myocarditis, and cardiomyopathy that can be permanent. [ 2 ] These conditions can greatly alter mortality and morbidity in patients meaning careful monitoring is necessary in patients exposed to cardiotoxic agents. The list of inciting agents is vast and involves various classes of medication as well as environmental agents. The effects of the cardiotoxic substances vary and are not all identical. Source: [ 12 ] Source: [ 17 ] These agents can lead to varying degrees of cardiotoxicity, and their effects may be dose-dependent and influenced by individual factors such as pre-existing cardiovascular disease and genetic predispositions that can foster greater sensitivity to any cardiac damage. The most likely effective treatment is to stop exposure to the inciting agent as soon as possible whether a pharmacologic or environmental agent. While some may fully recover from cardiotoxicity caused from exposure, many are left with permanent damage that may need further management. The management varies on the damage sustained, but generally follows guidelines for each condition such as heart failure, arrhythmias, and myocarditis. [ 20 ] Patients taking anthracyclines can take Dexrazoxane as a cardioprotective agent to prevent extensive cardiac damage. [ 21 ]	https://en.wikipedia.org/wiki/Cardiotoxicity
The Cardiovascular System Dynamics Society (CSDS), founded on 5 October 1976 in Philadelphia, Pennsylvania , by organ system physiologist and biomedical engineers , was a historic first in its mathematical and quantitative approach to cardiovascular mechanics. [ citation needed ] Currently the society includes investigators in muscle and vascular biology, subcellular and sarcomere dynamics, the microcirculation, cardiovascular biology, clinical disease, and modeling. The primary theme remains cardiovascular function, its physiologic and molecular mechanisms, with an aim to understand how these features integrate to achieve overall performance. An important component of the overall approach remains inclusion of mathematical predictive and causal models for the micro to the macro level. [ 1 ] Biannual conferences rotate between Europe, North America and Japan. [ citation needed ] This article about biomedical engineering is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cardiovascular_System_Dynamics_Society
Cardiovascular agents are drugs used to treat diseases associated with the heart or blood vessels. These medications are available for purchase only with a physician’s prescription . They include, but are not limited to, drugs that target hypertension ( antihypertensives ), hyperlipidemia ( antihyperlipidemics ) and blood clotting (blood-thinners) to reduce the risk of cardiovascular diseases . Antihypertensive agents are classified according to their mechanism of actions. The most common classes prescribed are diuretics , angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), calcium channel blockers (CCBs) and beta-blockers . Antihyperlipidemic agents most often prescribed are statins , ezetimibe and fibrates . They either lower low-density lipoprotein cholesterol (LDL-C) or triglyceride (TG) levels in blood to manage hypercholesterolaemia . Blood-thinning agents, particularly antiplatelets and anticoagulants , maintain smooth blood flow by preventing blood clot formation in blood vessels. Two main categories of antiplatelets are COX-1 inhibitors and ADP receptor inhibitors , while anticoagulants include vitamin K antagonists , direct oral anticoagulants (DOACs) and indirect thrombin inhibitors. Since cardiovascular agents have narrow therapeutic windows , a slight rise in dose may result in severe toxicity . Hence, monitoring at baseline and during therapy is needed. For drug overdose , stabilisation and antidotes help lower drug concentrations. Cardiovascular agents are drugs that affect the rate and intensity of cardiac contraction, blood vessel diameters, blood volume, blood clotting and blood cholesterol levels. [ 1 ] They are indicated to treat diseases related to the heart or the vascular system (blood vessels), such as hypertension , hyperlipidemia , coagulation disorders , heart failure and coronary artery disease . [ 1 ] These drugs are prescription-only medicines , meaning that they should be administered strictly under a doctor’s instruction and can only be obtained by means of a doctor’s prescription. Antihypertensive agents comprise multiple classes of compounds that are intended to manage hypertension (high blood pressure). Antihypertensive therapy aims to maintain a blood pressure goal of <140/90 mmHg in all patients, as well as to prevent the progression or recurrence of cardiovascular diseases (CVD) in hypertensive patients with established CVD. [ 2 ] An optimal blood pressure control is essential to prevent target-organ damage associated with complications of hypertension such as heart failure , ischemic heart diseases , stroke , and renal failure , ultimately reducing the risk of premature mortality. [ 2 ] Antihypertensives are classified by different mechanisms or sites of action. Some of the most commonly used drugs to treat hypertension include diuretics , angiotensin-converting enzyme inhibitors (ACEI), angiotensin II receptor blockers (ARBs), calcium channel blockers (CCBs), and beta-blockers . Diuretics act primarily by reducing the reabsorption of sodium at different sites of the renal tubular system and consequently promoting the elimination of sodium and water with increased urine output. [ 3 ] For loop diuretics, thiazide diuretics and thiazide-like diuretics, their common side effects include hypokalemia , hyponatremia , metabolic alkalosis and hyperglycaemia . [ 4 ] For potassium-sparing diuretics, its common side effects include hyponatremia , hyperkalemia , metabolic acidosis and sexual dysfunction specifically for spironolactone. [ 4 ] [ 5 ] The use of diuretics should be avoided in patients with severe dehydration, anuria (absence of urine production). [ 4 ] Diuretics are contraindicated in cases of severe electrolyte abnormalities and should not be administered until an electrolyte balance is restored. Special attention should be given to the use of thiazide and loop diuretics as they may exacerbate diabetes and gout . [ 4 ] Angiotensin-converting-enzyme inhibitors (ACEI) block the conversion of angiotensin I to angiotensin II by inhibiting the action of angiotensin-converting-enzyme, causing the reduction of blood volume and peripheral vascular resistance. [ 6 ] Some side effects of ACEI include hypotension, renal insufficiency , and hyperkalemia. [ 7 ] Dry cough is also a common side effect believed to be associated with decreased bradykinin breakdown. Angioedema is another possible but rare complication due to elevated levels of bradykinin. [ 6 ] ACEI should not be used in combinations with angiotensin II receptor blockers (ARBs) or direct renin inhibitors and is contraindicated in people with a history of angioedema and pregnancy. [ 6 ] [ 8 ] “Triple whammy”, the concurrent use of an ACEI with diuretics and non-steroidal anti-inflammatory drugs (NSAIDs), is also contraindicated as this combination has been correlated with an increased risk of acute kidney injury . [ 8 ] [ 7 ] ACEI should be used with caution in patients with renal impairment, and renal failure risk in severe bilateral renal stenosis . [ 8 ] Angiotensin II receptor blockers (ARBs) work by inhibiting the action of angiotensin II on, specifically AT1 receptors to prevent the vasoconstrictor effects of this receptor and block the peripheral sympathetic activity. [ 9 ] ARBs are generally well-tolerated, in which they are less likely to cause cough or angioedema compared to ACEI. Common side effects include hypotension, renal insufficiency , and hyperkalemia. [ 7 ] The contraindications of ARBs are similar to those of ACEI, including the contraindicated combinations with ACEI or direct renin inhibitors, "triple whammy" (the concurrent use of an ARB with diuretics and NSAIDs) and in patients with a history of angioedema and pregnancy. [ 6 ] [ 7 ] [ 8 ] In addition, ARB should be used with caution in patients with renal impairment and renal failure risk in severe bilateral renal stenosis [ 8 ] Calcium channel blockers (CCBs) preferentially block the L-type voltage-gated calcium channels to prevent the flow of calcium influx in the blood vessels and the heart, thereby reducing peripheral vascular resistance and cardiac output respectively. [ 10 ] In general, the side effects of CCBs include peripheral edema and gingival hyperplasia when CCBs are used chronically. [ 11 ] [ 12 ] To add on, DHP may cause reflex tachycardia and peripheral edema , while non-DHP may cause bradycardia and worsening of cardiac function due to reduced cardiac contractility and cardiac conduction. [ 12 ] [ 13 ] Non-dihydropyridines are contraindicated in patients with heart failure with reduced ejection fraction (HFrEF), and second- or third-degree atrioventricular block . [ 13 ] Special attention should be given to the coadministration of non-DHP with beta-blockers or ivabradine due to the increased risk of bradycardia. [ 13 ] Since both DHP and non-DHP are metabolized through the CYP3A4 system, grapefruit juice containing furanocoumarins (the potent inhibitors of the CYP3A4 enzyme) should be avoided. [ 13 ] Beta-blockers act as competitive antagonists that block the effects of catecholamines at beta-adrenergic receptor sites, resulting in reduced rate and force of contraction of the heart, as well as reduced peripheral vascular resistance. [ 14 ] Some common side effects include increased airway resistance for non-selective beta-blockers, exacerbation of peripheral vascular diseases, and hypotension [ 15 ] Beta-blockers are contraindicated in patients with second- or third-degree atrioventricular block . In particular, beta-blockers with intrinsic sympathomimetic activity are contraindicated in patients with myocardial infarction , heart failure or severe bradycardia . [ 15 ] [ 16 ] Beta-blockers should be used with caution in patients with asthma or chronic obstructive pulmonary disease (COPD) due to bronchoconstriction, and in patients with diabetes mellitus (DM) due to masking of hypoglycaemia . [ 16 ] Antihyperlipidemic agents are drugs used for the treatment of dyslipidemia , a condition of abnormal lipid levels in the body. It is characterised by elevations of low-density lipoprotein cholesterol (LDL-C) and triglycerides (TGs) in the blood. [ 17 ] Hypercholesterolaemia induces the formation of plaques due to the buildup of excess cholesterol within the arterial wall. This increases the risk of, or aggravate, atherosclerotic cardiovascular disease (ASCVD). Therefore, antihyperlipidemic drugs are introduced for primary and secondary coronary heart disease prevention, as well as for reduction in mortality from acute coronary outcomes. [ 18 ] These drugs include statins , ezetimibe and fibrates . Statins , also known as beta-hydroxy-beta-methylglutaryl-Coenzyme A (HMG-CoA) reductase inhibitors, are the first-line drugs for hypercholesterolaemia . [ 19 ] Examples of this drug class are atorvastatin , rosuvastatin , fluvastatin , simvastatin , pravastatin and lovastatin . Most efficacious in lowering LDL-C levels, statins block the action of HMG-CoA reductase through competitive inhibition . [ 18 ] HMG-CoA reductase, an enzyme found in hepatocytes , is responsible for the conversion of HMG-CoA to mevalonic acid for cholesterol biosynthesis. Inhibition of this enzyme reduces the synthesis and thus, availability of endogenous cholesterol. This reduction in intracellular cholesterol, in turn, causes an increase in the number of LDL receptors on hepatic cells. The elevation of LDL receptor expression decreases the plasma LDL-C level by promoting hepatic uptake of LDL from circulation. While statins are generally well-tolerated, severe adverse effects such as hepatotoxicity and myotoxicity may occur in rarity. Statin-induced hepatotoxicity can cause autoimmune hepatitis and an elevation in serum levels of hepatic enzymes such as alanine aminotransferase , impairing liver function. [ 20 ] Myotoxicity is commonly presented with statin-associated muscle symptoms (SAMS), which include myalgia and myositis . [ 21 ] In rare cases, they may progress into rhabdomyolysis , a condition manifested by muscle necrosis and myoglobinuria due to heightened creatine kinase levels. [ 22 ] [ 23 ] Another consequence of taking statins is the risk of developing new-onset diabetes, which is more prominent in individuals with high TG levels and body mass index (BMI). [ 19 ] However, the risk is far outweighed by the benefits from statin therapy for the reduction in cardiovascular outcomes. [ 20 ] Given the potential of statins to exacerbate liver and muscle abnormalities, contraindications of statins include decompensated liver cirrhosis , acute liver failure , unexplained and persistent elevations of serum transaminases, and myopathy. Moreover, statins are not recommended in pregnancy as they may cause foetal harm because of their mechanism of action. [ 19 ] Metabolised by the Cytochrome P450 (CYP450) enzyme, a major metabolic enzyme, simvastatin and lovastatin may accumulate in blood when administered with CYP450 inhibitors. [ 18 ] [ 24 ] Some of these inhibitors are azole antifungals , macrolides , CCBs , ticagrelor (antiplatelet) and grapefruit juice . Concomitant use of statins with CYP450 inhibitors, along with gemfibrozil (fibrate), increases the risk of myopathy . [ 20 ] [ 23 ] [ 25 ] This is especially significant in patients under polypharmacy . Ezetimibe is a selective cholesterol absorption inhibitor that inhibits the intestinal absorption of cholesterol by binding to the Niemann-Pick C1-Like 1 (NPC1L1) protein on the gastrointestinal epithelium. [ 23 ] This reduces the delivery of cholesterol to the liver, which then induces the upregulation of LDL receptor expression, lowering hepatic cholesterol stores and enhancing clearance of circulating LDL. More often prescribed as second-line therapy for dyslipidemia, ezetimibe is used in individuals with statin intolerance or those who failed to achieve the target LDL-C level on statin monotherapy . [ 26 ] [ 27 ] In particular, ezetimibe and statin dual therapy have shown a 15% greater LDL-C decrease compared with same-dose statins alone, favouring recovery from acute coronary syndrome . [ 23 ] Whilst ezetimibe intolerance is uncommon, some reports have been made regarding gastrointestinal and musculoskeletal effects. [ 28 ] Common adverse reactions of ezetimibe are nausea, abdominal pain, headache, fatigue, arthralgia , myalgia and hypersensitivity reactions . [ 29 ] On rare occasions, ezetimibe may cause cholecystitis , pancreatitis , elevation of serum transaminase level and rhabdomyolysis . As hepatic impairment hinders the rate of ezetimibe metabolism by the liver, ezetimibe is not recommended in individuals with moderate or severe hepatic insufficiency due to prolonged systemic exposure to the drug. [ 19 ] In addition, similar to combined statin and fibrate intake, individuals should avoid the concurrent use of ezetimibe with gemfibrozil as it would increase ezetimibe concentration in the body. [ 25 ] Fibrates , known as derivatives of fibric acids, are peroxisome proliferator-activated receptor alpha (PPAR-α) agonists primarily used for lowering TG levels and management of atherogenic dyslipidemia. [ 30 ] [ 31 ] [ 32 ] Typical drugs of the class include fenofibrate , bezafibrate , ciprofibrate and gemfibrozil . Through activation of PPAR-α receptors, fibrates decreases circulating TG via upregulation of lipoprotein lipase (LPL) expression and downregulation of apolipoprotein C-III (ApoC-III) gene expression. [ 23 ] [ 29 ] LPL is a hepatic enzyme involved in lipolysis , whereas ApoC-III is an inhibitor of LPL. Comparable to statins and ezetimibe, fibrates are usually well-tolerated with mild adverse reactions, with the exception of gemfibrozil. Some of the more prevalent side effects are minor gastrointestinal disturbances such as abdominal pain and cholithiasis on account of the increased excretion of biliary cholesterol. [ 23 ] Among atypical adverse effects, myositis can occur in patients under gemfibrozil therapy, especially in those with renal insufficiency or under co-treatment with statins. In contrast, the risk of myopathy is much lower if fenofibrate is used in replacement of gemfibrozil owing to its different pharmacokinetic pathway. Other rare effects are increased serum transaminase levels, agranulocytosis and anaemia . [ 31 ] As fenofibrate possess the same binding mechanism as warfarin in the blood, this combination should be addressed with caution as fenofibrate may potentiate the anticoagulant effect of warfarin. [ 33 ] Furthermore, fibrates are contraindicated in patients with active liver disease, severe renal impairment or pre-existing gallbladder disease , as well as in lactating mothers. [ 31 ] Blood-thinning agents are divided into two groups, antiplatelet drugs and anticoagulants . They are indicated to facilitate smooth blood flow within blood vessels by preventing the formation of blood clots and retarding their growth. [ 34 ] Blood clots are formed to prevent an injured blood vessel from excessive bleeding by a mechanism called hemostasis . The body has intrinsic mechanisms to dissolve the blood clot as the injury heals. However, it can be dangerous when clots do not dissolve naturally and develop within vessels, also known as thrombosis . Hence, blood-thinning medications can be prescribed to reduce the risk of cardiovascular diseases led by blood clots, such as myocardial infarction (heart attack), ischemic stroke , and venous thromboembolism . [ 35 ] Haemorrhage (internal bleeding) is the most prominent side effect of blood-thinning therapy. [ 36 ] Concomitant use of drugs that increase the risk of bleeding is not recommended. Meanwhile, patients should receive education about proper management of cuts, bruises and nosebleeds. The agents can be classified according to different mechanisms of action. Antiplatelet drugs inhibit blood cells called platelets from aggregating to form a clot. Potent antiplatelet medications that irreversibly inhibit the activity of cyclooxygenase (COX), an enzyme involved in the synthesis of thromboxane A 2 (TXA2) which is responsible for platelet activation and aggregation. The major member of this class is aspirin . Some common adverse effects associated with this class of medications include bronchospasm and gastrointestinal disturbances such as dyspepsia and nausea . Therefore, this class of drugs should be used with caution in patients with a history of peptic ulcer disease . [ 34 ] [ 37 ] Also known as P2Y12 receptor antagonists , they work by reversibly interacting with the P2Y12 receptor to inhibit the adenosine diphosphate (ADP) receptors on platelets, thus preventing the linkage of platelets by fibrinogen . [ 34 ] [ 35 ] ADP-induced platelet aggregation and activation are hence hindered. Examples include clopidogrel , prasugrel and ticagrelor . Clopidogrel has a common drug interaction with CYP2C19 inhibitors, particularly omeprazole and esomeprazole which are indicated for treatment of peptic ulcer and gastro-oesophageal reflux disease (GERD) . As the activation of clopidogrel requires an enzyme called CYP2C19, its inhibitors should be avoided. [ 38 ] Anticoagulants are considered more aggressive than antiplatelet drugs . [ 34 ] Anticoagulants work by interfering with various clotting factors to lengthen the time for coagulation . This can be achieved by either reducing the formation of bioactive clotting factors or accelerating the inactivation of clotting factors. Drugs that inhibit the formation of the vitamin K-dependent clotting factors and hence thrombin , an endogenous protein involved in the coagulation cascade . Vitamin K is an essential cofactor for the synthesis of clotting factors. By inhibiting vitamin K epoxide reductase , an enzyme for activating the vitamin K available in the body, the formation of bioactive clotting factors can be reduced. Although warfarin is commonly prescribed, it exhibits a delayed onset of action, which takes approximately 5 to 7 days to reach its full therapeutic effect. [ 39 ] Apart from haemorrhage , jaundice (yellowing of the skin and eyes) is also a common side effect caused by this class of drug. [ 34 ] DOACs are agents that inhibit the formation of thrombin which is the central effector of coagulation derived from factor Xa . They are categorised into direct thrombin inhibitors and direct factor Xa inhibitors . Direct thrombin inhibitors bind to the active sites of free or clot-bound thrombin to inhibit its effects. Dabigatran etexilate is a common example which has a rapid onset of action. [ 40 ] Whereas direct factor Xa inhibitors including apixaban and rivaroxaban directly bind to clotting factor Xa to block its activity, thus inhibiting thrombin formation. [ 34 ] DOACs are advantageous over warfarin because of a wider therapeutic window , which indicates safer and more effective use with minimal adverse effects. DOACs also have more stable and predictable anticoagulation effects. Therefore, routine coagulation monitoring is not required. [ 41 ] Indirect thrombin inhibitors bind to antithrombin to enhance the rate of inactivation of clotting factors, indirectly inactivating thrombin through actions on antithrombin. [ 42 ] Heparin is a widely used anticoagulant. It is administered intravenously (into a vein) or subcutaneously (below the skin). Heparin can exert an immediate anti-clotting effect which is useful for the treatment of acute symptoms. [ 36 ] Besides, heparin therapy is indicated for anticoagulation during pregnancy as it does not cross the placenta and is not associated with fetal malformations. [ 43 ] [ 44 ] Cardiovascular agents generally have narrow therapeutic indices , implying that small differences in dose or blood concentration may give rise to adverse drug reactions. [ 45 ] Serious acute toxicity may result from accidental, intentional or iatrogenic overdose. [ 46 ] Therefore, patients need to be aware of any unusual and serious side effects. Seek immediate medical attention if a drug overdose is suspected. General management of acute poisoning requires stabilisation of the airway, breathing, and circulation. [ citation needed ] Supportive treatment to reduce further absorption of the drug is achievable by the administration of activated charcoal . [ 47 ] Antidotes can be used to reverse effects of the overdosed medication if the exact poisoning agent is identified. However, only a few antidotes are available for cardiovascular medications. Table 1: antidotes for cardiovascular agent overdose For patients taking antihyperlipidemic agents, liver function tests have to be conducted before and during the therapy to monitor the elevation of liver enzymes which may result in hepatotoxicity , especially for those undergoing statin therapy . [ 52 ] For patients taking blood-thinners, signs of severe bleeding should be monitored. The effect of aspirin can be life-threatening if taken over 150 mg/kg of body weight. [ 47 ] The medication should be discontinued at the first sign of excessive bleeding.	https://en.wikipedia.org/wiki/Cardiovascular_agents
Cardiovascular disease , including heart disease , is a major cause of death in Australia. [ 1 ] Heart disease is an overall term used for any type of Cardiovascular disease that affects the heart reducing blood supply to the heart. It is also often referred as Cardiac disease and Coronary heart disease. It is generally a lifelong condition where damage to the artery and blood vessel cannot be cured. [ 2 ] Cardiovascular disease (CVD) continues to have a major impact on the health of Australians in terms of prevalence, mortality , morbidity , burden of disease and expenditure. From 2007 to 2008, an estimated 3.4 million Australians were diagnosed with CVD. [ 3 ] Cardiovascular disease remains Australia's leading cause of death. In 2009, 46,106 deaths in Australia were directly linked with CVD (21,935 males and 24,171 females); this figure represents a total of 33% of all deaths in Australia. [ 4 ] It was reported in 2010 that almost 16% of the total projected burden of disease was a result of CVD. [ 5 ] This then made individuals with CVD susceptible to co-morbid conditions later in life, making them "at risk" for depression and anxiety. There are number of conditions that involves the heart such as: According to Chenzbraun (2010), symptoms of the heart disease varies, and should not be ignored. The symptoms of heart disease are not always intense and varies according to factors such as age and gender. [ citation needed ] The most common symptoms of heart disease is: This is a major risk factor of heart disease resulting in death. The rate of smoking is low in Australia according to the health survey: 14% of women and 18% of men being daily smokers (Nichols, 2014). 58% of Australians lack physical activity. Those who undertake low levels of physical activity are at higher risk of developing heart disease. Men were classified as moderately active than women (Nichols & Peterson, 2014). Alcohol plays a huge role in Australian culture and its social circumstance. According to the Australian Bureau of statistics, 87.6% of males and 77.3% of females had consumed alcohol in the past year. Alcohol consumed at a limit, reduces the risk of developing heart disease. [ citation needed ] Being overweight and obese is very common in Australia especially children and teens. Almost 69.7% of male and 55.7% of female are overweight. The rate for both men and women of obesity is 27.5% (Australian Bureau of statistics). It is one of the leading cause of heart disease and cardiovascular disease . [ citation needed ] High blood pressure ( hypertension ) causes stress to the heart and its function that leads to heart disease. Males experience heart disease caused by hypertension than women. One in five Australians with high blood pressure has heart disease (Nichols, 2014). A key step to prevent any type of heart disease is addressing the risk factors. Such as not smoking or use of drugs, regular exercising, have healthy diet, maintain healthy weight and have regular health screening to check up on blood pressure. These lifestyle changes reduces the risk of developing heart disease (Wood & Gordon, 2011). Prescribed medications are given to help improve blood flow, low blood pressure and to relax blood vessel walls. [ citation needed ] A non-surgical procedure called, Angioplasty , could be done to help dilate the narrowed arteries. [ citation needed ] Coronary artery bypass surgery is also another way to treat coronary heart disease. [ citation needed ] Although there are treatments available to treat heart disease, it is a lifelong condition restricting some daily lifestyle routine and incurable. [ citation needed ] Heart disease is the leading cause of death in Australia. [ 7 ] In 2007-8 about 3.5 million people were diagnosed with heart disease (especially cardiovascular disease). Although there are significant advances in the treatments, heart disease still remains the lead cause of death in Australia especially with people in lower socioeconomic groups (AIHW, 2011). The number and rate of deaths from CVD have fallen considerably from the peak levels experienced in the late 1960s and early 1970s when CVD was responsible for around 60,000 deaths annually, or roughly 55% of all deaths each year. [ 8 ] These major gains have been attributed to a combination of research, improvements in prevention and detection of cardiovascular disease, and better clinical management of people with the disease. There is a close interrelationship between CVD and other important chronic conditions, including diabetes and chronic kidney disease . [ 9 ] Cardiovascular disease kills one Australian every 11 minutes, and 3·4 million of the country's population are affected, with the Indigenous Australians having a 30% higher rate. In their lifetime, 1·5 million Australians are estimated to have diabetes and one in six Australians are suspected to have a stroke. The Baker Heart and Diabetes Institute, based in Melbourne, is one of the most well known cardiovascular disease research institutes. [ citation needed ] One of the studies directed by an Australian-Dutch research team, led by, Karin Jandeleit-Dahm from Harald Schmidt from Maastricht University, Netherlands, has identified the role of an enzyme which accelerates the development of diabetic atherosclerosis . Researchers were able to substantially reduce the development of artery plaques by suppressing or inhibiting this enzyme with a new drug, which will allow prevention and treatment of cardiovascular disease in people with diabetes. [ citation needed ] Another team, led by Bronwyn Kingwell, [ 10 ] Head of the Baker Institute's Metabolic and Vascular Physiology, have found a new use for an old drug. The researchers found that after taking the standard anti-hypertensive drug Ramipril, patients with peripheral arterial disease (PAD), which restricts mobility due to leg pain, enjoyed a longer and less painful time on their feet. For some patients, this could be the difference between living independently and living under the care of others for the rest of their lives. [ 11 ]	https://en.wikipedia.org/wiki/Cardiovascular_disease_in_Australia
