In 1995,  Masimo  introduced Signal Extraction Technology (SET) that could measure accurately during patient motion and low perfusion by separating the arterial signal from the venous and other signals. Since then, pulse oximetry manufacturers have developed new algorithms to reduce some false alarms during motion, [ 54 ]  such as extending averaging times or freezing values on the screen, but they do not claim to measure changing conditions during motion and low perfusion. So there are still important differences in performance of pulse oximeters during challenging conditions. [ 19 ]  Also in 1995, Masimo introduced perfusion index, quantifying the amplitude of the peripheral  plethysmograph  waveform. Perfusion index has been shown to help clinicians predict illness severity and early adverse respiratory outcomes in neonates, [ 55 ] [ 56 ] [ 57 ]  predict low superior vena cava flow in very low birth weight infants, [ 58 ]  provide an early indicator of sympathectomy after epidural anesthesia, [ 59 ]  and improve detection of critical congenital heart disease in newborns. [ 60 ]


Published papers have compared signal extraction technology to other pulse oximetry technologies and have demonstrated consistently favorable results for signal extraction technology. [ 18 ] [ 19 ] [ 61 ]  Signal extraction technology pulse oximetry performance has also been shown to translate into helping clinicians improve patient outcomes. In one study, retinopathy of prematurity (eye damage) was reduced by 58% in very low birth weight neonates at a center using signal extraction technology, while there was no decrease in retinopathy of prematurity at another center with the same clinicians using the same protocol but with non-signal extraction technology. [ 62 ]  Other studies have shown that signal extraction technology pulse oximetry results in fewer arterial blood gas measurements, faster oxygen weaning time, lower sensor utilization, and lower length of stay. [ 63 ]  The measure-through motion and low perfusion capabilities it has also allow it to be used in previously unmonitored areas such as the general floor, where false alarms have plagued conventional pulse oximetry. As evidence of this, a landmark study was published in 2010 showing that clinicians at Dartmouth-Hitchcock Medical Center using signal extraction technology pulse oximetry on the general floor were able to decrease rapid response team activations, ICU transfers, and ICU days. [ 64 ]  In 2020, a follow-up retrospective study at the same institution showed that over ten years of using pulse oximetry with signal extraction technology, coupled with a patient surveillance system, there were zero patient deaths and no patients were harmed by opioid-induced respiratory depression while continuous monitoring was in use. [ 65 ]


In 2007, Masimo introduced the first measurement of the  pleth variability index  (PVI), which multiple clinical studies have shown provides a new method for automatic, noninvasive assessment of a patient's ability to respond to fluid administration. [ 41 ] [ 66 ] [ 67 ]  Appropriate fluid levels are vital to reducing postoperative risks and improving patient outcomes: fluid volumes that are too low (under-hydration) or too high (over-hydration) have been shown to decrease wound healing and increase the risk of infection or cardiac complications. [ 68 ]  Recently, the National Health Service in the United Kingdom and the French Anesthesia and Critical Care Society listed PVI monitoring as part of their suggested strategies for intra-operative fluid management. [ 69 ] [ 70 ]


In 2011, an expert workgroup recommended newborn screening with pulse oximetry to increase the detection of  critical congenital heart disease  (CCHD). [ 71 ]  The CCHD workgroup cited the results of two large, prospective studies of 59,876 subjects that exclusively used signal extraction technology to increase the identification of CCHD with minimal false positives. [ 72 ] [ 73 ]  The CCHD workgroup recommended newborn screening be performed with motion tolerant pulse oximetry that has also been validated in low perfusion conditions. In 2011, the US Secretary of Health and Human Services added pulse oximetry to the recommended uniform screening panel. [ 74 ]  Before the evidence for screening using signal extraction technology, less than 1% of newborns in the United States were screened. Today,  The Newborn Foundation  has documented near universal screening in the United States and international screening is rapidly expanding. [ 75 ]  In 2014, a third large study of 122,738 newborns that also exclusively used signal extraction technology showed similar, positive results as the first two large studies. [ 76 ]


High-resolution pulse oximetry (HRPO) has been developed for in-home sleep apnea screening and testing in patients for whom it is impractical to perform  polysomnography . [ 77 ] [ 78 ]  It stores and records both  pulse rate  and Sp O 2  in 1 second intervals and has been shown in one study to help to detect sleep disordered breathing in surgical patients. [ 79 ]


Pump thrombosis  ( PT ) is considered a specific case of a major device malfunction, and is classified as either suspected or confirmed pump  thrombus . Typically, the device is an implanted blood pump such as a  left ventricular assist device . The malfunction is a blockage in the flow of blood anywhere along a vessel (upstream or downstream) and it is mainly due to the bio-incompatible presence of a fairly complex mechanical apparatus. Pump thrombus is dreaded complication of CF LVAD technology [ 1 ]  that can require repeat surgery to replace the pump or lead to death. [ 2 ]


In suspected pump thrombus, the clinical patient condition or pump parameters suggest thrombus on any of the blood-contacting surfaces of the pump (inflow cannula, pump itself, or outflow graft). Confirmed pump thrombus is done by visual inspection (during device exchange, transplantation, autopsy), irrefutable radiographic evidence, or absence of Doppler inflow or outflow signals.Not all ventricular assist devices (VADs) are fully biocompatible, thus device thrombosis has always been a significant complication. Older generation pulsatile VADs were relatively large and it was practically impossible to thrombose the entire pump and cause hemodynamic consequences.Instead, any thrombus created in the pump could be dislodged, possibly resulting in an embolic stroke. In contrast, the newer continuous flow left ventricular assist devices (CF LVAD) are much smaller and have smaller gaps between the various components of the pump. These characteristics predispose CF LVAD to thrombosis of the entire pump where the clot stays in the device, leading to increased hemolysis and device dysfunction. [ citation needed ]


Thrombosis of CF LVADSs can occur as a result of various factors, [ 3 ]  which can be divided into three categories: the pump, the patient, and the clinician. Management protocols for VADs are usually institution-dependent and there is a large variability in clinician-related factors. A decrease in anticoagulation thresholds [ 4 ] [ 5 ] [ 6 ]  has been postulated to have resulted in an increase in CF LVAD thrombosis. [ 7 ] [ 8 ]


A complex balance exists between over-anticoagulation and under-anticoagulation, in a patient population where the coagulation system response to the CF LVAD device varies greatly between individuals. Common adverse events precipitated by over-anticoagulation include bleeding problems such as gastrointestinal bleeding and intracranial hemorrhage, while common complications due to under-anticoagulation include hemolysis, pump thrombosis and ischemic/embolic strokes. [ citation needed ]


Unfortunately, robust and individually-tailored anticoagulation therapy protocols do not exist in most institutions, which usually utilize a "one size fits all" approach. One anticoagulation protocol example targets the therapeutic window of  coumadin  of an  international normalized ratio  (INR) goal of 2–3 and full-dose aspirin for antiplatelet activity. In the complex dynamics of the interaction of patients' systems, there is no completely safe zone between thrombosis or bleeding, or both.


Pump thrombosis is defined as a specific case of a major device malfunction. In turn, device malfunction is as defined by  Interagency Registry for Mechanically Assisted Circulatory Support  (INTERMACS) as a failure of one or more of the components of the mechanical circulatory support systems which either directly causes or could potentially induce a state of inadequate circulatory support (low cardiac output state) or death. A failure that was iatrogenic or recipient-induced will be classified as an Iatrogenic/Recipient-Induced failure. [ citation needed ]


Device failure should be classified according to which component fails as follows:


The FDA is aware of serious adverse events associated with LVADs. It has received reports and information from a variety of sources indicating an increase in the rate of pump thrombosis events in patients implanted with LVADs. Information also shows that patients are experiencing pump thrombosis events earlier than observed during the clinical trials conducted to support product approvals in 2008 Bridge To Transplant (BTT) and 2010 Destination Therapy (DT). [ citation needed ]


Two analyses in scientific literature reported the confirmed (after explant) pump thrombosis rate as high as 8.4% of implanted devices at 3 months (Starling et al, 2013) and 6% of implanted devices at 6 months (Kirklin et al, 2014). This is compared to 1.6% of implanted devices at one year during the BTT clinical trial and 3.8% of implanted devices at 2 years during the DT clinical trial. [ 10 ]


The cause for PT are classified as either pump-related, patient-related, or management-related. But of particular concern is the emergence in some reports of  HIT syndrome  as an etiologic factor in some cases of PT. [ 11 ] [ 12 ] [ 13 ]


Inherent to the technology itself. Examples: Heat generated by pump rotor; Outflow graft kink.


Individual conditions that render patient more likely to have thrombotic complications. Examples: Atrial fibrillation; Infection.


Criteria should include the presence of hemolysis, presence of heart failure not explained by structural disease, and/or abnormal pump parameters. Imaging and functional studies (ramp) can confirm diagnosis. [ 14 ]  Elevated lactate dehydrogenase (LDH) levels. [ 15 ]


The complication itself, its prevention, or its treatment may lead to PT. Prevention of GI bleeding in VAD patients often includes keeping pump speeds lower to potentially minimize the proliferation of AV malformations.


In addition, bleeding, once it occurs, is managed at least temporarily by a halting or decrease in  AC . Efforts to decrease the development of AI in LVAD patients include keeping pump speeds on the lower side as well.


Right ventricular dysfunction, particularly in the early postoperative period, is likewise managed with lower pump speeds. Finally, infections and sepsis are known to be associated with a more hypercoagulable state in VAD patients. In the end, the occurrence of any of these complications may thus prove to be a surrogate for a higher risk of PT.


While the issue of biocompatibility is always at the forefront of critical issues of new pumps, the field of mechanical circulatory support is first focusing on adopting a standardized approach to this therapy so that valid analyses and comparisons can be made. [ 16 ]


No standardized protocol exist regarding the management of LVAD pump thrombosis. [ 17 ]


No standardized protocol exist regarding therapy of pump thrombosis. [ 18 ]


Beginning in 2011, centers and collaborative groups began to observe a significant increase in the
incidence of pump thrombosis, which led to pump modifications and the appreciation of more strict control of blood pressure and anticoagulation with this pump design. [ 19 ]


The unexpected abrupt increase in LVAD thrombosis was accompanied by elevated  lactate dehydrogenase  (LDH) levels with outcomes of different management strategies in a multi-institutional study. [ 20 ] [ 21 ] [ 22 ]  Elevation of lactate dehydrogenase during the first month offers an opportunity for early intervention strategies. [ 23 ]


Starting in approximately March 2011, the occurrence of confirmed pump thrombosis at 3 months after implantation increased from 2.2% to 8.4% by January 1, 2013. [ citation needed ]


Before March 1, 2011, the median time from implantation to thrombosis was 18.6 months, and from March 2011 onward, it was 2.7 months. The occurrence of elevated LDH levels within 3 months after implantation mirrored that of thrombosis. Thrombosis was presaged by LDH levels that more than doubled, from 540 IU per liter to 1490 IU per liter, within the weeks before diagnosis.


