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9,800 | [Treatment for perioperative arrhythmias with nifekalant hydrochloride]. | Ventricular tachycardia (VT), ventricular fibrillation (VF), and atrial flutter (AFL) are potentially fatal or serious complications arising after cardiac surgery. Generally, we treat these complications with class I antiarrhythmic agents and/or direct counter shock (DC). However, sometimes these complications do not respond to antiarrhythmic agents and require frequent DC. Moreover, these class I agents induce heart failure due to their negative inotropic effect. Nifekalant hydrochloride (NIF) is a class III antiarrhythmic agent that prolongs the refractory period of the atrial and ventricular myocardium without any negative inotropic action. From July 2003 to September 2004, we treated 11 patients with NIF for perioperative arrhythmias (VT 5, VF 2, and AFL 4). NIF was administered by continuous intravenous infusion (0.3 to 0.4 mg/ kg/h) to prevent the recurrence of VT/VF and AFL. NIF prevented the recurrence of VT in 3 of the 5 cases. No recurrence was observed in 2 cases with VF. Furthermore, NIF prevented the recurrence of AFL in all the 4 patients. None of the patients exhibited changes in heart rate, cardiac output, and QTc interval. Additionally, no occurrence of Torsades de pointes was observed in any of the cases. In conclusion, NIF is an effective and safe antiarrhythmic agent for the treatment of perioperative arrhythmias under continuous monitoring of the QTc interval. |
9,801 | [Atrail fibrillation and heart failure: a complex relationship]. | Atrial fibrillation (AF) and heart failure (HF) often coexist in the same patient, not only because they can result from the same heart disease, but also because each of them can directly lead to the other. In the genesis of AF, structural, electrical and functional factors share a key role, but the importance of any of them is variable, according to the different clinical situations. AF causes atrial changes, electrical, anatomical or both, that can result in maintenance, recurrence and even irreversibility of the arrhythmia. In addition, AF affects the ventricular function by: a) loss of atrioventricular synchrony; b) irregular ventricular response; c) rapid ventricular response, possibly leading to tachycardia-induced cardiomyopathy. AF, thus, can "beget" HF, even in subjects with a previously normal heart. On the other hand, HF often "begets" AF. The prevalence of AF in patients with HF, indeed, increases from 5% (NYHA class I) to 50% (NYHA class IV). The mechanisms of HF-induced AF, include: a) increase of "critical atrial mass"; b) atrial stretch, with mechanoelectrical feedback; c) neuroendocrine changes; and d) extracellular matrix fibrosis. In brief, there is an important association between HF and development of AF and vice versa. AF-induced prognosis worsening of HF patients is not always true: in advanced HF, thus, no evidence has been obtained that the arrhythmia is associated with a decreased survival. This observation, as well as the lesson from "rhythm" versus "rate" control clinical trials, can help the management of AF in HF. The so-called "non channel target therapy" could be of value in this context. |
9,802 | [Effects of combined mitral valve replacement and radiofrequency atrial ablation in chronic atrial fibrillation]. | The aim of the study is to find out the efficacy of radiofrequency catheter atrial ablation (RF) simultaneously done with mitral valve replacement (MVR) surgery in patients having rheumatic mitral valve disease with chronic atrial fibrillation and to evaluate the short-term postoperative results.</AbstractText>Seventeen patients underwent MVR surgery, and intraoperative RF procedures were done simultaneously with MVR to eight of these patients, whereas remaining nine of them were assigned to control group. Patients were assessed preoperatively, at time of discharge, and 1st, 6th and 12th months controls. Atrial and ventricular functions were evaluated with echocardiography, serum atrial natriuretic peptide (ANP) levels were investigated and electrocardiograms were recorded in all patients.</AbstractText>Demographically there were no significant differences between two groups. Radiofrequency ablation group had longer aortic cross-clamping and cardiopulmonary bypass times. Sinus rhythm was established in seven patients of RF group at postoperative 12th month. However, all patients of this group experienced sinus rhythm at postoperative sixth month whereas 'atrial kick' was detected in five of them. Significantly increased ejection fraction, decreased pulmonary artery pressure and decreased left atrial diameter were observed in RF group compared to control group. Serum ANP levels were found to be significantly decreased as compared to preoperative periods in both groups.</AbstractText>Although RF ablation has higher costs, this technique is efficient and useful to restore the sinus rhythm and to recover the atrial functions back in patients having rheumatic mitral valve disease.</AbstractText> |
9,803 | Evaluation of left ventricular function using Tei index in patients with preinfarction angina. | The study investigated whether preinfarction angina influences left ventricular functions assessed using Tei index, which is an independent predictor for left ventricular dysfunction in acute myocardial infarction.</AbstractText>We studied 96 patients with acute myocardial infarction with ST segment elevation (80 men, 16 women; mean age 57.5+/-9.9 years) who were assigned into 2 groups: with and without preinfarction angina. All patients were serially evaluated by 2-dimensional and Doppler echocardiography on the days 1, 6, and 30, and were followed up for 30 days for incidence of complications.</AbstractText>We observed that Tei index was lower on the days 1, 6 and 30 (0.49+/-0.20 vs. 0.59+/-0.20, p=0.003, 0.46+/-0.20 vs. 0.56+/-0.20, p=0.001, 0.44+/-0.20 vs. 0.53+/-0.10, p=0.01) in patients with preinfarction angina as compared with those without angina. Tei index significantly decreased during follow-up (0.49+/-0.20, 0.46+/-0.20, 0.44+/-0.20; p=0.02) in patients with preinfarction angina, while it did not change significantly in patients without preinfarction angina (p=0.2). Echocardiographically significant improvements were observed in E deceleration time, isovolumic relaxation time and ejection time in all patients, whereas significant improvements in ejection fraction, wall motion score index and isovolumic contraction time were observed only in patients with preinfarction angina during follow-up. Mortality, Killip class >or=2, pericarditis, atrial fibrillation, and left ventricular thrombus were lower in patients with preinfarction angina.</AbstractText>These data indicated that the patients with preinfarction angina had better preserved systolic left ventricular function and Tei index values. Also, it was observed that preinfarction angina may cause earlier and more prominent myocardial functional recovery and confer protection against complications on short-term after first acute myocardial infarction.</AbstractText> |
9,804 | Continuation of amiodarone therapy despite type II amiodarone-induced thyrotoxicosis. | Amiodarone is a powerful antiarrhythmic drug; however, its use may be complicated by thyrotoxicosis. When this occurs, clinicians must balance the continuation of amiodarone for antiarrhythmic purposes, and the discontinuation of treatment in order to prevent aggravation of the thyrotoxicosis. We studied the consequences of continuation or cessation of amiodarone in patients with type II amiodarone-induced thyrotoxicosis.</AbstractText>Consecutive patients who developed type II amiodarone-induced thyrotoxicosis between September 1997 and September 2000 were studied. Amiodarone was continued in patients with previous ventricular arrhythmia or supraventricular arrhythmia associated with severe haemodynamic changes and was withdrawn in the other patients. In patients with persistent, severe symptomatic thyrotoxicosis, corticosteroids were added to therapy.</AbstractText>Thirteen patients were studied (nine with previous atrial fibrillation/flutter and four with ventricular tachycardia). Amiodarone treatment was continued in ten patients, including eight patients who received corticosteroids, and was temporarily halted in three patients. All patients recovered, with no difference in the duration of thyrotoxicosis between the two groups. Corticosteroid treatment was well tolerated and seemed to hasten the return to a euthyroid state (mean of 3.7 +/- 0.7 months vs 6.3 +/- 1.7 months). No recurrence of hyperthyroidism occurred during long-term follow-up.</AbstractText>In patients who require amiodarone, treatment may be safely continued despite the development of type II amiodarone-induced thyrotoxicosis.</AbstractText> |
9,805 | The use of amiodarone for in-hospital cardiac arrest at two tertiary care centres. | Although amiodarone significantly increases survival to hospital admission when used in resuscitation of out-of-hospital pulseless ventricular tachycardia and fibrillation, there are limited data on its utility for in-hospital arrests.</AbstractText>To determine whether the use of amiodarone, as recommended by the year 2000 American Heart Association Advanced Cardiac Life Support guidelines, improved survival following its introduction to the resuscitation algorithm at two tertiary care institutions.</AbstractText>Charts of 374 cardiac resuscitations were retrospectively studied at the two institutions. Basic survival outcomes and demographic data were recorded for cardiac arrests with ventricular tachyarrhythmias qualifying for administration of antiarrhythmic agents.</AbstractText>Qualifying rhythms were present in 95 patients. Clinical uptake of amiodarone was limited. In the 36 patients who received amiodarone, survival of resuscitation was 67% versus 83% (P=0.07) in the 59 patients receiving only other antiarrhythmic agents (chiefly lidocaine [94%]), while survival to discharge was 36.1% and 55.9% (P=0.06) in these two groups, respectively.</AbstractText>Following two years' experience with the introduction of intravenous amiodarone for resuscitation in the institutions, use was less than 50% and no clinically observable survival benefit could be documented. Possible explanations for the difference between this experience and that found in out-of-hospital resuscitation trials include differing patient populations and operator bias during resuscitation. These results should provoke other institutions to question whether amiodarone has improved survival of cardiac arrest under the conditions prevailing in their hospitals. A patient registry or prospective, randomized trial will be required to assess what parameters affect the success of intravenous amiodarone for resuscitation in-hospital.</AbstractText> |
9,806 | Gemcitabine and atrial fibrillation: a rare manifestation of chemotherapy toxicity. | Gemcitabine is a purine analog with known activity in many solid tumors, namely lung, breast, pancreatic, genitourinary and head/neck cancers. Cardiac toxicity is a rare event and only one report previously described atrial fibrillation (AF) as a consequence of gemcitabine infusion. We report two cases of women suffering from lung cancer who were treated with gemcitabine. Both patients were admitted to hospital for paroxysmal AF occurring 12-24 h after the infusion of the drug. In the first case a sinus rhythm was spontaneously repristinated when AF occurred for the first time, while the second episode required an anti-arrhythmic drug to interrupt the dysrhythmia. In the second case, the patient had to be treated with digitalis glycoside to control the ventricular response without attaining a sinus rhythm. We could not recognize any other precipitating factor beyond the infusion of gemcitabine as a cause for the arrhythmia. Both cases were treated with gemcitabine for lung cancer and we observed the appearance of AF less than 24 h after drug administration. We assume that 2',2'-difluorodeoxyuridine, an active metabolite of gemcitabine, could be responsible for the toxic effect. We conclude that AF is an unusual, but potentially dangerous, side-effect of gemcitabine infusion. The arrhythmia should be suspected whenever patients complain of dyspnea and palpitations beginning 12-24 h after treatment. In these cases, the treatment of AF consists of anti-arrhythmic drugs in order to repristinate a sinus rhythm or control the heart rate. |
9,807 | Large emboli on their way through the heart - first live demonstration of large paradoxical embolisms through a patent foramen ovale. | We report a case of large paradoxical embolisms through a patent foramen ovale in a patient with acquired heparin-induced thrombocytopenia type II (HIT). One large ventricular thrombus embolizing through the aortic valve was documented on videotape for the first time while performing transesophageal echocardiography. A 56-year-old man was admitted with acute respiratory failure initially believed to have an exacerbated chronic obstructive pulmonary disease. Arterial oxygen saturation was only 33%. He received antibiotic and anti-obstructive treatments and was mechanically ventilated for 7 days. Few hours after extubation, he developed recurrent severe dyspnea accompanied by acute pain and pulselessness in his left leg. Transthoracic echocardiography revealed an enlarged right ventricle and suggested the presence of free-floating thrombi both in the right and in the left-heart cavities. During transesophageal echocardiography, a large serpentine left-heart thrombus embolized through the aortic valve and disappeared. The patient developed ventricular fibrillation and underwent successful cardiopulmonary resuscitation including emergency thrombolysis with alteplase. Four hours later, the surgeon retrieved a 20-cm long thrombus from the left femoral artery. |
9,808 | Pulmonary hypertension and predominant right heart failure in thyrotoxicosis. | In this report we discuss a patient with predominant right heart failure and pulmonary hypertension, caused by thyrotoxicosis due to Graves disease, which deteriorated to asystole, due to amiodarone administration for rapid atrial fibrillation. |