Cardiovascular physiology is the study of the cardiovascular system , specifically addressing the physiology of the heart ("cardio") and blood vessels ("vascular"). These subjects are sometimes addressed separately, under the names cardiac physiology and circulatory physiology . [ 1 ] Although the different aspects of cardiovascular physiology are closely interrelated, the subject is still usually divided into several subtopics. [ citation needed ] Under most circumstances, the body attempts to maintain a steady mean arterial pressure . [ 2 ] When there is a major and immediate decrease (such as that due to hemorrhage or standing up ), the body can increase the following: In turn, this can have a significant impact upon several other variables:	https://en.wikipedia.org/wiki/Cardiovascular_physiology
A cardiovascular technician , also known as a vascular technician , is health professional that deal with the circulatory system . Technicians who use ultrasound to examine the heart chambers , valves , and vessels are referred to as cardiac sonographers. [ 1 ] They use ultrasound instrumentation to create images called echocardiograms. An echocardiogram may be performed while the patient is either resting or physically active. Technicians may administer medication to physically active patients to assess their heart function. Cardiac sonographers also may assist transesophageal echocardiography , which involves placing a tube in the patient's esophagus to obtain ultrasound images. [ citation needed ] Those who assist in the diagnosis of disorders affecting the circulation are known as vascular technologist, vascular specialists or vascular sonographers. They obtain a medical history, evaluate pulses and assess blood flow in arteries and veins by listening to the vascular flow sounds for abnormalities. Then they perform a noninvasive procedure using ultrasound instrumentation to record vascular information such as vascular blood flow, blood pressure , changes in limb volume, oxygen saturation , cerebral circulation , peripheral circulation, and abdominal circulation. Many of these tests are performed during or immediately after surgery. Cardiovascular technicians who obtain EKGs are known as electrocardiograph (or EKG) technicians. To take a basic EKG , which traces electrical impulses transmitted by the heart, technicians attach electrodes to the patient's chest, arms, and legs, and then manipulate switches on an EKG machine to obtain a reading. An EKG is printed out for interpretation by the physician. This test is done before most kinds of surgery or as part of a routine physical examination, especially on persons who have reached middle age or who have a history of cardiovascular problems. EKG technicians with advanced training setup Holter monitor and stress testing. For Holter monitoring, technicians place electrodes on the patient's chest and attach a portable EKG monitor to the patient's belt. Following 24 or more hours of normal activity by the patient, the technician removes a tape from the monitor and places it in a scanner. After checking the quality of the recorded impulses on an electronic screen, the technician usually prints the information from the tape for analysis by a physician. Physicians use the output from the scanner to diagnose heart ailments, such as heart rhythm abnormalities or problems with pacemakers . For a treadmill stress test, EKG technicians document the patient's medical history, explain the procedure, connect the patient to an EKG monitor, and obtain a baseline reading and resting blood pressure. Next, they monitor the heart's performance while the patient is walking on a treadmill, gradually increasing the treadmill's speed to observe the effect of increased exertion. The position is generally unlicensed and skills are learned on the job; however, two- and four-year training programs to learn advanced ECG technical skills are available at junior colleges and community colleges. [ 2 ]	https://en.wikipedia.org/wiki/Cardiovascular_technologist
Cardioversion is a medical procedure by which an abnormally fast heart rate ( tachycardia ) or other cardiac arrhythmia is converted to a normal rhythm using electricity or drugs . Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle , restoring the activity of the electrical conduction system of the heart . ( Defibrillation uses a therapeutic dose of electric current to the heart at a random moment in the cardiac cycle , and is the most effective resuscitation measure for cardiac arrest associated with ventricular fibrillation and pulseless ventricular tachycardia . [ 1 ] ) Pharmacologic cardioversion , also called chemical cardioversion , uses antiarrhythmia medication instead of an electrical shock. [ 2 ] To perform synchronized electrical cardioversion, two electrode pads are used (or, alternatively, the traditional hand-held "paddles"), each comprising a metallic plate which is faced with a saline based conductive gel. The pads are placed on the chest of the patient, or one is placed on the chest and one on the back. These are connected by cables to a machine which has the combined functions of an ECG display screen and the electrical function of a defibrillator . A synchronizing function (either manually operated or automatic) allows the cardioverter to deliver a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R wave of the QRS complex on the ECG . Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle , which could induce ventricular fibrillation . If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable. However, if the patient is hemodynamically unstable or unconscious, the shock is given immediately upon confirmation of the arrhythmia . When synchronized electrical cardioversion is performed as an elective procedure, the shocks can be performed in conjunction with drug therapy until sinus rhythm is attained. After the procedure, the patient is monitored to ensure stability of the sinus rhythm. Synchronized electrical cardioversion is used to treat hemodynamically unstable supraventricular (or narrow complex) tachycardias , including atrial fibrillation and atrial flutter . It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia , when a pulse is present. Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation . Electrical therapy is inappropriate for sinus tachycardia , which should always be a part of the differential diagnosis . Various antiarrhythmic agents can be used to return the heart to normal sinus rhythm . [ 3 ] Pharmacological cardioversion is an especially good option in patients with atrial fibrillation of recent onset. Drugs that are effective at maintaining normal rhythm after electric cardioversion can also be used for pharmacological cardioversion. Drugs like amiodarone , diltiazem , verapamil and metoprolol are frequently given before electrical cardioversion to decrease the heart rate, stabilize the patient and increase the chance that cardioversion is successful. There are various classes of agents that are most effective for pharmacological cardioversion. Class I agents are sodium (Na) channel blockers (which slow conduction by blocking the Na+ channel) and are divided into 3 subclasses a, b and c. Class Ia slows phase 0 depolarization in the ventricles and increases the absolute refractory period. Procainamide , quinidine and disopyramide are Class Ia agents. Class 1b drugs lengthen phase 3 repolarization. They include lidocaine , mexiletine and phenytoin . Class Ic greatly slow phase 0 depolarization in the ventricles (however unlike 1a have no effect on the refractory period). Flecainide , moricizine and propafenone are Class Ic agents. [ 4 ] Class II agents are beta blockers which inhibit SA and AV node depolarization and slow heart rate. They also decrease cardiac oxygen demand and can prevent cardiac remodeling. Not all beta blockers are the same; some are cardio selective (affecting only beta 1 receptors) while others are non-selective (affecting beta 1 and 2 receptors). Beta blockers that target the beta-1 receptor are called cardio selective because beta-1 is responsible for increasing heart rate; hence a beta blocker will slow the heart rate. Class III agents (prolong repolarization by blocking outward K+ current): amiodarone and sotalol are effective class III agents. Ibutilide is another Class III agent but has a different mechanism of action (acts to promote influx of sodium through slow-sodium channels). It has been shown to be effective in acute cardioversion of recent-onset atrial fibrillation and atrial flutter. Class IV drugs are calcium (Ca) channel blockers. They work by inhibiting the action potential of the SA and AV nodes. If the patient is stable, adenosine may be used for restoration of sinus rhythm in patients with macro-reentrant supraventricular tachycardias. It causes a short-lived cessation of conduction through the atrio-ventricular node breaking the circus movement through the node and the macro-reentrant pathway restoring sinus rhythm. Cardioversion for restoration of sinus rhythm from an atrial rhythm is largely a scheduled procedure. In addition to cardiology, anesthesiology is also usually involved to ensure comfort of the patient for the duration of the shock therapy. The presence of registered nurses, physician associates, or other medical personnel may also be helpful during the procedure. Before starting the procedure, the patient's chest and back will be prepped for electrode placement. The skin should be free of any oily substances (e.g., lotions) and hair which may otherwise interfere with adhesion of the pads. [ 5 ] Once this is complete, the medical team will adhere the pads to the patient using a rolling motion to ensure the absence of air pockets. (see details on pad placement below) . The anesthesiology team will then administer a general anesthetic (e.g., Propofol ) in order to ensure patient comfort and amnesia during the procedure. Opioid analgesics (e.g., Fentanyl) may be combined with Propofol, although anesthesiology must weigh the benefits against adverse effects including apnea. [ 6 ] Bite blocks and extremity restraints are then utilized to prevent self-injury during cardioversion. Once these medications are administered, the glabellar reflex or eyelash reflex may be used to determine the patient's level of consciousness. The pads are connected to a machine that can interpret the patient's cardiac rate and rhythm and deliver a shock at the appropriate time. The machine should synchronize ('sync') with the R wave of the rhythm strip. Although uncommon, sometimes the machine will unintentionally sync to high amplitude T waves, so it is important to ensure that the machine is synced appropriately to R waves. [ 7 ] Interpretation of the patient's rhythm is imperative when using cardioversion to restore sinus rhythm from less emergent arrhythmias where a pulse is present (e.g., atrial flutter , atrial fibrillation ). However, if a patient is confirmed to be in pulseless ventricular tachycardia "v-tach" or ventricular fibrillation "v-fib", then a shock is delivered immediately upon connection of the pads. In this application, electrical cardioversion is more properly termed defibrillation . [ 7 ] Once the machine is synced with the patient's cardiac rhythm, the machine must be charged. To determine the amount of energy (measured in joules "J") the patient requires, many factors are considered. As a rule of thumb, recent-onset atrial arrhythmias require less energy compared to persistent atrial arrhythmias. If the cardiologist suspects that the patient may be less respondent to cardioversion, a higher energy may be utilized. Once the machine is synced and charged, a shock can be delivered to the patient. [ 8 ] Following electrical cardioversion, the cardiologist will determine if sinus rhythm has been restored. To confirm sinus rhythm, a distinct P wave should be seen preceding each QRS complex. Additionally, each R-R interval should be evenly spaced. If sinus rhythm is restored, the pads may be disconnected, and any other medical equipment is removed from the patients (e.g., bite blocks, restraints, etc.). The patient will regain consciousness soon thereafter (the effects of Propofol generally last for only 3–8 minutes). However, if the arrhythmia is persistent, the machine may be re-charged to a higher energy level, and the cardioversion attempt may be repeated. It is recommended to wait 60 seconds between subsequent cardioversion attempts, but this amount of time may be adjusted based on the patient and/or provider. Pad placement for electrical cardioversion a cardiac arrhythmia may be either anterior-posterior or anterior-lateral. In an anterior-posterior setup one pad is placed on the chest and the other pad is placed on the back. In an anterior-lateral setup, one pad is placed on the chest and the other pad is placed along the left midaxillary line. Choosing the right pad placement can be an important aspect when measuring the success of electrical cardioversion. For example, the anterior-posterior pad positioning is commonly used when attempting to restore an atrial arrhythmia as the vector between the pads predominately runs through the atria. The anterior-lateral pad positioning may be used when attempting to restore pulseless ventricular tachycardia or ventricular fibrillation as there may not be enough time or strength to apply an electrode the patient's back. The anterior pad should be placed inferior to the right clavicle while also being vertically centered over at the level of the right 4th intercostal space. The posterior pad should be placed just lateral to the left side of the spine and vertically centered at the level of T7. [ 12 ] [ 13 ] The inferior angle of the scapula can be used as a reference for the level of T7. The anterior pad should be placed inferior to the right clavicle while also being vertically centered over at the level of the right 4th intercostal space. The lateral pad should be placed along the left midaxillary line at the level of the left 5th intercostal space. [ 12 ] [ 13 ] The left nipple can be used as a reference for the level of the left 4th intercostal space. From here, the midaxillary 5th intercostal space is identified by moving inferiorly one intercostal space and laterally towards the midaxillary line.	https://en.wikipedia.org/wiki/Cardioversion
Carditis (pl. carditides ) is the inflammation of the heart . [ 1 ] It is usually studied and treated by specifying it as: [ citation needed ] This article about a medical condition affecting the circulatory system is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Carditis
Carestream Health, Inc. , formerly Eastman Kodak Company 's Health Group, is an American medical imaging company, owned by Canadian investment firm Onex Corporation . [ 3 ] Recently, Moody’s Investors Rating Service “downgraded” the Carestream Health financial outlook to negative from stable. Showing a credit rating of Caa1 with a Probability of Default. [ 4 ] In 2007, the Kodak Health Group was sold to Onex Corporation for $2.35 billion in cash. [ 5 ] [ 6 ] Around 8,100 employees transferred to Onex, and Kodak Health Group was renamed Carestream Health. In April 2017, Carestream Health announced an agreement to sell its Dental Digital business to private equity firms Clayton, Dubilier & Rice and the Hillhouse Capital Management group, part of CareCapital Advisors Limited. Carestream Dental provides imaging systems and practice management software for general and specialist dental practices. The dental X-ray film and anesthetics business were not included in the agreement and remain with Carestream Health. [ 7 ] On September 28, 2022 Carestream Health filed for Chapter 11 bankruptcy. [ 8 ] Carestream continues to have financial difficulty and stability as shown with the closure of the Colorado plant in February of 2024. [ 9 ] According to Carestream the declining analog print business accounts for almost half of its revenues. Since 2018, Carestream annual revenues declined by $100m. The other half of its revenues are attributed to its digital medical systems but are less profitable than its declining print business. [ 10 ] Products include: photothermographic laser imagers, photothermographic imaging film, computed radiography systems, digital radiography systems, [ 11 ] and other diagnostic imaging systems for the medical and dental imaging fields. Carestream Health owns more than 800 patents for medical and dental imaging technology. Digital imaging technologies include the DRX-1 series, which allows a wireless connection between the digital X-ray detector and computer system (whether part of their static system or a mobile/portable radiography system). [ 12 ] [ 13 ] The Carestream Health flagship product, DRX-Revolution, has been recalled by the FDA multiple times. The popular product has been reported to have unexpected and spontaneous internal system fires resulting in clinicians and patients exposed to toxic smoke in common areas. [ 14 ] Medical and Dental Products Non-Medical Products	https://en.wikipedia.org/wiki/Carestream_Health
A Cargile membrane was a sterile membrane made from the peritoneum of the ox , and was the first commercially available adhesion barrier. [ 1 ] Its first reported use was in 1905. [ 2 ] It was used in abdominal surgery to interpose between raw surfaces and thus prevent the formation of adhesions . [ 3 ] It was also used to envelop freshly sutured nerves or tendons , and to protect wounds. It was designed primarily to cover surfaces over which peritoneum has been removed, especially where a sterile membrane would lessen the formation of adhesion. It was available in the size of 4 × 6 inches, and sometimes used as packaging or a protective sheath. It was named for American surgeon Charles H. Cargile (1853–1930), [ 4 ] who first used it ca. 1900, according to Dorland's Medical Dictionary . This article incorporates text from a publication now in the public domain : Gilman, D. C. ; Peck, H. T.; Colby, F. M., eds. (1905). New International Encyclopedia (1st ed.). New York: Dodd, Mead. {{ cite encyclopedia }} : Missing or empty \|title= ( help ) This surgery article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cargile_membrane
A caries vaccine is a vaccine to prevent and protect against tooth decay . [ 1 ] Streptococcus mutans ( S. mutans ) has been identified as the major etiological agent of human dental caries. The development of a vaccine for tooth decay has been under investigation since the 1970s. In 1972, a caries vaccine was said to be in animal testing in England, and that it would have begun human testing soon. [ 2 ] However, intrinsic difficulties in developing it, coupled with lack of strong economic interests, are the reasons why still no such vaccine is commercially available today. [ citation needed ] Several types of vaccines are being developed at research centres, with some kind of caries vaccines being considered to diminish or prevent dental caries' impact on young people. [ 3 ] Early attempts followed a traditional approach to vaccination where normal S. mutans was introduced to promote a reaction from the immune system, stimulating antibody production. [ 4 ] [ non-primary source needed ] Planet Biotechnology developed a monoclonal antibody against S. mutans , branded CaroRx, produced with transgenic tobacco plants. It is a therapeutic vaccine , applied once every several months. Phase II clinical trials were discontinued in 2016. [ citation needed ] The International Associations for Dental Research and American Association for Dental Research announced a study performed by the Chinese Academy of Sciences which looked at using an inhaled vaccine that uses a protein filament as a delivery vehicle. Trials performed in rats showed an increase in antibody response along with a decrease in the amount of Streptococcus mutans adhering to teeth, leading to significantly fewer cavities observed among the test population. [ 5 ] [ non-primary source needed ] On a different line of research, Jeffrey Hillman from the University of Florida [ 6 ] developed a genetically modified strain of Streptococcus mutans called BCS3-L1, that is incapable of producing lactic acid – the acid that dissolves tooth enamel – and aggressively replaces native flora. In laboratory tests, rats who were given BCS3-L1 were conferred with a lifetime of protection against S. mutans . [ 7 ] [ non-primary source needed ] BCS3-L1 colonizes the mouth and produces a small amount of a lantibiotic , called MU1140, [ 7 ] which allows it to out-compete S. mutans . [ 8 ] Hillman suggested that treatment with BCS3-L1 in humans could also provide a lifetime of protection, or, at worst, require occasional re-applications. He stated that the treatment would be available in dentists' offices and "will probably cost less than $100." [ 9 ] The product was being developed by Oragenics, but was shelved in 2014, citing regulatory concerns and patent issues. [ 10 ] [ non-primary source needed ] In 2016, Oragenics received a 17-year patent for the product. [ 11 ] In 2023, the startup Lumina Probiotic began developing a BCS3-L1 application in Próspera, Honduras. [ 12 ] On rare occasions the native S. mutans strain escapes into the blood, potentially causing dangerous heart infections. It is unclear how likely BCS3-L1 is to do the same. [ 13 ] Another approach is being pursued by BASF , focused on replacing native lactobacillus flora with a variety dubbed L. anti-caries , which prevents S. mutans from binding to enamel. [ 14 ] However, it is not a long-term vaccination in that no attempt is being made to have a self-sustaining population of L. anti-caries . The intent is that the L. anti-caries population would be frequently replenished through use of a chewing gum containing the organism. [ citation needed ] The University of Leeds has also begun researching a recently discovered peptide known as P11-4 . When applied to a cavity and coming in contact with saliva, this peptide assembles itself in a fibrous matrix or scaffold, attracting calcium and thereby allowing the tooth to regenerate. [ 15 ] [ 16 ] The Swiss-based company Credentis has licensed the peptide and launched a product called Curodont Repair in 2013. [ 17 ] Recent studies show a positive clinical effect. [ 18 ] [ non-primary source needed ] DNA vaccine approaches for dental cavities have had a history of success in animal models. Dental cavity vaccines directed to key components of S. mutans colonization and enhanced by safe and effective adjuvants and optimal delivery vehicles, are likely to be forthcoming. Some believe that the rational target for developing an anti-caries vaccine is a protein antigen, which has adherent functional and important immunogenic regions. [ 19 ] [ clarification needed ] [ non-primary source needed ] The use of Enterococcus faecalis bacteriophages as a form of treatment for caries has been considered, as they are capable of maintaining persistent stability in human saliva. [ 20 ] [ non-primary source needed ]	https://en.wikipedia.org/wiki/Caries_vaccine
Caring for the Heart: Mayo Clinic and the Rise of Specialization is a historical account of the diagnosis and treatment of heart disease in the United States during the twentieth century, written by American historian and cardiologist W. Bruce Fye , and published in 2015 by Oxford University Press . It highlights major medical advancements and the contributions of key individuals and institutions in both the United States and Europe. The Mayo Clinic in Rochester , Minnesota , is used as a central case study due to its prominent role in the development of diagnostic and surgical techniques. These innovations include the electrocardiograph , cardiac catheterisation , heart surgery , and coronary angiography . The book also examines the medical care provided to Franklin D. Roosevelt for his severe hypertension and heart failure . [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] Caring for the Heart: Mayo Clinic and the Rise of Specialization was published in 2015 by Oxford University Press . The book has 704 pages covering three main areas: the development of heart disease treatment, the evolution of the Mayo Clinic, and the rise of medical specialisation and technology. It begins with the history of the Mayo Clinic from its founding to the 1940s, alongside the development of cardiology in the United States and at the Mayo. It then presents case studies on heart surgery, diagnostic technologies including catheterisation and echocardiography, coronary care units , nursing, angioplasty , electrophysiology , and heart failure treatment, including transplants. There is account of Mayo’s role in World War II aviation medicine and its early refusal of NIH funding due to concerns over government control. Key contributions from institutions like the University of Minnesota and the Cleveland Clinic are also discussed. The book also examines the medical care provided to Franklin D. Roosevelt for his severe hypertension and heart failure . This article about a medical book is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Caring_for_the_Heart