While starting in 2011 device failures due to clots forming inside the pumps appeared to rise dramatically, there is some indication that these failures may now be declining, but data analysis and interpretation are complex. [ 24 ]


Computational fluid dynamics  (CFD) is an invaluable tool in the development of VADs, enabling new designs to be tested rapidly and undesirable flow characteristics eliminated in successive versions before prototypes are manufactured. CFD is used for predicting pressure-flow characteristics and efficiency curves, revealing the detailed flow field to help eliminate regions of recirculation or stagnation and for calculating fluid dynamic forces. When combined with models of blood damage CFD has been used for predicting haemolysis and platelet activation by VADs. When combined with shape optimization algorithms it can be used in design optimization. [ 25 ]


The  Randomized Aldactone Evaluation Study  ( RALES ) trial is a landmark clinical study that assessed the impact of  spironolactone , an  aldosterone antagonist , on morbidity and mortality in patients with severe  heart failure  due to systolic dysfunction. [ 1 ]  The findings from this trial significantly influenced the treatment guidelines for heart failure. [ 2 ]


Heart failure, particularly with reduced  ejection fraction  (HFrEF), is a major cause of morbidity and mortality worldwide. Aldosterone, a hormone that promotes sodium retention and potassium excretion, plays a significant role in the pathophysiology of heart failure by contributing to fluid overload, myocardial fibrosis, and vascular damage. Spironolactone, a  potassium-sparing diuretic  and aldosterone antagonist was hypothesized to improve outcomes in patients with severe heart failure. [ 1 ] [ 2 ]


RALES trial was a randomized, double-blind, placebo-controlled trial that enrolled 1663 patients from 195 centers in 15 countries from March 1995 to December 1996. The average age of the patients was 65 years. Patients were eligible for enrollment if they had recently been diagnosed with severe heart failure (NYHA class III or IV) and a left ventricular ejection fraction (LVEF) of 35% or less, who were already receiving standard therapy (ACE inhibitors, loop diuretics, and, if tolerated, digoxin). The objective of this trial was to assess the impact of spironolactone on morbidity and mortality in patients with severe heart failure.  Patients were randomized to receive either spironolactone (25 to 50 mg) daily or placebo. Both groups were continued on standard therapy. The primary endpoint was all-cause mortality. Secondary endpoints included hospitalization for heart failure, changes in symptoms of heart failure, and serum potassium levels. [ 1 ] [ 2 ]


The trial was stopped early because the beneficial effect of spironolactone on all-cause death exceeded the prespecified discontinuation requirements. Spironolactone reduced the risk of death by 30% compared to placebo. Additionally, there was a 35% reduction in the risk of hospitalization for worsening heart failure in the spironolactone group. Finally, patients treated with spironolactone reported significant improvements in heart failure symptoms. Hyperkalemia was more common in the spironolactone group, but the incidence of severe hyperkalemia was relatively low. Gynecomastia or breast pain occurred in 10% of men treated with spironolactone vs 1% of men in the placebo group, otherwise there were no other differences in safety or adverse events. [ 1 ] [ 2 ]


The RALES trial had a profound impact on the management of heart failure. The results led to the inclusion of aldosterone antagonists, such as spironolactone, in treatment guidelines for patients with severe heart failure. Spironolactone has become a standard therapy for reducing mortality and morbidity in patients with severe heart failure with reduced ejection fraction. [ 2 ] [ 3 ]  The RALES trial has then paved the way for further studies on the role of aldosterone antagonists in heart failure and other cardiovascular conditions. [ 4 ] [ 5 ]


The RALES trial established spironolactone as a vital component of therapy for patients with severe heart failure, demonstrating significant reductions in mortality and hospitalization and improvements in symptoms. The trial's findings have been instrumental in shaping current heart failure treatment guidelines and improving patient outcomes. [ 1 ] [ 2 ] [ 3 ]


Reflex syncope  is a brief  loss of consciousness  due to a  neurologically  induced drop in  blood pressure  and/or a  decrease  in  heart  rate. [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 2 ]  Before an affected person passes out, there may be sweating, a decreased ability to see, or  ringing in the ears . [ 1 ]  Occasionally, the person may twitch while unconscious. [ 1 ]  Complications of reflex syncope include injury due to a fall. [ 1 ]


Reflex syncope is divided into three types: vasovagal, situational, and carotid sinus. [ 2 ]  Vasovagal syncope is typically triggered by seeing  blood , pain, emotional stress, or prolonged standing. [ 11 ]  Situational syncope is often triggered by  urination , swallowing, or coughing. [ 2 ]  Carotid sinus syncope is due to pressure on the  carotid sinus  in the neck. [ 2 ]  The underlying mechanism involves the  nervous system  slowing the heart rate and dilating blood vessels, resulting in low blood pressure and thus not enough blood flow to the brain. [ 2 ]  Diagnosis is based on the symptoms after ruling out other possible causes. [ 3 ]


Recovery from a reflex syncope episode happens without specific treatment. [ 2 ]  Prevention of episodes involves avoiding a person's triggers. [ 2 ]  Drinking sufficient fluids, salt, and exercise may also be useful. [ 2 ] [ 4 ]  If this is insufficient for treating vasovagal syncope, medications such as  midodrine  or  fludrocortisone  may be tried. [ 4 ]  Occasionally, a  cardiac pacemaker  may be used as treatment. [ 2 ]  Reflex syncope affects at least 1 in 1,000 people per year. [ 1 ]  It is the most common type of  syncope , making up more than 50% of all cases. [ 2 ]


Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Before losing consciousness, the individual frequently experiences early signs or symptoms such as  lightheadedness , nausea, the feeling of being extremely hot or cold (accompanied by sweating),  ringing in the ears , an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering), weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well. The symptoms may become more intense over several seconds to several minutes before the loss of consciousness (if it is lost). Onset usually occurs when a person is sitting up or standing. [ citation needed ]


When people lose consciousness, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a  seizure  may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense. [ citation needed ]


The  autonomic nervous system 's physiological state (see below) leading to loss of consciousness may persist for several minutes, so


Reflex syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows or blood pressure drops, the resulting lack of blood to the brain causes fainting. [ 12 ]


Typical triggers include:


Pressing upon a certain spot in the neck. [ 11 ]  This may happen when wearing a tight collar, shaving, or turning the head. [ 11 ]


Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. The  nucleus tractus solitarii  of the  brainstem  is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of  parasympathetic nervous system  ( vagal ) tone and withdrawal of  sympathetic nervous system  tone. [ citation needed ]


This results in a spectrum of hemodynamic responses: [ citation needed ]


One account for these physiological responses is the  Bezold-Jarisch reflex .


Vasovagal syncope may be part of an evolved response, specifically, the  fight-or-flight response . [ 16 ] [ 17 ]


In addition to the mechanism described above, a number of other medical conditions may cause  syncope . Making the correct diagnosis for loss of consciousness is difficult. The core of the diagnosis of vasovagal syncope rests upon a clear description of a typical pattern of triggers, symptoms, and time course. [ citation needed ]


It is pertinent to differentiate  lightheadedness , seizures,  vertigo , and  low blood sugar  as other causes. [ citation needed ]


In people with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:


Treatment for reflex syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures that interrupt or prevent the  pathophysiologic mechanism  described above. [ citation needed ]


Types of long-term therapy for vasovagal syncope include [ 18 ]


Brief periods of unconsciousness usually cause no lasting harm to health. Reflex syncope can occur in otherwise healthy individuals, and has many possible causes, often trivial ones such as prolonged standing with the legs locked. [ citation needed ]


The main danger of vasovagal syncope (or dizzy spells from vertigo) is the risk of injury by falling while unconscious. Medication therapy could possibly prevent future vasovagal responses; however, for some individuals medication is ineffective and they will continue to have fainting episodes. [ 29 ]


A  registered cardiovascular invasive specialist  or  RCIS  assists a  cardiologist  with  cardiac catheterization  procedures in the  United States . [ 1 ]   These procedures can determine if a blockage exists in the  blood vessels  that supply the heart muscle and can help diagnose other problems. [ citation needed ]


To become registered they have to pass the registry proctored by CCI (Cardiovascular Credentialing International). The exam consists of 170 multiple choice questions.  Some questions involve mathematical computation as well as pictures where one must identify  anatomy  and equipment.  To be registry eligible, they must have worked in the Cardiac Catheterization Laboratory for at least one year or have graduated from a registry–eligible program.


Regurgitation  is  blood flow  in the opposite direction from normal, as the backward flowing of blood into the  heart  or between heart chambers. It is the  circulatory  equivalent of  backflow  in engineered systems. It is sometimes called reflux.


The various types of heart valve regurgitation via insufficiency are as follows:


Regurgitation in or near the heart is often caused by valvular insufficiency (insufficient function, with incomplete closure, of the  heart valves ); for example,  aortic valve  insufficiency causes regurgitation through that valve, called aortic regurgitation, and the terms  aortic insufficiency  and  aortic regurgitation  are so closely linked as usually to be treated as  metonymically  interchangeable.


Regurgitant fraction is the percentage of blood that regurgitates back through the  aortic valve  to the  left ventricle  due to  aortic insufficiency , or through the  mitral valve  to the  atrium  due to  mitral insufficiency . It is measured as the amount of blood regurgitated into a cardiac chamber divided by the  stroke volume .


This fraction affords a quantitative measure of the severity of the valvular lesion. Normally, no blood regurgitates, so the regurgitant fraction is zero. In patients with severe valvular lesions, regurgitant fraction can approach 80%.