9,809 | Outcome and characteristics of out-of-hospital cardiac arrest according to location of arrest: A report from a large-scale, population-based study in Osaka, Japan. | To evaluate the outcome and the factors concerned with of out-of-hospital cardiac arrest patients according to the location of the collapse.</AbstractText>From May 1st, 1998 to April 30th, 2001, 15,211 consecutive out-of-hospital cardiac arrest cases considered for resuscitation were recorded. Of these cases 7540 arrests in subjects aged 18 years or older with cardiac aetiology were analyzed. The outcome and the related-factors, particularly incidence of ventricular fibrillation, were evaluated according to the location of the cardiac arrest. To analyze the factors that affect the incidence of ventricular fibrillation, a logistic regression model was used.</AbstractText>About three-quarters of out-of-hospital cardiac arrests occurred at private residences. The outcome and characteristics were significantly different according to the location of the arrest. Arrest patients in public or in the work place had a higher chance of being found in ventricular fibrillation and survival than those at a private residence. The multivariate adjusted odds ratios for ventricular fibrillation in a public or work place were significantly higher than that in private residences, after adjusting for covariates affecting initial rhythm, such as age, sex, witnessed status, bystander cardiopulmonary resuscitation, and response interval.</AbstractText>Although the majority of out-of-hospital cardiac arrests occur at private residences, arrests in public or in the work place had a higher chance of being found in ventricular fibrillation and survival than those at private residences. In order to establish a system to improve the outcome of out-of-hospital cardiac arrest, a well-considered strategy considering the location of arrest is necessary.</AbstractText> |
9,810 | Utility of N terminal pro brain natriuretic peptide in elderly patients. | To evaluate the utility of N terminal pro brain natriuretic peptide (NT-proBNP) as a diagnostic marker for diastolic dysfunction or failure, systolic dysfunction, and significant valve disorders in patients over 75 years.</AbstractText>Cohort study.</AbstractText>Outpatient echocardiography service in a district general hospital.</AbstractText>100 consecutive patients.</AbstractText>Sensitivity, specificity, positive predictive values, negative predictive values, and area under receiver operating characteristic curve for NT-proBNP assay in the diagnosis of left ventricular diastolic dysfunction or failure, systolic dysfunction, and significant valve disorders.</AbstractText>For diagnosis of systolic dysfunction NT-proBNP level of 424 pg/ml had a sensitivity of 96%, specificity of 45%, positive predictive value of 36%, and negative predictive value of 96%. The area under the curve was 0.71 (95% confidence intervals: 0.69 to 0.89). In valve heart disease, level of 227 pg/ml had sensitivity of 91%, specificity of 43%, positive predictive value of 40%, and negative predictive value of 92%. Patients with diastolic dysfunction/failure had lower plasma concentrations.</AbstractText>This study showed that NT-proBNP had excellent negative predictive value for systolic dysfunction and significant valve disorders in very elderly patients. It increased significantly in systolic dysfunction, valve heart disease, and atrial fibrillation. NT-proBNP is not useful in the diagnosis of diastolic dysfunction or diastolic heart failure using standard echocardiography criteria.</AbstractText> |
9,811 | Progress in cardiovascular disease: technical considerations in cardiac resynchronization therapy. | Cardiac resynchronization therapy (CRT) has been shown to improve symptoms, ventricular function, and survival in patients with left ventricular systolic dysfunction and ventricular conduction delay. Patients with moderate to severe drug-refractory heart failure symptoms along with ventricular dyssynchrony, manifested as prolongation of the QRS duration on the surface electrocardiogram, benefit from CRT. Owing to the growing awareness and application of CRT, a large number of patients have been identified as candidates for this therapy, making it necessary for clinicians involved in the care of such patients to be adequately knowledgeable of various aspects of CRT implementation. In particular, clinicians involved in the care of these patients must be aware of the practical considerations in preparing patients for the implantation procedure, careful surveillance for early or late procedure-related complications, and knowledge of the fundamental device features so as to tailor therapeutic and programming techniques to improve long-term response to CRT. This review addresses the technical considerations of the implantation procedure and device function with emphasis on the initial and long-term programming to ensure optimal delivery of CRT. |
9,812 | Challenging the rationale of three sequential shocks for defibrillation. | The 2000 guidelines for cardiopulmonary resuscitation (CPR) recommend up to three sequential shocks for persistent ventricular fibrillation (VF). We hypothesized that the time consumed for repetitive rhythm analyses and recharging of the capacitor compromises the success of the second and third shock of each sequence. In 60 domestic pigs, VF was electrically induced and untreated for 7 min. After 1 min of CPR, which includes precordial compression and ventilation, up to three sequential shocks were delivered. All animals were resuscitated. For purposes of the present study we determined the outcomes of the first, the second, and the third shock of each sequence during attempted defibrillation. Our criterion of success was the restoration of spontaneous circulation (ROSC). Forty-eight of the 60 animals (80%) attained ROSC after the first shock, 9/60 (15%) after the second shock, and only 3/60 (5%) after the third shock. In confirmation of the earlier observations, ROSC was highly predictive when the coronary perfusion pressure (CPP) exceeded 12 mmHg and end-tidal CO(2) (ETCO(2)) exceeded 11 mmHg. However, these criteria were never achieved after the second shock. The present study supports the rationale of delivering only a single shock, or at the most two shocks, prior to resuming chest compression, to re-establish the threshold levels of CPP and ETCO(2) before delivery of a subsequent electrical shock. |
9,813 | [Resuscitation from accidental hypothermia of 22 degrees C with circulatory arrest: importance of prehospital management]. | In winter, French Medicalised Ambulance Service rescued a 50-year-old patient after suicide attempts by jump from a bridge in the Seine. The body was discovered after more than 10 minutes of immersion. She was unconscious and in deep hypothermia with circulatory arrest. Basic CPR was started immediately and oral intubation and 100% oxygen ventilation was performed. Ventricular fibrillation appeared but repeated defibrillation failed due to profound hypothermia (rectal temperature: 28 degrees C). The patient was immediately transported to hospital. CPR and mechanical ventilation was continued during transport. The patient was taken in emergency room. The oesophageal temperature was 22 degrees C. Rewarming using extracorporeal circulation was immediately initiated after insertion of femoral access. At 27 degrees C, ventricular fibrillation started and was converted by external defibrillation to a pulse-generating cardiac rhythm. At 360 minutes, the patient's rectal temperature had reached 36 degrees C and she was disconnected from cardiopulmonary bypass with inotropic support. She was transferred to the intensive care unit after 9 hours of resuscitation, rewarming and stabilisation. Mechanical ventilation was needed for 15 days because of adult respiratory distress syndrome. Renal failure, pneumonia also occurred. She was successfully extubated on day 15 and was discharged from intensive care unit on day 21, suffering no neurological side effects. |
9,814 | Pharmacologic approaches to rhythm versus rate control in atrial fibrillation--where are we now? | Until recently, contemporary drug treatment of atrial fibrillation (AF) focused primarily on restoration and maintenance of sinus rhythm, predicated on the belief that if AF is abolished then problems associated with AF would be abolished too. Recently completed clinical trials using drug therapy and comparing maintenance of sinus rhythm with control of ventricular rate have challenged this assumption, showing that simple control of ventricular rate with anticoagulation is an acceptable primary therapy, notably in older patients with persistent AF, minimally symptomatic or asymptomatic, and at increased risk for thromboembolic events. However, rate control and anticoagulation is not a panacea; existing trial results should not be interpreted to mean all patients should be treated with the rate control approach. Despite the limited efficacy and poor safety of current antiarrhythmic drugs, strategies for maintenance of sinus rhythm remain justified in many patients, such as those with first-episode AF, highly symptomatic patients, younger patients, and those with a history of congestive heart failure (CHF). Commonly used current and some investigational agents designated for "rhythm control" have enough pharmacologic overlap with rate control agents to be considered to have a dual mode of action, simultaneously addressing both rhythm and rate control. Furthermore, there is much interest in non-pharmacologic therapies, such as radiofrequency ablation, for rhythm control. The lack of appropriately designed and controlled trials at this time makes it difficult to determine the place of radiofrequency ablation and its impact on the rhythm versus rate question. |
9,815 | Profound metoprolol-induced bradycardia precipitated by acetaminophen-propoxyphene. | Pharmacokinetic studies demonstrate that propoxyphene is a potent inhibitor of cytochrome P450 (CYP) 2D6. Clinically significant sequelae have not been previously reported. We report a case of this inhibition manifested by life-threatening bradycardia in a patient receiving a CYP2D6 substrate, metoprolol. A 48-year-old man came to the emergency department complaining of dizziness 3 hours after ingesting metoprolol, at his usual dose, and 2 tablets of propoxyphene, newly begun postoperatively. Four hours after ingestion of both drugs, the patient was noted to have a ventricular rate of about 30 beats/min with underlying atrial fibrillation. The patient's ventricular response returned to normal within 11 hours of ingestion. We have demonstrated the clinical importance of the interaction between propoxyphene and metoprolol likely resulting from inhibition of hepatic clearance of metoprolol by propoxyphene. Underscoring the clinical relevance of CYP2D6 inhibition by an analgesic of questionable efficacy should proscribe its use. |
9,816 | Influence of cardiac-resynchronization therapy on heart rate and blood pressure variability: 1-year follow-up. | Several studies have shown that cardiac-resynchronization therapy (CRT) improves haemodynamic function, cardiac symptoms, and heart rate variability (HRV) and reduces the risk of mortality and sudden death in subjects with chronic heart failure (CHF). In subjects with CHF, power spectral values for the low-frequency (LF) component of RR variability < or =13 ms2, are associated with an increased risk of sudden death.</AbstractText>To assess whether spectral indexes obtained by power spectral analysis of HRV and systolic blood pressure (SBP) variability could predict malignant ventricular arrhythmias in patients with severe CHF treated with an implantable cardioverter-defibrillator (ICD) alone or with ICD+CRT. In addition, changes in non-invasive spectral indices using short-term power spectral analysis of HRV and SBP variability during controlled breathing in 15 patients with CHF treated with an ICD alone and 16 patients receiving ICD+CRT, were assessed pre-treatment and at 1 year.</AbstractText>Arrhythmias necessitating an appropriate ICD shock were more frequent in subjects who had low LF power. CRT improved all spectral components, including LF power.</AbstractText>Low LF power values predict an increased risk of malignant ventricular arrhythmias; after 1 year of CRT most non-spectral and spectral data, including LF power, improved. Whether these improvements lead to better long-term survival in patients with CHF remains unclear.</AbstractText> |
9,817 | Acute coronary artery occlusion following intravascular ultrasound examination.<Pagination><StartPage>422</StartPage><EndPage>423</EndPage><MedlinePgn>422-3</MedlinePgn></Pagination><Abstract><AbstractText>Intravascular ultrasound is considered as having few complications, most of them are just a transient coronary spasm. However, we experienced one case of acute left anterior descending coronary artery occlusion following an intravascular ultrasound study during the intervention and this was treated successfully with cardiopulmonary resuscitation and stent implantation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nam</LastName><ForeName>Chang-Wook</ForeName><Initials>CW</Initials></Author><Author ValidYN="Y"><LastName>Hur</LastName><ForeName>Seung-Ho</ForeName><Initials>SH</Initials></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Seong-Wook</ForeName><Initials>SW</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Young-Soo</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Kee-Sik</ForeName><Initials>KS</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Yoon-Nyun</ForeName><Initials>YN</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Kwon-Bae</ForeName><Initials>KB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016422">Letter</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Cardiol</MedlineTA><NlmUniqueID>8200291</NlmUniqueID><ISSNLinking>0167-5273</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000208" MajorTopicYN="N">Acute Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015906" MajorTopicYN="N">Angioplasty, Balloon, Coronary</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003327" MajorTopicYN="N">Coronary Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018084" MajorTopicYN="N">Ultrasonography, Interventional</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>3</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2005</Year><Month>3</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>3</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>8</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>3</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16513193</ArticleId><ArticleId IdType="doi">10.1016/j.ijcard.2005.03.063</ArticleId><ArticleId IdType="pii">S0167-5273(05)00611-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16510914</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2008</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>130</Issue><PubDate><Year>2006</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal>[Prevention of paroxysms of atrial fibrillation in old and senile patients]. | Intravascular ultrasound is considered as having few complications, most of them are just a transient coronary spasm. However, we experienced one case of acute left anterior descending coronary artery occlusion following an intravascular ultrasound study during the intervention and this was treated successfully with cardiopulmonary resuscitation and stent implantation.