Carl Alfred Meier (19 April 1905 – 1995) was a Swiss psychiatrist , Jungian psychologist , scholar , and first president of the C. G. Jung Institute in Zürich . As a successor to Carl Jung , he held the Chair of Honorary Professor of Psychology at the Swiss Federal Institute of Technology in 1949. Later, co-founded the Clinic and Research Center for Jungian Psychology in Zürichberg . Meier was born in Schaffhausen , Switzerland , in 1905. He enrolled at the University of Zürich in 1924. In the winter semester of 1927, Meier traveled to Paris to study at the Medical Faculty of the University of Paris . Later, in 1928, he traveled to Vienna to study at the Steinhof (the Psychiatric Clinic of the University of Vienna), and to attend the lectures of Julius Wagner-Jauregg . A colleague at Steinhof invited him to attend a series of Wednesday seminars delivered by Sigmund Freud . In 1931, he began his study of psychiatry under Hans-Wolfgang Maier at Burghölzli . This article about a psychologist is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Carl_Alfred_Meier
Carl Frank Gugino is an American orthodontist who is known to develop the first computerized cephalometric and visual treatment objective (VTO) program with Dr. Robert M. Ricketts and Dr. Bench. He is mostly known, along with Peter R. Breads, to have founded Great Lakes Dental Technologies, formally known as Great Lakes Orthodontics, which is an orthodontic laboratory and product company. [ 1 ] [ 2 ] He graduated in 1953 from University at Buffalo . He then served dental officer in the United States Navy Dental Corps from 1953 to 1955. He was stationed at the naval hospital at Marine Corps Air Station Cherry Point in North Carolina and became a lieutenant in 1955. After serving in the Navy, Gugino worked as a dentist for several years before he specialized in orthodontics from the same university in 1961. He developed the first computerized cephalometric and visual treatment objective (VTO) program with Dr. Thomas Ricketts and Dr. Bench. He authored a textbook called Next Generation BioprogressiveTM Philosophy, ZeroBase OrthodonticsTM . [ 3 ] He worked with Dr. Suyehiro and founded the Millennium Society . This society is focused on the practice management aspect of orthodontics. [ 2 ] This dentistry article is a stub . You can help Wikipedia by expanding it . This biographical article related to medicine in the United States is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Carl_F._Gugino
Carl Gustav Jung ( / j ʊ ŋ / YUUNG ; [ 1 ] [ 2 ] Swiss Standard German: [karl jʊŋ] ; 26 July 1875 – 6 June 1961) was a Swiss psychiatrist , psychotherapist , and psychologist who founded the school of analytical psychology . [ 3 ] [ a ] A prolific author of over 20 books , illustrator, and correspondent, Jung was a complex and convoluted academic, best known for his concept of archetypes . Alongside contemporaries [ b ] Freud and Adler , Jung became one of the most influential psychologists of the early 20th century and has fostered not only scholarship, but also popular interest. [ 6 ] Jung's work has been influential in the fields of psychiatry , anthropology , archaeology , literature , philosophy , psychology , [ 7 ] and religious studies . He worked as a research scientist at the Burghölzli psychiatric hospital in Zurich , under Eugen Bleuler . Jung established himself as an influential mind, developing a friendship with Sigmund Freud , founder of psychoanalysis , conducting a lengthy correspondence paramount to their joint vision of human psychology. Jung is widely regarded as one of the most influential psychologists in history. [ 8 ] [ 9 ] Freud saw the younger Jung not only as the heir he had been seeking to take forward his "new science" of psychoanalysis but as a means to legitimize his own work: Freud and other contemporary psychoanalysts were Jews facing rising antisemitism in Europe, and Jung was Christian . [ 10 ] Freud secured Jung's appointment as president of Freud's newly founded International Psychoanalytical Association . Jung's research and personal vision, however, made it difficult to follow his older colleague's doctrine, and they parted ways. This division was painful for Jung and resulted in the establishment of Jung's analytical psychology, as a comprehensive system separate from psychoanalysis. Among the central concepts of analytical psychology is individuation —the lifelong psychological process of differentiation of the self out of each individual's conscious and unconscious elements. Jung considered it to be the main task of human development. He created some of the best-known psychological concepts, including synchronicity , archetypal phenomena , the collective unconscious , the psychological complex , and extraversion and introversion . His treatment of American businessman and politician Rowland Hazard in 1926 with his conviction that alcoholics may recover if they have a " vital spiritual (or religious) experience " played a crucial role in the chain of events that led to the formation of Alcoholics Anonymous . [ 11 ] Jung was an artist , craftsman , builder, and prolific writer. Many of his works were not published until after his death, and some remain unpublished. [ 12 ] Carl Gustav Jung [ c ] was born 26 July 1875 in Kesswil , in the Swiss canton of Thurgau , as the first surviving son of Paul Achilles Jung (1842–1896) and Emilie Preiswerk (1848–1923). [ 13 ] His birth was preceded by two stillbirths and that of a son named Paul, born in 1873, who survived only a few days. [ 14 ] [ 15 ] Paul Jung, Carl's father, was the youngest son of a noted German-Swiss professor of medicine at Basel , Karl Gustav Jung (1794–1864). [ 16 ] Paul's hopes of achieving a fortune never materialised, and he did not progress beyond the status of an impoverished rural pastor in the Swiss Reformed Church . Emilie Preiswerk, Carl's mother, had also grown up in a large family whose Swiss roots went back five centuries. Emilie was the youngest child of a distinguished Basel churchman and academic, Samuel Preiswerk (1799–1871), and his second wife. Samuel Preiswerk was an Antistes , the title given to the head of the Reformed clergy in the city, as well as a Hebraist , author, and editor, who taught Paul Jung as his professor of Hebrew at Basel University . [ 14 ] : 17–19 Jung's father was appointed to a more prosperous parish in Laufen when Jung was six months old. Tensions between father and mother had developed. Jung's mother was an eccentric and depressed woman; she spent considerable time in her bedroom, where she said spirits visited her at night. [ 17 ] Though she was normal during the day, Jung recalled that at night his mother became strange and mysterious. He said that one night, he saw a faintly luminous and indefinite figure coming from her room, with a head detached from the neck and floating in the air in front of the body. Jung had a better relationship with his father. [ 17 ] Jung's mother left Laufen for several months of hospitalization near Basel for an unknown physical ailment. His father took Carl to be cared for by Emilie Jung's unmarried sister in Basel, but he was later brought back to his father's residence. Emilie Jung's continuing bouts of absence and depression deeply troubled her son and caused him to associate women with "innate unreliability", whereas "father" meant for him reliability, but also powerlessness. [ 18 ] In his memoir, Jung would remark that this parental influence was the "handicap I started off with". Later, these early impressions were revised: "I have trusted men friends and been disappointed by them, and I have mistrusted women and was not disappointed." [ 19 ] After three years living in Laufen, Paul Jung requested a transfer. In 1879, he was called to Kleinhüningen, next to Basel, where his family lived in a church parsonage. [ 20 ] The relocation brought Emilie Jung closer to contact with her family and lifted her melancholy. [ 21 ] When he was 9, Jung's sister Johanna Gertrud (1884–1935) was born. Known in the family as "Trudi", she became a secretary to her brother. [ 14 ] : 349 Jung was a solitary and introverted child. From childhood, he believed that, like his mother, [ 22 ] he had two personalities—a modern Swiss citizen and a personality more suited to the 18th century. [ 23 ] "Personality Number 1", as he termed it, was a typical schoolboy living in the era of the time. "Personality Number 2" was a dignified, authoritative, and influential man from the past. Though Jung was close to both parents, he was disappointed by his father's academic approach to faith. [ 24 ] Some childhood memories made lifelong impressions on him. As a boy, he carved a tiny mannequin into the end of the wooden ruler from his pencil case and placed it inside it. He added a stone, which he had painted into upper and lower halves, and hid the case in the attic. Periodically, he would return to the mannequin, often bringing tiny sheets of paper with messages inscribed on them in his own secret language. [ 25 ] He later reflected that this ceremonial act brought him a feeling of inner peace and security. Years later, he discovered similarities between his personal experience and the practices associated with totems in Indigenous cultures , such as the collection of soul-stones near Arlesheim or the tjurungas of Australia. He concluded that his intuitive ceremonial act was an unconscious ritual, which he had practiced in a way that was strikingly similar to those in distant locations which he, as a young boy, knew nothing about. [ 26 ] His observations about symbols, archetypes , and the collective unconscious were inspired, in part, by these early experiences combined with his later research. [ 27 ] [ 28 ] At the age of 12, shortly before the end of his first year at the Humanistisches Gymnasium in Basel, Jung was pushed to the ground by another boy so hard he momentarily lost consciousness. (Jung later recognized the incident was indirectly his fault.) A thought then came to him—"Now you won't have to go to school anymore". [ 29 ] From then on, whenever he walked to school or began homework, he fainted. He remained home for six months until he overheard his father speaking hurriedly to a visitor about the boy's future ability to support himself. They suspected he had epilepsy . Confronted with his family's poverty, he realized the need for academic excellence. He entered his father's study and began poring over Latin grammar . He fainted three more times but eventually overcame the urge and did not faint again. This event, Jung later recalled, "was when I learned what a neurosis is". [ 30 ] Initially, Jung had aspirations of becoming a Christian minister. His household had a strong moral sense, and several of his family were clergy. Jung had wanted to study archaeology, but his family could not afford to send him further than the University of Basel, which did not teach it. After studying philosophy in his teens, Jung decided against the path of religious traditionalism and decided to pursue psychiatry and medicine. [ 31 ] His interest was captured—it combined the biological and spiritual, exactly what he was searching for. [ 32 ] In 1895 Jung began to study medicine at the University of Basel. Barely a year later, his father, Paul, died and left the family nearly destitute. They were helped by relatives who also contributed to Jung's studies. [ 33 ] During his student days, he entertained his contemporaries with the family legend that his paternal grandfather was the illegitimate son of Goethe and his German great-grandmother, Sophie Ziegler . In later life, he pulled back from this tale, saying only that Sophie was a friend of Goethe's niece. [ 34 ] It was during this early period when Jung was an assistant at the Anatomical Institute at Basel University, that he took an interest in palaeoanthropology and the revolutionary discoveries of Homo erectus and Neanderthal fossils. These formative experiences contributed to his fascination with the evolutionary past of humanity and his belief that an ancient evolutionary layer in the psyche, represented by early fossil hominins, is still evident in the psychology of modern humans. [ 35 ] In 1900, Jung moved to Zurich and began working at the Burghölzli psychiatric hospital under Eugen Bleuler . [ 36 ] Bleuler was already in communication with the Austrian neurologist Sigmund Freud . Jung's dissertation , published in 1903, was titled On the Psychology and Pathology of So-Called Occult Phenomena . It was based on the analysis of the supposed mediumship of Jung's cousin Hélène Preiswerk, under the influence of Freud's contemporary Théodore Flournoy . [ 37 ] Jung studied with Pierre Janet in Paris in 1902 [ 38 ] and later equated his view of the complex with Janet's idée fixe subconsciente . [ 39 ] In 1905, Jung was appointed as a permanent 'senior' doctor at the hospital and became a lecturer Privatdozent in the medical faculty of Zurich University. [ 40 ] In 1904, he published with Franz Riklin their Diagnostic Association Studies , of which Freud obtained a copy. [ 41 ] [ 42 ] In 1909, Jung left the psychiatric hospital and began a private practice in his home in Küsnacht . [ 43 ] Eventually, a close friendship and strong professional association developed between the elder Freud and Jung , which left a sizeable correspondence . In late summer 1909, the two sailed for the U.S., where Freud was the featured lecturer at the twentieth-anniversary celebration of the founding of Clark University in Worcester, Massachusetts , the Vicennial Conference on Psychology and Pedagogy, September 7–11. Jung spoke as well and received an honorary degree. [ 44 ] It was during this trip that Jung first began separating psychologically from Freud, his mentor, which occurred after intense communications around their individual dreams. It was during this visit that Jung was introduced to the elder philosopher and psychologist William James , known as the "Father of American psychology," whose ideas Jung would incorporate into his own work. [ 45 ] Jung connected with James around their mutual interests in mysticism , spiritualism and psychical phenomena . [ 46 ] James wrote to a friend after the conference stating Jung "left a favorable impression," while "his views of Freud were mixed." [ 47 ] James died about eleven months later. The ideas of both Jung and James, on topics including hopelessness, self-surrender, and spiritual experiences, were influential in the development and founding of the international altruistic, self-help movement Alcoholics Anonymous on June 10, 1935, in Akron, Ohio , a quarter of a century after James' death and in Jung's sixtieth year. For six years, Jung and Freud cooperated in their work. In 1912, however, Jung published Psychology of the Unconscious , which manifested the developing theoretical divergence between the two. Consequently, their personal and professional relationship fractured—each stating the other could not admit he could be wrong. After the culminating break in 1913, Jung went through a difficult and pivotal psychological transformation, exacerbated by the outbreak of the First World War. Henri Ellenberger called Jung's intense experience a "creative illness" and compared it favorably to Freud's own period of what he called neurasthenia and hysteria . [ 48 ] : 173 In 1903, Jung married Emma Rauschenbach (1882–1955), seven years his junior and the elder daughter of a wealthy industrialist in eastern Switzerland, Johannes Rauschenbach-Schenck. [ 49 ] Rauschenbach was the owner, among other concerns, of IWC Schaffhausen —the International Watch Company, manufacturer of luxury time-pieces. Upon his death in 1905, his two daughters and their husbands became owners of the business. Jung's brother-in-law— Ernst Homberger —became the principal proprietor, but the Jungs remained shareholders in a thriving business that ensured the family's financial security for decades. [ 50 ] Emma Jung, whose education had been limited, showed considerable ability and interest in her husband's research and threw herself into studies and acted as his assistant at Burghölzli. She eventually became a noted psychoanalyst in her own right. The marriage lasted until Emma died in 1955. [ 51 ] They had five children: None of the children continued their father's career. The daughters, Agathe and Marianne, assisted in publishing work. [ 52 ] During his marriage, Jung engaged in at least one extramarital relationship: his affair with his patient and, later, fellow psychoanalyst Sabina Spielrein . [ 53 ] [ 54 ] [ 55 ] A continuing affair with Toni Wolff is also alleged. [ 56 ] [ 57 ] Jung and Freud influenced each other during the intellectually formative years of Jung's life. Jung became interested in psychiatry as a student by reading Psychopathia Sexualis by Richard von Krafft-Ebing . In 1900, Jung completed his degree and started work as an intern (voluntary doctor) under the psychiatrist Eugen Bleuler at Burghölzli Hospital. [ 58 ] It was Bleuler who introduced him to the writings of Freud by asking him to write a review of The Interpretation of Dreams (1899). In the early 1900s psychology as a science was still in its early stages, but Jung became a qualified proponent of Freud's new "psycho-analysis". Freud needed collaborators and pupils to validate and spread his ideas. Burghölzli was a renowned psychiatric clinic in Zurich, and Jung's research had already gained him international recognition. Jung sent Freud a copy of his Studies in Word Association in 1906. [ 59 ] The same year, he published Diagnostic Association Studies , a copy of which he later sent to Freud, who had already purchased a copy. [ 42 ] Preceded by a lively correspondence, Jung met Freud for the first time in Vienna on 3 March 1907. [ 60 ] Jung recalled the discussion between himself and Freud as interminable and unceasing for 13 hours. [ 61 ] Six months later, the then 50-year-old Freud sent a collection of his latest published essays to Jung in Zurich. This began an intense correspondence and collaboration that lasted six years. [ 62 ] In 1908, Jung became an editor of the newly founded Yearbook for Psychoanalytical and Psychopathological Research . In 1909, Jung traveled with Freud and Hungarian psychoanalyst Sándor Ferenczi to the United States; in September, they took part in a conference at Clark University in Worcester , Massachusetts. The conference at Clark University was planned by the psychologist G. Stanley Hall and included 27 distinguished psychiatrists, neurologists, and psychologists. It represented a watershed in the acceptance of psychoanalysis in North America. This forged welcome links between Jung and influential Americans. [ 63 ] Jung returned to the United States the next year for a brief visit. In 1910, Freud proposed Jung, "his adopted eldest son, his crown prince, and successor," for the position of lifetime President of the newly formed International Psychoanalytical Association . However, after forceful objections from his Viennese colleagues, it was agreed Jung would be elected to serve a two-year term of office. [ 64 ] While Jung worked on his Psychology of the Unconscious: a study of the transformations and symbolisms of the libido , tensions manifested between him and Freud because of various disagreements, including those concerning the nature of libido . [ 65 ] Jung de-emphasized the importance of sexual development and focused on the collective unconscious: the part of the unconscious that contains memories and ideas that Jung believed were inherited from ancestors. While he did think that the libido was an important source of personal growth, unlike Freud, Jung did not think that the libido alone was responsible for the formation of the core personality. [ 66 ] In 1912, these tensions came to a peak because Jung felt severely slighted after Freud visited his colleague Ludwig Binswanger in Kreuzlingen without paying him a visit in nearby Zurich, an incident Jung referred to as "the Kreuzlingen gesture". Shortly thereafter, Jung again traveled to the US and gave the Fordham University lectures, a six-week series, which were published later in the year as Psychology of the Unconscious , subsequently republished as Symbols of Transformation . While they contain remarks on Jung's dissenting view on the libido, they represent largely a "psychoanalytical Jung" and not the theory of analytical psychology, for which he became famous in the following decades. Nonetheless, it was their publication which, Jung declared, "cost me my friendship with Freud". [ 67 ] Another disagreement with Freud stemmed from their differing concepts of the unconscious. [ 68 ] Jung saw Freud's theory of the unconscious as incomplete, unnecessarily negative, and inelastic. According to Jung, Freud conceived the unconscious solely as a repository of repressed emotions and desires. [ 69 ] Jung's observations overlap to an extent with Freud's model of the unconscious, what Jung called the " personal unconscious ", but his hypothesis is more about a process than a static model, and he also proposed the existence of a second, overarching form of the unconscious beyond the personal, that he named the psychoid—a term borrowed from neo-vitalist philosopher and embryologist Hans Driesch (1867–1941)—but with a somewhat altered meaning. [ 70 ] The collective unconscious is not so much a 'geographical location', but a deduction from the alleged ubiquity of archetypes over space and time. [ clarification needed ] In November 1912, Jung and Freud met in Munich for a meeting among prominent colleagues to discuss psychoanalytical journals. [ 71 ] At a talk about a new psychoanalytic essay on Amenhotep IV , Jung expressed his views on how it related to actual conflicts in the psychoanalytic movement. While Jung spoke, Freud suddenly fainted, and Jung carried him to a couch. [ 72 ] Jung and Freud personally met for the last time in September 1913 at the Fourth International Psychoanalytical Congress in Munich. Jung gave a talk on psychological types, the introvert and extraverted types, in analytical psychology . It was the publication of Jung's book The Psychology of the Unconscious in 1912 that led to the final break with Freud. The letters they exchanged show Freud's refusal to consider Jung's ideas. This rejection caused what Jung described in his posthumously published autobiography, Memories, Dreams, Reflections (1962) as a "resounding censure". Everyone he knew dropped away from him except two of his colleagues. After the Munich congress, he was on the verge of a suicidal psychosis that precipitated his writing of his Red Book, his seven-volume personal diaries that were only published partially and posthumously in 2009. Eleven years later, in 2020, they were published as his Black Books. Jung described his 1912 book as "an attempt, only partially successful, to create a wider setting for medical psychology and to bring the whole of the psychic phenomena within its purview". The book was later revised and retitled Symbols of Transformation in 1952. [ 73 ] Jung spoke at meetings of the Psycho-Medical Society in London in 1913 and 1914. His travels were soon interrupted by the war, but his ideas continued to receive attention in England primarily through the efforts of Constance Long , who translated and published the first English volume of his collected writings. [ 74 ] [ 75 ] In 1913, at the age of 38, Jung experienced a horrible "confrontation with the unconscious". He saw visions and heard voices. He worried at times that he was "menaced by a psychosis" or was "doing a schizophrenia". He decided that it was a valuable experience and, in private, he induced hallucinations or, in his words, a process of " active imagination ". He recorded everything he experienced in small journals, which Jung referred to in the singular as his Black Book , [ 76 ] considering it a "single integral whole", even though some of these original journals have a brown cover. [ 76 ] The material Jung wrote was subjected to several edits, hand-written and typed, including another, "second layer" of text, his continual psychological interpretations during the process of editing. [ 77 ] [ 78 ] Around 1915, Jung commissioned a large red leather-bound book, [ 79 ] [ 80 ] and began to transcribe his notes and paint, working intermittently for sixteen years. [ 81 ] Jung left no posthumous instructions about the final disposition of what he called the Liber Novus or Red Book . Sonu Shamdasani , a historian of psychology from London, tried for three years to persuade Jung's resistant heirs to have it published. Ulrich Hoerni, Jung's grandson who manages the Jung archives, decided to publish it when the necessary additional funds were raised through the Philemon Foundation . [ 81 ] Up to September 2008, fewer than about two dozen people had ever seen it. In 2007, two technicians for DigitalFusion, working with New York City publishers W. W. Norton & Company , scanned the manuscript with a 10,200-pixel scanner. It was published on 7 October 2009 in German, with a "separate English translation along with Shamdasani's introduction and footnotes" at the back of the book. According to Sara Corbett, reviewing the text for The New York Times , "The book is bombastic, baroque and like so much else about Carl Jung, a willful oddity, synched with an antediluvian and mystical reality." [ 81 ] The Rubin Museum of Art in New York City displayed Jung's Red Book leather folio, as well as some of his original "Black Book" journals, from 7 October 2009 to 15 February 2010. [ 82 ] According to them, "During the period in which he worked on this book Jung developed his principal theories of archetypes, collective unconscious, and the process of individuation." Two-thirds of the pages bear Jung's illuminations and illustrations to the text. [ 82 ] During World War I, Jung was drafted as an army doctor and soon made commandant of an internment camp for British officers and soldiers. The Swiss were neutral and obliged to intern personnel from either side of the conflict, who crossed their frontier to evade capture. Jung worked to improve the conditions of soldiers stranded in Switzerland and encouraged them to attend university courses. [ 83 ] [ 84 ] Jung emerged from his period of isolation in the late 1910s with the publication of several journal articles, followed in 1921 with Psychological Types , one of his most influential books. There followed a decade of active publication, interspersed with overseas travels. Constance Long arranged for Jung to deliver a seminar in Cornwall in 1920. Another seminar was held in 1923, this one organized by Jung's British protégé Helton Godwin Baynes (known as "Peter") (1882–1943), and another in 1925. [ 85 ] In 1935, at the invitation of his close British friends and colleagues, H. G. Baynes , E. A. Bennet and Hugh Crichton-Miller , Jung gave a series of lectures at the Tavistock Clinic in London, later published as part of the Collected Works . [ 86 ] In 1938, Jung was awarded an honorary degree by the University of Oxford . [ 87 ] At the tenth International Medical Congress