Tricuspid regurgitation is common and is estimated to occur in 65–85% of the population. [ 1 ]  In The  Framingham Heart Study  presence of any severity of tricuspid regurgitation, ranging from trace to above moderate was in 82% of men and in 85.7% of women. [ 2 ]  Mild tricuspid regurgitation tend to be common and benign and in structurally normal tricuspid valve apparatus can be considered a normal variant. [ 1 ]  Moderate or severe tricuspid regurgitation is usually associated with tricuspid valve leaflet abnormalities and/or possibly annular dilation and is usually pathologic which can lead to irreversible damage of  cardiac muscle  and worse outcomes due to chronic prolonged  right ventricular volume overload . [ 1 ]


In a study of 595 male elite football players aged 18–38, and 47 sedentary non-athletes, it was found that 58% of the athletes had tricuspid regurgitation vs. 36% in non-athletes and mitral regurgitation was found in 20% football players and 15% in controls. Football players with tricuspid regurgitation had larger tricuspid annulus diameter, compared to athletes without tricuspid regurgitation. Athletes with tricuspid regurgitation also had enlarged right atrium diameter when compared to control group. In athletes with mitral regurgitation it was found they had larger mitral annulus diameter, compared to athletes without regurgitation. Also left atrium diameter was larger in athletes with mitral regurgitation. [ 3 ]


Remnant cholesterol , also known as  remnant lipoprotein  and  triglyceride-rich lipoprotein cholesterol  is an  atherogenic   lipoprotein  composed primarily of  very low-density lipoprotein  (VLDL) and  intermediate-density lipoprotein  (IDL) with  chylomicron  remnants. [ 1 ] [ 2 ] [ 3 ]  Elevated remnant cholesterol is associated with increased risk of atherosclerotic cardiovascular disease and stroke. [ 3 ] [ 4 ]


Remnant cholesterol is the cholesterol content of triglyceride-rich lipoproteins, which consist of very low-density lipoproteins and intermediate-density lipoproteins with chylomicron remnants. [ 2 ] [ 5 ]  Remnant cholesterol is primarily chylomicron and VLDL, and each remnant particle contains about 40 times more cholesterol than LDL. [ 6 ]


Remnant cholesterol corresponds to all cholesterol not found in high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C). It is calculated as total cholesterol minus HDL-C and LDL-C. [ 7 ]


Elevated remnant cholesterol is associated with an increased risk of atherosclerotic cardiovascular disease, chronic inflammation,  myocardial infarction  and stroke. [ 4 ] [ 5 ] [ 8 ] [ 9 ]  Remnant cholesterol is especially predictive of  coronary artery disease  in patients with normal total cholesterol. [ 10 ] [ 11 ]


High plasma remnant cholesterol is associated with increased plasma triglyceride levels. [ 12 ]   Hypertriglyceridemia  is characteristic of high plasma remnant cholesterol, but persons with high plasma triglycerides without high remnant cholesterol rarely have coronary artery disease. [ 13 ]


Remnant cholesterol has about twice the association with  ischemic heart disease  as LDL cholesterol. [ 14 ]  Although remnant cholesterol tends to be higher in people who are overweight (high  body mass index ), normal-weight persons with high remnant cholesterol tend to have a higher risk of myocardial infarction. [ 15 ]


Vupanorsen, an  ANGPTL3  inhibitor has been shown to lower remnant cholesterol up to 59%. [ 16 ]


Restenosis  is the recurrence of  stenosis , a narrowing of a  blood vessel , leading to restricted blood flow. Restenosis usually pertains to an  artery  or other large  blood vessel  that has become narrowed, received treatment to clear the blockage, and subsequently become re-narrowed. This is usually restenosis of an  artery , or other blood vessel, or possibly a vessel within an  organ .


Restenosis is a common adverse event of endovascular procedures. Procedures frequently used to treat vascular damage from  atherosclerosis  and related narrowing and re-narrowing (restenosis) of blood vessels include  vascular surgery ,  cardiac surgery , and  angioplasty . [ 1 ]


When a stent is used and restenosis occurs, this is called  in-stent restenosis  or  ISR . [ 2 ]  If it occurs following balloon angioplasty, this is called post-angioplasty restenosis or  PARS . The diagnostic threshold for restenosis in both ISR  and PARS is ≥50% stenosis. [ 3 ]


If restenosis occurs after a procedure, follow-up imaging is not the only way to initially detect compromised blood flow. Symptoms may also suggest or signal restenosis, but this should be confirmed by imaging. For instance, a coronary stent patient who develops restenosis may experience recurrent chest pain ( angina ) or have a minor or major heart attack ( myocardial infarction ), though they may not report it. This is why it is important that a patient comply with follow-up screenings and the clinician follows through with a thorough clinical assessment. But it is also important to note that not all cases of restenosis lead to clinical symptoms, nor are they asymptomatic. [ 3 ]


Surgery to widen or unblock a  blood vessel  usually has a long-lasting beneficial effect on the patient. However, in some cases, the procedure itself can cause further narrowing of the vessel, or restenosis.  Angioplasty , also called  percutaneous transluminal coronary angioplasty  (PTCA), is commonly used to treat blockages of the  coronary  or  peripheral arteries  (such as in the limbs). The balloon inserted into the narrowing 'smashes' the  cholesterol  plaques ( atherosclerosis ) against the  artery walls , thus widening the size of the  lumen  and increasing blood flow. However the action damages the artery walls, and they respond by using  physiological  mechanisms to repair the damage. (See physiology below.)  [ 4 ]


A  stent  is a mesh, tube-like structure often used in conjunction with  angioplasty  to permanently hold open an artery, allowing for unrestricted blood flow, or to support a weakness in the artery wall called an  aneurysm . The artery can react to the stent, perceive it as a foreign body, and respond by mounting an  immune system  response which leads to further narrowing near or inside the stent. [ citation needed ]


Damage to the blood vessel wall by angioplasty triggers a physiological response that can be divided into two stages. The first stage that occurs immediately after tissue  trauma , is  thrombosis . A  blood clot  forms at the site of damage and further hinders blood flow. This is accompanied by an inflammatory  immune response . [ citation needed ]


The second stage tends to occur 3–6 months after surgery and is the result of the  proliferation of cells  in the media, a smooth muscle wall in the vessel. This is also known as  Neointimal Hyperplasia  (NIHA). [ 5 ]


Vessel restenosis is typically detected by  angiography , but can also be detected by duplex  ultrasound  and other imaging techniques. [ 6 ]


Late loss  is synonymous with  restenosis  and means loss of the  lumen   after  a procedure intended to open the vessel. It measures either the percent (relative) or absolute change in minimum luminal diameter (MLD) over the months following a  vascular procedure , such as the implantation of a stent graft. Late loss is one metric that is useful in determining the effectiveness of vascular interventions in clinical trials for either an individual patient or a group of patients. [ citation needed ]


However  late loss  is only part of the terminology in describing the outcomes of vascular interventions. For instance, the implantation of a stent graft will first provide an  acute gain  in lumen diameter. In other words, there is an immediate gain in lumen size because the implanted stent opens up the vessel. However, over time, the body's inflammatory immune response (described below in the "Causes" section) reacts to the stent graft via smooth muscle proliferation, etc., which pushes the stent graft back, narrowing the vessel and  losing  at least a percentage of what was previously  gained , or  late loss. [ citation needed ]


The  net gain  of lumen diameter is the difference between  acute gain  and  late loss  and is a measure of stent-graft effectiveness. [ 7 ]


Percent diameter restenosis (or just percent diameter stenosis) is a measure observed in individual patients and is typically calculated as the difference between the minimal (or minimum) luminal diameter (MLD) from the target reference vessel diameter (RVD), divided by the RVD, and multiplied by 100 to get the percentage of stenosis. It is an important measure needed to calculate binary restenosis (see Binary Restenosis section below). The RVD is typically calculated by averaging the MLD of the healthy part of the vessel both proximal and distal to the vessel lesion. [ 8 ]


There is some controversy over the accuracy of observing the lesion MLD itself, since many atherosclerotic lesions may create uneven "hills and valleys" within the lumen, making a true MLD difficult to obtain or estimate. Some research indicates calculating "area stenosis" is also a valid measure of actual vessel stenosis compared to diameter stenosis alone, but this requires additional analysis because a tracing of the lumen border must be performed. However, there are computer programs available to automatically perform this function. It may be helpful to obtain both percent diameter and area percent stenosis, especially since the two percentages may not always correlate with each other. [ 9 ]


An  occlusion , or the blocking of all blood flow through a vessel, is considered 100% percent diameter stenosis.


Binary restenosis is traditionally defined as a reduction in the percent diameter stenosis of 50% or more (≥50%). It is also known as just "binary stenosis". [ 10 ]  The term "binary" means that patients are placed in 2 groups, those who have ≥50% stenosis and those who have <50% stenosis. Binary restenosis is an epidemiological method of analyzing percent diameter stenosis for observing not only an individual patient, but also performing statistical techniques on a group of patients to determine averages (descriptive measures of central tendency) or as a predictive variable. [ citation needed ]


In the first stage of restenosis, administering anti- platelet  drugs (called IIb/IIIa inhibitors) immediately after surgery greatly reduces the chance of a  thrombosis  occurring. [ citation needed ]


Drug-eluting stents , coated with  pharmaceuticals  that inhibit tissue growth and thus reduce the risk of restenosis from scar tissue and cell proliferation, are now widely used. [ 11 ]  These  stents  reduce the occurrence of restenosis, with clinical studies showing an incidence rate of 5% or lower. [ 3 ] [ 12 ] [ 13 ]


If restenosis occurs without a  stent , it is usually treated with more  angioplasty . [ citation needed ]  This treatment is also used if restenosis occurs at either the proximal or distal end of the  stent . [ citation needed ]


If restenosis occurs within a  stent  (also known as in-stent stenosis), it may be treated with repeated  angioplasty  and insertion of another stent inside the original, often with a drug-eluting stent. [ 14 ]


Over the past 5 years, ISR has been increasingly treated with a  drug-coated balloon  (DCB), which is a balloon coated with the same anti-cancer drugs that prevent restenosis, such as  Paclitaxel . [ 15 ] [ 16 ]  The balloon avoids the need for a double layer of metal which is used when an in-stent restenosis is treated with another stent within the original stent. Additionally, DCB treatment does not leave an implant in the body and is designed for faster drug delivery.