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nam</LastName><ForeName>Chang-Wook</ForeName><Initials>CW</Initials></Author><Author ValidYN="Y"><LastName>Hur</LastName><ForeName>Seung-Ho</ForeName><Initials>SH</Initials></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Seong-Wook</ForeName><Initials>SW</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Young-Soo</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Kee-Sik</ForeName><Initials>KS</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Yoon-Nyun</ForeName><Initials>YN</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Kwon-Bae</ForeName><Initials>KB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016422">Letter</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Cardiol</MedlineTA><NlmUniqueID>8200291</NlmUniqueID><ISSNLinking>0167-5273</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000208" MajorTopicYN="N">Acute Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015906" MajorTopicYN="N">Angioplasty, Balloon, Coronary</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003327" MajorTopicYN="N">Coronary Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018084" MajorTopicYN="N">Ultrasonography, Interventional</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>3</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2005</Year><Month>3</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>3</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>8</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>3</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16513193</ArticleId><ArticleId IdType="doi">10.1016/j.ijcard.2005.03.063</ArticleId><ArticleId IdType="pii">S0167-5273(05)00611-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16510914</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2008</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>130</Issue><PubDate><Year>2006</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal><ArticleTitle>[Prevention of paroxysms of atrial fibrillation in old and senile patients].</ArticleTitle><Pagination><StartPage>57</StartPage><EndPage>61</EndPage><MedlinePgn>57-61</MedlinePgn></Pagination><Abstract>It is known that the atrial fibrillation is a sorrow "privilege" of the senile groups of people. The aim of the given paper was to study the reasons of atrial fibrillation arising in old (60-74 years) and senile (75-89 years) patients and possibility of prevention paroxysms of atrial fibrillation and its complications with help of prolonged selective beta-blocker egilok retard pro daily doses 50-100 mg. The results which were received after the examination and treatment of 147 patients who were under stationary and dispensary treatment at the Research Institute of Experimental and Clinical therapy for 12 months. We have achieved full absence of paroxysmal atrial fibrillation in 89.8% patients (132 patients). The use of egilok retard gives stable hypotensive effect in old and senile patients, provides the regression of the left ventricular hypertrophy with improvement of its parameters and diastolic function, which is especially important for the studied contingent of the patients. |
9,818 | Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. | Sudden cardiac death that results from chest wall blows (commotio cordis) the second leading cause of death in young athletes. Most events are caused by blows from projectiles, such as baseballs or lacrosse balls, with a substantial proportion occurring despite the use of a chest protector. In the present experiment, we tested the effectiveness of commercially available chest protectors in preventing ventricular fibrillation (VF) that results from chest wall strikes with baseballs and lacrosse balls.</AbstractText>Twelve different baseball or lacrosse chest protectors were evaluated in juvenile swines that were subjected to 40-mph baseball or lacrosse ball blows to the precordium during the vulnerable period of repolarization for VF and were compared with control impacts without chest protectors. Seven baseball chest protectors were hit by regulation baseballs, and 5 lacrosse chest protectors were tested by blows with standard lacrosse balls. Each animal received 2 chest blows for each protector and 2 control impacts without a chest protector, with the sequence of impacts assigned randomly.</AbstractText>VF was elicited by 12 (32%) of 37 strikes in control animals without baseball chest protectors. None of the baseball chest wall protectors tested were shown to decrease significantly the occurrence of VF when compared with controls. VF was elicited by 11 (46%) of 24 strikes in control animals without lacrosse chest protectors. None of the lacrosse chest wall protectors tested decreased significantly the occurrence of VF when compared with controls.</AbstractText>In our experimental animal model of commotio cordis, commercially available baseball and lacrosse chest wall protectors were ineffective in protecting against VF that was triggered by chest blows and, by inference, sudden cardiac death. Improvements in materials and design of chest wall barriers are necessary to reduce the occurrence of these tragic events and make the athletic field safer for youths.</AbstractText> |
9,819 | Obesity in diabetic patients undergoing coronary artery bypass graft surgery is associated with increased postoperative morbidity. | Despite the fact that obesity is a known risk factor for cardiovascular disease, many studies have failed to demonstrate that obesity is independently associated with an increased risk of cardiovascular morbidity and mortality in nondiabetic patients undergoing coronary artery bypass graft surgery. The authors investigated the influence of obesity on adverse postoperative outcomes in diabetic and nondiabetic patients after primary coronary artery bypass surgery.</AbstractText>A retrospective cohort study of patients undergoing primary coronary artery bypass surgery (n = 9,862) between January 1995 and December 2004 at the Texas Heart Institute was performed. Diabetic (n = 3,374) and nondiabetic patients (n = 6,488) were classified into five groups, according to their body mass index: normal weight (n = 2,148), overweight (n = 4,257), mild obesity (n = 2,298), moderate obesity (n = 785), or morbid obesity (n = 338). Multivariate, stepwise logistic regression was performed controlling for patient demographics, medical history, and preoperative medications to determine whether obesity was independently associated with an increased risk of adverse postoperative outcomes.</AbstractText>Obesity in nondiabetic patients was not independently associated with an increased risk of adverse postoperative outcomes. In contrast, obesity in diabetic patients was independently associated with a significantly increased risk of postoperative respiratory failure (odds ratio [OR], 2.26; 95% confidence interval [CI], 1.41-3.61; P < 0.001), ventricular tachycardia (OR, 2.27; 95% CI, 1.18-4.35; P < 0.02), atrial fibrillation (OR, 1.56; 95% CI, 1.03-2.38; P < 0.04), atrial flutter (OR, 2.38; 95% CI, 1.29-4.40; P < 0.01), renal insufficiency (OR, 1.66; 95% CI, 1.10-3.41; P < 0.03), and leg wound infection (OR, 5.34; 95% CI, 2.27-12.54; P < 0.001). Obesity in diabetic patients was not independently associated with an increased risk of mortality, stroke, myocardial infarction, sepsis, or sternal wound infection.</AbstractText>Obesity in diabetic patients is an independent predictor of worsened postoperative outcomes after primary coronary artery bypass graft surgery.</AbstractText> |
9,820 | Can heart rate variation rule out sleep-disordered breathing in heart failure? | In patients with obstructive sleep apnoea (OSA), the very low frequency power spectral density index (VLFI) derived from analysis of heart rate correlates with the severity of obstructive apnoeas. VLFI is also associated with Cheyne-Stokes respiration/central sleep apnoea (CSR/CSA) in congestive heart failure (CHF). The present authors have tested the hypothesis that per cent VLFI, derived from a standard Holter ECG recording, can be used to detect the presence of OSA and CSR/CSA in patients with mild-to-moderate CHF. In total, 60 CHF patients underwent polysomnography with monitoring of heart rate. Data from 33 patients were analysed for per cent VLFI. Of the 60 patients, 27 were excluded due to atrial fibrillation, extensive pacing or frequent ventricular extra systoles. Receiver operator characteristic curves were constructed to establish the per cent VLFI that would optimally identify the presence or absence of sleep-disordered breathing. Using an apnoea-hypopnoea index>20 events.h-1 and setting the per cent VLFI at 2.23% yielded a sensitivity of 85%, specificity of 65%, positive predictive value of 61% and a negative predictive value of 87%. The latter increased to 100% when using an apnoea-hypopnoea cut-off of 30 events.h-1. In conclusion, these results suggest that spectral analysis of heart rate may be useful as a "rule-out test" for sleep-disordered breathing in patients with mild-to-moderate congestive heart failure. |
9,821 | Previously known and newly diagnosed atrial fibrillation: a major risk indicator after a myocardial infarction complicated by heart failure or left ventricular dysfunction. | To characterize the relationship between known and newly diagnosed atrial fibrillation (AF) and the risk of death and major cardiovascular (CV) events in patients with acute myocardial infarction (MI) complicated by heart failure (HF) and/or left ventricular systolic dysfunction (LVSD).</AbstractText>The VALIANT trial enrolled 14,703 individuals with acute MI complicated by HF and/or LVSD. AF was assessed at presentation and at randomization (median 4.9 days after symptom onset). Primary outcomes were risk of death and major CV events 3 years following acute MI.</AbstractText>A total of 1812 with current AF (AF between presentation and randomization), 339 patients with prior AF (history of AF without current AF), and 12,509 without AF were enrolled. Patients with AF were older; had more prior HF, angina, and MI, and received beta-blockers and thrombolytics less often than those without AF. Three-year mortality estimates were 20% in those without AF, 37% with current AF, and 38% with prior AF. Compared with patients without AF, the multivariable adjusted HR of death was 1.25 (1.03-1.52; p=0.03) for prior AF and 1.32 (1.20-1.45; p<0.0001) for current AF. HR for major CV events was 1.15 (0.98-1.35; p=0.08) and 1.21 (1.12-1.31; p<0.0001).</AbstractText>AF is associated with greater long-term mortality and adverse CV events with acute MI complicated by HF or LVSD.</AbstractText> |
9,822 | Monitoring of cerebral oxygenation with near infrared spectroscopy and tissue oxygen partial pressure during cardiopulmonary resuscitation in pigs. | The present study was designed to compare cerebral oxygenation measured with near infrared spectroscopy and local brain tissue oxygen partial pressure, respectively, in pigs during cardiopulmonary resuscitation. Since tissue overlying the brain may have an impact on near infrared spectroscopy readings, we tested whether optode placement on intact skin or on the skull yielded comparable results.</AbstractText>Twelve healthy pigs were anaesthetized and subjected to continuous haemodynamic, near infrared spectroscopy and brain tissue oxygen partial pressure monitoring. After 4 min of untreated ventricular fibrillation, cardiopulmonary resuscitation was started and arginine vasopressin was administered repeatedly three times. Near infrared spectroscopy values recorded were both the tissue oxygenation index and the tissue haemoglobin index as well as relative changes of chromophores (haemoglobin and cytochrome oxidase). Four animals served as control and were measured with both near infrared spectroscopy optodes mounted on the intact skin of the forehead, while in the remaining eight animals, one near infrared spectroscopy optode was implanted directly on the skull.</AbstractText>Near infrared spectroscopy readings at the skin or at the skull differed consistently throughout the study period. After arginine vasopressin administration, near infrared spectroscopy values at the different locations showed a transient dissociation. In contrast to near infrared spectroscopy measured on intact skin, near infrared spectroscopy readings obtained from skull showed a significant correlation to brain tissue oxygen partial pressure values (r = 0.67, P < 0.001).</AbstractText>Near infrared spectroscopy readings obtained from skin and skull differed largely after vasopressor administration. Near infrared spectroscopy optode placement therefore may have an important influence on the tissue region investigated.</AbstractText> |
9,823 | Biventricular pacing reduces ventricular arrhythmic burden and defibrillator therapies in patients with heart failure. | Cardiac resynchronization therapy (CRT) has recently emerged as a new modality for the treatment of patients with advanced heart failure (HF).</AbstractText>Cardiac resynchronization therapy reduces atrial and ventricular arrhythmia burdens.</AbstractText>We analyzed the clinical data of patients who underwent an upgrade from a dual-chamber to a biventricular implantable cardioverter-defibrillator (ICD) at a tertiary care center.</AbstractText>Nineteen patients (age 67 +/- 10 years, 18 men, left ventricular [LV] ejection fraction 0.24 +/- 0.07) underwent an upgrade to CRT-ICD. The LV lead was placed in a lateral position in 11, posterolateral in 4, and anterolateral in 3 patients. Baseline New York Heart Association class of HF improved in 11 (58%) patients who were considered "responders." After adjusting for the duration of follow-up before and after the upgrade, the number of patients receiving any ICD therapy decreased significantly from 13 to 4 (p = 0.004) and the total number of therapies decreased from 72 to 17 (p = 0.067). Also, the number of detections of sustained ventricular arrhythmias decreased from 40 to 11 episodes (p = 0.05), but the decrease in the number of detected supraventricular arrhythmias and mode switch episodes was not significant. The reduction in the ventricular arrhythmia load was independent of whether or not the patient responded to CRT.</AbstractText>Our data suggest that CRT reduces ventricular but not atrial arrhythmia burden in patients with HF irrespective of their clinical response. This suggests that the reduction in arrhythmia is primarily an electrical phenomenon. Further studies are needed to confirm these findings and to uncover their underlying mechanisms.</AbstractText> |