for Psychotherapy held at Oxford from 29 July to 2 August 1938, Jung gave the presidential address, followed by a visit to Cheshire to stay with the Bailey family at Lawton Mere. [ 88 ] In 1946, Jung agreed to become the first Honorary President of the newly formed Society of Analytical Psychology in London, having previously approved its training programme devised by Michael Fordham . [ 89 ] During the period of Jung's collaboration with Freud , both visited the US in 1909 to lecture at Clark University, Worcester, Massachusetts, [ 63 ] where both were awarded honorary degrees. In 1912, Jung gave a series of lectures at Fordham University, New York, which were published later in the year as Psychology of the Unconscious . [ 67 ] Jung made a more extensive trip westward in the winter of 1924–5, financed and organized by Fowler McCormick and George Porter. Of particular value to Jung was a visit with Chief Mountain Lake of the Taos Pueblo near Taos, New Mexico . [ 85 ] Jung made another trip to America in 1936, receiving an honorary degree at Harvard [ 90 ] and giving lectures in New York and New England for his growing group of American followers. He returned in 1937 to deliver the Terry Lectures at Yale University , later published as Psychology and Religion . [ 91 ] In October 1925, Jung embarked on his most ambitious expedition, the "Bugishu Psychological Expedition" to East Africa. He was accompanied by his English friend, "Peter" Baynes , and an American associate, George Beckwith . On the voyage to Africa, they became acquainted with an English woman named Ruth Bailey, who joined their safari a few weeks later. The group traveled through Kenya and Uganda to the slopes of Mount Elgon , where Jung hoped to increase his understanding of "primitive psychology" through conversations with the culturally isolated residents of that area. Later, he concluded that the major insights he had gleaned had to do with himself and the European psychology in which he had been raised. [ 92 ] [ 93 ] One of Jung's most famous proposed constructs is kinship libido. Jung defined this as an instinctive feeling of belonging to a particular group or family and believed it was vital to the human experience and used this as an endogamous aspect of the libido and what lies amongst the family. This is similar to a Bantu term called Ubuntu that emphasizes humanity and almost the same meaning as kinship libido, which is, "I am because you are." [ 94 ] In December 1937, Jung left Zurich again for an extensive tour of India with Fowler McCormick. In India, he felt himself "under the direct influence of a foreign culture" for the first time. In Africa, his conversations had been strictly limited by the language barrier, but he could converse extensively in India. Hindu philosophy became an important element in his understanding of the role of symbolism and the life of the unconscious, though he avoided a meeting with Ramana Maharshi . He described Ramana as being absorbed in "the self". During these travels, he visited the Vedagiriswarar Temple , where he had a conversation with a local expert about the symbols and sculptures on the gopuram of this temple. He later wrote about this conversation [ 95 ] in his book Aion . [ 96 ] Jung became seriously ill on this trip and endured two weeks of delirium in a Calcutta hospital. After 1938, his travels were confined to Europe. [ 97 ] Jung became a full professor of medical psychology at the University of Basel in 1943 but resigned after a heart attack the next year to lead a more private life. In 1945, he began corresponding with an English Roman Catholic priest, Father Victor White , who became a close friend, regularly visiting the Jungs at the Bollingen estate. [ 1 ] Jung became ill again in 1952. [ 98 ] Jung continued to publish books until the end of his life, including Flying Saucers: A Modern Myth of Things Seen in the Skies (1959), which analyzed the archetypal meaning and possible psychological significance of the reported observations of UFOs . [ 99 ] In 1961, he wrote his last work, a contribution to Man and His Symbols entitled "Approaching the Unconscious" (published posthumously in 1964). [ 98 ] Jung died on 6 June 1961 at Küsnacht after a short illness. [ 48 ] : 450 [ 100 ] He had been beset by circulatory diseases . [ 101 ] Among his principal distinctions are honorary doctorates from: In addition, he was: Jung's thought derived from the classical education he received at school and from early family influences, which on the maternal side were a combination of Reformed Protestant academic theology with an interest in occult phenomena. On his father's side was a dedication to academic discipline emanating from his grandfather, the physician, scientist, and first Basel Professor of Medicine, Karl Gustav Jung , a one-time student activist and convert from Catholicism to Swiss Reformed Protestantism. Family lore suggested there was at least a social connection to the German polymath , Johann Wolfgang Goethe , through the latter's niece, Lotte Kestner, known as "Lottchen" who was a frequent visitor in Jung senior's household. [ 103 ] Carl Jung, the practicing clinician, writer, and founder of analytical psychology, had, through his marriage, the economic security to pursue interests in other intellectual topics of the moment. His early celebrity as a research scientist through the Word Association Test led to the start of prolific correspondence and worldwide travel. It opened academic as well as social avenues, supported by his explorations into anthropology , quantum physics , vitalism , Eastern and Western philosophy . He delved into epistemology , alchemy , astrology , and sociology, as well as literature and the arts. Jung's interest in philosophy and spiritual subjects led many to label him a mystic, although he preferred to be seen as a man of science. Jung, unlike Freud, was deeply knowledgeable about philosophical concepts and sought links between epistemology and emergent theories of psychology. [ 104 ] [ 105 ] Within the field of analytical psychology , a brief survey of major concepts developed by Jung include (alphabetical): [ 106 ] Since the establishment of psychoanalytic theory , the notion and meaning of individuals having a personal unconscious has gradually come to be commonly accepted. This was popularised by both Freud and Jung. Whereas an individual's personal unconscious is made up of thoughts and emotions that have, at some time, been experienced or held in mind but which have been repressed or forgotten, in contrast, the collective unconscious is neither acquired by activities within an individual's life nor a container of things that are thoughts, memories or ideas which are capable of being conscious during one's life. The contents of it were never naturally "known" through physical or cognitive experience and then forgotten. The collective unconscious consists of universal heritable elements common to all humans, distinct from other species. [ 111 ] However, this does not necessarily imply a genetic cause. It encapsulates fields of evolutionary biology, history of civilization, ethnology, brain and nervous system development, and general psychological development. [ 112 ] Considering its composition in practical physiological and psychological terms, "it consists of pre-existent forms, the archetypes, which can only become conscious secondarily and which give definite form to certain psychic contents." [ 112 ] Jung writes about causal factors in personal psychology as stemming from, influenced by an abstraction of the impersonal physical layer, the common and universal physiology among all humans. [ 113 ] Jung considers that science would hardly deny the existence and basic nature of "instincts", existing as a whole set of motivating urges. The collective unconscious acts as the frame where science can distinguish individual motivating urges, thought to be universal across all individuals of the human species, while instincts are present in all species. Jung contends, "The hypothesis of the collective unconscious is, therefore, no more daring than to assume there are instincts." [ 112 ] The archetype is a concept "borrowed" from anthropology to denote a process of nature. Jung's definitions of archetypes varied over time and have been the subject of debate regarding their usefulness. Archetypal images , also referred to as motifs in mythology , [ d ] are universal symbols that can mediate opposites in the psyche, are often found in religious art, mythology and fairy tales across cultures. Jung saw archetypes as pre-configurations in nature that give rise to repeating, understandable, describable experiences. In addition, the concept considers the passage of time and patterns resulting from transformation. [ 114 ] Archetypes are said to exist independently of any current event or its effect. They are said to exert influence both across all domains of experience and throughout the stages of each individual's unique development. Being in part based on heritable physiology, they are thought to have "existed" since humans became a differentiated species. They have been deduced through the development of storytelling over tens of thousands of years, indicating repeating patterns of individual and group experience, behaviors, and effects across the planet, apparently displaying common themes. [ 112 ] The concept did not originate with Jung but with Plato , who first conceived of primordial patterns. Later contributions came from Adolf Bastian and Hermann Usener , among others. [ 115 ] In the first half of the twentieth century, it proved impossible to objectively isolate and categorize the notion of an archetype within a materialist frame. According to Jung, there are "as many archetypes as there are typical situations in life", [ 116 ] and he asserted that they have a dynamic mutual influence on one another. Their alleged presence could be extracted from thousand-year-old narratives, from comparative religion, and from mythology. [ 117 ] Jung elaborated on many archetypes in " The Archetypes and the Collective Unconscious " and in " Aion: Researches into the Phenomenology of the Self ". Examples of archetypes might be the shadow, the hero, the self, anima, animus, mother, father, child, and trickster. The shadow exists as part of the unconscious mind and is composed of the traits individuals instinctively or consciously resist identifying as their own and would rather ignore, typically repressed ideas, weaknesses, desires, instincts, and shortcomings. Much of the shadow comes as a result of an individual's adaptation to cultural norms and expectations. [ 109 ] Thus, this archetype not only consists of all the things deemed unacceptable by society but also those things that are not aligned with one's own personal morals and values. Jung argues that the shadow plays a distinctive role in balancing one's overall psyche, the counter-balancing to consciousness—"where there is light, there must also be shadow". Without a well-developed shadow (often "shadow work", "integrating one's shadow"), an individual can become shallow and extremely preoccupied with the opinions of others; that is, a walking persona . [ 109 ] Not wanting to look at their shadows directly, Jung argues, often results in psychological projection . Individuals project imagined attitudes onto others without awareness. The qualities an individual may hate (or love) in another may manifest in those who do not see the external, material truth. [ 109 ] In order to truly grow as an individual, Jung believed that both the persona and shadow should be balanced. [ 109 ] The shadow can often appear as a dark, wild, exotic figure in dreams or visions. [ 118 ] Jung was one of the first people to define introversion and extraversion in a psychological context. In Jung's Psychological Types , he theorizes that each person falls into one of two categories: the introvert or the extravert. Jung compares these two psychological types to ancient archetypes, Apollo and Dionysus . The introvert is likened to Apollo, who shines a light on understanding. The introvert is focused on the internal world of reflection, dreaming, and vision. Thoughtful and insightful, the introvert can sometimes be uninterested in joining the activities of others. The extravert is associated with Dionysus, interested in joining the activities of the world. The extravert is focused on the outside world of objects, sensory perception, and action. Energetic and lively, the extravert may lose their sense of self in the intoxication of Dionysian pursuits. [ 119 ] Jungian introversion and extraversion is quite different from the modern idea of introversion and extraversion. [ 120 ] Modern theories often stay true to behaviourist means of describing such a trait (sociability, talkativeness, assertiveness, etc.), whereas Jungian introversion and extraversion are expressed as a perspective: introverts interpret the world subjectively , whereas extraverts interpret the world objectively . [ 121 ] In his psychological theory—which is not necessarily linked to a particular theory of social structure —the persona appears as a consciously created personality or identity, fashioned out of part of the collective psyche through socialization , acculturation and experience. [ 122 ] Jung applied the term persona explicitly because, in Latin, it means both personality and the masks worn by Roman actors of the classical period , expressive of the individual roles played. The persona , he argues, is a mask for the "collective psyche", a mask that 'pretends' individuality so that both self and others believe in that identity, even if it is really no more than a well-played role through which the collective psyche is expressed. Jung regarded the "persona-mask" as a complicated system that mediates between individual consciousness and the social community: it is "a compromise between the individual and society as to what a man should appear to be". [ 123 ] But he also makes it quite explicit that it is, in substance, a character mask in the classical sense known to theatre, with its double function: both intended to make a certain impression on others and to hide (part of) the true nature of the individual. [ 124 ] The therapist then aims to assist the individuation process through which the client (re)gains their "own self"—by liberating the self, both from the deceptive cover of the persona and from the power of unconscious impulses. Jung has influenced management theory because managers and executives create an appropriate "management persona" (a corporate mask) and a persuasive identity, [ 125 ] and they have to evaluate what sort of people the workers are, to manage them (for example, using personality tests and peer reviews ). [ 126 ] Of his early years, Jung would write that "mentally my greatest adventure had been the study of Kant and Schopenhauer. The great news of the day was the work of Charles Darwin." [ 127 ] While Jung’s conception of human psychology is grounded in Darwinian evolutionary theory it is important to note that his evolutionary thought had a distinctively German quality to it. This is because the idiosyncratic reception of Darwin in late nineteenth and early twentieth century Germany resulted in the integration of Darwin's ideas with German embryological and developmental traditions formulated by the Naturphilosophen and theorists such as Ernst Haeckel . It was these traditions that formed the intellectual background of Jung’s evolutionary thought. [ 128 ] The result was that Jung's evolutionary conception of mind focused on embryology and development. From this perspective, the emergence of consciousness both in ontogeny (development) and phylogeny (evolution) was built upon much more archaic, affect-based subcortical brain systems. It was this developmental approach to evolution that underpinned his "archaeological" conception of the human psyche consisting of different evolutionary layers, from the deeply archaic to the more evolutionarily recent. Those more archaic structures in the brain Jung believed to be the basis of the “collective unconscious” - an aspect of human psychology shared by all members of the species Homo sapiens . [ 129 ] In commenting on humanity's evolution from an ancient primate ancestor, Jung wrote: 'We keep forgetting that we are primates and that we have to make allowances for these primitive layers in our psyche.' [ 130 ] Jung also developed the notion of different evolutionary layers in the psyche in his discussion of fossil hominins such as Pithecanthropus ( Homo erectus ). As he writes: For just as a man has a body that is no different in principle from that of an animal, so also his psychology has a whole series of lower storeys [ sic ] in which the spectres from humanity’s past epochs still dwell, then the animal souls from the age of Pithecanthropus and the hominids, then the “psyche” of the cold-blooded saurian. [ 131 ] Jung’s notion of different evolutionary layers in the human mind has been compared with the work of neuroscientist Jaak Panksepp, particularly as outlined in his book The Archaeology of Mind: Neuroevolutionary Origins of Human Emotions . [ 3 ] Of these affinities it has been suggested that ‘Jung and Panksepp have, independently it seems, developed similar metaphors of an archeologically layered psyche in which jewels and treasures are discoverable in the deepest phylogenetically ancient regions of the brain – for Jung they are archetypal structures for Panksepp cross-species homologies.' [ 3 ] Significantly, in a 2017 article entitled "The Affective Core of the Self: A Neuro-Archetypical Perspective on the Foundations of Human (and Animal) Subjectivity", when noting Jung’s belief that archetypes may be related to evolutionarily ancient subcortical brain systems, Panksepp and colleagues wrote that "such assertions by Jung were not only quite farsighted, but they actually open ways to connect his theory of the psyche with the most advanced scientific theories and discoveries of our day." [ 132 ] Jung's work on himself and his patients convinced him that life has a spiritual purpose beyond material goals. [ 133 ] [ 134 ] The main task for people, he believed, is to discover and fulfill their deep, innate potential. Based on his study of Christianity , Hinduism , Buddhism , Gnosticism , Taoism , and other traditions, Jung believed this journey of transformation, which he called individuation , is at the mystical heart of all religions. It is a journey to meet the self and at the same time to meet the Divine . [ 135 ] Unlike Freud's atheistic worldview, Jung's pantheism may have led him to believe that spiritual experience was essential to well-being, as he specifically identifies individual human life with the universe as a whole. [ 136 ] [ 137 ] In 1959, Jung was asked by the host, John Freeman , on the BBC interview program Face to Face whether he believed in God, to which Jung answered, "I do not need to believe. I know ." [ 138 ] [ 139 ] Jung's ideas on religion counterbalance Freudian skepticism. Jung's idea of religion as a practical road to individuation is still treated in modern textbooks on the psychology of religion , though his ideas have been criticized. [ 140 ] Jung recommended spirituality as a cure for alcoholism , and is considered to have had an indirect role in establishing Alcoholics Anonymous . [ 141 ] Jung treated an American patient named Rowland Hazard III who had chronic alcoholism. After working with the patient for some time and achieving no significant progress, Jung told the man that his alcoholic condition was near to hopeless, save only the possibility of a spiritual experience. Jung noted that, occasionally, such experiences had been known to reform alcoholics when all other options had failed. Hazard took Jung's advice seriously and sought a personal, spiritual experience. He returned to the United States and joined a Christian evangelical movement known as the Oxford Group . He told other alcoholics what Jung had told him about the importance of a spiritual experience. One of the alcoholics he brought into the Oxford Group was Ebby Thacher , a long-time friend and drinking buddy of William Griffith Wilson , later co-founder of Alcoholics Anonymous. Thacher told Wilson about the Oxford Group, and through them, Wilson became aware of Hazard's experience with Jung. The influence of Jung thus indirectly found its way into the formation of Alcoholics Anonymous, the original twelve-step program . The above claims are documented in the letters of Jung and Wilson. [ 142 ] Although some historians dispute the detail, Jung discussed an Oxford Group member, who may have been the same person, in talks around 1940. The remarks were distributed privately in transcript form, from shorthand taken by an attender (Jung reportedly approved the transcript), and later recorded in his Collected Works , "For instance, when a member of the Oxford Group comes to me in order to get treatment, I say, 'You are in the Oxford Group; so long as you are there, you settle your affair with the Oxford Group. I can't do it better than Jesus. ' " [ 143 ] Jung goes on to state he has seen similar cures among Roman Catholics . The 12-step program of Alcoholics Anonymous has a psychological backdrop involving the human ego and the dichotomy between the conscious and unconscious mind. [ 144 ] Jung had an apparent interest in the paranormal and occult. For decades he attended seances and claimed to have witnessed "parapsychic phenomena". Initially, he attributed these to psychological causes, even delivering a 1919 lecture in England for the Society for Psychical Research on "The Psychological Foundations for the belief in spirits". [ 145 ] However, he began to "doubt whether an exclusively psychological approach can do justice to the phenomena in question" [ 145 ] and stated that "the spirit hypothesis yields better results". [ 146 ] But he retained some skepticism toward his own postulation, as he could not find material evidence of the existence of spirits. [ 146 ] Jung's ideas about the paranormal culminated in " synchronicity ". [ 147 ] This is the idea that certain coincidences manifest in the world, have exceptionally intense meaning to observers. Such coincidences have a great effect on the observer from multiple cumulative aspects: from the immediate personal relevance of the coincidence to the observer, from the peculiarities of (the nature of, the character, novelty, curiosity of) any such coincidence; from the sheer improbability of the coincidence, having no apparent causal link (hence Jung's essay subtitle "An Acausal Connecting Principle"). Despite his own experiments failing to confirm the phenomenon [ 148 ] he held on to the idea as an explanation for apparent ESP . [ 149 ] In addition, he proposed it as a functional explanation for how the I-Ching worked. However, he was never clear about how synchronicity worked. [ 150 ] Jung influenced one philosophical interpretation (not the science) of quantum physics with the concept of synchronicity regarding some events as non-causal . That idea influenced the physicist Wolfgang Pauli (with whom, via a letter correspondence, Jung developed the notion of unus mundus in connection with the idea of nonlocality) and some other physicists . [ 151 ] Jung's acquaintance with alchemy came between 1928 and 1930 when he was introduced to a manuscript of The Secret of the Golden Flower , translated by Richard Wilhelm . [ 152 ] The work and writings of Jung from the 1930s onwards shifted to a focus on the psychological significance of alchemy . [ 153 ] In 1944, Jung published Psychology and Alchemy , in which he analyzed the alchemical symbols and came to the conclusion that there is a direct relationship between them and the psychoanalytical process. [ e ] He argued that the alchemical process was the transformation of the impure soul (lead) to perfected soul (gold), and a metaphor for the individuation process. [ 32 ] In 1963, Mysterium Coniunctionis first appeared in English as part of The Collected Works of C. G. Jung . Mysterium Coniunctionis was Jung's last major book and focused on the " Mysterium Coniunctionis " archetype, known as the sacred marriage between the sun and moon. Jung argued that the stages of the alchemists, the blackening, the whitening, the reddening, and the yellowing, could be taken as symbolic of individuation—his chosen term for personal growth (75). [ 154 ] Jung proposed that art can be used to alleviate or contain feelings of trauma, fear, or anxiety and also to repair, restore, and heal. [ 25 ] In his work with patients and his own personal explorations, Jung wrote that art expression and images found in dreams could help recover from trauma and emotional distress. At times of emotional distress, he often drew, painted, or made objects and constructions, which he recognized as more than recreational. [ 25 ] Dance and movement therapy , as a form of active imagination, was developed by Jung and Toni Wolff in 1916 [ 155 ] and practiced by Tina Keller-Jenny and other analysts. It remained largely unknown until the 1950s when it was rediscovered by Marian Chace and therapist Mary Whitehouse. Whitehouse, after studying with Martha Graham and Mary Wigman , became a dancer and teacher of modern dance, [ 156 ] and, along with Swiss dancer Trudi Schoop , is considered one of the founders of dance/movement therapy in the U.S. Jung stressed the importance of individual rights in a person's relation to the state and society. He saw that the state was treated as "a quasi-animate personality from whom everything is expected" but that this personality was "only camouflage for those individuals who know how to manipulate it". [ 157 ] He referred to the state as a form of slavery. [ 158 ] [ 159 ] [ 160 ] [ 161 ] He also thought that the state "swallowed up [people's] religious forces", [ 162 ] and therefore that the state had "taken the place of God"—making it comparable to a religion in which "state slavery is a form of worship". [ 160 ] Jung observed that "stage acts of [the] state" are comparable to religious displays: Brass bands, flags, banners, parades and monster demonstrations are no different in principle from ecclesiastical processions, cannonades and fire to scare off demons. [ 163 ] From Jung's perspective, this replacement of God with the state in a mass society leads to the dislocation of the religious drive and results in the same fanaticism of the church-states of the Dark Ages —wherein the more the state is 'worshipped', the more freedom and morality are suppressed; [ 164 ] this ultimately leaves the individual psychically undeveloped with extreme feelings of marginalization. [ 165 ] Jung was in contact with Allen Dulles of the Office of Strategic Services (predecessor of the Central Intelligence Agency ) and provided valuable intelligence on the psychological condition of Hitler . Dulles referred to Jung as "Agent 488" and offered the following description of his service: "Nobody will probably ever know how much Professor Jung contributed to the Allied Cause during the war, by seeing people who were connected somehow with the other side". Jung's service to the Allied cause