Alternative treatments include  brachytherapy , or intracoronary radiation. The radiation kills cells and inhibits tissue growth (similar to a patient undergoing cancer therapy). [ 17 ]


Rates of restenosis differ between devices (e.g., stent-grafts, balloon angioplasty, etc.) and location of procedure (i.e., centrally located in the heart, such as the coronary artery, or in peripheral vessels such as the popliteal artery in the leg, the pudendal artery in the pelvis, or the carotid artery in the neck). [ citation needed ]


In cardiac procedures, balloon angioplasty without stent implantation has been associated with a high incidence of restenosis, with rates ranging from 25% to 50%, and the majority of these patients need further angioplasty within 6 months. [ 18 ]


A 2010 study in India comparing coronary  drug-eluting stents  (DES) with coronary  bare-metal stents  (BMS) reported that restenosis developed in 23.1% of DES patients vs 48.8% in BMS patients, and female sex was found to be a statistically significant risk factor for developing restenosis. [ 19 ]


However, in newer-generation DES and BMS the restenosis rates are much lower. For example, the NORSTENT trial, presented in 2016, reports target-lesion revascularization rates of 5.3% and 10.3% for DES and BMS respectively. [ 13 ]


In peripheral procedures, rates are still high. A 2003 study of selective and systematic stenting for limb-threatening ischemia reported restenosis rates at 1year follow-up in 32.3% of selective stenting patients and 34.7% of systematic stenting patients. [ 20 ]


The 2006 SIROCCO trial compared the sirolimus drug-eluting stent with a bare nitinol stent for atherosclerotic lesions of the  subsartorial artery , reporting restenosis at 2 year follow-up was 22.9% and 21.1%, respectively. [ 21 ]


A 2009 study compared bare nitinol stents with percutaneous transluminal angioplasty (PTA) in  subsartorial artery  disease. At 1 year follow-up, restenosis was reported in 34.4% of stented patients versus 61.1% of PTA patients. [ 22 ]


Return of spontaneous circulation  ( ROSC ) is the resumption of a sustained  heart rhythm  that perfuses the body after  cardiac arrest . It is commonly associated with significant respiratory effort. Signs of return of spontaneous circulation include breathing, coughing, or movement and a palpable pulse or a measurable blood pressure. Someone is considered to have sustained return of spontaneous circulation when circulation persists and  cardiopulmonary resuscitation  has ceased for at least 20 consecutive minutes. [ 1 ]


There are multiple factors during cardiopulmonary resuscitation (CPR) and  defibrillation  that are associated with success of achieving return of spontaneous circulation. One of the factors in CPR is the chest compression fraction, which is a measure of how much time during cardiac arrest are chest compressions performed. A study measured the effects of chest compression fraction on return of spontaneous circulation in out-of-hospital cardiac arrest patients with a non-ventricular fibrillation arrhythmia and it showed a trend to achieving return of spontaneous circulation with an increased chest compression fraction. [ 2 ]  Another study highlighted the benefits of minimizing chest compression intervals before and after shocking a patient's rhythm, which would in turn increase chest compression fraction. [ 3 ]  A  coronary perfusion pressure  of 15 mmHg is thought to be the minimum necessary to achieve ROSC. [ 4 ]


Pertaining to defibrillation, the presence of a shockable rhythm ( ventricular fibrillation  or pulseless  ventricular tachycardia ) is associated with increased chances of return of spontaneous circulation. [ 5 ]  Although a shockable rhythm increases chances for return of spontaneous circulation, a cardiac arrest can present with  pulseless electrical activity  or  asystole , which are non-shockable cardiac rhythms. [ 6 ]


Return of spontaneous circulation can be achieved through cardiopulmonary resuscitation and defibrillation. Though ROSC is necessary for survival, it is not, itself, a predictor of a favorable medium- or long-term outcome. [ 7 ]  Patients have died not long after their circulation has returned. One study showed that those who had had an out-of-hospital cardiac arrest and had achieved return of spontaneous circulation, 38% of those people had a cardiac re-arrest before arriving at the hospital with an average time of 3 minutes to re-arrest. [ 8 ]  Patients with sustained ROSC generally present with  post-cardiac arrest syndrome  (PCAS). Longer time-to-ROSC is associated with a worse presentation of PCAS. [ 9 ]


Lazarus phenomenon  is the rare spontaneous return of circulation after cardiopulmonary  resuscitation  attempts have stopped in someone with cardiac arrest. This phenomenon most frequently occurs within 10 minutes of cessation of resuscitation, thus passive monitoring is recommended for 10 minutes following CPR cessation. [ 10 ]


Rhythm interpretation  is an important part of healthcare in Emergency Medical Services ( EMS ). Trained medical personnel can determine different treatment options based on the  cardiac rhythm  of a patient.  There are many common heart rhythms that are part of a few different categories,  sinus arrhythmia , atrial arrhythmia,  ventricular arrhythmia .   Rhythms can be evaluated by measuring a few key components of a rhythm strip, the  PQRST  sequence, which represents one cardiac cycle, the  ventricular rate , which is the rate at which the  ventricles  contract, and the  atrial rate , which is the rate at which the atria contract.


The 5 deviations from the base line on a rhythm strip make up the  PQRST sequence .  There are a few key intervals that must be measured for proper analysis of a heart rhythm,  The  PR  interval is the interval between the end of the  P wave  and the beginning of the  Q wave .  This represents the conduction of the atria of the heart, the speed at which they are able to conduct an electrical impulse.  The  QRS complex  represents the conduction of the ventricles of the heart, the speed at which they are able to conduct an  electrical impulse .  The interval between each  R wave  represents the heart rate, which is critical for determining different rhythms within the defined categories. [ citation needed ]


There are 6 different sinus arrhythmia. [ 1 ] [ 2 ]


A normal heart should have a  normal sinus rhythm , this rhythm can be identified by a ventricular rate of 60-100 bpm, at a regular rate, with a normal PR interval (0.12 to 0.20 second) and a normal QRS complex (0.12 second and less).


Sinus bradycardia   is another regular rhythm however the ventricular rate is only between 40 and 60 bpm, with a normal PR interval and a normal QRS complex.


Sinus tachycardia   is another regular rhythm however the ventricular rate is quicker, between 100 - 160 bpm, with a normal PR interval and normal QRS complex.


Sinus arrhythmia   is an irregular rhythm with a ventricular rate of 60 - 100 normally, however a slow rhythm can be distinguished when the rate is less than 60, the PR interval and QRS complex are normal.


Sinus pause  is a regular rhythm however a sudden pause occurs in the rhythm which makes it miss a few beats, if the rhythm resumes on time after the pause then this is known as a  sinus block , if the rhythm does not resume on time after the pause this is known as a  sinus arrest.


There are 5 different atrial arrhythmias. [ 1 ] [ 2 ]


A  wandering atrial pacemaker  can be either normal or irregular in rate, much like a sinus arrhythmia the rate is normally between 60 - 100 bpm when it is normal and less than 60 when it is slow, the distinguishing feature of this rhythm is a p wave that varies in size, shape, and direction, the PR interval can either be normal or irregular depending on the location of conduction of the PR interval, the QRS complex is normal.


A  premature atrial pacemaker  has a regular underlying rhythm however there is a premature beat which can be identified by an irregular p wave with a different size, shape, and direction often found within a T wave, the PR interval is generally normal however can be hard to measure, the QRS complex is premature for the PAC, but is generally normal.


Paroxysmal  atrial tachycardia  has a regular rate, however a high rate of about 140-250 bpm, p waves are generally hidden and the PR interval is not measurable.


Atrial flutter  has an atrial rate of 250-400 and can be identified by p waves with saw tooth deflections.


Atrial fibrillation  has an atrial rate of 400+ and is distinguishable due to its irregular ventricular rate and wavy deflections.


Ventricular arrhythmias are some of the most dangerous heart rhythms requiring  cardiopulmonary resuscitation  ( CPR ) and defibrillation in cases of symptomatic  ventricular tachycardia  and  ventricular fibrillation .


There are 5 different ventricular arrhymia. [ 1 ] [ 2 ]


Ventricular tachycardia  is a regular rhythm with a rate of 140-250 bpm, there are no P waves and the main feature is a wide QRS complex (0.12 and greater)


Ventricular fibrillation  has no p waves or QRS complexes, there are only wavy irregular deflections throughout the heart rhythm, at this point the heart would have a rate of 0 and be supplying no blood through the body.


Idioventricular rhythm  this is a regular rhythm identifiable by a wide QRS complex with absent P waves, and a rate between 30 and 40 bpm.


Accelerated idioventricular rhythm  is a regular rhythm with a wide QRS complex and absent P waves, and a rate between 50 and 100 bpm.


The final rhythm is  ventricular standstill  this rhythm will appear as a flat line, but may have a few non conducted p waves, the heart rate of this will be 0 and be supplying no blood through the body like ventricular fibrillation.


The  Roseto effect  is the phenomenon by which a close-knit community experiences a reduced rate of heart disease.  The effect is named for  Roseto, Pennsylvania .  The Roseto effect was first noticed in 1961 when the local Roseto doctor encountered  Stewart Wolf , then head of Medicine of the  University of Oklahoma , and they discussed, over a couple of beers, the unusually low rate of  myocardial infarction  in the  Italian American  community of Roseto compared with other locations. [ 1 ] [ 2 ] [ 3 ]   Many studies followed, including a 50-year study comparing Roseto to nearby  Bangor .  As the original authors had predicted, as the Roseto cohort shed their Italian social structure and became more Americanized in the years following the initial study, heart disease rates increased, becoming similar to those of neighboring towns. [ 4 ]


From 1954 to 1961, Roseto had nearly no heart attacks for the otherwise high-risk group of men 55 to 64, and men over 65 had a death rate of 1% while the national average was 2%.  Widowers outnumbered widows, as well. [ 1 ]


These statistics were at odds with a number of other factors observed in the community.  They smoked unfiltered  stogies , drank  wine  "with seeming abandon" in lieu of  milk  and  soft drinks , skipped the  Mediterranean diet  in favor of meatballs and sausages fried in lard with hard and soft cheeses.  The men worked in the  slate  quarries where they contracted illnesses from gases and dust. [ 5 ]   Roseto also had very little crime, and very few applications for public assistance. [ 5 ]


Wolf attributed Rosetans' lower heart disease rate to lower stress.  "'The community,' Wolf says, 'was very cohesive. There was no  keeping up with the Joneses . Houses were very close together, and everyone lived more or less alike.'"  Elders were revered and incorporated into community life.  Housewives were respected, and fathers ran the families. [ 2 ] [ 6 ]


The  San Francisco Syncope Rule  (SFSR) is a rule for evaluating the risk of adverse outcomes in patients presenting with  fainting  or  syncope .


The mnemonic for features of the rule is CHESS:


•  C  - History of  congestive heart failure


•  H  -  Hematocrit  < 30%


•  E  - Abnormal  ECG


•  S  - Shortness of breath


•  S  - Triage systolic  blood pressure  < 90


A patient with any of the above measures is considered at high risk for a serious outcome such as death,  myocardial infarction ,  arrhythmia ,  pulmonary embolism ,  stroke ,  subarachnoid hemorrhage , significant  hemorrhage , or any condition causing a return Emergency Department visit and hospitalization for a related event. [ citation needed ]


SFSR was retrospectively found to have 98% sensitivity and specificity of 56% for serious causes of syncope. [ 1 ]  However, external prospective validation of the criteria found sensitivity to be 74%, substantially lower than the initial study. [ 2 ]  This means that in patients with none of the above criteria, potentially serious causes of syncope were missed in over a quarter of patients. Syncope accounts for 1-2%  emergency department  visits. Half are hospitalized and of these, 50% have unclear diagnosis and 85% will be simply monitored. [ citation needed ]


SATRO-EKG  - a  computer program  analysing electro-cardiology signals. It is based on the  SFHAM model . It facilitates the evaluation of electrical activity of myocardium, and therefore, early detection of  ischemic changes in the heart .