9,824 | Noncardiac surgery and the risk of death and other cardiovascular events in patients with hypertrophic cardiomyopathy. | There is a paucity of reports evaluating the perioperative risk of noncardiac surgery in patients with hypertrophic cardiomyopathy (HCM).</AbstractText>The study was undertaken to evaluate the incidence of acute myocardial infarction (MI) and all-cause inhospital mortality following noncardiac surgery in patients with HCM.</AbstractText>We searched the National Hospital Discharge Survey database for patients with a diagnosis of HCM who had undergone noncardiac surgery. Cases were matched by age, gender, and year of surgery. Death or acute MI were used as endpoints for analysis.</AbstractText>From 1996 to 2002, 227 patients with HCM were matched with 554 controls (representing national estimates of 25,874 HCM and 50,326 controls patients). Patients with HCM were more likely than controls to have a history of atrial fibrillation (22.7 vs. 10.6%, p < 0.001) and of congestive heart failure (CHF) (24.2 vs. 14.1%, p < 0.001). The in-hospital incidence of death or MI was higher in patients with HCM than in controls (6.7 vs. 2.5%, p < 0.001 for death and 2.2 vs. 0.3%, p < 0.001 for MI). After correcting for age, gender, race, presence of hypertension, diabetes mellitus, history of coronary artery-disease, history of CHF, atrial fibrillation, and ventricular arrhythmias in a multivariate binary logistic regression model, the presence of HCM increased the odds of death by 61% (odds ratio [OR] = 1.61, 95% confidence interval [CI] 1.46-1.77, p < 0.001), and almost tripled the odds of the combined endpoint of death or MI (OR = 2.82, 95% CI 2.59-3.07, p < 0.001).</AbstractText>The presence of HCM significantly increases the risk of death and MI associated with noncardiac surgery. Patients with HCM undergoing elective procedures may require more careful preoperative assessment and perioperative monitoring. The impact of the severity of HCM on outcomes of noncardiac surgery needs further study.</AbstractText> |
9,825 | Health-related quality of life relative to clinical outcomes in patients with atrial fibrillation treated with ventricular rate stabilisation pacing. | It is uncertain whether patient perception of atrial fibrillation (AF) is based on the fast ventricular rate as such or the irregularity of the ventricular responses. This trial was designed to confirm the effectiveness of a ventricular rate stabilisation (VRS) algorithm in reducing ventricular irregularity during permanent pacing in patients with AF and to assess the patient preference and effect on quality of life (QoL).</AbstractText>In this multicentre single-blind randomised crossover trial, 184 patients with drug-refractory permanent (n=91) or paroxysmal (n=93) AF received a VVI(R) or DDD(R) pacemaker respectively and were paced in a randomised sequence with VRS on or off for two months. Clinical assessments (QoL, New York Heart Association (NYHA) classification, echocardiography, six-minute walk test and Holter recording) were carried out at baseline, at randomisation and after each crossover period. QoL assessment was performed using Aquarel, a new disease-specific QoL questionnaire for pacemaker patients, the Short Form 36 survey (SF-36), the Duke Activity Status Index (DASI) and the Symptom Checklist frequency and severity scores. At the end of the study patients preferences for VRS-on or VRS-off were recorded.</AbstractText>VRS pacing reduced ventricular irregularity without increasing the mean ventricular rate. VRS-on was preferred by 65.8% of patients with paroxysmal AF; patients with permanent AF had no preference. QoL did not show improvement during VRS pacing on any of the instruments.</AbstractText>VRS pacing is effective in reducing ventricular rhythm irregularity. QoL does not improve during VRS pacing but preference for VRS pacing appears particularly outspoken for patients with paroxysmal AF.</AbstractText> |
9,826 | Ventricular tachycardia in arrhythmogenic right ventricular dysplasia/cardiomyopathy: clinical presentation, risk stratification and results of long-term follow-up. | Not all patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) are at risk for sudden cardiac death. The aim of the study was to evaluate the risk stratification in patients with ARVD/C.</AbstractText>Programmed ventricular stimulation (PVS) was performed in 34 ARVD/C patients. Twenty-two, 7 and 4 patients had documented sustained monomorphic ventricular tachycardia (smVT), non-smVT and ventricular fibrillation, respectively. One patient experienced syncope only. An implantable cardioverter defibrillator (ICD) was implanted in 11 patients inducible in smVT with hemodynamic compromise, in 4 patients with documented ventricular fibrillation and in one patient with non-smVT (194 ms tachycardia cycle length) (ICD group, n = 16). Ten patients were left without any antiarrhythmic therapy, 5 patients received antiarrhythmic drugs and 3 patients underwent successful VT ablation (non-ICD group, n = 18). Thirteen patients had an abnormal signal averaged ECG. During 6.5 +/- 2.4 years 69% of ICD patients received appropriate discharges and one non-ICD patient had a hemodynamically tolerated smVT recurrence (no sudden cardiac death in both groups). Comparison between the cycle lengths of clinical VT, induced VT and follow-up VT revealed a strong relationship (R = 0.62-0.88). On multivariate analysis abnormal signal averaged ECG and decreased left ventricular ejection fraction were statistically significant predictors for VT recurrence.</AbstractText>In ARVD/C the tachycardia cycle length of clinical VT, PVS-induced VT and follow-up VT correlate well implicating that a PVS-guided approach does not provide additional information. Spontaneous arrhythmia in combination with clinical presentation allows identification of patients in need for an ICD.</AbstractText> |
9,827 | Enhanced expression of platelet CD40-ligand by in vitro lipopolysaccharide-challenge in patients with ventricular fibrillation complicating acute myocardial infarction. | Acute myocardial infarction can be complicated by ventricular arrhythmias due to electrophysiological changes in the ischemic myocardium, but the exact predisposing factors causing ventricular fibrillation during myocardial infarction still remain unclear. A role of inflammatory stimulation on platelets as a potential risk factor for ventricular fibrillation during acute myocardial infarction has not been described yet.</AbstractText>Whole blood samples of 21 patients with a history of acute myocardial infarction (AMI) and ventricular fibrillation (VF) were incubated with lipopolysaccharide (LPS). As a control group, we studied 19 patients without VF during AMI. CD40-ligand and CD62P expression on platelets and tissue factor binding on monocytes were measured by flow cytometry. Platelet-monocyte aggregates were measured by CD41 expression on platelets adherent to monocytes. Soluble CD40-ligand plasma levels were measured with an ELISA. Without LPS, no significant difference between the patient groups concerning CD40L expression on platelets was observed, but plasma levels of soluble CD40L were significantly higher in patients with a history of AMI with VF. After LPS stimulation, patients with a history of VF showed a significantly increased expression of CD40L in comparison to the patients without ventricular fibrillation, based on a significantly higher increase of CD40L expression. CD62P expression on platelets was significantly increased in patients with a history of VF.</AbstractText>Patients with a history of VF complicating AMI show an enhanced expression of CD40L on platelets after in vitro lipopolysaccharide-challenge with an enhanced platelet activation.</AbstractText> |
9,828 | Effects of n-3 polyunsaturated fatty acid on upper limit of vulnerability shocks. | Ventricular fibrillation (VF) can be induced when a strong shock is delivered during the vulnerable period of a cardiac cycle. VF, however, cannot be induced if the shock strength is increased to the "upper limit of vulnerability" (ULV) level. Docosahexaenoic acid (DHA) has been shown to prevent the occurrence of VF after coronary occlusion. However, its effects on the ULV have not been verified. We tested the hypothesis that ULV shock strength is decreased after DHA administration.</AbstractText>In 10 pigs, 10 S1s (square, 5-ms) were delivered from the RV apex electrode at 300 ms cycle length. Shocks (S2, biphasic) were delivered from the RV-SVC electrodes after the last S1. The ULV was determined using an up/down protocol. In group 1 (n = 5), after the control ULV was determined at the beginning of the study, a solution containing 1.0 gm of DHA was infused intravenously within 90 min. The ULV (DHA-ULV) was determined again after the end of infusion. In group 2 (n = 5), the vehicle for DHA was infused instead of DHA to confirm that the vehicle did not have an effect on the ULV.</AbstractText>DHA-ULV (412 +/- 58 V, 12 +/- 3 J) was significantly decreased (P < 0.04) compared to the control ULV (478 +/- 32 V, 16 +/- 3 J). The ULV before (483 +/- 28 V, 16 +/- 1 J) and after (463 +/- 28 V, 15 +/- 2 J) the vehicle infusion was not different (P = 0.4). There was no change in the systolic blood pressure as well as heart rate in both groups.</AbstractText>DHA significantly decreases the ULV (13% by voltage and 25% by energy), suggesting that DHA can help to prevent VF induced by a strong stimulus delivered during the vulnerable period.</AbstractText> |
9,829 | [New aspects in the management of asymptomatic patients with mitral regurgitation]. | With 31%, mitral insufficiency (MI) represents the second most common valve lesion and is most commonly of degenerative etiology. Sudden death is rare, in asymptomatic patients with flail leaflet and in sinus rhythm it occurs at a rate of 0.8%/year, and increases to a rate of 4.8%/ year when atrial fibrillation occurs. The effective regurgitant orifice area (ERO) is an important determinator of severity of MI and is of prognostic importance. An ERO of >or=40 mm(2) implies severe MI. These patients require further evaluation with exercise testing to determine functional and objective symptom status and exercise hemodynamics to identify pulmonary hypertension at rest or during exercise. This is of particular importance in patients with absent tricuspid insufficiency. Coronary angiography is indicated when symptoms or pathologic hemodynamics occur during exercise. Surgery in asymptomatic, severe MI is recommended when ejection fraction drops to <60%; left ventricular end-systolic diameter (LVESD) increases to >45 mm (LVESD index >26 mm/m(2)), when atrial fibrillation occurs or pulmonary hypertension with PAP syst >50 mmHg at rest and >60 mmHg during exercise), and if the valve is reparable.Patients without an indication for surgery need careful cardiac follow-up. Patients who underwent surgery according to guidelines had an 8-year survival rate of 89%. Clinical assessment together with echocardiography and exercise hemodynamics determine the optimal timing of surgery in asymptomatic patients with severe MI. |
9,830 | Blockade of angiotensin II type 1 receptor improves the arrhythmia morbidity in mice with left ventricular hypertrophy. | Stimulation of angiotensin II type 1 (AT(1)) receptors has been shown to generate the arrhythmogenic substrate in ventricular hypertrophy. We examined whether candesartan, an AT1 receptor blocker, has antiarrhythmic effects on mouse model of left ventricular hypertrophy created by transverse aorta constriction (TAC).</AbstractText>Forty-eight male mice were divided into 3 groups: TAC, candesartan (TAC plus candesartan) and control groups. Echocardiographic examination was performed before the operation and 2 and 4 weeks after the operation. Four weeks after the operation, electrophysiological studies were conducted by inserting a 1.7 F octapolar electrode catheter through the right external jugular vein into the right ventricle. The effective refractory period of the atrioventricular node (AVNERP) in TAC group was significantly prolonged, and short episodes of ventricular tachycardia (VT) and atrial fibrillation (AF) could be induced in 12 of 16 mice (75%) and 8 of 16 (50%), respectively. In contrast, in candesartan group, the incidence of VT was significantly reduced (12.5%) and no AF was induced. Moreover, the drug produced a significant left ventricular hypertrophy regression and restored the AVNERP to normal.</AbstractText>Candesartan reduced both ventricular and atrial arrhythmias in the TAC mice, presumably by preventing the electrical remodeling by inhibiting the AT(1) receptor.</AbstractText> |
9,831 | Japanese randomized trial for investigation of a combined therapy of amiodarone and implantable cardioverter defibrillator in patients with ventricular tachycardia and fibrillation: the Nippon ICD Plus Pharmachologic Option Necessity study design. | Implantable cardioverter-defibrillators (ICDs) are the most effective therapy in reducing the mortality of patients with life-threatening ventricular tachyarrhythmias. However, the ICD cannot prevent the recurrence of tachycarida attacks and that limits the clinical usefulness of them. The Nippon ICD Plus Pharmachologic Option Necessity (NIPPON) trial was designed as the first prospective randomized study to test the hypothesis whether amiodarone could improve the patient's clinical outcome by reducing the amount of ICD therapy in the Japanese patient population.</AbstractText>Approximately 400 patients with organic heart disease and spontaneous episode(s) of sustained ventricular tachycardia/fibrillation (VT/VF) will be randomly assigned to one of 2 groups; the amiodarone group and non-amiodarone group. Both groups of patients will be followed at least for 24 months. The end-point committee will adjudicate events in a blinded fashion. The primary end-points of this study are determination of the appropriate therapy from the ICD and alteration of the assigned treatment because of its harmful effects and/or frequent ICD therapies.</AbstractText>The NIPPON study is expected to confirm our understanding of the prognostic and therapeutic usefulness of adjuvant amiodarone therapy for patients with an ICD and with a history of sustained VT/VF.</AbstractText> |
9,832 | Long-term follow-up of transvenous defibrillation leads: high incidence of fracture in coaxial polyurethane lead. | As a result of longer follow-up after implantation of cardioverter defibrillators (ICD), fatigue of the leads has become a concern. The aim of this study was to determine the incidence and clinical presentation of ICD lead failures.</AbstractText>The study population consisted of 241 patients with 249 ICD leads who underwent implantation of an ICD with a transvenous lead system. After device implantation, the patients were routinely followed up every 4 months. Five lead failures (2.0%) occurred as an oversensing of artifact during the follow-up period (2.6+/-2.1 years); 4 of those 5 patients received inappropriate shocks and 1 case of lead failure was identified in a patient with frequent episodes of non-sustained ventricular fibrillation. In particular, the right ventricular polyurethane transvenous lead in the Medtronic model 6936 failed in 4 (13%) of 31 cases. Percutaneous lead extraction was not available in all cases, so an additional ICD lead was inserted through the same site of the subclavian vein.</AbstractText>Lead failures may occur 5 years after ICD implantation and polyurethane leads have an especially high incidence of failure. However, there were no follow-up parameters observed that predicted lead failures.</AbstractText> |