through the OSS remained classified after the war. [ 166 ] In "The State of Psychotherapy Today", [ 167 ] published in 1934 in the Zentralblatt für Psychotherapie , Jung wrote: "The Aryan unconscious has a greater potential than the Jewish unconscious" and "The Jew, who is something of a nomad, has never yet created a cultural form of his own and as far as we can see never will". [ 168 ] Andrew Samuels argues that his remarks on the "Aryan unconscious" and the "corrosive character" of Freud's "Jewish gospel" [ 169 ] demonstrate a form of antisemitism "fundamental to the structure of Jung's thought" but also argues that there is a "pioneering nature of Jung's contributions" and that "his intuition of the importance of exploring difference remains intact." [ 170 ] In 1933, after the Nazis gained power in Germany, Jung became the president of the new International General Medical Society for Psychotherapy ( Allgemeine Ärztliche Gesellschaft für Psychotherapie ), a professional body which aimed to have affiliated organizations in different countries. [ 171 ] The German affiliated organization, the Deutsche Allgemeine Ärztliche Gesellschaft für Psychotherapie, led by Matthias Göring , an Adlerian psychotherapist [ 172 ] and a cousin of the prominent Nazi Hermann Göring , excluded Jews. In 1933, the society's Zentralblatt für Psychotherapie journal published a statement endorsing Nazi positions [ 173 ] and Hitler's book Mein Kampf . [ 174 ] In 1934, Jung wrote in a Swiss publication, the Neue Zürcher Zeitung , that he experienced "great surprise and disappointment" [ 175 ] when the Zentralblatt associated his name with the pro-Nazi statement. He did not end his relationship with the Zentralblatt at this time, but he did arrange the appointment of a new managing editor, Carl Alfred Meier of Switzerland. For the next few years, the Zentralblatt under Jung and Meier maintained a position distinct from that of the Nazis in that it continued to acknowledge the contributions of Jewish doctors to psychotherapy. [ 176 ] In the face of energetic German attempts to Nazify the international body, Jung resigned from its presidency in 1939, [ 176 ] the year the Second World War started. The International Society's constitution permitted individual doctors to join it directly rather than through one of the national affiliated societies, a provision to which Jung drew attention in a circular in 1934. [ 177 ] This implied that German Jewish doctors could maintain their professional status as individual members of the international body, even though they were excluded from the German affiliate, as well as from other German medical societies operating under the Nazis. [ 178 ] Jung went on to say, "The main point is to get a young and insecure science into a place of safety during an earthquake." [ 179 ] Scholar Yosef Hayim Yerushalmi believed that Jung's antisemitism may have contributed to the schism between Freud and his circle of psychoanalysts, who were predominantly Jews. [ 180 ] Jung's interest in European mythology and folk psychology was shared by the Nazis . [ 181 ] [ 182 ] [ 72 ] Richard Noll describes Jung's own reaction to this connection: Jung clearly identifies himself with the spirit of German Volkstumsbewegung throughout this period and well into the 1920s and 1930s, until the horrors of Nazism finally compelled him to reframe these neopagan metaphors in a negative light in his 1936 essay on Wotan . [ 183 ] Various statements made by Jung in the 1930s have been cited as evidence of both contempt for Nazism and sympathy for Nazism. [ 184 ] In the 1936 essay "Wotan", Jung described the influence of Adolf Hitler on Germany as "one man who is obviously 'possessed' has infected a whole nation to such an extent that everything is set in motion and has started rolling on its course towards perdition." [ 185 ] [ 186 ] He would later say, during a lengthy interview with H. R. Knickerbocker in October 1938: [ 187 ] [ 188 ] Hitler seemed like the 'double' of a real person, as if Hitler the man might be hiding inside like an appendix, and deliberately so concealed in order not to disturb the mechanism ... You know you could never talk to this man; because there is nobody there ... It is not an individual; it is an entire nation. In an interview in 1949, Carl Jung said, It must be clear to anyone who has read any of my books that I have never been a Nazi sympathizer and I never have been anti-Semitic, and no amount of misquotation, mistranslation, or rearrangement of what I have written can alter the record of my true point of view. Nearly every one of these passages has been tampered with, either by malice or by ignorance. Furthermore, my friendly relations with a large group of Jewish colleagues and patients over a period of many years in itself disproves the charge of anti-Semitism. [ 189 ] Jung is also known to have possessed an interest in the Jewish mystic tradition of Kabbalah. [ 190 ] Jung addressed homosexuality in his published writings, in one comment specifying that homosexuality should not be a concern of legal authorities nor be considered a crime. He also stated that homosexuality does not reduce the value of a person as a member of society. Jung also said that homosexuality is a result of psychological immaturity ( "nurture" ), but only if one's sexuality is not an aspect of their constitutional characteristics ( "nature" ). [ 191 ] Jung's theories are considered to be a useful therapeutic framework for the analysis of unconscious phenomena that become manifest in the acute psychedelic state. [ 3 ] [ 192 ] [ 193 ] [ 194 ] [ 195 ] This view is based on correspondence Jung had with researchers involved in psychedelic research in the 1950s, as well as more recent neuroimaging research where subjects who are administered psychedelic compounds seem to have archetypal religious experiences of "unity" and "ego dissolution" associated with reduced activity in the default mode network. [ 193 ] [ 194 ] [ 196 ] This research has led to a re-evaluation of Jung's work, particularly the visions detailed in The Red Book , in the context of contemporary psychedelic, evolutionary, and developmental neuroscience . For example, in a chapter entitled "Integrating the Archaic and the Modern: The Red Book, Visual Cognitive Modalities and the Neuroscience of Altered States of Consciousness", in the 2020 volume Jung's Red Book for Our Time: Searching for Soul Under Postmodern Conditions, Volume 4 , it is argued Jung was a pioneer who explored uncharted "cognitive domains" that are alien to Western modes of thought. While such domains of experience are not part of mainstream Western culture and thought, they are central to various Indigenous cultures that use psychedelics such as Iboga and Ayahuasca during rituals to alter consciousness. The author writes: "Jung seems to have been dealing with modes of consciousness alien to mainstream Western thought, exploring the terrain of uncharted cognitive domains. I argue that science is beginning to catch up with Jung who was a pioneer whose insights contribute a great deal to our emerging understanding of human consciousness." [ 197 ] In this analysis, Jung's paintings of his visions in The Red Book were compared to the paintings of Ayahuasca visions by the Peruvian shaman Pablo Amaringo . [ 198 ] Commenting on research that was being undertaken during the 1950s, Jung wrote the following in a letter to Betty Eisner, a psychologist who was involved in LSD research at the University of California: "Experiments along the line of mescaline and related drugs are certainly most interesting since such drugs lay bare a level of the unconscious that is otherwise accessible only under peculiar psychic conditions. It is a fact that you get certain perceptions and experiences of things appearing either in mystical states or in the analysis of unconscious phenomena." [ 199 ] An account of Jung and psychedelics, as well as the importance of Jungian psychology to psychedelic-assisted therapies, is outlined in Scott Hill's 2013 book Confrontation with the Unconscious: Jungian Depth Psychology and Psychedelic Experience . [ 200 ] A 2021 article discusses Jung's attitude towards psychedelics, as well as the applicability of his ideas to current research. [ 196 ] As the author writes, Jung's "...legitimate reservations about the clinical use of psychedelics are no longer relevant as the field has progressed significantly, devising robust clinical and experimental protocols for psychedelic-assisted therapies. That said Jung's concept of individuation—that is the integration of the archaic unconscious with consciousness—seems extremely pertinent to modern psychedelic research." [ 196 ] The author also uses work in evolutionary and psychedelic neuroscience, and specifically the latter's ability to make manifest ancient subcortical brain systems, to illuminate Jung's concept of an archaic collective unconscious that evolved before the ego complex and the uniquely human default mode network. [ 196 ] The Myers–Briggs Type Indicator (MBTI), a psychometric instrument mostly popular with non-psychologists, as well as the concepts of socionics , were developed from Jung's model of psychological types . The MBTI is considered pseudoscience [ 201 ] and is not widely accepted by researchers in the field of psychology. [ 202 ] Jung is considered a "godparent" of the altruistic, mutual self-help movement, Alcoholics Anonymous . [ 203 ] Jung told Rhode Island businessman and politician Rowland Hazard III, who had come under his care for the first time in 1926, that the only chance he might have to recover was through a "spiritual or religious experience" or "genuine conversion," which Hazard later had, through the Oxford Group and the Emmanuel Movement , and, according to some sources, never drank again. [ 204 ] [ 205 ] Hazard, in turn, helped Ebby Thatcher , another alcoholic, get sober, with help from the Oxford Group. Thatcher brought Jung's ideas to a third alcoholic, Bill W. , who consequently co-founded Alcoholics Anonymous with Dr. Bob . Years later, Bill W. corresponded with Jung, in 1961, thanking him for helping to inspire the organization. Of Hazard, the alcoholic who came under his care, Jung wrote: "His craving for alcohol was the equivalent, on a low level, of the spiritual thirst of our being for wholeness, expressed in medieval language: the union with God." [ 203 ] Jung concludes his letter to Bill W.: "You see, "alcohol" in Latin is spiritus , and you use the same word for the highest religious experience as well as for the most depraving poison. The helpful formula therefore is: spiritus contra spiritum ." [ 206 ] Jung saw the human psyche as "by nature religious" and made this idea a principal focus of his explorations. Jung is one of the best-known contemporary contributors to dream analysis and symbolization. His influence on popular psychology, the "psychologization of religion", spirituality , and the New Age movement has been immense. A Review of General Psychology survey, published in 2002, ranked Jung as the 23rd most cited psychologist of the 20th century. The list however focused on U.S. journals and was made by the psychology department of Arkansas State University . [ 207 ] Although psychoanalysis is still studied in the humanities, a 2008 study in The Journal of the American Psychoanalytic Association found that psychology departments and textbooks treat it as "desiccated and dead". [ 208 ] Similarly, Alan Stone noted, "As academic psychology becomes more 'scientific' and psychiatry more biological, psychoanalysis is being brushed aside." [ 209 ] In a 2024 book-length reappraisal of Jung’s theories entitled Carl Jung and the Evolutionary Sciences: A New Vision for Analytical Psychology , it has been suggested that Jung was far ahead of his time in his evolutionary conception of the human mind. This thesis asserts that recent work in developmental biology, as well as experimental and psychedelic neuroscience, have provided empirical evidence that supports some of Jung’s central claims about the nature and evolution of consciousness. More specifically, trance states or altered states of consciousness (what Jung often referred to as the numinous ) have become a central concern in contemporary neuroscientific investigation of the nature and origins of consciousness. In this sense, as an evolutionary theorist of the mind, Jung was far ahead of his own time. It was only during the first decades of the 21st Century, as scientists began investigating altered, trance, and psychedelic states, that Jung’s far-seeing and wide-ranging theories found increasing support from the empirically based mind sciences. In this sense, the authors suggest audiences can appreciate how revolutionary and prescient Jung’s evolutionary conception of human psychology really was. [ 3 ] Editors: Herbert Read , Michael Fordham , Gerhard Adler . Executive ed.: W. McGuire. Trans.: R.F.C. Hull . London: Routledge Kegan Paul (1953–1980). Supplementary volumes Seminars Houses and institutions Organizations Introductory texts Texts in various areas of Jungian thought Academic texts Journals Jung-Freud relationship Others recollections of Jung Critical scholarship	https://en.wikipedia.org/wiki/Carl_Jung
Carl Schneider (December 19, 1891 in Gembitz, Kreis Mogilno , Province of Posen – December 11, 1946 in Frankfurt ), professor at Heidelberg University , (1933–1945) [ 1 ] chairman of its department of Psychiatry , [ 2 ] director of its clinic, was a senior researcher for the Action T4 euthanasia program. Schneider is said to exemplify the descent of a distinguished academic psychiatrist into the Nazi worldview. Some described him as having once shown great empathy in his psychiatric rehabilitation work, and having a great idealism about transforming the 'horror' of psychiatric patients thought to be regressed, isolated and backward. He would sometimes put forward two possible ways of helping a patient – one of them 'work therapy', and the other to sterilize or kill them. [ 3 ] Schneider joined the Nazi Party in 1932. He defined and elaborated the psychological assumptions of Nazi ideology and science. He coined the term national therapy for ethnic cleansing : ridding the populace of genetic and blood contaminants threatening the psychological and physical health of the German / Aryan population. [ 4 ] He collected the brains of murdered Jews , [ 2 ] mentally handicapped children, and other victims, for research in his clinic and for instruction. He taught a technique of replacing spinal fluid with air, to get clearer x-rays of the brain. [ citation needed ] Schneider, along with Konrad Zucker , helped Heidelberg become one of the two leading training centres for the killing of children for theoretically scientific purposes, which went on at thirty clinics for three years. [ 5 ] At the end of the war, Schneider flew out of Heidelberg on the 29 March 1945. The U.S. occupation authorities barred his reinstatement to the university's medical faculty , even before they learned of his role in the euthanasia program. Later Schneider was arrested and moved to Lager in Moosburg . On 29 November 1946, Schneider was given to the German justice authorities in Frankfurt am Main , to be a witness in the trial against Werner Heyde . Prosecutors allegedly told Schneider that in a trial his position would be very bad. On 11 December 1946, Schneider hanged himself in his prison cell awaiting trial in Frankfurt am Main. His co-workers were not punished and could continue their work. [ 6 ] [ 7 ] His membership in the Heidelberg academy of sciences was deleted. [ 8 ] [ 9 ] [ 10 ] [ 11 ]	https://en.wikipedia.org/wiki/Carl_Schneider
The Carlo Besta Neurological Institute is a hospital and research institute in Milan . Is known to be one of the most important neurological hospitals in the world. [ 1 ] The Carlo Besta Neurological Institute was founded in 1918. [ 2 ] In 1981 the Italian government designated it as an Institute of Research and Treatment (IRCCS). [ 2 ] The Carlo Besta Neurological Institute is a member of EuroBioBank 's biobank program. [ citation needed ] Here is active the first, and the most important, neurosurgical simulation center in Europe and the most equipped in the world (Besta NeuroSim) that enable the neurosurgeons residents to practice before to operate on a person. [ 3 ] The other activities regard neurological disorders, brain cancer, neuromuscular disorders, vascular, functional and oncological neurosurgery and pediatric neurology and neurosurgery. The oncological neurology ward is one of the most active in Europe for number of patients treated and number of clinical trials available. [ 4 ]	https://en.wikipedia.org/wiki/Carlo_Besta_Neurological_Institute
Carlos Enrique Soto Menegazzo (born August 26, 1951) is a Guatemalan cardiologist and politician who served as Minister of Public Health and Social Assistance from 2017 to 2020 under the government of Jimmy Morales . [ 1 ] [ 2 ] On August 29, 2017 he was appointed to replace Lucrecia Hernández Mack as Minister of Public Health. [ 2 ] Hernández had announced her resignation the sunday before, in protest over President Jimmy Morales ordering the expulsion of United Nations anti-corruption investigator Iván Velásquez Gómez . [ 3 ] Since February 2014, he had served as director of Roosevelt Hospital until that day. [ 4 ] He is son of Carlos Armando Soto Gómez y Odilia Perina Menegazzo Vanfrette, his father was Minister of Health too from 1986 to 1990 and deputy of the Guatemalan National Constituent assembly of 1984. [ 5 ] He married whit Beatriz Díaz in 1969 and they divorced in 1989. He married for the second time with Lucrecia Torcelli in 1989. [ 5 ] This article about a Guatemalan politician is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Carlos_Soto_Menegazzo
Carney complex and its subsets LAMB syndrome [ 1 ] and NAME syndrome [ 1 ] are autosomal dominant conditions comprising myxomas of the heart and skin, hyperpigmentation of the skin ( lentiginosis ), and endocrine overactivity. [ 2 ] [ 3 ] It is distinct from Carney triad . Approximately 7% of all cardiac myxomas are associated with Carney complex. [ 4 ] The spotty skin pigmentation and lentigines occur most commonly on the face, especially on the lips, eyelids, conjunctiva and oral mucosa. [ 3 ] Cardiac myxomas may lead to embolic strokes and heart failure [ 4 ] and may present with fever, joint pain, shortness of breath, diastolic rumble and tumor plop. Myxomas may also occur outside the heart, usually in the skin and breast. Endocrine tumors may manifest as disorders such as Cushing syndrome . The most common endocrine gland manifestation is an ACTH-independent Cushing's syndrome due to primary pigmented nodular adrenocortical disease (PPNAD). [ 5 ] The LAMB acronym refers to lentigines , atrial myxomas , and blue nevi . [ 1 ] NAME refers to nevi , atrial myxoma, myxoid neurofibromas, and ephelides . [ 1 ] Testicular cancer, particularly Sertoli cell type, is associated with Carney syndrome. [ 7 ] Thyroid and pancreas cancer may also occur. [ 8 ] [ 9 ] Although J Aidan Carney also described Carney's triad it is entirely different. [ 10 ] Carney complex is most commonly caused by mutations in the PRKAR1A gene on chromosome 17 (17q23-q24) [ 11 ] which may function as a tumor-suppressor gene . The encoded protein is a type 1A regulatory subunit of protein kinase A. Inactivating germline mutations of this gene are found in 70% of people with Carney complex. [ 12 ] Less commonly, the molecular pathogenesis of Carney complex is a variety of genetic changes at chromosome 2 (2p16). [ 13 ] [ 14 ] Both types of Carney complex are autosomal dominant . Despite dissimilar genetics, there appears to be no phenotypic difference between PRKAR1A and chromosome 2p16 mutations. [ 13 ] Cardiac myxomas can be difficult to manage surgically because of recurrence within the heart, often far away from the site of the initial tumor. [ 3 ] [ 4 ] In 1914 an American neurosurgeon, Harvey Cushing , reported on a patient with a pituitary tumour on whom he had operated. The post mortem findings as reported were consistent with Carney complex, though at the time this condition had yet to be described. In 2017 archived tissue from the operation in Cushing's report was subjected to DNA sequencing, revealing an Arg74His ( arginine to histidine : guanine (G)-> adenosine (A) transition in the second codon position of the 74th codon in the protein) mutation in the PRKAR1A gene, confirming a diagnosis of Carney complex. Therefore, Cushing's paper appears to be the first report of this complex. [ 15 ]	https://en.wikipedia.org/wiki/Carney_complex
Carol Weihrer (August 21, 1951 - April 27, 2024 [ 1 ] ) was an activist for victims of anesthesia awareness . Beginning in 1989, Weihrer had chronic pain from recurrent corneal erosion syndrome. After 14 unsuccessful surgeries to relieve the increasing severity of the pain , in 1998 she underwent an enucleation of the eye and reportedly woke up from anesthesia during the procedure. [ 2 ] Although she didn't feel any pain during the surgery, [ 2 ] she remembered the entire experience afterwards. Weihrer received an out-of-court settlement and maintained that she had post-traumatic stress disorder as result of her experience. [ 3 ] Weihrer died on April 27, 2024. [ 1 ]	https://en.wikipedia.org/wiki/Carol_Weihrer
Carole Wilbourn (March 19, 1940 – December 23, 2024) was an American cat therapist. [ 1 ] [ 2 ] [ 3 ] Wilbourn was born in Flushing, Queens to parents Harriet Greenwald and Gustave Engel, a taxi driver. [ 1 ] She attended Bayside High School . [ 1 ] She went on to study at State University of New York at Albany , but later transferred to New York University , where she studied psychology. [ 1 ] She was awarded a BSc degree in business education in 1964. [ 1 ] She was married twice. Her first marriage to David Willbourn, a photographer, ended in divorce. [ 1 ] She later married Paul Rowan, a veterinarian , with whom she founded The Cat Practice, a cats-only hospital in Manhattan. [ 1 ] Their marriage ended in divorce. [ 1 ] Veterinary medicine The Cat Practice	https://en.wikipedia.org/wiki/Carole_Wilbourn
Carpal tunnel surgery , also called carpal tunnel release (CTR) and carpal tunnel decompression surgery , is a nerve decompression in which the transverse carpal ligament is divided. It is a surgical treatment for carpal tunnel syndrome (CTS) and recommended when there is constant (not just intermittent) numbness, muscle weakness, or atrophy, and when night-splinting no longer controls intermittent symptoms of pain in the carpal tunnel . [ 1 ] In general, milder cases can be controlled for months to years, but severe cases are unrelenting symptomatically and are likely to result in surgical treatment. [ 2 ] [ 3 ] In the United States , approximately 500,000 surgical procedures are performed each year, and the economic impact of this condition is estimated to exceed $2 billion annually. [ 4 ] The procedure is used as a treatment for carpal tunnel syndrome and according to the American Academy of Orthopaedic Surgeons (AAOS) treatment guidelines, early surgery is an option when there is clinical evidence of median nerve denervation or the patient elects to proceed directly to surgical treatment. [ 5 ] Management decisions rely on several factors, including the etiology and chronicity of CTS, symptom severity, and individual patient choices. Nonsurgical treatment measures are appropriate in the initial management of most idiopathic cases of CTS. Splinting and corticosteroid injections may be prescribed, and they have proven benefits. Steroid injections can provide relief if symptoms are of short duration. If no improvement is seen following steroid injection, carpal tunnel release may not be as effective. [ 6 ] Surgical treatment is indicated in acute cases of CTS from trauma or infection, in chronic cases with denervation of the abductor pollicis brevis muscle or a pronounced sensory loss, and in cases unresponsive to conservative management. [ 7 ] Before pursuing CTR, confirmation of the diagnosis of carpal tunnel syndrome is recommended, given that the symptoms of median nerve entrapment can overlap with other disorders including: cervical radiculopathy , thoracic outlet syndrome , and pronator syndrome . [ 8 ] Beyond physical exam testing, confirmatory electrodiagnostic studies are recommended for all patients being considered for surgery. [ 9 ] Nerve conduction studies are reported to be 90% sensitive and 60% specific for the diagnosis of carpal tunnel syndrome. [ 10 ] These studies provide the surgeon with a patient baseline and can rule out other syndromes that present similarly. Specifically, a distal motor latency of more than 4.5 ms and a sensory latency of more than 3.5 ms are considered abnormal. [ 10 ] Of note, these electrodiagnostic studies can yield normal results despite symptomatic median nerve compression. In this scenario, CTR should be considered only if physical signs of median nerve dysfunction are present in addition to classical symptoms of CTS. [ 8 ] The goal of any carpal tunnel release surgery is to divide the transverse carpal ligament and the distal aspect of the volar ante brachial fascia, thereby decompressing the median nerve and providing relief. [ 8 ] The transverse carpal ligament is a wide ligament that runs across the hand, from the scaphoid bone to the hamate bone and pisiform. It forms the roof of the carpal tunnel, and when the surgeon cuts across it (i.e., in a line with the ring finger) it no longer presses down on the nerve inside, relieving the pressure. [ 11 ] [ unreliable medical source? ] The two major types of surgery are open carpal tunnel release and endoscopic carpal tunnel release . Open carpal tunnel release can be performed through a standard incision or a limited incision. Endoscopic carpal tunnel release, which can be performed through a single or double portal. Most surgeons historically have performed the open procedure, widely considered to be the gold standard. [ citation needed ] However, since the 1990s, a growing number of surgeons now offer endoscopic carpal tunnel release. [ 12 ] Existing research does not show significant differences in outcomes of one kind of surgery versus the other, so patients can choose a surgeon they like and the surgeon also will practice the technique they like. [ 13 ] Historically, carpal tunnel release was performed under general anesthesia with a tourniquet, however the worldwide trend is now for 'wide awake hand surgery': with no tourniquet, no general or regional anesthesia and no sedation; which also enables carpal tunnel release to be performed under local anesthesia as a one stop procedure. [ 14 ] After carpal tunnel surgery, the long term use of a splint on the wrist should not be used for relief. [ 15 ] Splints do not improve grip strength , lateral pinch strength, or bowstringing. [ 15 ] While splints may protect people working with their hands, using a splint does not change complication rates or patient satisfaction. [ 15 ] Using splints can cause problems including adhesion and lack of flexibility . [ 15 ] Carpal tunnel surgery is usually performed by a hand surgeon , orthopaedic surgeon, or plastic surgeon . [ citation needed ] Open carpal tunnel release (OCTR) has long been considered the gold-standard surgical treatment for CTS. This approach allows for direct visualization of the anatomy and possible anatomical variants, which minimizes the risk of damaging critical structures. It also provides the surgeon with the option of probing the carpal canal for other structures that may be contributing to the compression of the median nerve, including ganglions and tumors. The technique involves placement of a longitudinal incision at the base of the hand. There are a few ways to determine where the incision can be placed. One of the ways is to make an incision over the carpal tunnel where it lines up with the 3rd web space of the hand. The other way is to bring the ring finger down and where that lays is where the incision can be made. [ 16 ] The length of the skin incision varies but typically is <4 cm. The subcutaneous tissue, the superficial palmar fascia, and the muscle of the palmaris brevis (if present) are also incised in line with the incision, thereby exposing the TCL. [ 17 ] With the incision of the transverse carpal ligament [ 18 ] [ 19 ] longitudinally, the median nerve is exposed. The release is extended to the superficial palmar arterial arch distally and for a limited distance proximally beneath the wrist flexion creases. [ 7 ] For optimal outcomes, the TCL must be completely released while avoiding damage to the vital structures. The flexor tendons can be retracted to inspect the floor of the canal for lesions. Scar tenderness, pillar pain, weakness, and delays in return to work can occasionally be seen following an OCTR. [ citation needed ] The open release technique has been compared to other treatments. [ 20 ] A light compression dressing and a volar splint may be applied. The hand is actively used as soon as possible after surgery, but the dependent position is avoided. Usually, the dressing can be removed by the patient at home 2 or 3 days after the surgery, and then gentle washing and showering of the hand is permitted. Gradual resumption of normal hand use is encouraged. If non-absorbable sutures are used, they are removed after 10 to 14 days. A splint may be continued for comfort as needed for 14 to 21 days. Limited-incision carpal tunnel release techniques similar to endoscopic surgery were developed to decrease palmar discomfort and hasten the return to activities. It allows for adequate exposure to avoid complications and keeps the incision out of the painful portion of the palm. The surgical approach involves a small skin incision in the palm followed by release of the distal end of the TCL under direct visualization. [ 7 ] Patients experience reduced post-operative pain as this techniques leaves the palmar fascia intact over the proximal TCL. [ 8 ] Sayed Issa's approach [ 21 ] is a carpal tunnel release through a small approach on the distal wrist crease; it is about 1.5 cm; the benefits of this technique are less surgical traumatic and more tender, it takes less time for rehabilitation, so the patient can work next day of operation, and it has very cosmetic and gentle scar in results and outcome. [ 22 ] A skin incision is made and the surgeon will dissect through fat and the superficial palmar fascia. Once the superficial palmar fascia has been released the transverse carpal ligament will be exposed. The transverse carpal ligament will be cut longitudinally to release it. [ 16 ] Endoscopic techniques for carpal tunnel release involve one or two smaller incisions (less than half inch each) through which instrumentation is introduced including a synovial elevator, probes, knives, and an endoscope used to visualize the underside of the transverse carpal ligament. [ 23 ] [ unreliable medical source? ] The endoscopic methods do not divide the subcutaneous tissues or the palmar fascia to the same degree as does the open method. [ 24 ] Advocates of endoscopic carpal tunnel release cite less palmar scarring and ulnar “pillar” pain, rapid and complete return of strength, and return to work and activities at least 2 weeks sooner than for open release. Some studies comparing open and endoscopic carpal tunnel release found no significant differences in function. The advantages of the endoscopic technique in grip strength and pain relief are realized within the first 12 weeks and seem to benefit those patients not involved in compensable injuries. However, problems related to endoscopic carpal tunnel release include (1) a technically demanding procedure; (2) a limited visual field that prevents inspection of other structures; (3) the vulnerability of the median nerve, flexor tendons, and superficial palmar arterial arch; (4) the inability to control bleeding easily; and (5) the limitations imposed by mechanical failure. [ 10 ] Although this technique has proved to be effective, it may not be applicable to every patient with carpal tunnel syndrome. If an endoscopic release cannot be accomplished safely, the procedure should be converted to an open technique. Briefly, the endoscopic method can be performed using either one portal, [ 25 ] or two portals. [ 26 ] In the Agee single-portal technique, a small transverse skin incision is made at the ulnar border of the palamaris longus tendon. A distally based flap of forearm fascia is elevated to expose the proximal end of the carpal canal. With the wrist held in slight extension, the endoscopic blade is inserted into the canal, the distal edge of the TCL is identified, and the ligament is sectioned distally to proximally. The two portal technique requires a proximal incision and a distal incision deep to the TCL. [ citation needed ] Many surgeons have embraced limited incision methods. It is considered to be the procedure of choice for many of these surgeons with respect to idiopathic carpal tunnel syndrome. [ citation needed ] Supporting this are the results of some of the previously mentioned series that cite no difference in the rate of complications for either method of surgery. Thus, there has been broad support for either surgical procedure using a variety of devices or incisions. [ citation needed ] The thread carpal tunnel release (TCTR) is a minimally invasive procedure for transecting the transverse carpal ligament (TCL) by sawing a piece of thread looped percutaneously under the guidance of ultrasound. The TCTR is performed under local anesthesia in a clinic based procedure room, and results in only one needle entry point at the palm and one needle exit point in the wrist. The technique ensures that the division happens only inside the loop of the thread around the TCL without injuring adjacent tissues. The features of the procedure includes the potentials of reduced risk of iatrogenic injury, reduced surgical cost, and reduced patient recovery time. [ 27 ] [ 28 ] [ 29 ] The sono-guided percutaneous surgical technique approach involves the use of ultrasound visibility by a surgeon in a day clinic setting, under local anesthesia, and without the use of a tourniquet or sedation. Before the operation, a thorough sonographic evaluation is conducted to identify important landmarks, structures at risk, and anatomical variations. Specific classifications, such as the Lanz classification for the median nerve motor branch, the Ferrari and Gilbert classification for Berrettini anastomosis, and the Lippert and Pabst classification for the superficial palmar arch, are assessed. The cross-sectional area (CSA) of the median nerve and the transverse carpal ligament's (TCL) thickness are measured at several anatomically significant points. [ 30 ] The limb is disinfected and draped during the procedure, ensuring sterility with a covered ultrasound probe and sterile gel. Local anesthesia is applied under sonographic control. A small skin puncture opening is made with a 14-gauge catheter, followed by the introduction of a 1.5mm probe to palpate the TCL and establish the safe zone for release. The surgical instrument, similar to a bent needle, is then used for the gradual release of the Transverse Carpal Ligament, monitored by sonographic imaging to confirm completeness. If uncertainty remains regarding the full release of the TCL, the procedure may be repeated. [ 30 ] Carpal tunnel syndrome cannot be cured, but surgery to alleviate symptoms can be successful. Success is greatest in patients with the most typical symptoms. The most common cause of failure is incorrect diagnosis, and this surgery will only mitigate carpal tunnel syndrome, and will not relieve symptoms with alternative causes. The recurrence rate after primary carpal tunnel release is approximately 2%. The success rate of surgery to relieve symptoms depends on the definition of “success” and the metrics applied. For example, with respect to alleviation of symptoms, up to 90% success is reported. Yet with respect to patient satisfaction, approximately 50% is reported. The rate at which patients return to their former employer also is less than 90%. Yet approximately 25% of those patients are re-tasked to another duty in order to minimize further stress on their hands. [ 31 ] [ 32 ] [ 33 ] In general, endoscopic techniques are as effective as traditional open carpal surgeries, [ 34 ] [ 35 ] though the faster recovery time (2–3 weeks) typically noted in endoscopic procedures is felt by some to possibly be offset by higher complication rates. [ 36 ] [ 37 ] A recent Cochrane Review showed that the use of absorbable sutures (stitches that the body dissolves) provide the same outcomes (i.e. scar quality, pain levels, etc.) as non-absorbable sutures [ 38 ] but are much cheaper. [ 39 ] [ 40 ] Complications and failures are estimated to be 3% to 19%. Unrelieved symptoms may lead to repeat operation in 12% of patients. [ 10 ] Because most patients obtain relief in the early postoperative period, it is difficult to attribute one anatomical cause to recurrent symptoms. Findings reported at reoperation include incomplete release of the transverse carpal ligament, re-formation of the flexor retinaculum, scarring in the carpal tunnel, median or palmar cutaneous neuroma, palmar cutaneous nerve entrapment, recurrent granulomatous or inflammatory tenosynovitis, and hypertrophic scar in the skin. [ 10 ] As with most soft-tissue surgeries of the hand, postoperative wound infection is rare after CTR, occurring in only 0.36% of cases. [ 41 ] Most of these are superficial, with only 0.13% of cases having deep infections. The most common complication with open carpal tunnel release surgery is pillar pain (pain in the thenar or hypothenar eminence that is worse with pressure or grasping), followed by laceration of the palmar cutaneous branch of the median nerve. Pillar pain occurs in approximately 25% of surgical cases, with symptom resolution reported in most patients by 3 months. There is no difference in the rates of pillar pain between patients undergoing open or endoscopic release. Incomplete release of the TCL with persistent or recurrent CTS symptoms is the most frequent complication attributed to endoscopic carpal tunnel release surgery. Recurrent CTS develops in 7% to 20% of surgical cases. [ 42 ] The problem is difficult to address, and revision surgery is less successful than primary carpal tunnel release surgery. [ 43 ] Injury to the median nerve proper occurs in 0.06% of cases. [ 44 ] Risk of nerve injury has been found to be higher in patients undergoing endoscopic CTR compared with open, though most are temporary neurapraxias. [ 45 ] The palmar cutaneous branch of the median nerve may be injured during superficial skin dissection or while releasing the proximal portion of the transverse carpal ligament with scissors or an endoscopic device. Nerve injury can lead to persistent paresthesias or painful neuroma formation. [ 41 ] In addition to pain, patients may have mechanical symptoms related to the flexor tendons contained in the carpal tunnel after release of the transverse carpal ligament. Damage to the tendons during release may cause inflammation and adhesions leading to triggering at the wrist. Balloon carpal tunnelplasty is an experimental technique that uses a minimally invasive balloon catheter director to access the carpal tunnel. As with a traditional tissue elevator-expander, balloon carpal tunnelplasty elevates the carpal ligament, increasing the space in the carpal tunnel. As an experiment it has been described but there are no peer-reviewed series available in the current hand surgical literature that review or comment upon the procedure. The technique is performed through a one-centimeter incision at the distal wrist crease. It is monitored and expansion is confirmed by direct or endoscopic visualization. The technique's secondary goals are to avoid to incision in the palm of the hand, to avoid cutting of the transverse carpal ligament, and to maintain the biomechanics of the hand. [ 46 ]	https://en.wikipedia.org/wiki/Carpal_tunnel_surgery
Carphologia (or carphology ) is a lint -picking behavior that is often a symptom of a delirious state . Often seen in delirious or semiconscious patients, carphologia describes the actions of picking or grasping at imaginary objects, as well as the patient's own clothes or bed linens . This can be a grave symptom in cases of extreme exhaustion or approaching death. [ 1 ] The word carphology is derived from the ancient Greek " καρφολογία " ( karphologia ), as a compound of the two Greek elements: "κάρΦος" ( karphos , "straw"), and "λέγειν" ( legein ), here in its sense of "to collect" rather than the more usual sense of "to say, profess". Thus, carphology literally means "to behave as though one were collecting straw". This refers to the involuntary picking or grasping movements sometimes seen in delirious patients in exhaustion, stupor, or high fever. [ 2 ] The Latin-derived equivalent is floccillation which derives from floccus , "a piece of wool or straw". The late Latin crocydismus , still used in continental European psychiatry, is also synonymous and derived from the ancient Greek "κροκύς" ( krokus , "bit of fluff" or "dust"). It appears first in the writings of Aretaeus and later of Galen .	https://en.wikipedia.org/wiki/Carphologia
Carprofen is a nonsteroidal anti-inflammatory drug (NSAID) of the carbazole and propionic acid class that was previously for use in humans and animals but is now only available to veterinarians for prescribing as a supportive treatment for various conditions in animals. [ 1 ] Carprofen reduces inflammation by inhibition of COX-1 and COX-2 ; its specificity for COX-2 varies from species to species. [ 1 ] Marketed under many brand names worldwide, [ 3 ] carprofen is used as a treatment for inflammation and pain , including joint pain and postoperative pain . [ 1 ] Carprofen was used in humans for almost ten years, starting in 1988, for the same conditions as in dogs; namely, joint pain and inflammation. Side effects tended to be mild, usually consisting of nausea or gastrointestinal pain and diarrhoea . It was available by prescription in 150 mg to 600 mg doses. [ 4 ] Dosages over 250 mg were reserved for pain caused by severe trauma , such as postoperative inflammation; 150 mg doses were commonly used to relieve arthritis pain, while 200 mg doses were commonly prescribed for severe arthritis or inflammatory pain. The drug was taken orally. Pfizer voluntarily removed the medication from the market for human use on commercial grounds. [ 4 ] In November 2024, the Committee for Veterinary Medicinal Products of the European Medicines Agency adopted a positive opinion, recommending the granting of a marketing authorization for the veterinary medicinal product Carprofen Orion, Chewable tablet; Solution for injection, intended for Cat and Dog. [ 2 ] The applicant for this veterinary medicinal product is Orion Corporation. [ 2 ] Carprofen Orion is a generic of Rimadyl vet, which has been authorized in the EU since January 2003. [ 2 ] Carprofen is a nonsteroidal anti-inflammatory drug approved for use in dogs. [ 5 ] It aids in the relief of inflammation, pain, and fever . Carprofen can be administered in pill , chewable tablet , or injection form. [ 6 ] Carprofen can be used for long-term pain management of such conditions as osteoarthritis , which is common in canine patients, or after surgical procedures for relief of acute pain and inflammation. [ 6 ] [ 7 ] In animals suffering from pain, carprofen has been shown to improve energy, activity level , comfort, and general well-being . [ 7 ] Most dogs respond well to carprofen use, but like all NSAIDs, it can cause gastrointestinal, liver, and kidney problems. [ 8 ] In 1999, the Food and Drug Administration (FDA) received more than six thousand anecdotal reports of sudden animal death after usage of Pfizer 's Rimadyl brand of carprofen. In response, the FDA requested that Pfizer advise consumers in their advertising that death is a possible side effect ; [ 9 ] Pfizer refused and pulled their advertising, later including death as a possible side effect on the drug label . [ 10 ] Adverse effects can include: Effects of overdose include gastritis and ulcer formation. [ 14 ] In healthy dogs given carprofen, no perioperative adverse effects on the cardiovascular system have been reported at recommended dosages. [ 15 ] [ 16 ] Perioperative administration of carprofen to cats did not affect postoperative respiratory rate nor heart rate. [ 17 ] Carprofen should not be administered concurrently with steroids , as this can cause ulcers in the stomach. Dogs should be taken off carprofen for three full days before ingesting a steroid (such as prednisolone ). Carprofen should not be given at the same time with other types of medications, such as other NSAIDs ( aspirin , etodolac , deracoxib , meloxicam , tepoxalin ), or steroids such as dexamethasone , triamcinolone , cortisone , or prednisone . [ medical citation needed ] Carprofen must be used with caution within the supervision of a veterinarian in dogs with liver or kidney disease, dehydration , bleeding deficits, or other health problems. It is not recommended for use in dogs with bleeding disorders (such as Von Willebrand's disease ), as safety has not been established in dogs with these disorders. [ 18 ] It has not been established whether carprofen can be safely used in pregnant dogs, dogs used for breeding purposes, or in lactating dogs. Several laboratory studies and clinical trials have been conducted to establish the safety of using carprofen. Clinical studies were conducted in nearly 300 dogs of different breeds . The dogs were treated with Rimadyl at the recommended dose for two weeks. According to these studies, the drug was clinically well tolerated, and the treated dogs did not have a greater incidence of adverse reactions when compared to the control group. [ 19 ] [ medical citation needed ] A number of factors may contribute to the high incidence of adverse reports received for carprofen by the Center for Veterinary Medicine in the late 1990s. These include: Carprofen may be administered intravenously to horses. [ 21 ] A single dose has been shown to reduce prostaglandin E2 production and inflammatory exudate for up to 15 hours, [ 22 ] although there was less effect on eicosanoid production when compared to the effects produced by NSAIDs such as phenylbutazone or flunixin . [ 23 ] Prostaglandin E2 and inflammatory exudate are also reduced and leukotriene B4 is inhibited. Carprofen can also be given orally, but intramuscular use may produce muscle damage. [ 24 ] Carprofen is used as an analgesic for mouse surgical procedures. [ 25 ] Carprofen may also be used on adult fish. [ 26 ] It is marketed under many brand names including: Acticarp, Artriofin, Austiofen, Bomazeal, Canidryl, Carporal, Carprieve, Carprocow, Carprodolor, Carprodyl, Carprofelican, Carprofen, Carprofène, Carprofeno, Carprofenum, Carprogesic, Carprosol, Carprotab, Carprox, Comforion, Dolagis, Dolocarp, Dolox, Eurofen, Kelaprofen, Librevia, Norocarp, Norodyl, Novocox, Ostifen, Prolet, Quellin, Reproval, Rimadyl, Rimifin, Rofeniflex, Rovera, Rycarfa, Scanodyl, Tergive, Vetprofen, and Xelcor. [ 3 ] Veterinary dosage forms include 25 mg , 75 mg, and 100 mg tablets, and 50 mg per mL injectable form. [ 1 ] [ 27 ] and more recent a 50 mg Caplet called Carprox for senior dogs aged 10 years+. Media related to Carprofen at Wikimedia Commons	https://en.wikipedia.org/wiki/Carprofen
Carrion insects are insects associated with decomposing remains. The processes of decomposition begin within a few minutes of death. [ 1 ] Decomposing remains offer a temporary, changing site of concentrated resources which are exploited by a wide range of organisms, of which arthropods are often the first to arrive and the predominant exploitive group. However, not all arthropods found on or near decomposing remains will have an active role in the decay process. [ 2 ] Carrion insects are commonly described based on their ecological role. [ 2 ] [ 3 ] Four commonly described roles are: Necrophagous species are insects/arthropods that feed directly on remains, or the fluids released from remains during the decomposition process. [ 2 ] [ 3 ] This ecological classification includes many species of the order Diptera (true flies) from the families Calliphoridae (blowflies) and Sarcophagidae (flesh flies), and some species of the order Coleoptera (beetles). Although specific arthropod species present at remains will vary by geographic location, some examples of common blowflies are Calliphora vicina , Phormia regina , Protophormia terraenovae and Lucilia sericata Necrophagous blowfly species are often the first to arrive and colonize at a site of decomposing remains. [ 2 ] These species develop from eggs laid directly on the carcass and complete their life cycle on or near the remains. Because of this, necrophagous species are considered to be the most important for post-mortem interval estimations. [ 4 ] [ 5 ] The initial colonizers of greatest importance are those of the family Calliphoridae, Sarcophagidae and Muscidae (house flies), as these are typically the first insects to lay eggs at remains. [ 5 ] The fresh stage of decomposition is characterized by the arrival of necrophagous blowflies and flesh flies. These blowflies are also strongly attracted during the bloat stage of decomposition. [ 2 ] Many Dipterans, especially their larval forms, are involved in removal of material from the carcass, though not in an appreciable amount. [ 6 ] Necrophagous species of Coleoptera are most strongly attracted during the active stage of decomposition. [ 2 ] This role includes those insects which feed on, or act as parasites of, necrophagous species. These insects do not feed directly on the decomposing remains or its fluids, but are considered to be the second most forensically important ecological role. [ 3 ] [ 7 ] Predators of necrophagous insects include species from the Coleoptera families Silphidae (carrion beetles) and Staphylinidae (rove beetles). [ 3 ] Parasites may include species of parasitic wasps, from the order Hymenoptera (family Braconidae ). Some species of blowflies may begin their larval development in the necrophagous role, feeding directly on remains, but become predaceous during later larval stages. These species are listed as being schizophagous, and are included in the predators and parasites ecological role. [ 3 ] The majority of beetles present at remains are there as predators of blowfly larvae, and are not directly concerned with the removal of carcass materials. [ 6 ] Predaceous beetles may arrive at a site of remains as early as the bloat stage of decomposition, when there is a strong attraction of their necrophagous prey. Some of these species may also remain during active decay. During the advanced stage of decay there is an increase in those insects which are predaceous and/or parasitic on necrophagous beetles. [ 2 ] Omnivorous species feed on both the decomposing remains as well as other carrion associated insects, usually necrophagous species. [ 2 ] [ 3 ] Large numbers of omnivorous insects can slow the rate at which carcass materials are removed by depleting the number of necrophagous larvae. [ 8 ] This category includes species of ants , wasps , and some species of carrion beetles. [ 2 ] Adventive species may or may not play a significant role in the decomposition of remains. Arthropods in this ecological role are not necessarily attracted to decaying remains, but use it as an extension of their natural habitats. Adventive species originate within the vegetation and soils surrounding decomposing remains. These insects may visit remains from time to time, or use them for concealment, [ 9 ] but their presence can only be accounted for by chance. [ 2 ] They may also become predators of necrophagous species found at remains. [ 9 ] Adventive species include springtails , centipedes and spiders . [ 3 ] The diagram below shows the relationship between each ecological role and a site of decaying remains. The ecological roles described above can further be condensed into two broad, general classifications: [ 10 ] This classification consists of necrobiont insects which use decaying remains as a permanent environment necessary for their life and development. Necrobiont insects includes necrophagous and entomophagous trophic specializations, [ 10 ] or necrophagous, predaceous/parasitic and omnivorous species. Some insects or arthropods visit sites of carrion, but do not colonize them. [ 5 ] This classification consists of those insects for which decomposing remains are not a permanent feature for development. [ 10 ] The adventive trophic specialization falls into this category. Each group or species of insect will be attracted to decomposing remains at different stages of decomposition, as changes within the remains result in the availability of different resources. The predictable order in which the above described insect groups are attracted to and observed on remains is referred to as a succession pattern, and can be used in forensic investigations to estimate the post-mortem interval (PMI) or time since death. [ 11 ] This method of PMI estimation is most useful in the later stages of decomposition. [ 12 ] A second method of PMI determination, in early stages of decomposition, by insect evidence utilizes the development rate of colonizing arthropods. This method is usually applied to necrophagous blowflies, as they are often the first to colonize and are associated with remains for the longest period. Development rates are only useful in forensic investigations until the first new generation has completed development and left the remains. [ 2 ]	https://en.wikipedia.org/wiki/Carrion_insects
Cartilage tumors , also known as chondrogenic tumors , are a type of bone tumor that develop in cartilage , and are divided into non-cancerous , cancerous and intermediate locally aggressive types. [ 1 ] [ 2 ] [ 3 ] This oncology article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cartilage_tumor