The reference tests of the SATRO-ECG method in relation to  perfusive scintigraphy SPECT  conducted in Military Medical Institute in  Warsaw  and  Medical University of Wroclaw  proved the possibility to use this method to detect  coronary heart disease (CHD) .  A very high  Sensitivity and specificity  in detecting this disease were obtained. [ citation needed ]


Sensitivity (Se), specificity (Sp),  predictive value of positive values results  (PV(+)) and  negative values results  (PV(-)) are presented in the grid below: [ citation needed ]


Comparison of SATRO-ECG results -  SPECT  (exercise) for particular parts of the cardiac muscle is presented in the grid below:  [ 1 ]


The results of the tests prove a high correlation the between SATRO-ECG results and  SPECT  in the case of detection of  coronary heart disease (CHD)   [ 1 ]


An advantage of this method is a fast and precise analysis of the ECG results in the rest, which enables:  [ citation needed ]


The method is a diagnostic element of the Program of Universal Prevention and Therapy of Ischemic Heart Disease in the international project developed for  United Nations Economic and Social Council   [ 2 ] .


The  Scandinavian Simvastatin Survival Study  (also known as the  4S  study), was a multicentre,  randomized, double-blind ,  placebo-controlled clinical trial , which provided the initial data that supported the use of the  cholesterol-lowering drug ,  simvastatin , in people with a moderately raised  cholesterol  and  coronary heart disease  (CHD); that is people who had previously had a  heart attack  or  angina . The study was sponsored by the pharmaceutical company  Merck  and enrolled 4,444 people from 94 centres in  Scandinavia . [ 1 ] [ 2 ]


Before the 4S study, it was not proven that lowering cholesterol could prolong life in people who had CHD. [ 3 ]  The study concluded that  secondary prevention  with simvastatin in a high risk group with CHD reduced overall mortality by 30%. [ 3 ]  Published in  The Lancet  in 1994, it is considered a "landmark paper". [ 3 ] [ 4 ]


The 4S multicentre,  randomized, double-blind ,  placebo-controlled clinical trial  enrolled 4,444 people chosen from 7,027 people who had been followed up for two months after being given dietary advice. [ 2 ]  The objective of the study was to assess the effect of a  cholesterol-lowering drug  called  simvastatin  on  mortality  and morbidity in people with a history of a previous  heart attack  or  angina , who also had a moderately  raised cholesterol ; between 5.5 and 8.0 mmol/L. [ 1 ] [ 5 ] [ 6 ]


A second objective was to investigate whether the incidence of major coronary artery disease events (fatal and nonfatal myocardial infarction and sudden death) could be reduced with simvastatin. [ 2 ]


The participants, all at high risk of death from CHD and death in general, [ 5 ]  were selected from 94 clinical centers in Denmark, Finland, Iceland, Norway, and Sweden from 1988 to 1989, and were aged between 35 and 70 years, with the average age being 59. [ 2 ] [ 7 ]  Of the 4,444 people enrolled in the study, 3,617 were men and 827 women, [ 5 ]  2,223 were randomly assigned a  placebo  and 2,221 were given 20 to 40 mg of simvastatin daily. [ 1 ]  The plan was to follow the participants for a minimum of three years or until such a time as total mortality reached 440 deaths. [ 2 ] [ 5 ]  In practice, the study carried for a median period of 5.4 years. [ 3 ]


After 5.4 years, compared to the group that were given placebo, the simvastatin group demonstrated a 35% reduction in  LDL-C  and 30% reduction in overall mortality. [ 1 ] [ 3 ]  The risk of hospital-verified non-fatal myocardial infarction reduced by 37% and fatal and non-fatal  cerebrovascular events  ( stroke  and  TIA ) lessened by 28%. [ 1 ]  30 people would need to be treated with simvastatin for about five years, to prevent one death;  number needed to treat  around 30. [ 3 ]  There were no extra deaths from other non-cardiac causes such as  cancer  or trauma. [ 3 ] [ 9 ]  The trial also showed benefits in diabetes, women and older people. [ 3 ]


A follow-up of treatment with simvastatin for up to eight years was published in 2000. [ 7 ]  Ten years after the start of the 4S trial, a follow-up study published on 28 August 2004 in  The Lancet , revealed that of those 2,221 people who continued to take simvastatin, there was a further reduction in number of deaths from CHD when compared to those who had switched from placebo to statin at the five year mark. [ 7 ] [ 10 ]  The overall mortality also reduced by 15% at the 10 year mark. [ 3 ] [ 7 ]


The study concluded that  secondary prevention  with simvastatin in a high risk group with CHD reduced overall mortality by 30%. Non-fatal CHD events and fatal and non-fatal cerebrovascular events were reduced without an increase in risk of cancer. [ 3 ]


Published in  The Lancet  in 1994, the 4S trial, had an immediate influence on medical opinion, [ 9 ]  and is considered a "landmark paper". [ 3 ] [ 4 ] [ 11 ]  Several other large multicenter clinical trials followed, leading to widespread use of simvastatin. [ 3 ]


Data from the 4S trial has frequently been used to analyse the cost-effectiveness of simvastatin in secondary prevention. [ 12 ] [ 13 ]


SCP-ECG , which stands for  Standard communications protocol for computer assisted electrocardiography , is a standard for  ECG  traces, [ 1 ]  annotations, and  metadata , that specifies the interchange format and a messaging procedure for  ECG  cart-to-host communication and for retrieval of SCP-ECG records from the host to the ECG cart.   It is defined in the joint  ANSI / AAMI  standard EC71:2001  and in the  CEN  standard EN 1064:2005.


The SCP Standard was first developed between 1989 and 1991 during a European AIM R&D project. [ citation needed ]


DICOM ,  HL7 aECG , MFER (ISO 22077) [ citation needed ]


The  Sensei X robotic catheter  is a medical  robot  designed to enhance a physician’s ability to perform complex  operations  using a small flexible tube called a  catheter . As open surgical procedures that require large incisions have given way to minimally invasive surgeries in which the surgeon gains access to the target organs through small incisions using specialized surgical tools.  One important tool used in many of these procedures is a catheter used to deliver many of things a surgeon needs to do his work, to impact target tissue and deliver a variety of medicines or disinfecting agents to treat disease or infection.


Manufactured by  Hansen Medical , Sensei X is a specialized robotic catheter system that is controlled by a physician and is designed for accurate positioning, manipulation and stable control of catheter and catheter-based technologies during  cardiovascular procedures . The Sensei system obtained U.S.  Food and Drug Administration  (FDA) clearance in 2007, after which the  Cleveland Clinic 's  electrophysiology  program, then directed by Dr. Andrea Natale, received the first placement. The  Sensei Robotic Catheter System  and Artisan Extend Control Catheter allow physicians to navigate flexible catheters with greater stability and control during complex  cardiac arrhythmia  procedures. Hansen Medical has related co-development agreements with the following industry leaders:  St. Jude Medical ,  GE Healthcare ,  Siemens Healthcare , and  Philips  Medical Systems.


Hansen Medical was founded by Dr. Frederic Moll, who had also co-founded Intuitive Surgical, manufacturer of the Da Vinci Surgical System, whose use has propelled medicinal robotics to the forefront of patient care. The Sensei system is indicated for use during the cardiac mapping phase of cardiac arrhythmia treatment in the US. Meanwhile, it has CE mark approval for facilitating the navigation of ablation catheters within the atria of the heart during complex arrhythmia procedures such as Atrial Fibrillation (AF).


In November 2010, Hansen Medical received unconditional Investigational Device Exemption (IDE) approval from the FDA initiating  a clinical trial to investigate the use of the Sensei X Robotic Catheter System and the Artisan Control Catheter for treatment of AF, the most common cardiac arrhythmia. The Principal Investigator of the ARTISAN AF Trial is Dr. Andrea Natale, executive medical director for Texas Cardiac Arrhythmia Institute (TCAI). The first case in the trial was completed by Dr. Joseph Gallinghouse, an electrophysiologist, at the TCAI at St. David's Medical Center. [ 1 ]


By the end of 2010, nearly 100 Sensei systems have been shipped worldwide since its 2007 release. The system has been used to perform almost 5,000 procedures. [ 2 ]  The Sensei system operates by guiding standard catheters through a manipulated robotically steerable sheath (hollow tube) in the patient's vasculature. The doctor performs the procedure at a control station with a technology called "IntelliSense" to proximally measure the forces applied along the shaft of the catheter as a result of catheter tissue contact. The Artisan catheter has two robotically controlled segments which provides six degrees of freedom and 270 degrees of bend articulation which can assist physicians in accessing  hard-to-reach cardiac anatomy. The open lumen Artisan catheter accommodates 8F percutaneous EP catheters. Centers have reported acute and long term success rates consistent with manual procedures. [ 3 ] [ 4 ] [ 5 ] [ 6 ]


Although the Sensei system was initially tested in a range of ablation procedures including SVT and typical atrial flutter, [ 7 ] [ 8 ]  there is most excitement about its role in complex ablation procedures  such as for atrial fibrillation (AF), where the ability to manipulate catheters to precise locations within the heart and keep them stable in the desired position is crucial. Achieving adequate tissue contact, ideally with a small amount of pressure being applied by the catheter during ablation, is also essential to effectively destroy the heart tissue responsible for arrhythmia. The ability to titrate catheter contact force using the Sensei system’s built-in pressure sensor technology (called intellisense) may allow operators to maximise the chance of creating effective burns across the thickness of the atrial wall, whilst minimising the risk of complication. [ 9 ]  Intracardiac echocardiography has also demonstrated that greater catheter stability is achieved with robotic compared to manual catheter delivery. [ 10 ]  Consequently, there is evidence that robotic ablation causes more effective and more efficient burns. [ 11 ]


Use of robotic navigation for  catheter ablation  was also designed to allow  Electrophysiology  to perform most of the procedure without being exposed to X-rays (or radiation). The radiation dose to the operator during a conventional manual ablation procedure is relatively small, although there is cumulative exposure that becomes an important consideration for operators performing procedures on a daily basis. By performing procedures a few metres away using a robotic system and seated in the leaded anteroom, the operator is shielded from X-rays and is less vulnerable to operator fatigue, which may affect operator performance in long complex cases. Use of robotic navigation has been shown to reduce fluoroscopy times in  catheter ablation  of AF, resulting in reduced X-ray exposure for patients and other health care professionals present in the catheter laboratory. [ 12 ] [ 13 ] [ 14 ]