9,833 | Clinical significance of the electrophysiologic study (EPS)-guided therapy for the secondary prevention of ventricular tachycardia. | Although electrophysiologic study (EPS) is one of the most reliable methods for selecting preventive therapy for patients with sustained ventricular tachycardia (VT), VT may recur during EPS-guided effective therapy; therefore, the importance of implantable cardioverter-defibrillator (ICD) has been emphasized. In this study, the prognoses of VT patients were evaluated to clarify the importance of EPS-guided therapy for the secondary prevention of VT.</AbstractText>The study population consisted of 99 consecutive patients with a history of sustained VT, which was inducible in EPS. The VT induction protocol used 1-3 extrastimuli and rapid ventricular pacing at 2 right ventricular sites and included additional isoproterenol infusion. ICD implantation was applied to all patients with an episode of hemodynamically unstable VT, regardless of the result of preventive therapy. For preventive therapy, an antiarrhythmic drug and/or catheter ablation were selected, and they were defined as being effective in the EPS-guided therapy when the induction of VT was completely prevented. When no therapy was effective for prevention, an antiarrhythmic drug was prescribed under ICD implantation. During the follow-up period of 19+/-20 months, VT recurred in 17 of 32 patients (53%) in the ineffective group and in 10 of 67 patients (15%) in the effective group (p=0.0001). The therapies used in the effective group were class I antiarrhythmic drug in 9, class III in 15, and catheter ablation in 35 patients. Between the patients with and without VT recurrence, there were no significant differences in the left ventricular ejection fraction and the maximum number of repetitive ventricular responses that remained in VT induction in EPS.</AbstractText>Although VT may recur in up to 15% of patients with EPS-guided effective therapy, the recurrence rate was significantly reduced in comparison to that in the ineffective group. EPS-guided therapy may be useful to reduce the clinical recurrence of VT, as well as the action of ICD.</AbstractText> |
9,834 | Heart rate response to onset of exercise: evidence for enhanced cardiac sympathetic activity in animals susceptible to ventricular fibrillation. | A large heart rate (HR) increase at the onset of exercise has been linked to an increased risk for adverse cardiovascular events, including cardiac death. However, the relationship between changes in cardiac autonomic regulation induced by exercise onset and the confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, a retrospective analysis of the HR response to exercise onset was made in mongrel dogs with healed myocardial infarctions that were either susceptible (S, n = 131) or resistant (R, n = 114) to VF (induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise). The ECG was recorded, and time series analysis of HR variability (vagal activity index, the 0.24-1.04-Hz frequency component of R-R interval variability) was measured before and 30, 60, and 120 s after the onset of exercise (treadmill running). Exercise elicited significantly (ANOVA, P < 0.0001) greater increases in HR in susceptible dogs at all three times (e.g., at 60 s: R, 46.8 +/- 2.3 vs. S, 57.1 +/- 2.2 beats/min). However, the vagal activity index decreased to a similar extent in both groups of dogs (at 60 s: R, -2.8 +/- 0.1 vs. S, -3.0 +/- 0.2 ln ms2). Beta-adrenoceptor blockade (BB, propranolol 1.0 mg/kg iv) reduced the HR increase and eliminated the differences noted between the groups [at 60 s: R (n = 26), 40.4 +/- 3.2 vs. S (n = 31), 37.5 +/- 2.4 beats/min]. After BB, exercise once again elicited similar declines in vagal activity in both groups (at 60 s: R, -3.6 +/- 0.5 vs. S, -3.2 +/- 0.4 ln ms2). When considered together, these data suggest that at the onset of exercise HR increases to a greater extent in animals prone to VF compared with dogs resistant to this malignant arrhythmia due to an enhanced cardiac sympathetic activation in the susceptible dogs. |
9,835 | Warfarin versus aspirin in patients with reduced cardiac ejection fraction (WARCEF): rationale, objectives, and design. | Warfarin is widely prescribed for patients with heart failure without level 1 evidence, and an adequately powered randomized study is needed.</AbstractText>The Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction study is a National Institutes of Health-funded, randomized, double-blind clinical trial with a target enrollment of 2860 patients. It is designed to test with 90% power the 2-sided primary null hypothesis of no difference between warfarin (International Normalized Ratio 2.5-3) and aspirin (325 mg) in 3- to 5-year event-free survival for the composite endpoint of death, or stroke (ischemic or hemorrhagic) among patients with cardiac ejection fraction < or =35% who do not have atrial fibrillation or mechanical prosthetic heart valves. Secondary analyses will compare warfarin and aspirin for reduction of all-cause mortality, ischemic stroke, and myocardial infarction (MI), balanced against the risk of intracerebral hemorrhage, among women and African Americans; and compare warfarin and aspirin for prevention of stroke alone. Randomization is stratified by site, New York Heart Association (NYHA) heart class (I vs II-IV), and stroke or transient ischemic attack (TIA) within 1 year before randomization versus no stroke or TIA in that period. NYHA class I patients will not exceed 20%, and the study has a target of 20% (or more) patients with stroke or TIA within 12 months. Randomized patients receive active warfarin plus placebo or active aspirin plus placebo, double-blind.</AbstractText>The results should help guide the selection of optimum antithrombotic therapy for patients with left ventricular dysfunction.</AbstractText> |
9,836 | Preserved heart rate variability identifies low-risk patients with nonischemic dilated cardiomyopathy: results from the DEFINITE trial. | The recent expansion of indications for prophylactic implantable cardioverter-defibrillator (ICD) placement in subjects with nonischemic dilated cardiomyopathy has raised concerns about the cost-effectiveness of this therapy.</AbstractText>The purpose of this study was to identify low-risk patients with nonischemic dilated cardiomyopathy who may not require prophylactic ICD placement.</AbstractText>This was a prospective study of 274 participants in the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial, a randomized controlled trial that evaluated the role of prophylactic ICD placement in patients with nonischemic dilated cardiomyopathy. The patients underwent 24-hour Holter recording for analysis of heart rate variability (HRV). The primary HRV variable was the standard deviation of normal R-R intervals (SDNN). Patients with atrial fibrillation and frequent ventricular ectopy (>25% of beats) were excluded from HRV analysis (23% of patients). SDNN was categorized in tertiles, and Kaplan-Meier analysis was performed to compare survival in the three tertiles and excluded patients.</AbstractText>The study population was 73% male, with a mean age of 59 +/- 12 years and mean left ventricular ejection fraction of 21% +/- 6%. After 3-year follow-up, significant differences in mortality rates were observed: SDNN >113 ms: 0 (0%), SDNN 81-113 ms: 5 (7%), SDNN <81 ms: 7 (10%), excluded patients: 11 (17%) (P = .03). There were no deaths in the tertile with SDNN >113 ms regardless of treatment assignment (ICD vs control).</AbstractText>Patients with nonischemic dilated cardiomyopathy and preserved HRV have an excellent prognosis and may not benefit from prophylactic ICD placement. Patients with severely depressed HRV and patients who are excluded from HRV analysis because of atrial fibrillation and frequent ventricular ectopy have the highest mortality.</AbstractText> |
9,837 | Comparison of 30 and the 100% inspired oxygen concentrations during early post-resuscitation period: a randomised controlled pilot study. | High oxygen concentration in blood may be harmful in the reperfusion phase after cardiopulmonary resuscitation. We compared the effect of 30 and 100% inspired oxygen concentrations on blood oxygenation and the level of serum markers (NSE, S-100) of neuronal injury during the early post-resuscitation period in humans.</AbstractText>Patients resuscitated from witnessed out-of-hospital ventricular fibrillation were randomised after the return of spontaneous circulation (ROSC) to be ventilated either with 30% (group A) or 100% (group B) oxygen for 60 min. Main outcome measures were NSE and S-100 levels at 24 and 48 h after ROSC, the adequacy of oxygenation at 10 and 60 min after ROSC and, in group A, the need to raise FiO(2) to avoid hypoxaemia. Blood oxygen saturation <95% was the threshold for this intervention.</AbstractText>Thirty-two patients were randomised and 28 (14 in group A and 14 in group B) remained eligible for the final analysis. The mean PaO(2) at 10 min was 21.1 kPa in group A and 49.7 kPa in group B. The corresponding values at 60 min were 14.6 and 46.5 kPa. PaO(2) values did not fall to the hypoxaemic level in group A. In another group FiO(2) had to be raised in five cases (36%) but in two cases it was returned to 0.30 rapidly. The mean NSE at 24 and 48 h was 10.9 and 14.2 microg/l in group A and 13.0 and 18.6 microg/l in group B (ns). S-100 at corresponding time points was 0.21 and 0.23 microg/l in group A and 0.73 and 0.49 microg/l in group B (ns). In the subgroup not treated with therapeutic hypothermia in hospital NSE at 24h was higher in group B (mean 7.6 versus 13.5 microg/l, p=0.0487).</AbstractText>Most patients had acceptable arterial oxygenation when ventilated with 30% oxygen during the immediate post-resuscitation period. There was no indication that 30% oxygen with SpO(2) monitoring and oxygen backup to avoid SpO(2)<95% did worse that the group receiving 100% oxygen. The use of 100% oxygen was associated with increased level of NSE at 24h in patients not treated with therapeutic hypothermia. The clinical significance of this finding is unknown and an outcome-powered study is feasible.</AbstractText> |
9,838 | Atrial natriuretic peptide predicts impaired atrial remodeling and occurrence of late postoperative atrial fibrillation after surgery for symptomatic aortic stenosis. | Aortic stenosis (AS) and atrial fibrillation (AF) are commonly encountered in clinical practice. Natriuretic peptides (NP) are endogenous cardiac hormones, which have been shown to increase in patients with heart failure, and valvular or congenital heart disease. We aimed to determine the association between atrial NP (ANP) and late postoperative AF after surgery for AS along with temporal changes in plasma ANP levels and left atrial (LA) volumes.</AbstractText>22 patients (16 males/6 females, mean age: 61 years) with symptomatic AS and 8 healthy volunteers (5 males/3 females) were enrolled into our study. All the patients studied underwent transthoracic echocardiography, which was repeated during the follow-up. N-terminal ANP (N-ANP) was studied initially and at the 2-month follow-up. Postoperatively, the patients were followed up for 12 months for AF attacks.</AbstractText>Patients with AS had significantly higher levels of N-ANP, left ventricular (LV) end-diastolic pressure, E/A ratio, LV mass and LA volumes compared to the controls. Patients with postoperative AF attacks were significantly older, had higher N-ANP levels and LV end-diastolic pressure in addition to higher LA volumes and longer symptom duration compared to patients without AF. Age at the time of operation (p = 0.011) and N-ANP at the 2nd month (p = 0.047) were found to be independent predictors for late AF attacks during follow-up in regression analysis. Besides, N-ANP (p < 0.001) at the 2-month follow-up independently predicted impaired LA remodeling.</AbstractText>ANP might be an important factor to identify AS patients at risk for late postoperative AF attacks.</AbstractText>Copyright 2006 S. Karger AG, Basel.</CopyrightInformation> |
9,839 | Effects of the blockade of cardiac sarcolemmal ATP-sensitive potassium channels on arrhythmias and coronary flow in ischemia-reperfusion model in isolated rat hearts. | Activation of ATP-sensitive K+ channels (K ATP) during ischemia leads to arrhythmias and blockade of these channels exert antiarrhythmic action. In this study, we investigated the effects of HMR1098, a sarcolemmal K ATP channel blocker and 5-hydroxydeconoate (5-HD), a mitochondrial K ATP channel blocker on cardiac function and arrhythmias in isolated rat hearts. The hearts were subjected to 30 min coronary occlusion, followed by 30 min reperfusion. In the preischemic period, both HMR 1098 and 5-HD slightly increased coronary perfusion pressure. Coronary occlusion increased the perfusion pressure and decreased the left ventricular developed pressure (LVDP) in both control and drug-treated hearts. However, inhibition of LVDP was greater and recovery of the perfusion pressure was lower in 30 micromol/l HMR1098 and 100 micromol/l 5-HD-treated hearts compared to control (P < 0.05). HMR1098, at 3 micromol/l, but not at 30 micromol/l, significantly reduced the ratio of bigeminis, couplets and salvos (P < 0.05). Ventricular tachycardia and ventricular fibrillation were not prevented by HMR1098, at both concentrations, and with 5-HD (100 micromol/l). These results suggest that blockade of sarcK ATP and mitoK ATP channels exert weak antiarrhythmic action, but reduce the recovery of coronary perfusion and contractile force, implying that both types of K(ATP) channels have beneficial role in the recovery of ischemic rat myocardium. |