A cartwheel pattern is a histopathologic architectural pattern . Microscopically, cartwheel arrangements appear to have center points that radiate cells or connective tissue outward. Cartwheel patterns may be irregular and, at lower magnification, can cause tissue to appear tangled into clumps. [ 1 ] Skin tumors that can be classified as "storiform," having spindle cells with elongated nuclei radiating from a center point, are mainly: [ 2 ] This article related to pathology is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Cartwheel_pattern
The Case of Aimée concerned the Frenchwoman Marguerite Pantaine, who in 1931 attacked the celebrity actress Huguette Duflos . Marguerite was hospitalised in a mental hospital, and was treated by Jacques Lacan , becoming the subject of his doctoral thesis. [ 1 ] Lacan used the pseudonym "Aimée" to protect the identity of Marguerite Pantaine. In his thesis, he linked "Aimée"'s psychosis to her life experience, developing an innovative theory of psychogenic psychosis which drew heavily on psychoanalysis to explain phenomena not usually tractable by psychoanalytic methods. [ 2 ] [ 3 ] Lacan argued that Aimée regarded her attack on the actress as an attack against a persecutory aspect of her own psyche, namely the image of her own Ideal ego ; and that she carried out the attack in a sort of narcissistic trance. [ 4 ] He used her case to develop a theory of self-punishing paranoia . [ 5 ] It was, however, primarily in the form of ego psychology that Lacan's psychoanalytic thinking was at this point framed: "The therapeutic problem regarding psychosis seems to me to make a psychoanalysis of the ego more necessary than a psychology of the unconscious." [ 6 ] Ten years after Marguerite was discharged from hospital, she went to work for Lacan's father, and her estranged son Didier Anzieu went into analysis with Lacan. When the two Anzieus reunited, Didier realised his mother had been the subject of Lacan's thesis the decade before. [ 7 ] Elisabeth Roudinesco reports the mother's complaint that Lacan, instead of helping her, "had stolen her life story and turned it into a thesis," and that she "had been observed, ransacked, fabricated, travestied, and made into a myth for the benefit of psychiatry." [ 8 ]	https://en.wikipedia.org/wiki/Case_of_Aimée
A case presentation is a formal communication between health care professionals such as doctors and nurses regarding a patient's clinical information. [ 1 ] [ 2 ] [ 3 ] Essential parts of a case presentation include: This medical treatment –related article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Case_presentation
In medicine , a case report is a detailed report of the symptoms , signs , diagnosis , treatment, and follow-up of an individual patient . Case reports may contain a demographic profile of the patient, but usually describe an unusual or novel occurrence. Some case reports also contain a literature review of other reported cases. Case reports are professional narratives that provide feedback on clinical practice guidelines and offer a framework for early signals of effectiveness, adverse events , and cost. They can be shared for medical, scientific, or educational purposes. Most case reports are on one of six topics: [ 1 ] A case report is generally considered a type of anecdotal evidence . [ 2 ] Given their intrinsic methodological limitations, including lack of statistical sampling , case reports are placed at the bottom of the hierarchy of clinical evidence , together with case series . [ 3 ] Nevertheless, case reports do have genuinely useful roles in medical research and evidence-based medicine . [ 4 ] In particular, they have facilitated recognition of new diseases and adverse effects of treatments [ 5 ] (e.g., recognition of the link between administration of thalidomide to mothers and malformations in their babies was triggered by a case report [ 6 ] ). Case reports have a role in pharmacovigilance . [ 5 ] They can also help understand the clinical spectrum of rare diseases as well as unusual presentations of common diseases. [ 4 ] They can help generate study hypotheses , including plausible mechanisms of disease . [ 4 ] Case reports may also have a role to play in guiding the personalization of treatments in clinical practice. [ 4 ] Proponents of case reports have outlined some particular advantages of the format. Case reports and series have a high sensitivity for detecting novelty and therefore remain one of the cornerstones of medical progress; they provide many new ideas in medicine. [ 7 ] Whereas randomized clinical trials usually only inspect one variable or very few variables, rarely reflecting the full picture of a complicated medical situation, the case report can detail many different aspects of the patient's medical situation (e.g. patient history , physical examination , diagnosis , psychosocial aspects, follow up). [ 8 ] Because typical, unremarkable cases are less likely to be published, use of case reports as scientific evidence must take into account publication bias . Some case reports also contain an extensive review of the relevant literature on the topic at-hand (and sometimes a systematic review of available evidence). Reports adopting this sort of approach can be identified by terms such as a "case report and review of the literature". Reports containing broader active research such as this might be considered case studies in the true definition of the term. Case reports can also play a relevant role in medical education, providing a structure for case-based learning. [ 4 ] A particular attraction of case reports is the possibility of quick publication (with respect to more extensive studies such as randomized control trials), allowing them to act as a kind of rapid short communication between busy clinicians who may not have the time or resources to conduct large scale research. [ 8 ] The quality of the scientific reporting of case reports is variable, and sub-optimal reporting hinders the use of case reports to inform research design or help guide clinical practice. [ 4 ] In response to these issues, reporting guidelines are under development to facilitate greater transparency and completeness in the provision of relevant information for individual cases. [ 4 ] The CARE (i.e. CAse REport) guidelines include a reporting checklist that is listed on the EQUATOR Network , [ 9 ] an international initiative aimed at promoting transparent and accurate reporting of health research studies to enhance the value and reliability of medical research literature. This 13-item checklist includes indications regarding the title, key words, abstract , introduction, patient information, clinical findings, timeline, diagnostic assessment, therapeutic interventions, follow-up and outcomes, discussion, patient perspective, and informed consent . [ 4 ] An explanation and elaboration article (a manual for writing case reports following the CARE guidelines) was published in the Journal of Clinical Epidemiology in 2017. [ 10 ] Many international journals publish case reports, but they restrict the number that appear in the print run because this has an adverse effect on the journal's impact factor . [ 11 ] Case reports are often published online, and there is often still a requirement for a subscription to access them. However, an increasing number of journals are devoted to publishing case reports alone, most of which are open access . [ 12 ] [ 11 ] The first of these to start publishing, in 2001, was Grand Rounds . [ 13 ] [ 14 ] There are a number of websites that allow patients to submit and share their own patient case reports with other people. PatientsLikeMe [ 15 ] and Treatment Report [ 16 ] are two such sites. The term is also used to describe non-scientific reports usually prepared for educational reasons.	https://en.wikipedia.org/wiki/Case_report
A case series (also known as a clinical series ) is a type of medical research study that tracks subjects with a known exposure, such as patients who have received a similar treatment, [ 1 ] or examines their medical records for exposure and outcome. Case series may be consecutive [ 2 ] or non-consecutive , [ 3 ] depending on whether all cases presenting to the reporting authors over a period were included, or only a selection. When information on more than three patients is included, the case series is considered to be a systematic investigation designed to contribute to generalizable knowledge (i.e., research ), and therefore submission is required to an institutional review board (IRB). [ 4 ] Case series usually contain demographic information about the patient(s), for example, age, gender, ethnic origin. etc. Case series have a descriptive study design ; unlike studies that employ an analytic design (e.g. cohort studies , case-control studies or randomized controlled trials ), case series do not, in themselves, involve hypothesis testing to look for evidence of cause and effect (though case-only analyses are sometimes performed in genetic epidemiology to investigate the association between an exposure and a genotype [ 5 ] ). Case series are especially vulnerable to selection bias ; for example, studies that report on a series of patients with a certain illness and/or a suspected linked exposure draw their patients from a particular population (such as a hospital or clinic) which may not appropriately represent the wider population. Internal validity of case series studies is usually very low, due to the lack of a comparator group exposed to the same array of intervening variables. For example, the effects seen may be wholly or partly due to intervening effects such as the placebo effect, Hawthorne effect , Rosenthal effect , time effects, practice effects or the natural history effect. Calculating the difference in effects between two treatment groups assumed to be exposed to a very similar array of such intervening effects allows the effects of these intervening variables to cancel out. Hence only the presence of a comparator group, which is not a feature of case-series studies, will allow a valid estimate of the true treatment effect. [ 6 ] This medical article is a stub . You can help Wikipedia by expanding it .	https://en.wikipedia.org/wiki/Case_series
In the Soviet Union , a systematic political abuse of psychiatry took place [ 1 ] and was based on the interpretation of political dissent as a psychiatric problem. [ 2 ] It was called "psychopathological mechanisms" of dissent. [ 3 ] During the leadership of General Secretary Leonid Brezhnev , psychiatry was used as a tool to eliminate political opponents ("dissidents") who openly expressed beliefs that contradicted official dogma. [ 4 ] The term "philosophical intoxication" was widely used to diagnose mental disorders in cases where people disagreed with leaders and made them the target of criticism that used the writings by Karl Marx , Friedrich Engels , and Vladimir Lenin . [ 5 ] Article 58 -10 of the Stalin Criminal Code—which as Article 70 had been shifted into the RSFSR Criminal Code of 1962—and Article 190-1 of the RSFSR Criminal Code along with the system of diagnosing mental illness, developed by academician Andrei Snezhnevsky , created the very preconditions under which non-standard beliefs could easily be transformed into a criminal case, and it, in its turn, into a psychiatric diagnosis. [ 6 ] Anti-Soviet political behavior, in particular, being outspoken in opposition to the authorities, demonstrating for reform, writing books were defined in some persons as being simultaneously a criminal act (e.g., violation of Articles 70 or 190–1), a symptom (e.g., "delusion of reformism"), and a diagnosis (e.g., " sluggish schizophrenia "). [ 7 ] Within the boundaries of the diagnostic category, the symptoms of pessimism, poor social adaptation and conflict with authorities were themselves sufficient for a formal diagnosis of "sluggish schizophrenia." [ 8 ] The process of psychiatric incarceration was instigated by attempts to emigrate; distribution or possession of prohibited documents or books; participation in civil rights actions and demonstrations, and involvement in forbidden religious activity. [ 9 ] The religious faith of prisoners, including well-educated former atheists who adopted a religion, was determined to be a form of mental illness that needed to be cured. [ 10 ] The KGB routinely sent dissenters to psychiatrists for diagnosing to avoid embarrassing public trials and to discredit dissidence as the product of ill minds. [ 11 ] Formerly highly classified government documents published after the dissolution of the Soviet Union demonstrate that the authorities used psychiatry as a tool to suppress dissent. [ 12 ] According to the Commentary on the Russian Federation Law on Psychiatric Care , persons who were subjected to repressions in the form of commitment for compulsory treatment to psychiatric medical institutions and were rehabilitated in accordance with the established procedure receive compensation. The Russian Federation acknowledged that psychiatry was used for political purposes and took responsibility for the victims of "political psychiatry." [ 13 ] Political abuse of psychiatry in Russia continues after the fall of the Soviet Union [ 14 ] and threatens human rights activists with a psychiatric diagnosis. [ 15 ] Political abuse of psychiatry is the misuse of psychiatric diagnosis, detention and treatment for the purposes of obstructing the fundamental human rights of certain groups and individuals in a society. [ 16 ] It entails the exculpation and committal of citizens to psychiatric facilities based upon political rather than mental health-based criteria. [ 17 ] Many authors, including psychiatrists, also use the terms "Soviet political psychiatry" [ 18 ] or "punitive psychiatry" to refer to this phenomenon. [ 19 ] In the book Punitive Medicine by Alexander Podrabinek , the term "punitive medicine", which is identified with "punitive psychiatry," is defined as "a tool in the struggle against dissidents who cannot be punished by legal means." [ 20 ] Punitive psychiatry is neither a discrete subject nor a psychiatric specialty but, rather, it is an emergency arising within many applied sciences in totalitarian countries where members of a profession may feel themselves compelled to service the diktats of power. [ 21 ] Psychiatric confinement of sane people is uniformly considered a particularly pernicious form of repression [ 22 ] and Soviet punitive psychiatry was one of the key weapons of both illegal and legal repression. [ 23 ] As Vladimir Bukovsky and Semyon Gluzman wrote in their joint A Manual on Psychiatry for Dissenters , "the Soviet use of psychiatry as a punitive means is based upon the deliberate interpretation of dissent… as a psychiatric problem." [ 24 ] This work was published in Russian, [ 25 ] English, [ 26 ] French, [ 27 ] Italian, [ 28 ] German [ 29 ] and Danish. [ 30 ] Psychiatry possesses an inherent capacity for abuse that is greater than in other areas of medicine. [ 31 ] The diagnosis of mental disease can give the state license to detain persons against their will and insist upon therapy both in the interest of the detainee and in the broader interests of society. [ 31 ] In addition, receiving a psychiatric diagnosis can in itself be regarded as oppressive. [ 32 ] In a monolithic state, psychiatry can be used to bypass standard legal procedures for establishing guilt or innocence and allow political incarceration without the ordinary odium attaching to such political trials. [ 31 ] In the period from the 1960s to 1986, the abuse of psychiatry for political purposes was reported to have been systematic in the Soviet Union and episodic in other Eastern European countries such as Romania , Hungary , Czechoslovakia , and Yugoslavia . [ 33 ] The practice of incarceration of political dissidents in mental hospitals in Eastern Europe and the former USSR damaged the credibility of psychiatric practice in these states and entailed strong condemnation from the international community. [ 34 ] Psychiatrists have been involved in human rights abuses in states across the world when the definitions of mental disease were expanded to include political disobedience. [ 35 ] As scholars have long argued, governmental and medical institutions have at times coded threats to authority as mental disease during periods of political disturbance and instability. [ 36 ] Nowadays, in many countries, political prisoners are still sometimes confined and abused in mental institutions. [ 37 ] In the Soviet Union dissidents were often confined in the so-called psikhushka , or psychiatric wards. [ 38 ] Psikhushka is the Russian ironic diminutive for "mental hospital". [ 39 ] One of the first psikhushkas was the Psychiatric Prison Hospital in the city of Kazan . In 1939 it was transferred to the control of the NKVD , the secret police and the precursor organization to the KGB , under the order of Lavrentiy Beria , who was the head of the NKVD. [ 40 ] International human rights defenders such as Walter Reich have long recorded the methods by which Soviet psychiatrists in Psikhushka hospitals diagnosed schizophrenia in political dissenters. [ 36 ] Western scholars examined no aspect of Soviet psychiatry as thoroughly as its involvement in the social control of political dissenters. [ 41 ] Cases of political abuse of psychiatry have been known since the 1940s and 1950s. One of these early cases was that of party official Sergei Pisarev . Pisarev was arrested after criticizing the work of the Soviet secret police in the context of the so-called Doctors' Plot , an anti-Semitic campaign waged at Stalin's instructions that should have brought about a new terror wave in the Soviet Union and possibly the extermination of the remaining Jewish communes that had outlived the Second World War. [ 42 ] Pisarev was committed to the Special Psychiatric Hospital in Leningrad which along with an analogous hospital in Sychevka has started functioning since the Second World War . [ 42 ] After his discharge, Pisarev began a campaign against political abuse of psychiatry, concentrating on the Serbsky Institute which he viewed to be the seat of the trouble. [ 42 ] As a consequence of his efforts, the Central Committee of the Communist Party formed a committee which investigated the situation and came to the conclusion that political abuse of psychiatry was actually taking place. [ 42 ] The report, however, vanished in a desk drawer and never brought about any action. [ 42 ] In 1961, Soviet general Pyotr Grigorenko started to openly criticize what he considered the excesses of the Khrushchev regime. [ 43 ] He maintained that the special privileges of the political elite did not comply with the principles laid down by Lenin . [ 43 ] Grigorenko formed a dissident group — The Group for the Struggle to Revive Leninism . [ 43 ] Soviet psychiatrists from commissions instituted to inquire into his sanity diagnosed him at least three times — in April 1964, August 1969, and November 1969. [ 44 ] When arrested, Grigorenko was sent to Moscow's Lubyanka prison , and from there for psychiatric examination to the Serbsky Institute [ 43 ] where the first commission, which included Snezhnevsky and Lunts, diagnosed him with the mental disease in the form of a paranoid delusional development of his personality, accompanied by early signs of cerebral arteriosclerosis. [ 44 ] Lunts, reporting later on this diagnosis, mentioned that the symptoms of paranoid development were "an overestimation of his own personality reaching messianic proportions" and "reformist ideas." [ 44 ] Grigorenko was irresponsible for his actions and was thereby forcibly committed to a special psychiatric hospital. [ 43 ] While there, the government deprived him of his pension despite the fact that, by law, a mentally sick military officer was entitled to a pension. [ 45 ] After six months, Grigorenko was found to be in remission and was released for outpatient follow-up. [ 45 ] He required that his pension be restored. [ 45 ] Although he began to draw pension again, it was severely cut. [ 45 ] He became much more active in his dissidence, stirred other people to protest some of the State's actions and received several warnings from the KGB. [ 45 ] As Grigorenko had followers in Moscow, he was lured to Tashkent , half a continent away. [ 45 ] Again he was arrested and examined by psychiatric team. [ 45 ] None of the manifestations or symptoms cited by the Lunts commission were found by the second commission held in Tashkent under the chairmanship of Fyodor Detengof . [ 46 ] The diagnosis and evaluation made by the commission was that "Grigorenko's [criminal] activity had a purposeful character, it was related to concrete events and facts... It did not reveal any signs of illness or delusions." [ 46 ] The psychiatrists reported that he was not mentally sick, but responsible for his actions. [ 45 ] He had firm convictions which were shared by many of his colleagues and were not delusional. [ 45 ] Having evaluated the records of his preceding hospitalization, they concluded that he had not been sick at that time either. [ 45 ] The KGB brought Grigorenko back in Moscow and, three months later, arranged a second examination at the Serbsky Institute. [ 45 ] Once again, these psychiatrists found that he had "a paranoid development of the personality" manifested by reformist ideas. [ 45 ] The commission, which included Lunts and was chaired by Morozov, recommended that he be recommitted to a special psychiatric hospital for the socially dangerous. [ 46 ] Eventually, after almost four years, he was transferred to a usual mental hospital. [ 45 ] In 1971, Dr. Semyon Gluzman wrote a psychiatric report on Grigorenko. [ 47 ] Gluzman came to the conclusion that Grigorenko was mentally sane and had been taken to mental hospitals for political reasons. [ 48 ] In the late 1970s and early 1980s, Gluzman was forced to serve seven years in labor camp and three years in Siberian exile for refusing to diagnose Grigorenko with a mental illness. [ 49 ] Andrew, Grigorenko's son, was declared a hereditary madman in 1975 and was expelled from the USSR to the USA where he lives now. [ 50 ] Andrew was repeatedly told that since his father was mentally ill, then he was hereditarily mentally ill as well, and if he would not stop his appearances in defense of human rights and his father, he was told to go to psikhushka . [ 51 ] In 1979 in New York , Grigorenko was examined by the team of psychologists and psychiatrists including Alan A. Stone , the then President of American Psychiatric Association . [ 52 ] The team came to the conclusion that they could find no evidence of mental disease in Grigorenko and his history consistent with mental disease in the past. [ 52 ] The conclusion was drawn up by Walter Reich . [ 53 ] Stone said Grigorenko's case confirms some of the accusations that psychiatry in the Soviet Union is sometimes employed as a tool of political repression. [ 54 ] In 1981, Pyotr Grigorenko told about his psychiatric examinations and hospitalizations in his memoirs V Podpolye Mozhno Vstretit Tolko Krys ( In The Underground One Can Meet Only Rats ) [ 55 ] translated into English under the title Memoirs in 1982. [ 56 ] In 1991, a commission, composed of psychiatrists from all over the Soviet Union and led by Modest Kabanov, director of the Bekhterev Psychoneurological Institute in St Petersburg, spent six months reviewing the Grigorenko files, drew up 29 thick volumes of legal proceedings, [ 57 ] and reversed the official diagnosis on Grigorenko in October 1991. [ 48 ] In 1992, the official post-mortem forensic psychiatric commission of experts met at Grigorenko's homeland removed the stigma of mental patient from him and confirmed that the debilitating treatment he underwent in high security psychiatric hospitals for many years was groundless. [ 58 ] The 1992 psychiatric examination of Grigorenko was described by the Nezavisimiy Psikhiatricheskiy Zhurnal in its numbers 1–4 of 1992. [ 59 ] Viktor Rafalsky , a political prisoner, dissident and author of unpublished plays, novels, and short stories, was committed to Soviet psychiatric prisons in Lviv , Dnipropetrovsk , and Leningrad for 24 years because of belonging to a clandestine Marxist group (from 1954 to 1959), writing anti-Soviet prose (from 1962 to 1965), and possessing anti-Soviet literature (from 1968 to 1983). [ 60 ] In the winter of 1987, he was discharged and pronounced sane. [ 60 ] In 1988, Viktor Rafalsky published the first version of his memoirs Reportazh iz Niotkuda ( Reportage from Nowhere ) [ 61 ] describing his confinement in Soviet psychiatric hospitals. [ 62 ] In his memoirs, he writes, "I will say plain: when I got into a prison (it happened quite often), I, whether you believe or not, had a rest. So what was a prison in comparison with the horror of prison psikhushkas?!" [ 63 ] Some pages below, he adds, "In a prison, you can read, write, lastly do something to kill time. In prison psikhushkas, you have the right only to look at the ceiling: it is forbidden to keep paper, pencils, and even a book." [ 64 ] At the very end of 1963, the poet Joseph Brodsky was committed for observation to the Kashchenko psychiatric clinic in Moscow where he stayed for several days. [ 65 ] A few weeks later, his second hospitalization took place: on 13 February he was arrested in Leningrad. [ 65 ] Brought to trial for "pursuing a parasitic way of life", Brodsky was accused of being a poet and of not doing more "productive" work. [ 66 ] There were two hearings of the trial dated 18 February and 13 March 1964. [ 66 ] The judge ordered to send him "for an official psychiatric examination during which it will be determined whether Brodsky is suffering from some sort of psychological illness or not and whether this illness will prevent Brodsky from being sent to a distant locality for forced labor. Taking into consideration that from the history of his illness it is apparent that Brodsky has evaded hospitalization, it is hereby ordered that division No. 18 of the militia be in charge of bringing him to the official psychiatric examination." [ 67 ] On 18 February, the Dzerzhinsky District Court sent Brodsky for psychiatric examination to "Pryazhka," Psychiatric Hospital No. 2 where he spent about three weeks, from 18 February to 13 March. [ 65 ] In the mental hospitals, Brodsky was given "tranquilizing" injections, wakened in the middle of the night, immersed into a cold bath, wrapped in a wet sheet, and put next to the heater so that the sheet would cut into his body when it dried. [ 68 ] These two stints at psychiatric establishments formed the experience underlying Gorbunov and Gorchakov written and called by Brodsky "an extremely serious work." [ 69 ] In 1972, when the authorities considered Brodsky for exile and sought an expert opinion on his mental health, they consulted Snezhnevsky who, without examining him personally, diagnosed him with schizophrenia and concluded that he was "not a valuable person at all and may be let go." [ 70 ] In 1965 in the West, strong public awareness that Soviet psychiatry could be subject to political abuse arose with publication of the book Ward 7 [ 71 ] by Valery Tarsis , a writer born in 1906 in Kiev . [ 72 ] He based the book upon his own experiences in 1963–1964 when he was detained in the Moscow Kashchenko psychiatric hospital for political