The system has been the subject of several  clinical trials  in the USA and Europe, particularly for the catheter ablation of AF. There were early safety concerns after the ‘first-in-human’ studies suggested high complication rates. Wazni et al. reported experience with the first 71 catheter ablations for AF in their centre using the Hansen robotic navigation system starting from 2005. [ 15 ]


These early studies have allowed others to incorporate changes to their technique, [ 16 ]  and hence recent work has produced complication rates for catheter ablation of AF comparable to procedures performed manually. [ 17 ] [ 18 ] [ 19 ]  The field of robotic ablation is growing and evolving rapidly, and randomised controlled trials comparing robotic to manual ablation are ongoing in Europe and the USA to see if these potential advantages will translate into better clinical outcomes. [ citation needed ]


Since there are no completed randomised controlled trials comparing robotic ablation to manual ablation, comparing the modalities remains difficult. Techniques, complication rates and clinical results vary widely between centres for both manual and robotic procedures, making registry data difficult to compare. Typical ranges for procedures performed manually are: major complication rates of 3-5%, and success rates of approximately 80-90% for paroxysmal AF and 70-75% for persistent AF (depending on the length of follow-up). [ 20 ] [ 21 ]  The following are recent reports in medical journals detailing experience of the Sensei system in the catheter ablation of AF, and demonstrate approximate success and complication rates at the time of writing:


All paroxysmal


(Freedom from AF )


86% after 21 patients had a repeat procedure


135 paroxysmal
55 persistent
6 long-lasting persistent


127 paroxysmal
55 persistent
11 long-lasting persistent


Paroxysmal AF 90%
Persistent AF 71%
Long-lasting 100% (of only 6)


Paroxysmal AF 85%
Persistent AF 73%
Long lasting 67%


(Freedom from AF)


Paroxysmal 43
Persistent 22


(remainder completed manually)


76% Paroxysmal
78% persistent


Tamponade 1.5%


Paroxysmal 29
Persistent 11


Tamponade 5% (nil else)


SFHAM (single fibre based heart activity model)  is a physical model describing the electric activity of the  left ventricle  of the heart during its  depolarisation . It facilitates a precise analysis of  electric potentials  of different parts of the ventricle. [ 1 ]


The  SFHAM model  is based on the following principles: [ citation needed ]


The model constitutes a theoretical basis for  SATRO-ECG  being a system to  non-invasive diagnosing  facilitating early detection  ischemic changes in the heart . [ citation needed ]


Samin K. Sharma  (born May 28, 1955) is an American  philanthropist  of Indian descent and an  interventional cardiologist [ 1 ] [ 2 ]  who co-founded the Eternal Heart Care Centre and Research Institute in  Jaipur  (EHCC). [ 3 ]  Sharma has served on New York State’s Cardiac Advisory Board since 2004. As of 2021, he is Senior Vice-President, Operations & Quality at The  Mount Sinai Hospital  in New York [ 4 ]  and runs the  Dr. Samin K. Sharma Family Foundation Cardiac  Catheterization  Laboratory . [ 5 ]  As of 2018, he is Chairman Board of Trustees, Association of Indians in America (AIA). [ 6 ]  As of 2022, he has been an investigator on 86 grants and multi-center trials and authored 486 peer-reviewed articles that have been cited 21,734 times.


Sharma was born to a  Brahmin  family in  Alwar , India. [ 7 ]  He graduated from Rajgarh Higher Secondary School in  Alwar . In 1972, he received his bachelor of science degree from University  Maharaja College  then his MBBS degree from  SMS  Medical Department of  Pharmacy , Jaipur in 1978.


Sharma traveled to New York in 1983 [ 8 ]  for a three-year residency in  internal medicine  at the  NY Infirmary-Beekman Downtown Hospital  (1983-1986), a two-year fellowship in cardiology at  Elmhurst Hospital  in Queens (1986-1988). He trained with Mount Sinai's chief of cardiology, Dr.  Valentín Fuster . He was concurrently an emergency department physician in  Queens  and was later hired to Mount Sinai's cardiology department. He is the director of the  Mount Sinai Hospital   Cardiac Catheterization  Laboratory. [ 9 ] [ 10 ]


Sharma specializes in the non-surgical treatment of  mitral  and  aortic stenosis . [ 11 ] [ 12 ]  He reportedly performed 3,722  angioplasties  over three years (2005-2007) according to a study by the  New York State Department of Health . [ 13 ]  He also performs rotational  atherectomy , an alternative to angioplasty for complex, calcified coronary lesions. [ 14 ]   He has published extensively on the procedure [ 15 ]  and he is a principal investigator (PI) on scores of clinical trials and research grants analyzing and contrasting forms of interventional cardiology. In 2009, he performed a coronary  angiography  and angioplasty procedure on Indian Prime Minister  Shri Manmohan Singh .


As of 2022, Sharma participated as an investigator on more than 80 grants and  multi-center trials . Recent and current trials focus on  transcatheter aortic valve replacement , protracted  percutaneous coronary interventions , outcomes of moderate to severely calcified coronary lesions, best practices, the performance of self-expanding vs balloon-expandable  transcatheter   aortic valve  replacement, post-market device and procedural outcomes, refractory  angina  and rotational  atherectomy . [ 16 ] [ 17 ] [ 18 ] [ 19 ] [ 20 ] [ 21 ]


A partial listing of his awards and recognition includes  Businessman of the Year  by national  Republican Congressional Committee  for 2001-2002, Rajasthan Gaurav award in Jaipur by Rajasthan Government, India (2002),  Rajive Gandhi  Memorial Award for outstanding community service and medical excellence for India (2005), Governor’s award of excellence for outstanding contribution to Medicine, New York State (2006),  Ellis Island Medal of Honor  (2011). [ citation needed ]


Sharma co-founded the Eternal Heart Care Center in 2004 [ 22 ]  with his wife, Manju Sharma. This 250-bed tertiary   multidisciplinary hospital offers care to patients of any  socioeconomic  status. The plan for this hospital was conceived in 2007 when the Sharmas met then-Chief Minister of  Rajasthan ,  Vasundhara Raje . Sharma is as of 2021 documented as one of the organization's directors. [ 23 ]


Under Sharma’s leadership, the cardiac catheterization lab at Mount Sinai has been implicated in allegations of Medicaid fraud, coaching emergency room patients to say they were having symptoms of a heart attack in order to receive reimbursement for advance scheduled interventional procedures. He has also been accused of inflating procedural numbers to unattainable records by having trainees perform his procedures without supervision. He received $4.8 million from billing for these procedures himself in 2012. [ 24 ] [ 25 ]


According to  ResearchGate , Sharma published 165 articles while affiliated with Icahn School of Medicine. According to Scopus, he has 486 publications as of 2022 that were cited 21,734 times across 18,988 documents. His h-index is listed as 60. [ 26 ]


A  sinus rhythm  is any  cardiac rhythm  in which  depolarisation  of the  cardiac muscle  begins at the  sinus node . [ 1 ]   It is necessary, but not sufficient, for normal electrical activity within the  heart . [ 2 ]  On the  electrocardiogram  (ECG), a sinus rhythm is characterised by the presence of  P waves  that are normal in morphology. [ 2 ]


The term  normal sinus rhythm  ( NSR ) is sometimes used to denote a specific type of sinus rhythm where all other measurements on the ECG also fall within designated normal limits, giving rise to the characteristic appearance of the ECG when the  electrical conduction system of the heart  is functioning normally; however, other sinus rhythms can be entirely normal in particular patient groups and clinical contexts, so the term is sometimes considered a misnomer and its use is sometimes discouraged. [ 3 ] [ 4 ]


Other types of sinus rhythm that can be normal include  sinus tachycardia ,  sinus bradycardia , and  sinus arrhythmia . Sinus rhythms may be present together with various other  cardiac arrhythmias  on the same ECG.


In humans, for an ECG to be described as showing a sinus rhythm, the shape of the P wave in each of the 12 standard  ECG leads  should be consistent with a "typical P  vector " of +50° to +80°. [ 2 ]  This means that the P wave should be:


If the P waves do not meet these criteria, they must be originating from an abnormal site elsewhere in the atria and not from the sinus node; the ECG cannot, therefore, be classed as showing a sinus rhythm. [ 2 ]


In general, each P wave in a sinus rhythm is followed by a QRS complex, and the sinus rhythm therefore gives rise to the whole heart's depolarization. Exceptions to this include  complete heart block  and certain ventricular  artificial pacemaker  rhythms, where the P waves may be completely normal in shape, but ventricular depolarization bears no relation to them; in these cases, the speed of the "sinus rhythm of the atria" and the speed of the ventricular rhythm must be calculated separately. [ 2 ]


By convention, the term "normal sinus rhythm" is taken to imply that not only are the P waves (reflecting activity of the sinus node itself) normal in morphology but that all other ECG measurements are also normal. [ 3 ] [ 5 ]  Criteria therefore include:


A  sonographer  is an  allied healthcare professional  who specializes in the use of  ultrasonic  imaging devices to produce diagnostic images, scans, videos or three-dimensional volumes of anatomy and diagnostic data. The requirements for clinical practice vary greatly by country. Sonography requires specialized education and skills to acquire, analyze and optimize information in the image. Due to the high levels of decisional latitude and diagnostic input, sonographers have a high degree of responsibility in the diagnostic process. Many countries require medical sonographers to have professional certification. Sonographers have core knowledge in ultrasound physics, cross-sectional anatomy, physiology, and pathology.


A  sonologist  is a  medical doctor  who has undergone additional  medical ultrasound  training to diagnose and treat diseases. [ 1 ] [ 2 ]  Sonologist is licensed to perform and write ultrasound imaging reports independently or verifies a sonographer's report, prescribe medications and medical certificates, and give clinical consultations.


A sonologist may practice in multiple modalities or specialize in only one field, such as  obstetric ,  gynecology ,  heart ,  emergency  and  vascular  ultrasound.