9,840 | Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation.<Pagination><StartPage>329</StartPage><EndPage>334</EndPage><MedlinePgn>329-34</MedlinePgn></Pagination><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Spontaneous gasping is associated with increased survival in animal models of cardiac arrest and in observational studies of humans. The potential beneficial effect of gasping on cerebral perfusion may underlie the observed survival benefit, but mechanisms remain unknown.</AbstractText><AbstractText Label="HYPOTHESIS" NlmCategory="OBJECTIVE">We hypothesized that spontaneous gasping in a pig model of ventricular fibrillation (VF) decreases intracranial pressure (ICP) and increases cerebral perfusion pressure (CePP) during VF in a pig model.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The 13 female farm pigs, weighing between 16 and 33 kg, were anesthetized with propofol and intubated, and then had VF induced for 8 min without intervention. Intrathoracic pressure (ITP), aortic pressure (AoP), and ICP were measured continuously. CePP and ITP were recorded simultaneously during three maximal gasps and correlated with gasping by Spearman rank correlation.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Gasping during VF occurred in 13/13 pigs and followed a crescendo-decrescendo pattern. Each gasp was associated with a biphasic AoP (initial fall, then rise) and ICP (initial rise, then fall) morphology. Time to first gasp (r(2)=0.06), time to maximal gasp (r(2)=0.02), duration of gasping (r(2)=0.11) and frequency of gasping (r(2)=0.32) did not correlate significantly with CePP during gasping while depth of gasping exhibited a weak but significant correlation with CePP (r(2)=0.35, p=0.05). Maximal gasping occurred at 202+/-34 s from onset of VF and resulted in an average decrease in ICP from 27.4+/-5.8 to 20+/-6.7 mmHg, p<0.01 along with an increase in CePP from -0.05+/-10.9 to 11.5+/-12.6 mmHg, p<0.05.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Spontaneous gasping during cardiac arrest decreased intra-cranial pressure and increased cerebral perfusion pressure significantly. These results may help explain why gasping is associated with improved cardiac arrest survival rates. Based upon this new understanding of the physiology of gasping, we speculate that investigation of devices that can enhance the physiological effects of gasping on intracranial pressure and cerebral perfusion should be prioritized.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Srinivasan</LastName><ForeName>Vijay</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Anesthesia and Critical Care Medicine, Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, PA 19104, USA. srinivasan@email.chop.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nadkarni</LastName><ForeName>Vinay M</ForeName><Initials>VM</Initials></Author><Author ValidYN="Y"><LastName>Yannopoulos</LastName><ForeName>Demetris</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Marino</LastName><ForeName>Bradley S</ForeName><Initials>BS</Initials></Author><Author ValidYN="Y"><LastName>Sigurdsson</LastName><ForeName>Gardar</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>McKnite</LastName><ForeName>Scott H</ForeName><Initials>SH</Initials></Author><Author ValidYN="Y"><LastName>Zook</LastName><ForeName>Maureen</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Benditt</LastName><ForeName>David G</ForeName><Initials>DG</Initials></Author><Author ValidYN="Y"><LastName>Lurie</LastName><ForeName>Keith G</ForeName><Initials>KG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>02</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Resuscitation</MedlineTA><NlmUniqueID>0332173</NlmUniqueID><ISSNLinking>0300-9572</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002560" MajorTopicYN="N">Cerebrovascular Circulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006323" MajorTopicYN="N">Heart Arrest</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007427" MajorTopicYN="N">Intracranial Pressure</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012119" MajorTopicYN="Y">Respiration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013534" MajorTopicYN="N">Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D034421" MajorTopicYN="N">Sus scrofa</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>5</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2005</Year><Month>8</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2005</Year><Month>8</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>2</Month><Day>24</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>11</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>2</Month><Day>24</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16494991</ArticleId><ArticleId IdType="doi">10.1016/j.resuscitation.2005.08.013</ArticleId><ArticleId IdType="pii">S0300-9572(05)00356-4</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16493932</PMID><DateCompleted><Year>2006</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2006</Year><Month>02</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0038-0814</ISSN><JournalIssue CitedMedium="Print"><Issue>702 Suppl</Issue><PubDate><Year>2006</Year><Season>Jan-Feb</Season></PubDate></JournalIssue><Title>Soins; la revue de reference infirmiere</Title><ISOAbbreviation>Soins</ISOAbbreviation></Journal>[Nursing care for automatic implantable defibrillators]. | Spontaneous gasping is associated with increased survival in animal models of cardiac arrest and in observational studies of humans. The potential beneficial effect of gasping on cerebral perfusion may underlie the observed survival benefit, but mechanisms remain unknown.</AbstractText>We hypothesized that spontaneous gasping in a pig model of ventricular fibrillation (VF) decreases intracranial pressure (ICP) and increases cerebral perfusion pressure (CePP) during VF in a pig model.</AbstractText>The 13 female farm pigs, weighing between 16 and 33 kg, were anesthetized with propofol and intubated, and then had VF induced for 8 min without intervention. Intrathoracic pressure (ITP), aortic pressure (AoP), and ICP were measured continuously. CePP and ITP were recorded simultaneously during three maximal gasps and correlated with gasping by Spearman rank correlation.</AbstractText>Gasping during VF occurred in 13/13 pigs and followed a crescendo-decrescendo pattern. Each gasp was associated with a biphasic AoP (initial fall, then rise) and ICP (initial rise, then fall) morphology. Time to first gasp (r(2)=0.06), time to maximal gasp (r(2)=0.02), duration of gasping (r(2)=0.11) and frequency of gasping (r(2)=0.32) did not correlate significantly with CePP during gasping while depth of gasping exhibited a weak but significant correlation with CePP (r(2)=0.35, p=0.05). Maximal gasping occurred at 202+/-34 s from onset of VF and resulted in an average decrease in ICP from 27.4+/-5.8 to 20+/-6.7 mmHg, p<0.01 along with an increase in CePP from -0.05+/-10.9 to 11.5+/-12.6 mmHg, p<0.05.</AbstractText>Spontaneous gasping during cardiac arrest decreased intra-cranial pressure and increased cerebral perfusion pressure significantly. These results may help explain why gasping is associated with improved cardiac arrest survival rates. Based upon this new understanding of the physiology of gasping, we speculate that investigation of devices that can enhance the physiological effects of gasping on intracranial pressure and cerebral perfusion should be prioritized.</AbstractText> |
9,841 | Acute pericarditis unmasks ST-segment elevation in asymptomatic Brugada syndrome. | A 26-year-old man was admitted to our hospital because of acute pericarditis. The current patient had a saddle-back type ST-segment elevation shortly after the onset of acute pericarditis. Interestingly, it converted into a coved type ST-segment elevation, subsequently regressed gradually as acute inflammation improved. After 3 months, right ventricular rapid pacing induced ventricular fibrillation, and intravenous sodium channel blocker induced a coved type ST-segment elevation. The current case implies that a Brugada-type ST-segment elevation, which is thought to be false in acute pericarditis, may be true in some patients with asymptomatic Brugada syndrome. |
9,842 | Sleep parameters in patients using pacemakers with sleep rate function on. | The cardiovascular system (CVS) is heavily influenced by the autonomic nervous system. Additionally, there is a functional alteration during the various stages of sleep. In nonrapid eye movement (NREM), a state of cardiovascular relaxation occurs during stages three and four. A large amount of rapid ocular movements is concentrated in rapid eye movement (REM) sleep. During this phase, fluctuations in arterial pressure (AP) and heart rate (HR) can be readily noted. Sleep disordered breathing (SDB) has been associated with cardiac rhythm disorders. Recently, cardiac rhythm disorder treatment with pacemaker (PM) highlighted a reduction in abnormal respiratory events during sleep.</AbstractText>Comparison of sleep parameters of patients using PM with a sleep rate (SR) algorithm based on its rate-modulated capability during physical activity (Integrity PM with SR function on and off).</AbstractText>Twenty-two patients (14 women, 8 men), implanted with an Integrity PM (St. Jude Medical Cardiac Rhythm Management Division, Sylmar, CA) with SR function for standard clinical indications, were evaluated utilizing a double-blind protocol. The indication for pacing included sinus node disease (SND), atrium ventricular blockage (AVB), and atrial fibrillation (AF). Following randomization, half of our patients had SR function switched to "on" mode while the other half were on "off" mode. During the first stage of the protocol, all patients underwent two consecutive nights of polysomnographic sleep recordings (PSG). During the first night patients slept in the sleep lab only for adaptation purpose. PSG full recording was carried out in the subsequent night. At a later stage, the programing of SR functions was shifted to "on" or "off" modes. One week later, a third assessment was undertaken.</AbstractText>Twelve patients (54%) showed sleep efficiency improvement (total sleeping time/recording time) with PM SR on. This group had the least effective sleep efficiency with PM off, if compared with the others who highlighted no change in this sleep parameter (72 +/- 12 vs 81 +/- 7%, P = 0.01, respectively). This first group displayed a lower latency for REM sleep than the last one (89 +/- 55 vs 174 +/- 107 minutes, P = 0.01, respectively). In 11 (50%) patients, the number per sleep hour of microarousals was reduced when PM SR was switched on. When we compared such findings to the group whose parameters had not changed, we noted that the first set of patients were sleepier (ESE: 9 +/- 4 vs 5 +/- 5, P = 0.04, respectively), and showed more microarousals with PM SR off (20 +/- 14 vs 7 +/- 5 microarousal/hour, P = 0.007).</AbstractText>In PM patients with sleep-related issues, the SR function activation improved sleep both from a qualitative and quantitative perspective.</AbstractText> |
9,843 | [Anesthetic management for patients with Brugada syndrome]. | Brugada syndrome should not be neglected in terms of anesthetic management because its perioperative autonomic imbalance may cause ventricular fibrillation and sudden cardiac arrest. Diagnosis of Brugada syndrome is easily made by unique electrocardiographic pattern of right bundle branch block and ST segment elevation in the right precordial leads. Thus the number of patients with Brugada syndrome for anesthetic management tends to increase. We review current concept of anesthetic management for patients with Brugada syndrome including fourteen cases in our institution, two out of which developed VF during operation. |
9,844 | Prognostic value of a restrictive mitral filling pattern in patients with systolic heart failure and an implantable cardioverter-defibrillator. | In patients with chronic heart failure and reduced systolic function, an implantable cardioverter-defibrillator (ICD) improves the prognosis, but morbidity and mortality remain high. We attempted to identify the prognostic impact of Doppler echocardiography and QRS duration in such patients. We prospectively enrolled 84 patients with chronic heart failure, an ICD, and impaired systolic function (mean ejection fraction 29 +/- 10%). Echocardiographic measurements included left ventricular dimensions/volumes, ejection fraction, mitral E/A ratio, deceleration time, and tissue Doppler analysis of mitral annular velocities (S', E', A'). A cardiac event (death from pump failure or appropriate ICD therapy, i.e., antitachycardia pacing/shock due to sustained ventricular tachycardia or ventricular fibrillation) was defined as the study end point. During a follow-up of 373 +/- 254 days, 22 patients (26%) had an event (death from pump failure, n = 7; patients who received an appropriate ICD therapy, n = 16). In patients with an event, the QRS duration was longer (169 +/- 41 vs 146 +/- 37 ms, p = 0.023), the mitral E/E' ratio was higher (16.0 +/- 6.5 vs 12.8 +/- 5.9, p = 0.044), and a restrictive filling pattern was more frequent (44% vs 9%, p = 0.017). Stepwise multivariate Cox regression analysis identified a restrictive filling pattern as the only independent predictor of an event (hazard ratio 3.65, 95% confidence interval 1.54 to 8.64, p = 0.003). For patients with a restrictive filling pattern, the outcome was markedly poorer than that for patients with a nonrestrictive pattern (event-free survival rate 38% vs 72%, p = 0.005). In conclusion, in patients with chronic heart failure, an ICD, and systolic dysfunction, a restrictive filling pattern is an independent predictor of adverse cardiac events. |
9,845 | Vasopressin during cardiopulmonary resuscitation and different shock states: a review of the literature. | Vasopressin administration may be a promising therapy in the management of various shock states. In laboratory models of cardiac arrest, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the rate of return of spontaneous circulation, and neurological recovery compared with epinephrine (adrenaline). In a study of 1219 adult patients with cardiac arrest, the effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity; however, vasopressin was superior to epinephrine in patients with asystole. Furthermore, vasopressin followed by epinephrine resulted in significantly higher rates of survival to hospital admission and hospital discharge. The current cardiopulmonary resuscitation guidelines recommend intravenous vasopressin 40 IU or epinephrine 1mg in adult patients refractory to electrical countershock. Several investigations have demonstrated that vasopressin can successfully stabilize hemodynamic variables in advanced vasodilatory shock. Use of vasopressin in vasodilatory shock should be guided by strict hemodynamic indications, such as hypotension despite norepinephrine (noradrenaline) dosages >0.5 mug/kg/min. Vasopressin must never be used as the sole vasopressor agent. In our institutional routine, a fixed vasopressin dosage of 0.067 IU/min (i.e. 100 IU/50 mL at 2 mL/h) is administered and mean arterial pressure is regulated by adjusting norepinephrine infusion. When norepinephrine dosages decrease to 0.2 microg/kg/min, vasopressin is withdrawn in small steps according to the response in mean arterial pressure. Vasopressin also improved short- and long-term survival in various porcine models of uncontrolled hemorrhagic shock. In the clinical setting, we observed positive effects of vasopressin in some patients with life-threatening hemorrhagic shock, which had no longer responded to adrenergic catecholamines and fluid resuscitation. Clinical employment of vasopressin during hemorrhagic shock is experimental at this point in time. |