reasons. [ 72 ] The fictionalised documentary Ward No. 7 by Tarsis was the first literary work to deal with the Soviet authorities' abuse of psychiatry. [ 73 ] In a parallel with the story Ward No. 6 by Anton Chekhov , Tarsis implies that it is the doctors who are mad, whereas the patients are completely sane, although unsuited to a life of slavery. [ 73 ] Individuals in ward No. 7 are not cured, but persistently maimed; the hospital is a jail and the doctors are gaolers and police spies. [ 73 ] Most doctors know nothing about psychiatry, but make diagnoses arbitrarily and give all patients the same medication — an algogenic injection or the anti-psychotic drug Aminazin [ 73 ] known in the USA under trade name Thorazine . [ 74 ] Tarsis denounces Soviet psychiatry as pseudo-science and charlatanism and writes that, firstly, it has pretenses of curing the sickness of men's souls, but denies the existence of the soul; secondly, since there is no satisfactory definition of mental health, there can be no acceptable definition of mental disease in Soviet society. [ 73 ] In 1966, Tarsis was permitted to emigrate to the West, and was soon deprived of his Soviet citizenship. [ 75 ] The KGB had plans to compromise the literary career of Tarsis abroad through labelling him as a mentally ill person. [ 76 ] As the 1966 memorandum to the Politburo of the Central Committee of the Communist Party of the Soviet Union reported, "KGB continues arrangements for further compromising Tarsis abroad as a mentally ill person." [ 77 ] Among all the victims of Soviet psychiatry, Tarsis was the sole exception in the sense that he did not emphasize the 'injustice' of confining 'sane dissidents' to psychiatric hospitals and did not thereby imply that the psychiatric confinement of 'insane patients' was proper and just. [ 78 ] Shortly after publishing Ward 7 , a second case of political abuse of psychiatry gave rise to attention in Great Britain . [ 72 ] Evgeni Belov , a young Moscow interpreter contracted by a group of four British students, made friends with them. [ 72 ] At first he was positive about Soviet system, but gradually became more critical and began to voice demand for more freedom. [ 72 ] Calling for a free press and free trade unions, Belov began to write letters to the Party. [ 72 ] As a consequence, his membership in the Party was suspended and he was summoned to appear before a committee. [ 72 ] He declined, and instead sought justice higher up by writing protest letters to Leonid Brezhnev himself. [ 72 ] When British students returned from a short trip to Tokyo , Belov had vanished. [ 72 ] To their shock, it emerged that he had been committed to a mental hospital. [ 72 ] A campaign to get him out yielded no results. [ 72 ] A British newspaper published a letter in which Belov's father stated that his son was really sick, and the campaign came to a grinding halt. [ 72 ] However, the public interest had been activated. [ 72 ] Awareness in the West was also raised by the case of Alexander Esenin-Volpin , a son of the famous Russian poet Sergei Esenin and born in 1924. [ 72 ] In 1946, he was first committed to the Leningrad Special Psychiatric Hospital for writing a poem considered anti-Soviet. [ 72 ] During Khrushchev's reign, Esenin-Volpin was later hospitalized three times: in 1957, in 1959–1960 in the same the Leningrad Special Psychiatric Hospital and, finally, in 1962–1963. [ 79 ] In 1968, Esenin-Volpin was again hospitalized, and for this once his case achieved the attention in the West. [ 79 ] In February 1968, 99 Soviet mathematicians and scientists sent a letter [ ru ] to the Soviet officials demanding his release. [ 80 ] After a wave of protests, he was discharged and permitted to immigrate to the USA where he obtained the position of professor of mathematics. [ 79 ] In 2010, Alexander Magalif , who hospitalized Esenin-Volpin, recollected that he had seen a little mark made by a pencil in the corner of the referral to treatment of Esenin-Volpin: "not to discharge from the hospital without coordination with KGB." [ 81 ] In 1965, the writer Yuli Daniel was arrested due to his satirical anti-Stalinist works and outspoken protest at the human rights abuse in the USSR. [ 82 ] Daniel was kept in a mental hospital of the Gulag where he was refused medical treatment in order to destroy his will. [ 82 ] Viktor Fainberg was one of the seven participants of the 1968 Red Square demonstration against the Soviet intervention into Czechoslovakia . [ 85 ] He was committed for compulsory treatment to the Special Psychiatric Hospital in Leningrad where he was confined for five years. [ 85 ] During his confinement, a psychiatrist working in the establishment, Marina Voikhanskaya, fell in love with him and helped him as much as she could. [ 85 ] After his discharge, they married and emigrated to the United Kingdom [ 85 ] where Fainberg organized the Campaign Against Psychiatric Abuse [ 86 ] and was its director. [ 87 ] When Fainberg and Voikhanskaya had divorced, Viktor moved to Paris and Marina remained in the United Kingdom. [ 85 ] In 1968, Valeriya Novodvorskaya created an underground student organization whose purpose was to overthrow the Soviet state. [ 88 ] On 5 December 1969, she was arrested in the Kremlin Palace of Congresses , where before the start of a performance of the opera October she was handing out and scattering leaflets written in verse form until she was approached by KGB men. [ 89 ] She was later sentenced to indefinite detention in the prison psychiatric hospital in Kazan . [ 89 ] Her experience in this hospital was described [ 90 ] in her largest collection of writings entitled Po Tu Storonu Otchayaniya ( Beyond Despair ). [ 91 ] Novodvorskaya was also committed in a mental hospital later, in 1978 as a member of the Free Interprofessional Association of Workers [ 92 ] and as a person arrested "for insulting President" in September 1990; that time she was discharged after the 1991 putsch . [ 93 ] In the early 1990s, psychiatrists of the Independent Psychiatric Association of Russia and G. N. Sotsevich proved the absence of mental illness in Novodvorskaya. [ 94 ] After the 1968 Red Square demonstration against the Soviet invasion into Czechoslovakia , August 1968 saw the arrest of Natalya Gorbanevskaya well known in the West due to her book Red Square at Noon describing the demonstration. [ 95 ] A few days later, the Serbsky Institute found her non-accountable and made diagnosis of "deep psychopathy—the presence of mild, chronic schizophrenic process cannot be excluded." [ 95 ] She was allowed to return to the care of her mother. [ 95 ] In November 1969, a psychiatric commission again examined her, diagnosed "psychopathic personality with symptoms of hysteria and a tendency to decompensation", but considered that psychiatric hospitalization was not required. [ 95 ] A month later, she was again arrested and sent to the Serbsky Institute for psychiatric examination in April 1970. [ 95 ] The investigating commission chaired by Morozov found her non-responsible and that she had a "chronic, mental illness in the form of schizophrenia." [ 95 ] The commission found in her the presence of changes in the thinking processes and in the critical and emotional faculties characteristic of schizophrenia. [ 95 ] It was concluded that Gorbanevskaya took part in the Red Square demonstration in a state of the mental disease. [ 95 ] In Paris, French psychiatrists at their request examined Gorbanevskaya and found her to be mentally normal. [ 96 ] They concluded that in 1969–1972 she had been committed to a psychiatric hospital for political, not medical reasons. [ 96 ] On 29 May 1970, Zhores Medvedev , an internationally respected and prominent scientist, was forcibly taken from his apartment in Obninsk and committed to a mental hospital where he was held, without legitimate medical justification, until 17 June 1970. [ 97 ] The leadership was instantly faced with the action of strong collective protest initiated by top Soviet scientists including Igor Tamm and Pyotr Kapitsa . [ 98 ] Medvedev's release was achieved only after intense pressure from intellectuals and scientists both within and outside of the USSR. [ 97 ] He was largely hospitalized because of the publication abroad of his book of Trofim Lysenko . [ 99 ] In widely circulated books, Zhores Medvedev had criticized the "geneticist" Lysenko and had also expressed his straightforward disagreement with restrictions on communication with scientists abroad. [ 100 ] He was removed from his position as head of a laboratory at the Institute of Medical Radiology and this removal was illegal, he said. [ 100 ] The diagnosis in the case-notes was "incipient schizophrenia," the diagnosis made by the psychiatric commission was "psychopathic personality with paranoid tendencies." [ 100 ] What happened to Medvedev was not a separate incident; rather, it was part, in Medvedev's words, of "the dangerous tendency of using psychiatry for political purposes, the exploitation of medicine in an alien role as a means of intimidation and punishment — a new and illegal way of isolating people for their views and convictions." [ 97 ] This experience was reflected in Zhores Medvedev's and Roy Medvedev 's book A Question of Madness: Repression by Psychiatry in the Soviet Union published by Macmillan in London in 1971. [ 101 ] In 1971, renowned Soviet physicist Andrei Sakharov supported a protest of two political prisoners, V. Fainberg and V. Borisov, who announced a hunger strike against "compulsory therapeutic treatment with medications injurious to mental activity" in a Leningrad psychiatric institution. [ 102 ] In 1984, after publishing an article by Andrei Sakharov in the United States urging a buildup of nuclear weapons in the West, Soviet officials declared him "a talented, but sick man." [ 103 ] When sent into internal exile to Gorky "for his own peace of mind," according to officials, "Soviet medics are taking all necessary measures to restore his health." [ 103 ] One day in a selected auditorium, when discussing the situation in the country, Snezhnevsky, in the words of some of his clinical staff, diagnosed Sakharov with sluggish schizophrenia in absentia. [ 104 ] The director of KGB political police department (Fifth Directorate) Philipp Bobkov concluded, "Sakharov is objectively a mentally ill person. The complication with regards to operational consequences lies in the fact that for political reasons he cannot be committed to a psychiatric hospital." [ 105 ] Soviet authorities compulsorily committed Sakharov to a closed ward of the Semashko Hospital in Gorky, where he was force-fed and given drugs to change the state of his mind. [ citation needed ] Viktor Nekipelov , a well-known dissident poet, was arrested in 1973, sent to the Section 4 of the Serbsky Institute of Forensic Psychiatry for psychiatric evaluation, which lasted from 15 January to 12 March 1974, was judged sane (which he was), tried, and sentenced to two years' imprisonment. [ 106 ] In 1976, he published in samizdat his book Institute of Fools: Notes on the Serbsky Institute [ 107 ] based on his personal experience at Psychiatric Hospital of the Serbsky Institute [ 108 ] and translated into English in 1980. [ 109 ] In this account, he wrote compassionately, engagingly, and observantly of the doctors and other patients; most of the latters were ordinary criminals feigning insanity in order to be sent to a mental hospital, because hospital was a "cushy number" as against prison camps. [ 106 ] According to the President of the Independent Psychiatric Association of Russia Yuri Savenko , Nekipelov's book is a highly dramatic humane document, a fair story about the nest of Soviet punitive psychiatry, a mirror that psychiatrists always need to look into. [ 110 ] However, according to Malcolm Lader, this book as an indictment of the Serbsky Institute hardly rises above tittle-tattle and gossip, and Nekipelov destroys his own credibility by presenting no real evidence but invariably putting the most sinister connotation on events. [ 106 ] After publishing his book, he was sentenced to the maximum punishment for "anti-Soviet agitation and propaganda" of seven years in a labor camp and then five years in internal exile. [ 106 ] In 1968, the human rights movement in the USSR focused directly on Soviet political psychiatry, organizing public protests and writing international bodies. [ 111 ] In 1969, a group of about 14 activists including Sergei Kovalyov , a future Russian human rights ombudsman, constituted the Action Group for the Defense of Human Rights in the USSR . [ 112 ] The group composed the first samizdat (self-published) human rights bulletin, A Chronicle of Current Events . [ 112 ] Among the members of the Action Group were individuals who subsequently fell victim to psychiatric abuse themselves: the poet Natalya Gorbanevskaya who in 1968 demonstrated on Red Square against bringing Soviet tanks into Czechoslovakia ; Vladimir Borisov who later was one of the founders of the independent labor movement in the Soviet Union; Vladimir Maltsev , a translator; and Leonid Plyushch , a Ukrainian cyberneticist who was committed to the Special Psychiatric Hospital of Dnepropetrovsk and was awfully tortured with neuroleptics . [ 79 ] Later three senior Fellows of the Royal College of Psychiatrists examined Leonid Plyushch and "saw no indication of schizophrenia or other mental illness." [ 113 ] In November 1977, a group of unemployed and workers led by Vladimir Klebanov , a former coalminer from the Donbas region of Ukraine , announced the formation in the Soviet Union of the Association of Free Trade Unions of Workers (AFTU) whose purposes were to meet obligations achieved by collective bargaining; to induce workers and other employees to join free trade union associations; to implement those decisions of the Association which concern the seeking of justice and the defense of rights; to educate Association members in the spirit of irreconcilability toward wastefulness, inefficiency, deception, bureaucracy, deficiencies, and a negligent attitude toward national wealth. [ 92 ] These purposes show that AFTU was in all respects an organization whose right to exist is guaranteed by the international obligations of the Soviet Union. [ 114 ] On 19 December 1977, Klebanov along with two other workers in Donetsk was arrested by the Soviet militia and released nine days later, after international protests against his incarceration. [ 114 ] Worker Gavriil Yankov was incarcerated in Moscow mental hospital for two weeks. [ 114 ] On 1 February 1978, AFTU publicly announced the institution of its organizational Charter. [ 114 ] Several days later, Klebanov was again detained by Soviet police and sent from Moscow to psychiatric prison hospital in Donetsk. [ 114 ] Group member Nikolaev and workers Pelekh and Dvoretsky were also placed under psychiatric detention. [ 114 ] By October 1978 it was apparent that arrests and repressions had resulted in the dissolution of AFTU. [ 114 ] But the cause of trade union rights was to be invigorated by a new group, the Free Interprofessional Association of Workers known by its Russian acronym, SMOT, whose first press conference was held in Moscow on 28 October 1978. [ 114 ] The objectives of SMOT were to defend its members in cases of violation of their rights in different spheres of their daily activities: political, domestic, religious, spiritual, cultural, social, and economic; to look into the legal basis of the workers' complaints; to ensure that these complains were brought to the notice of relevant organizations; to facilitate a quick solution to complaints of workers; and in cases of negative results, to publicize them widely before international and Soviet public. [ 115 ] The leadership of SMOT was headed by a native of Leningrad electrician Vladimir Evgenievich Borisov , who was incarcerated in Soviet mental hospitals because of his human rights activism for a total of nine years in the 1960s and 1970s. [ 114 ] In November and December 1978, Soviet police searched the homes of SMOT activists, and SMOT members Vladimir Borisov, Valeriya Novodvorskaya , Albina Yakoreva , and Lev Volokhonsky were arrested and detained by Soviet authorities. [ 116 ] Both Borisov and Novodvorskaya were held in mental hospitals. [ 116 ]	https://en.wikipedia.org/wiki/Cases_of_political_abuse_of_psychiatry_in_the_Soviet_Union
Castle Connolly Medical is a publishing organization [ 1 ] dealing with healthcare research and information services in the US . [ 2 ] [ 3 ] The organization publishes an annual list of top doctors [ 4 ] in the United States based on different quality aspects. [ 5 ] [ 6 ] The publisher is also known for its consumer guide pieces. [ 7 ] John K Castle and John J Connolly [ 8 ] while being the Chairman and President [ 9 ] respectively of the board of trustees of the New York Medical College , [ 10 ] founded Castle Connolly Medical in 1991. [ 11 ] [ 12 ] Castle Connolly Graduate Medical , a separate organization that publishes books and guidebooks, was established in 1999. [ 13 ] A sister organization was established in 2006 with the name Castle Connolly Healthcare Navigation [ 14 ] , to provide guidance in health and insurance. [ 15 ] The sister organization was later merged with Castle Connolly Medical . Everyday Health Group acquired the organization in 2019. [ 16 ] The publisher works in collaboration with different news media and journal publication houses. [ 17 ]	https://en.wikipedia.org/wiki/Castle_Connolly_Medical
Catharyn Johanna Stern AO is a clinical associate professor, and gynaecologist at Waverley Private Hospital in Melbourne, Victoria. She was appointed an Officer of the Order of Australia for distinguished service to gynaecology , reproductive medicine and fertility research. Stern has been a member of the Australian Medical Association (AMA) member for 23 years. Her award was for her services to gynaecology, to reproductive medicine and fertility research, and to the community. [ 1 ] [ 2 ] [ 3 ] Stern was awarded a Bachelor of Medicine and Bachelor of Surgery at the University of Melbourne in 1987. She is a specialist in gynaecology and obstetrics, and specialises in reproductive fertility. She initially trained at The Women's Hospital, as well at The Mercy hospital, and subsequently obtained experience and training while in the United Kingdom for two years. Stern next spent three years working and obtaining experience in reproductive endocrinology and infertility. She is the head of the Fertility Preservation Service within the Melbourne IVF and The Women's Hospital. She works at the Melbourne IVF clinical research program, as well as working in clinical practice. Stern is leading a national trial within Australia, with the goal of protecting the fertility of women who are undergoing treatment with chemotherapy, and cancer patients. [ 4 ] [ user-generated source ] [ 5 ] Stern started the Australian and New Zealand group in fertility preservation, "Special Interest Group". The group is made up of national and international experts who specialise in the preservation of fertility, and was started in 2009. Stern was also appointed to be the chair of the Clinical Oncological Society of Australia, which is a fertility guidance group. The group has been involved in writing guidelines and practices that provide recommendations, based on evidence, as well as 'good practice' which then helps enable medical practitioners and health professionals to have conversations and discussions about fertility, to efficiently and effectively make informed decisions around the treatment of fertility with patients and their families. [ 6 ] [ 7 ] Stern has also worked on an IVF success comparator, which is an online website that allows women and their families to compare the success rates of different IVF clinics within Australia. [ 8 ] Stern has also published on the difficulties of young rural women in receiving treatment for their fertility. [ 9 ] Stern has published 49 peer-reviewed publications, as at July 2022, with an H-index of 20, and over 1700 citations. [ 10 ] Select publications include: 2022 – Officer of the Order of Australia, Queen's Birthday Honours [ 14 ] 2004 - FRANZCOG - Fellow of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists	https://en.wikipedia.org/wiki/Catharyn_Johanna_Stern
Catherine Alison Geissler, Lady Auld [ 1 ] is a prominent British nutritionist and author and co-author of widely recognised reference textbooks on human nutrition. [ 2 ] [ 3 ] [ 4 ] Geissler was born in Edinburgh and educated at the Mary Erskine School for girls. On leaving school she attended Edinburgh University , where she studied dentistry, obtaining her Bachelor of Dental Surgery BDS in 1963. In 1963-64 she spent a research year in Paris, followed by a year as a dental surgeon in Scotland before moving to California, where she initially taught dental radiography in San Francisco City College . She was then appointed to a research position in the Department of Nutrition, University of California, Berkeley , which led to a Masters in Nutrition (1971). After her Master's degree she went to the National Nutrition and Food Technology Research Institute in Teheran (under Habibollah Hedayat ), where she participated in studies of energy expenditure of agricultural workers, [ 5 ] carpet weavers [ 6 ] and rural women. [ 7 ] as well as her personal work for her PhD on lactation in different socio-economic groups in Teheran. Her PhD in Human Nutrition at Berkeley was based on her lactation studies in Teheran , Iran . [ 8 ] [ 9 ] [ 10 ] Professor of Human Nutrition, King's College London ; [ 11 ] Head of department of Nutrition and Dietetics, King's College London ; Head, Division of Health Sciences, School of Health and Life Sciences, King's College London ; Director of UK Higher Education Academy, Centre for Health Sciences and Practice. She has worked as Attachée de recherche, Laboratoire de Nutrition Humaine ( INSERM ), Hôpital Bichat , Paris (1972-1974) in the group of Jean Trémolières, [ 12 ] Visiting Professor at the Division of Nutritional Sciences Cornell University Ithaca, New York (1989–90) and at MRC Human Nutrition Research , and associate at Darwin College, Cambridge (2010). She is Professor Emerita of Human Nutrition, King's College London , Past President of The Nutrition Society of the UK & Ireland (2013–16) [ 13 ] and is currently Secretary General of the International Union of Nutritional Sciences (IUNS) (2013–2022). Her principal research interests are in international public health nutrition; [ 14 ] energy metabolism and obesity; [ 15 ] [ 16 ] [ 17 ] [ 18 ] and iron metabolism. [ 19 ] [ 20 ] In 2003 she was invited by the Belgian government to give expert evidence on the role of ephedrine in the treatment of obesity. A recognized authority on human nutrition and public health, [ 21 ] Geissler has served on many professional committees including the Ministry of Agriculture, Food and Fisheries (MAFF) Food Advisory Committee, the World Cancer Research Fund grants committee, and the British and American Nutrition Societies, and extensively as consultant to international development agencies including the World Bank (Senegal, Diourbel 1980, Senegal, Casamance 1980, Ghana 1981, Syria 1984, Niger 1991, Niger 1992, Benin 1993, Madagascar 1995, Armenia 1997), CGIAR , FAO (Mauritius 1974, Haiti 1982), WHO , the International Livestock Centre for Africa , Addis Ababa, Ethiopia 1982, UNICEF (Iran 1998), the British Council (Sierra Leone 1984, Syria 1984), in many countries including Iran , Haiti , Mauritius , Sierra Leone , Niger , Benin , Senegal , Ghana , Ethiopia , Yemen , [ 22 ] Thailand , Philippines , [ 23 ] Singapore , Indonesia , Malaysia and China . [ 24 ] [ 25 ] [ 26 ] Geissler has over 200 academic publications, in addition to her text books. She is the daughter of the artist William Geissler and the glass engraver Alison Geissler . She lived for extended periods in several different countries before her appointment in 1976 to a lectureship in human nutrition at Queen Elizabeth College , London, [ 27 ] which in 1985 merged with King's College, London. [ 28 ] 2003 Fellow of the Higher Education Academy (FHEA) (Nº25241) 2015 XI International Nutrition and Health Prize (Premio Internacional Alimentación y Salud), Facultad de Farmacia, Universidad de Navarra [ 29 ] 2016 Elected Fellow of The Nutrition Society of the UK & Ireland [ 13 ] 2018 American Society for Nutrition Kellogg Prize for Lifetime Achievements in International Nutrition [ 30 ] 2020 Elected Fellow of the American Society for Nutrition [ 31 ]	https://en.wikipedia.org/wiki/Catherine_Geissler
Catherine Naliaka Nyongesa Watta (née Catherine Naliaka ) (born in 1970), is a Kenyan physician and radiation oncologist , who is the founder, owner and chief executive of Texas Cancer Centre , in Nairobi , the capital and largest city in the country. [ 1 ] She was born in Kenya, c. 1970 . [ 2 ] She attended Kenyan elementary and secondary schools. She studied at the University of Nairobi School of Medicine , graduating with a Bachelor of Medicine and Bachelor of Surgery (MBChB) degree. In 2002, she was admitted to the University of the Witwatersrand in Johannesburg , South Africa . There, she was enrolled into a three-year residency program to study to become a radiation oncologist, graduating in 2005 with a Master of Medicine (MMed) degree, in Radiation Oncology . Later she was elected as a Fellow of the College of Radiation Oncologists of South Africa (FCRO (SA)). [ 3 ] Following her specialized training in South Africa, she returned to Kenya and was hired as a Consultant radiation oncologist at Kenyatta National Hospital , the largest tertiary-care public referral hospital in the country. The case load was heavy, and all patients could not be helped, in the public setting. [ 1 ] [ 2 ] In 2010, Nyongesa and her husband, a practicing pharmacist in the Houston -area, Texas , United States, started Texas Cancer Centre Nairobi. Initially the Centre only offered chemotherapy treatment as an outpatient service. Later, the couple borrowed KSh100 million (approx. US$1 million), to build an inpatient facility at a second location in Nairobi. With assistance from the University of Texas MD Anderson Cancer Center , the Nairobi center acquired and installed a radiotherapy machine, set up a diagnostic laboratory and acquired x-ray machines and ultrasound equipment. As of March 2015, the centre had over 70 full-time staff, handling over 150 outpatients daily, and offered accommodation at a reasonable fee to out-of-town outpatients. [ 1 ] [ 2 ] As of July 2017, the Texas Cancer Centre has expanded to a total of four locations in Nairobi and Eldoret. [ 4 ] Dr. Catherine Nyongesa is a married mother of three children. [ 2 ] [ 4 ] She is the first woman radiation oncologist in Kenya. She serves as Chairwoman of the Kenya Society of Hematology and Oncology (KESHO). She is the clinical coordinator at the Cancer Treatment Centre of Kenyatta National Hospital. She is also an honorary lecturer at the University of Nairobi . [ 3 ]	https://en.wikipedia.org/wiki/Catherine_Nyongesa

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