Prior to 1970, many individuals performed sonography for research purposes and those assisting with the imaging were considered technicians or technologists, and in 1973 in the United States the occupation of diagnostic medical technology was established as sonography become more widely used within healthcare settings. [ 3 ]  Today,  sonographer  is the preferred term for the  allied healthcare professionals  who perform  diagnostic medical sonography , or diagnostic  ultrasound . The alternative term "ultrasonographer" is much less commonly used. [ 4 ] [ 5 ]


The  Australasian Sonographers Association (ASA)  was formed in 1992 in response to the desire of sonographers across Australia for an organisation that represents and considers issues important to sonographers in the Australian healthcare environment. The ASA has more than 5000 individual member sonographers from Australia and New Zealand, and about 30 corporate partners. The ASA has pledged to pursue high standards within the practice of medical sonography, and has a structure of a board of directors and multiple representative branches in all Australian states and New Zealand. [ citation needed ]


Australian sonographers must be accredited by the Australian Sonographers Accreditation Registry (ASAR), whose brief is to accredit and reaccredit on a regular basis, postgraduate ultrasound programs offered by Australian universities, and to establish the criteria against which those programs and any other future Australian and New Zealand programs are to be judged. In addition, a register of accredited medical sonographers  and accredited student sonographers  is maintained and their continuing professional development activities monitored and recorded. [ citation needed ]


The Health Insurance Commissison in association with the ASAR introduced in 2002 a program of accreditation and continuing professional education for sonographers. The ASAR recognises registration with the Australian Orthoptic Board as appropriate accreditation for  orthoptists  to undertake sonography in relation to ocular structures. [ citation needed ]


The vast majority of Canadian sonographers have received their education through an accredited sonography program. Many programs are available across the country and may include direct-entry programs for degrees, advanced diplomas, and second-discipline graduate certificate programs. Sonography Canada registers sonographers in three credentials: generalist, cardiac, and vascular. To become registered, eligible candidates must successfully meet Sonography Canada's clinical (Canadian Clinical Skills Assessment) and academic requirements. Sonography Canada-credentialed sonographers must also document their continuing education by maintaining a minimum 40 continuing professional development credits every three years. [ citation needed ]


The  Nova Scotia Society of Diagnostic Medical Sonographers  is currently working with the  Nova Scotia Association of Medical Radiation Technologists  to add diagnostic ultrasound as a new discipline in the proposed college. This means that diagnostic sonography would become a self-regulated profession in Nova Scotia, along with radiography, nuclear medicine, magnetic resonance imaging, and radiation therapy. The Department of Health is now considering their application; the appropriate act and associated regulations have been drafted, and the associations are aiming for approval at the spring 2012 session of the legislature.


In the UK, sonographers are also responsible for the interpretation of the images and issue diagnostic reports. They are educated to a high level, and their training is delivered as a MSc/PGDip/PGCert by the universities and overseen by the Consortium for Accreditation of Sonographic Education; as training is delivered at postgraduate level, all sonographers must have a bachelor's degree or equivalent prior to undertaking this specialty, and this means training can take a minimum of 4 years. Currently, no requirement exists for a sonographer to be state registered in the UK, although the majority are registered with the  Health and Care Professions Council  (HCPC) as a radiographer. State registration of sonographers in their own right is being eagerly sought by the profession. However, the HCPC has previously sought to require statutory registration of sonographers, a motion supported by a number of professional bodies, and the HCPC was rejected by the Department of Health. [ 6 ]  The rationale for this rejection remains controversial, but a voluntary registry is currently maintained by the  College of Radiographers . [ 7 ]


Within the United Kingdom, sonographers are employed by hospitals within the  National Health Service  and by private companies offering healthcare services.


The profession is subdivided in specialties such as  cardiac , obstetrical, vascular, and general sonographers. General sonographers are registered in abdominal and/or obstetric and gynecologic sonography. [ 8 ]  Around 1 1/2 years may be needed to get a degree in diagnostic medical sonography. [ 9 ]  In the United States, the most widely accepted sonographic education is provided by CAAHEP/JRC-DMS accredited programs.


The American Society of Ultrasound Technical Specialists, now the  Society of Diagnostic Medical Sonography , was founded in 1970 as the primary professional society for sonographers. [ 3 ]   The two credentialing bodies in the United States for sonographers are the Cardiovascular Credentialing International established in 1968 and the American Registry for Diagnostic Medical Sonography (ARDMS) established in 1975. Accreditation is granted through the American National Standards Institute. Recognition of ARDMS programs in providing credentials has also earned the ARDMS accreditation with the  National Commission for Certifying Agencies , which is the accrediting arm of the National Organization for Competency Assurance (NOCA). Established in 1977 as a nonprofit organization, NOCA sets quality standards for certifying organizations. [ citation needed ]


In 2009, New Mexico and Oregon became the first two states to require licensure of sonographers, and as of 2023, licensure is also required in New Hampshire and North Dakota. [ 10 ]


The occupational risk associated with performing sonography was reported as early as 1985, [ 11 ]  but it wasn't until the mid-1990's those work-related injuries were widely recognized as a significant problem among sonographers that persists today. [ 12 ]  During their careers, up to 90% of sonographers report experiencing some form of work-related musculoskeletal discomfort. [ 13 ] [ 14 ]  Work-related musculoskeletal injuries are most common in the hand, shoulder, and neck. [ 15 ] [ 16 ]  Injuries are often due to scanning in compromised positions, incorrect gripping of the transducer, spending too much time manipulating the transducer on technically difficult exams such as obese or large pregnant patients, and a lack of upper body fitness, [ 17 ] [ 18 ]  but injuries also result from various organizational, administrative, equipment and other factors that are outside of the sonographer's control. [ 19 ] [ 20 ]   Implementation of ergonomic principles, including adjustments to equipment, to perform imaging tasks in low-strain postures is critical to reducing the risk of injury. [ 21 ]  Additionally, stretching and exercise protocols have been suggested to be a useful tool in reducing the risk of musculoskeletal injury, pain, and repetitive strain injury in sonographers. [ 22 ] [ 23 ]  Finally, sonographer health requires representation and acknowledgment of challenges facing the workforce across the entire work organization to promote the development and implementation of supportive policies and administrative procedures within the work setting, such as allowance for regular work breaks, uninterrupted workflow, and supervisor support. [ 14 ] [ 24 ] [ 25 ] [ 26 ]


Multiple professional societies have developed guidelines to address the pervasive problem of work-related injuries among sonographers. The first of these actions was a consensus conference held in 2003 and repeated in 2016 by the  Society of Diagnostic Medical Sonography  that resulted in the development of Industry Standards for the Prevention of Work-Related Musculoskeletal Disorders in Sonography. [ 27 ]  These standards primarily focused on the ergonomic design of equipment and the responsibilities of employers and employees in addressing injury prevention. [ 27 ]  The  American Institute of Ultrasound in Medicine  has also released guidelines that extend these standards by describing imaging exam-specific recommendations and discussing the role of quality improvement practices by healthcare organizations. [ 28 ]


In 2019, an alliance of eight professional societies, credentialing bodies, and accreditation organizations in the United States came together to create the  Work-Related Musculoskeletal Disorder (WRMSD) Grand Challenge  with a goal to stop WRMSDs resulting from the performance of diagnostic medical ultrasound. This alliance has supported design challenges and the creation of a research registry of sonographers to monitor the status of work-related injuries in the profession, examine risk factors, and develop solutions to remediate the pervasive issue. [ 14 ] [ 29 ]


A  split S2  is a finding upon auscultation of the  S2 heart sound . [ 1 ]


It is caused when the closure of the  aortic valve  (A 2 ) and the closure of the  pulmonary valve  (P 2 ) are not synchronized during inspiration. The second heart sound (S2) is caused by the closure of the aortic and pulmonic valves, which causes vibration of the valve leaflets and the adjacent structures. The aortic valve closes slightly before the pulmonic, and this difference is accentuated during inspiration when S2 splits into two distinct components (physiological splitting). During expiration, the pulmonic valve closes at nearly the same time as the aortic, and splitting of S2 cannot be heard.


Exercise increases the intensity of both the aortic and pulmonic components of S2, whereas deep inspiration increases the intensity of the pulmonic component only.


During inspiration , the chest wall expands and causes the intrathoracic pressure to become more negative (akin to a vacuum).  The increased negative pressure allows the lungs to fill with air and expand.  While doing so, it also induces an increase in venous blood return from the body into the right atrium via the superior and inferior venae cavae, and into the right ventricle by increasing the pressure gradient (blood is being pulled by the vacuum from the body and towards the right side of the heart).  Simultaneously, there is a reduction in blood volume returning from the lungs into the left atrium (the blood wants to stay in the lungs because of the vacuum surrounding the lungs, and  PVR  is lower because of lung expansion). Since there is an increase in blood volume in the right ventricle during inspiration, the pulmonary valve (P 2  component of S 2 ) stays open longer during ventricular systole due to an increase in ventricular emptying time, whereas the aortic valve (A 2  component of S 2 ) closes slightly earlier due to a reduction in left ventricular volume and ventricular emptying time. Thus the P 2  component of S 2  is delayed relative to that of the A 2  component. This delay in P 2  versus A 2  is heard as a slight broadening or even "splitting" of the second heart sound; though it is usually only heard in the pulmonic area of the chest because the P 2  is soft and not heard in other areas. [ citation needed ]


During expiration , the chest wall collapses and decreases the negative intrathoracic pressure (compared to inspiration).  Therefore, there is no longer an increase in blood return to the right ventricle versus the left ventricle and the right ventricle volume is no longer increased.  This allows the pulmonary valve to close earlier such that it overlaps the closing of the aortic valve, and the split is no longer heard. [ citation needed ]


It is physiologically normal to hear a "splitting" of the second heart tone in younger people, during inspiration and in the "pulmonary area", i.e. the second ICS (intercostal space) at the left edge of the sternum.


According to Harrison's Principles of Internal Medicine, "Normally, blood pressure falls during inspiration (equal or less than 10 mmHg), due to an increase in blood flow into the right ventricle with displacement of the interventricular septum to the left, decreasing left ventricular filling and cardiac output". [ 2 ]


The pressure in the right ventricle tries to open the pulmonary valve. The pressure in the pulmonary artery tries to close the pulmonary valve.  The higher pressure will "win". Hence, the closure of the pulmonary valve (P 2 ) will be delayed since the pressure in the right ventricle is increased in inspiration, opposing the pressure in the pulmonary artery and keeping it open longer than in expiration. The change in A 2  is not that evident. Thus P 2  appears after A 2  in inspiration. [ citation needed ]


The different types of split S 2  can be associated with medical conditions:


When the pulmonary valve closes  before  the aortic valve, this is known as a "paradoxically split S 2 ". [ 6 ]  On physical exam, paradoxical splitting is appreciated as increased splitting on expiration relative to inspiration, versus normal splitting where inspiration will increase splitting. It is seen in conditions that delay left ventricular emptying (e.g., aortic stenosis, left bundle branch block).


Sports cardiology  is an emerging subspecialty field of  Cardiology . [ 1 ] [ 2 ] [ 3 ]  It may also be considered a subspecialty field of  Sports medicine  (or Sport & Exercise Medicine), or alternatively a hybrid subspecialty that spans cardiology and  sports medicine .  Emergency medicine  is another medical specialty that has some overlap with Sports Cardiology. Sports cardiology is now considered to be a distinct subspecialty in Europe and the USA, with a core curriculum developed in both regions. [ 4 ] [ 5 ] [ 6 ]  In Europe it has traditionally been grouped under Preventive Cardiology, but the subspecialty of Sports Cardiology is now considered a distinct field. In the USA, it has developed from being a special interest area to a distinct subspecialty as well.