9,846 | Pharmacological prevention of thromboembolism in patients with left ventricular dysfunction. | Chronic left ventricular systolic dysfunction is a well recognized problem with an increasingly significant impact on healthcare in the form of congestive heart failure (CHF). Advances in medicine have led to improved survival after myocardial infarction (MI) and as a result, an increased prevalence of left ventricular systolic dysfunction. An increased incidence of thromboembolism, especially stroke, in patients with left ventricular systolic dysfunction is also well recognized. Pharmacological strategies to prevent stroke have been proposed in numerous studies. For example, anticoagulation in patients with atrial fibrillation and heart failure has been shown to reduce mortality rates and the incidence of stroke; however, its role in patients with left ventricular dysfunction and normal sinus rhythm is unclear and utilization of anticoagulation in these patients varies widely. The role of aspirin to prevent thromboembolism in patients with CHF is controversial. The relatively new pharmacological agent ximelagatran, which has an advantage of unmonitored oral administration has the potential to change the anticoagulation strategy in patients with heart failure. Important trials to define optimal therapy for reducing the risk of thromboembolism and death in patients with left ventricular systolic dysfunction and sinus rhythm include the recently reported WATCH (Warfarin and Antiplatelet Therapy in Chronic Heart failure) trial and the WARCEF (Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction) trial, which is currently underway. The WATCH trial failed to outline significant differences between aspirin (acetylsalicylic acid), warfarin, and clopidogrel in the primary composite endpoint of all-cause mortality, nonfatal MI, and nonfatal stroke. Combined data from WATCH and WARCEF may provide sufficient statistical power to clarify outcomes such as stroke and death in patients with reduced cardiac ejection fraction. The pooled data may also help define optimal preventative measures for thromboembolism in patients with left ventricular systolic dysfunction and sinus rhythm. |
9,847 | Conversion to sinus rhythm by ablation improves quality of life in patients submitted to mitral valve surgery. | Atrial fibrillation can be successfully treated with surgical ablation, but the effect of restoring sinus rhythm on the quality of life has yet to be established. We evaluate the effects of left atrial ablation combined with mitral valve surgery on health-related quality of life in patients with permanent atrial fibrillation.</AbstractText>Ninety-one consecutive patients with permanent atrial fibrillation underwent mitral valve surgery at our division. The last 53 also received left atrial ablation by means of monopolar radiofrequency and excision of the left appendage. The patients were divided into two groups according to the median total score obtained at the Short Form 36 Health Survey used to evaluate their quality of life (ie, the good quality of life group [n = 54] and the poor quality of life group [n = 37]).</AbstractText>Preoperative and intraoperative data of the two groups were similar. In-hospital mortality and morbidity were similar in both groups. Sinus rhythm was obtained in 68% of patients (36 of 53) treated with left atrial ablation and it occurred spontaneously in 10% of patients (4 of 38) treated for the mitral pathology only. At follow-up, there was no difference between the groups in ejection fraction, left atrial diameter, mitral dysfunction, tricuspidal regurgitation, and New York Heart Association functional class. Using stepwise logistic regression, only the presence of sinus rhythm was associated with better quality of life.</AbstractText>In patients submitted to mitral surgery, conversion to sinus rhythm by left atrial ablation can significantly improve the health-related quality of life.</AbstractText> |
9,848 | Rapid induction of cerebral hypothermia is enhanced with active compression-decompression plus inspiratory impedance threshold device cardiopulmonary resusitation in a porcine model of cardiac arrest. | A rapid, ice-cold saline flush combined with active compression-decompression (ACD) plus an inspiratory impedance threshold device (ITD) cardiopulmonary resusitation (CPR) will cool brain tissue more effectively than with standard CPR (S-CPR) during cardiac arrest (CA).</AbstractText>Early institution of hypothermia after CPR and return of spontaneous circulation improves survival and outcomes after CA in humans.</AbstractText>Ventricular fibrillation (VF) was induced for 8 min in anesthetized and tracheally intubated pigs. Pigs were randomized to receive either ACD + ITD CPR (n = 8) or S-CPR (n = 8). After 2 min of CPR, 30 ml/kg ice-cold saline (3 degrees C) was infused over the next 3 min of CPR via femoral vein followed by up to three defibrillation attempts (150 J, biphasic). If VF persisted, epinephrine (40 microg/kg) and vasopressin (0.3 U/kg) were administered followed by three additional defibrillation attempts. Hemodynamic variables and temperatures were continuously recorded.</AbstractText>All ACD + ITD CPR pigs (8 of 8) survived (defined as 15 min of return of spontaneous circulation [ROSC]) versus 3 of 8 pigs with S-CPR (p < 0.05). In survivors, brain temperature (degrees C) measured at 2-cm depth in brain cortex 1 min after ROSC decreased from 37.6 +/- 0.2 to 35.8 +/- 0.3 in ACD + ITD CPR versus 37.8 +/- 0.2 to 37.3 +/- 0.3 in S-CPR (p < 0.005). Immediately before defibrillation: 1) right atrial systolic/diastolic pressures (mm Hg) were lower (85 +/- 19, 4 +/- 1) in ACD + ITD CPR than S-CPR pigs (141 +/- 12, 8 +/- 3, p < 0.01); and 2) coronary perfusion pressures (mm Hg) were higher in ACD + ITD CPR (28.3 +/- 2) than S-CPR pigs (17.4 +/- 3, p < 0.01).</AbstractText>A rapid ice-cold saline infusion combined with ACD + ITD CPR during cardiac arrest induces cerebral hypothermia more rapidly immediately after ROSC than with S-CPR.</AbstractText> |
9,849 | Reduction in ventricular tachyarrhythmias with statins in the Multicenter Automatic Defibrillator Implantation Trial (MADIT)-II. | We evaluated whether statins have anti-arrhythmic effects by exploring the association of statin use with appropriate implantable cardioverter-defibrillator (ICD) therapy for ventricular tachycardia/ventricular fibrillation (VT/VF) in the Multicenter Automatic Defibrillator Implantation Trial (MADIT)-II.</AbstractText>A few studies have suggested that lipid-lowering drugs may have anti-arrhythmic effects in patients with coronary artery disease.</AbstractText>Patients receiving an ICD (n = 654; U.S. centers only) in the MADIT-II study were categorized by the percentage of days each patient received statins during follow-up (90% to 100%, n = 386; 11% to 89%, n = 116; and 0% to 10%, n = 152). The Kaplan-Meier method with significance testing by the log-rank statistic and time-dependent proportional hazards regression analysis were used to evaluate the effect of statin use on the probability of ICD therapy for the combined end point VT/VF or cardiac death and for the end point VT/VF.</AbstractText>The cumulative rate of ICD therapy for VT/VF or cardiac death, whichever occurred first, was significantly reduced in those with > or =90% statin usage compared to those with lower statin usage (p = 0.01). The time-dependent statin:no statin therapy hazard ratio was 0.65 (p < 0.01) for the end point of VT/VF or cardiac death and 0.72 (p = 0.046) for VT/VF after adjusting for relevant covariates.</AbstractText>Statin use in patients with an ICD was associated with a reduction in the risk of cardiac death or VT/VF, whichever occurred first, and was associated with a reduction in VT/VF episodes. These findings suggest that statins have anti-arrhythmic properties.</AbstractText> |
9,850 | Pediatric dysrhythmias. | Arrhythmias in children are less common than in adults but are increasing because of successful repair of congenital heart diseases. Supraventricular tachycardia is the most common symptomatic pediatric tachyarrhythmia. Atrial flutter and atrial fibrillation in children are attributed largely to structural heart disease. Bradycardia is defined as a heart rate less than the lower limit of normal for a child's age, and the most common cause is sinus bradycardia. Despite the infrequent occurrence of arrhythmias, it is crucial to expeditiously identify and treat certain rhythm abnormalities because they can lead to further decompensation. |
9,851 | Comparison of atrial signal extraction algorithms in 12-lead ECGs with atrial fibrillation. | Analysis of atrial rhythm is important in the treatment and management of patients with atrial fibrillation. Several algorithms exist for extracting the atrial signal from the electrocardiogram (ECG) in atrial fibrillation, but there are few reports on how well these techniques are able to recover the atrial signal. We assessed and compared three algorithms for extracting the atrial signal from the 12-lead ECG. The 12-lead ECGs of 30 patients in atrial fibrillation were analyzed. Atrial activity was extracted by three algorithms, Spatiotemporal QRST cancellation (STC), principal component analysis (PCA), and independent component analysis (ICA). The amplitude and frequency characteristics of the extracted atrial signals were compared between algorithms and against reference data. Mean (standard deviation) amplitude of QRST segments of V1 was 0.99 (0.54) mV, compared to 0.18 (0.11) mV (STC), 0.19 (0.13) mV (PCA), and 0.29 (0.22) mV (ICA). Hence, for all algorithms there were significant reductions in the amplitude of the ventricular activity compared with that in V1. Reference atrial signal amplitude in V1 was 0.18 (0.11) mV, compared to 0.17 (0.10) mV (STC), 0.12 (0.09) mV (PCA), and 0.18 (0.13) mV (ICA) in the extracted atrial signals. PCA tended to attenuate the atrial signal in these segments. There were no significant differences for any of the algorithms when comparing the amplitude of the reference atrial signal with that of the extracted atrial signals in segments in which ventricular activity had been removed. There were no significant differences between algorithms in the frequency characteristics of the extracted atrial signals. There were discrepancies in amplitude and frequency characteristics of the atrial signal in only a few cases resulting from notable residual ventricular activity for PCA and ICA algorithms. In conclusion, the extracted atrial signals from these algorithms exhibit very similar amplitude and frequency characteristics. Users of these algorithms should be observant of residual ventricular activities which can affect the analysis of the fibrillatory waveform in clinical practice. |
9,852 | Two cases of Brugada syndrome associated with spontaneous clinical episodes of coronary vasospasm. | Two patients with life-threatening episodes of ventricular fibrillation (VF) showed typical ST elevation in V1-V3 leads. Both had spontaneous clinical episodes of resting angina. Intracoronary injection of acetylcholine provoked coronary vasospasm and ST elevation was the same as Brugada-type ST elevation in 1 case but not in the other. Calcium channel antagonist was prescribed to prevent coronary vasospasm but Brugada-type ST elevation and the occurrence of VF could not be prevented. The symptoms accompanied both cases. Considering these cases, the pathogenesis of Brugada syndrome should differ from that of coronary vasospasm because it could not be prevented by calcium channel antagonist. |
9,853 | A comprehensive review and analysis of 25 years of data from an in vivo canine model of sudden cardiac death: implications for future anti-arrhythmic drug development. | Sudden cardiac death resulting from ventricular tachyarrhythmias remains the leading cause of death in industrially developed countries, accounting for between 300,000 and 500,000 deaths each year in the United States. Yet, despite the enormity of this problem, the development of safe and effective anti-arrhythmic agents remains elusive. The identification of effective anti-arrhythmic agents is critically dependent upon the use of appropriate animal models of human disease. During the last 25 years, a canine model of sudden cardiac death has proven to be useful in both the identification of factors contributing to ventricular fibrillation (VF) and the evaluation of potential anti-arrhythmic therapies. The present review provides a detailed retrospective analysis of the data obtained with this model. Briefly, VF was reliably and reproducibly induced by the combination of acute myocardial ischemia at site distant from a previous myocardial infarction during submaximal exercise (to activate the autonomic nervous system). This exercise plus ischemia test identified 2 stable populations of dogs: those that development malignant arrhythmias (susceptible, n=303) and those that rarely developed even single premature ventricular activation (resistant, n=209). The susceptible animals exhibited an elevated sympathetic activation (due to an enhanced beta2-adrenoceptor responsiveness) and a subnormal parasympathetic regulation. Several interventions have proven to be particularly effective in preventing VF in the susceptible dogs; including calcium channel antagonists, left stellate ganglion disruption, ATP-sensitive potassium channel antagonists, beta-adrenoceptor antagonists, and non-pharmacological interventions (endurance exercise training and dietary omega-3 fatty acids). |
9,854 | Flow-reversal device for cerebral protection during carotid artery stenting--acute and long-term results. | Several types of cerebral (embolic) protection devices have been used in patients undergoing carotid stenting. This study assessed results achieved with a flow-reversal system.</AbstractText>Carotid stenting was performed in 56 patients (mean age, 68 +/- 9 years). The mean percentage of stenosis was 77%+/- 10%. During the procedure, cerebral protection was achieved by means of balloon occlusion of the common and external carotid artery with use of a Parodi Anti-Emboli System. The patients' neurologic status was assessed during the intervention; at discharge; 1, 6, and 12 months after the procedure; and yearly thereafter.</AbstractText>The procedure was technically successful in all cases. One patient had a minor stroke 6 hours after the intervention. No major strokes, deaths, or myocardial infarctions occurred. During long-term follow-up (to 40 months), 2 patients died of a secondary complication after intracerebral bleeding and stroke and 1 died as a result of ventricular fibrillation. Restenosis did not exceed 50% of vessel diameter in any patient.</AbstractText>The acute results indicate that proximal occlusion and flow reversal for cerebral protection during carotid stenting is a safe and effective method. The low restenosis and complication rate during long-term follow-up is in accordance with other series of carotid angioplasty and shows that the occlusion balloons do not cause any long-term side effects.</AbstractText> |