Sports cardiology can be roughly divided into two areas itself:


The preventive aspect of Sports Cardiology aligns slightly more with the speciality of  Sports Medicine  (doctors who look after athletes and exercising people), acute response with  Emergency medicine , whereas the management of athletes with known heart disease is more aligned with the  Cardiology  side of Sports Cardiology.
Sports Cardiology as a cardiology subspecialty overlaps with  Electrophysiology , Cardiac Stress Testing,  Echocardiography  and other cardiac imaging,  Genetic testing , and  Cardiomyopathy .


Formal education for doctors is now available in Sports Cardiology, such as a Masters Degree in Sports Cardiology at St George's, University of London [ 7 ]  and at the University of Padua, in Italy (director prof. Domenico Corrado). [ 8 ]


Sudden cardiac death  (SCD) is a very rare event but particularly tragic affecting apparently healthy young or early middle-aged people. Sudden cardiac death occurs in approximately one per 100,000 young athletes per year, generally in matches or training, but also occasionally at rest. [ 9 ]


Common categories of sudden cardiac death causes are: [ 10 ]


Cardiomyopathies and conduction diseases are responsible for the majority of sudden cardiac death in young athletes (< 30 years old), whereas Coronary artery disease (often latent in a relatively young person) increases in risk with age and is by far the most common cause of sudden cardiac death in an athlete >35 years old.  Commotio cordis  is less common but caused by an external force rather than an intrinsic abnormality of the heart. [ 11 ]


Sports have been classified into varying risks for Sudden Cardiac Death for competitive athletes. [ 12 ] [ 13 ]  Sports with high static and dynamic forces are those that present the greatest risk, bearing in mind that for individual athletes playing in these sports the risks are still very small. Rowing, cycling and basketball are amongst the sports with the highest annual risk. [ 14 ]  Football (soccer) provides the highest number of young athletes who suffer cardiac arrest, being a medium risk sport that is played extensively worldwide. The risk is higher in male athletes than female athletes. [ 15 ] [ 16 ]


Screening of athletes to prevent SCD is a controversial area. Generally, medical screening is considered to be potentially valuable for conditions or diseases that are relatively common and not useful for conditions that are rare, due to the likely high number of false positives. SCD is rare and hence screening necessarily has a high rate of false positives (that is, athletes flagged as being potentially unsafe to participate in high-level sport but who would not die if they did continue to play sport). Nevertheless, because of the fear of SCD and occupational requirement to train and compete at extremely high intensity in professional and elite sport, screening is established as a standard of care in many countries of the world. [ 17 ]
The country with the most established program of screening for cardiac disease in athletes is Italy, which requires this to be done by law. Over many decades the rate of SCD in Italy has reduced, probably due to nationwide screening. [ 18 ]  Some experts question whether the rate may have been reduced through other means, and whether the disqualification of many young people from playing vigorous sport annually is worth it. [ 19 ]


International guidelines have been agreed to regarding what constitutes a normal and abnormal athletic ECG when screening asymptomatic athletes. [ 20 ] [ 21 ]


In Europe, the UK and Australia, [ 22 ]  the standard of care is generally to include an ECG as part of the standard screening program. Whilst ECGs are done for many athletes in the USA, the standard of care is more likely to be an annual history & physical examination, with an ECG only performed if any item of concern with the clinical presentation. [ 23 ]


A major charity in the UK is  Cardiac Risk in the Young (CRY)  which performs regular screenings.


In theory, cardiac arrest at a sporting event whilst very rare can be predicted and hence the survival rate from arrest should be higher if a good emergency management plan has been implemented. Not all stadia and athletic fields have  AEDs  present, particularly at amateur level. And not all events have well-trained event staff (doctors, paramedics and staff qualified in basic life support). Finally, even with AEDs and staff present, because of the rarity of cardiac arrest in the community especially in young people, event staff may not be well or recently trained to respond, or may not be concentrating at the time of an arrest. [ 24 ]


Event planning is therefore a key component of Sports Cardiology, even though event planning would not normally be a concern of a medical speciality. Making sure that there are sufficiently trained medical, paramedical and other trained staff or volunteers at sporting events, ready availability of AEDs or ambulances or both, and that those qualified people are ready to respond to an arrest, probably leads to a greater lowering of the rates of sudden cardiac death in sport than any other measure. Hence, having an excellent understanding of the parameters of safe event planning is a core subject in Sports Cardiology. [ 25 ]


Hypertrophic cardiomyopathy (HCM) or HOCM (O = obstructive) is considered the most common cause of sudden cardiac death in young athletes that may be preventable. However, the difficulty is that it overlaps with the more  Athlete Heart syndrome  and vast majority of discovered cases are mild, making it unclear about whether it is safe to continue playing intense sport. [ 26 ]


Arrhythmogenic right ventricular cardiomyopathy (ARVC) is less common than HCM but usually more clearly progressive, associated with intense activity and usually has more clear indication to avoid highly intense sporting activities. It is more common in certain genetic backgrounds. Much of the reduction in deaths in Italy since the advent of nationwide screening has been thought to be due to ARVC reduction. [ 27 ]


Long QT syndrome is a familial condition that is uncommon but is a known source of sudden death in young people. It can cause cardiac arrest during athletic activity but also when doing other activities that raise heart rate. [ 28 ]


Brugada syndrome is a familial condition that is also very uncommon, and also a known source of sudden death in young people. Many of the deaths occur when inactive and it is less commonly a cause of sudden death playing sport. [ 29 ]


Atrial fibrillation  (AF) is more common in the inactive, elderly population than the inactive young population. There is a reverse J-shaped curve, however, in that elite athletes doing very arduous sport have a higher rate of AF than moderately active people. Whereas the AF that occurs in the inactive elderly population is known to be associated with increased risk of stroke, it is unknown whether athletic AF increases the risk of sudden death or stroke. AF in athletes can be treated with a minimally-invasive procedure known as ablation. [ 30 ]


Wolff–Parkinson–White syndrome (WPW) syndrome is a known cause of arrhythmia in young people. It causes supraventricular tachycardia during exercise. Most of the time this causes cessation of exercise when the SVT occurs. It can lead to cardiac arrest but generally does not. It can also be successfully treated by a minimally-invasive procedure known as ablation. [ 31 ] [ 32 ]


An Implantable cardioverter-defibrillators (ICD device) can be used in an athlete who has either had a previous cardiac arrest or is known to be at very high risk for cardiac arrest to trigger an internal shock to cardiovert the heart in the event of a fatal rhythm occurring. [ 33 ]


Still ' s murmur  (also known as  vibratory murmur ) is a common type of benign or "innocent"  functional heart murmur  that is not associated with any sort of cardiac disorder or any other medical condition. [ 1 ]   It can occur at any age although it is most common among children two to seven years of age and it is rare in adulthood. [ 2 ]


Still's murmur was initially described by  Dr. George Frederic Still , England's first professor of childhood medicine at the  Great Ormond Street Hospital for Children .  In his pediatric textbook Common Disorders and Diseases of Childhood (published 1909) Dr. Still noted:


“I should like to draw attention to a particular bruit which has somewhat of a musical character, but is neither of sinister omen nor does it indicate endocarditis of any sort.  …its characteristic feature is a twangy sound, very like that made by twanging a piece of tense string...  Whenever may be its origin, I think it is clearly functional, that is to say, not due to any organic disease of the heart either congenital or acquired.” [ 3 ]


Still's murmur is detected via auscultation with a  stethoscope . It has a peculiar "musical", "resonant" or "vibratory" quality that is quite unique. [ 1 ] [ 2 ]  It is generally most easily heard at the left middle or lower sternal border and the right upper sternal border, often with radiation to the carotid arteries, although other locations are common. The murmur is usually louder in the  supine position  and may only be audible in the supine position. [ citation needed ]


The Still's murmur can be differentiated from pathological murmurs by this musical quality and lack of extra snaps or  clicks  in the heart sounds.


Because the Still's murmur has never been associated with any sort of cardiac disorder, it has no associated symptoms. [ 1 ] [ 2 ]


Heart murmurs are sounds generated by blood flowing through the structures of the heart.  The location of the Still's murmur on examination suggests resonation of blood in the left ventricular outflow tract and  aorta , and this is supported by studies that have shown that the murmur is more intense over the  aortic valve  than the  pulmonary valve . [ 4 ]    There has been conjecture that the vibratory or musical quality of the murmur is caused by vibration of “false chordae” of the left ventricle, which are a common finding in normal individuals, but no relationship between the two has been proven. [ 5 ]    There is some evidence that a smaller aorta with higher peak flow velocities are associated with Still's murmur, [ 6 ] [ 7 ] [ 8 ]  which certainly fits in well with the concept that the murmur is a musical phenomenon. [ citation needed ]


Still's murmur is diagnosed in the course of a physical examination of the patient, usually using a  stethoscope .  The murmur has a vibratory quality that can be detected as a regular frequency on  phonocardiography , [ 9 ]  although this type of testing is now rarely used.  Additional testing including  electrocardiography  (ECG or EKG) or  echocardiography  may be helpful in ruling out other conditions, particularly if the physical examination is not completely characteristic of Still's murmur.  When additional testing is done in the setting of Still's murmur the results are normal, since Still's murmur is not associated with any sort of cardiovascular pathology. [ citation needed ]


Still's murmur does not represent any sort of disorder and does not present a health risk, so no treatment is necessary. [ 1 ] [ 2 ]


Still's murmurs may occur in as many as a third of all children.  This type of murmur occurs most often in children two to seven years of age, but can occur in younger or older children.  In most cases, the innocent Still's murmur is present on and off during childhood and resolves on its own by young adulthood. [ 2 ]


The Still's murmur is a harmless finding that does not suggest any medical disorder.  In most cases, Still's murmur disappears around adolescence without medical intervention. [ 2 ]


However, families are often anxious when told their child has a heart murmur.  Parents of children diagnosed with Still's murmur may experience significantly greater anxiety than the children themselves. In a study conducted on the families impacted by Still's murmur, the parents were worried about a variety of issues.  Their concerns included: the need for medicine (49%), facing sports restrictions (41%), the need for  heart surgery  (29%), other offspring also having Still's murmur (20%), and early death (13%). Mothers worried that they did something during pregnancy that caused the murmur (19%). Even after being reassured by the child's physician, 17% of parents were still anxious. After hearing from a  cardiologist  that the children would be fine, only 7% of the parents were still nervous. [ 10 ]