9,855 | Induction of atrial fibrillation after the routine use of adenosine. | We report a case of atrial fibrillation induction after the use of adenosine for the termination of supraventricular tachycardia in the emergency department. Atrial fibrillation is not an uncommon side effect of adenosine administration. Hemodynamic collapse may occur if an antegrade-conducting accessory pathway allows for a rapid ventricular response. Therefore, we would recommend that the use of adenosine be limited to situations in which there is appropriate electrocardiographic monitoring and emergency resuscitative capabilities. |
9,856 | [The best of arrhythmia in 2005]. | In 2005, one of the major areas of interest in the field of electrophysiology remains ablation of atrial fibrillation (AF). Identification of specific atrial sites, likely playing a role in the perpetuation of this arrhythmia has taken part in the ablation technique refinement. An increase in the rate of asymptomatic AF following ablation has been reported this year, which underlined the need for long lasting ECG recordings to demonstrate ablation success. The role of ventricular programmed stimulation remained controversial in the management of Brugada syndrome. Nevertheless, in the report of the second consensus conference, result of ventricular programmed stimulation was still considered as important in the decision making process. The third form of short QT syndrome (SQT3) has been found to be caused by a mutation in the KCNJ2 gene, leading to an increase in the function of Ik1 channel. Right ventricular dilation seemed to be the most frequent echocardiography anomaly in patients with right ventricular dysplasia as defined by the criteria published in 1994. Ablation of frequent (>20% on Holter monitoring) ventricular premature beats has been shown to improve hemodynamics in patients with left ventricular dilation and impaired ejection fraction. Safety and efficacy of implantable cardioverter defibrillator (ICD) have been demonstrated in high risk patients with hypertrophic cardiomyopathy in a large clinical study. However, the use of high energy ICD and the systematic determination of the defibrillation threshold were recommended. Despite the presence of sophisticated algorithms to discriminate VT from SVT, high rates of inappropriate therapies were still reported in recent ICD studies. |
9,857 | [Prevalence of supraventricular tachycardia and tachyarrhythmias in resuscitated cardiac arrest]. | Supraventricular arrhythmias are considered to be benign when the ventricular rate is slowed and treated by anticoagulants. The aim of this study was to determine the possible influence of these arrhythmias in resuscitated cardiac arrest. Between 1980 and 2002, 151 patients were admitted after a cardiac arrest. Supraventricular arrhythrmias were identified as a possible cause of the cardiac arrest in 21 patients. They underwent echocardiography, exercise stress test, Holter ECG monitoring , coronary angiography and electrophysiological investigation. After these investigations, three patients had a malignant form of the Wolff-Parkinson-White syndrome, two were asymptomatic and, in the third patient, ventricular fibrillation was induced by treatment with diltiazem. In 8 patients, a rapid supraventricular arrhythmia was considered to be the cause of cardiac arrest by cardiogenic shock; 2 patients had hypertrophic cardiomyopathy, 5 had severe dilated cardiomyopathy which regressed in one patient. In ten patients, cardiac arrest due to ventricular tachycardia or fibrillation was provoked by a rapid (> 220 beats/min) supraventricular arrhythmia; two patients had no apparent underlying cardiac pathology. In the others, myocardial ischaemia or acute cardiac failure were considered to be the cause of the cardiac arrest. The authors conclude that rapid supraventricular arrhythmias may cause cardiac arrest either by cardiogenic shock or degenerescence to ventricular tachycardia or fibrillation. Usually, this event occurs in patients with severe cardiac disease but it may occur in subjects without cardiac disease or by an arrhythmia-induced cardiomyopathy. |
9,858 | The independent effects of eicosapentaenoic acid and docosahexaenoic acid on cardiovascular risk factors in humans. | This review details the independent effects of purified eicosapentaenoic acid and docosahexaenoic acid on cardiovascular risk factors in humans. We report data from the recent literature and our own controlled clinical trials which compared the independent effects of these fatty acids in individuals at increased risk of cardiovascular disease, namely overweight hyperlipidaemic men and treated-hypertensive, type 2 diabetic men and women. We discuss the biological effects of these fatty acids and the potential mechanisms through which they may affect cardiovascular disease risk factors.</AbstractText>A cardioprotective effect for omega3 fatty acids is supported by prospective studies demonstrating an inverse association between fish intake and coronary heart disease mortality. Data from secondary prevention trials support a reduction in ventricular fibrillation as a primary mechanism for the decreased incidence of myocardial infarction. Clinical trials and experimental studies have shown that omega3 fatty acids have many other potentially important antiatherogenic and antithrombotic effects. Omega-3 fatty acids lower blood pressure and heart rate, improve dyslipidaemia, reduce inflammation, and improve vascular and platelet function. These favourable effects have until recently been primarily attributed to the omega3 fatty acid eicosapentaenoic acid, which is present in large amounts in fish oil. Controlled studies in humans now demonstrate that docosahexaenoic acid, although often present in lower quantities, has equally important anti-arrhythmic, anti-thrombotic and anti-atherogenic effects.</AbstractText>Available evidence strongly suggests that eicosapentaenoic acid and docosahexaenoic acid have differing haemodynamic and anti-atherogenic properties. The effects of the two fatty acids may also differ depending on the target population.</AbstractText> |
9,859 | Biventricular pacing improves the blunted force-frequency relation present during univentricular pacing in patients with heart failure and conduction delay. | In patients with chronic heart failure (CHF) and conduction delay, biventricular (BiV) and left ventricular (LV) pacing similarly improve systolic function at resting heart rates. We hypothesized that BiV and univentricular pacing differentially affect contractile function at increasing heart rates.</AbstractText>Twenty-two patients (aged 66+/-2 years, QRS 179+/-8 ms, LV ejection fraction 23+/-1%) underwent cardiac catheterization before device implantation to measure LV hemodynamics at baseline (rate 68+/-2 bpm; sinus rhythm n=18; atrial fibrillation n=4) and during BiV, LV, and right ventricular (RV) stimulation at 80, 100, 120, and 140 bpm. BiV and LV pacing at 80 bpm equally augmented dP/dtmax as compared with baseline and RV pacing (P<0.001). Stimulation rate significantly interacted with the effect of BiV, LV, and RV pacing on LV end-diastolic pressure (LVEDP), systolic pressure (LVSP), and dP/dtmax. Increasing the rate from 80 to 140 bpm enhanced dP/dtmax from 913+/-28 to 1119+/-50 mm Hg/s during BiV stimulation (P<0.001) but had no significant effect on contractility during single-site LV (951+/-47 versus 1002+/-54 mm Hg/s) or RV (800+/-46 versus 881+/-49 mm Hg/s) pacing. At 140 bpm, LVEDP was lower and LVSP higher during BiV pacing than during RV and LV pacing (LVEDP 12+/-1 versus 17+/-1 and 16+/-1 mm Hg, P<0.001; LVSP 112+/-5 versus 106+/-5 and 108+/-6 mm Hg, P<0.01 and P=0.09; BiV versus RV and LV pacing, respectively).</AbstractText>Different modes of ventricular stimulation alter the in vivo force-frequency relation of CHF patients. In contrast to single-site LV and RV pacing, contractile function improves with increasing heart rates during BiV stimulation. This effect may contribute to the enhanced exercise capacity during BiV pacing and could provide a functional benefit over LV-only pacing in patients for whom resynchronization therapy is indicated.</AbstractText> |
9,860 | Acute onset of halos and glare: bilateral corneal epithelial edema with cystic eruptions--atypical presentation of amiodarone keratopathy. | Amiodarone (Cordarone; Wyeth, Ayerst, New York) is a potassium channel blocking antiarrythmal medication indicated for recurrent ventricular fibrillation and recurrent hemodynamically unstable ventricular tachycardia. Chemically, it is classified as an iodinated benzofuran derivate antiarrythmal drug not chemically related to any other available antiarrhythmic drug. Documented side effects of amiodarone include neurologic, gastrointestinal, dermatologic, cardiovascular, and ophthalmic. The ophthalmic abnormalities include optic neuropathy, optic neuritis, papilledema, corneal deposits, photosensitivity, lens opacities, and macular degeneration. Corneal microdeposits are seen in virtually all patients who receive amiodarone for more than 6 months. Corneal microdeposits result secondary to the secretion of amiodarone by the lacrimal gland with accumulation on, and absorption by, the corneal epithelium. Approximately 10% of these patients become symptomatic with glare and halos; however, that alone is usually not enough to precipitate intervention.</AbstractText>A 69-year-old woman presented to our office with a 2-week history of halos and glare in both eyes (OU). Her ocular history was significant for occasional contact lens wear. Her systemic history was significant for atrial fibrillation, for which she was taking amiodarone daily for the last 6 years. Six weeks before the onset of her chief complaint, her daily amiodarone dosage was increased from 100 mg to 300 mg. Ophthalmic examination found decreased visual acuities OU, amiodarone keratopathy (subepithelial verticillata), and diffuse corneal epithelial edema with diffuse sodium fluorescein staining OU. The corneal compromise was treated in 2 ways: the source medication was discontinued, and the ocular signs were medicated with a prophylactic topical antibiotic along with supportive preparations (tears/lubricants) and monitored over 2 weeks until full elimination of the pathologic signs and their symptoms. Even after complete resolution of the acute keratitis, the infiltrative keratopathy persisted along with the initial complaints of halos and glare. The supportive treatments were maintained over the course of 2 months until full recovery.</AbstractText>By exclusion, it was determined that the subepithelial depositions and cystic formations were secondary to an acute amiodarone dosage increase by a new practitioner. Prompt communication resulted in the physician discontinuing that medicine.</AbstractText> |
9,861 | [Therapeutic hypothermia after cardiac arrest--status]. | Induced hypothermia in comatose patients resuscitated from cardiac arrest improves survival and neurological outcome when the initial rhythm is ventricular fibrillation. Results from 26 patients treated with early prehospital cooling, continued in hospital with cold fluids and body surface cooling, are presented. Sixteen patients had no or only minor neurological defects at discharge. Thirteen of 17 patients treated for ventricular fibrillation had a good cerebral outcome at discharge. Two patients had minor complications resulting from the treatment. |
9,862 | New approaches to out-of-hospital cardiac arrest. | Out-of-hospital cardiac arrest (OOH-CA) is a leading cause of mortality and the focus of significant research. Recent studies provide new evidence that may change our management of OOH-CA and improve outcomes. The findings of two recently published studies of OOH-CA are reviewed in this article. The first, the Public Access Defibrillation Trial, was a randomized, controlled trial of public access defibrillation in 993 community facilities in the U.S. and Canada . It demonstrated that a community strategy to train laypersons to respond to cardiac arrests significantly increased survival to hospital discharge following OOH-CA in nonresidential community units with community members trained and equipped to provide public access defibrillation, compared to community units with community members trained to provide cardiopulmonary resuscitation (CPR) without any capacity for defibrillation. The second, the European Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation Study, was a randomized, controlled, double-blinded trial that compared vasopressin to epinephrine as the initial pharmacological therapy for 1,219 patients who sustained OOH-CA. The study demonstrated that vasopressin is similar to epinephrine for OOH-CA due to ventricular fibrillation or pulseless electrical activity, and superior to epinephrine for the initial treatment of asystolic arrest; it also demonstrated that the combination of vasopressin and epinephrine is superior to epinephrine alone in the treatment of refractory, out-of-hospital cardiac arrest. Studies on alternative CPR techniques and adjunctive devices for CPR were also reviewed. We conclude that pre-hospital access to defibrillators and the use of vasopressin in the management of asystole hold promise for improving survival for patients with out-of-hospital cardiac arrest. |
9,863 | Rate control in atrial fibrillation: looking beyond the average heart rate. | The aim of this article is to provide a perspective on rate control in atrial fibrillation which emphasizes patient wellbeing (exercise tolerance, symptoms, quality of life) over attempts to reduce resting or exercise heart rate to an arbitrary range.</AbstractText>Recent trials of rhythm versus rate control strategies of treatment in patients with atrial fibrillation suggest that rate control is a viable first line strategy in many patients. The adverse consequences of atrial fibrillation with rapid ventricular response are partly due to factors other than rate itself, such as irregularity of ventricular response, and variable changes in autonomic nervous system output. Digoxin, calcium channel blockers, and beta-blockers cause a similar reduction in resting heart rate. Beta blockers are the most potent at reducing exercise heart rate, followed by calcium channel blockers and digoxin. Exercise tolerance is occasionally improved by digoxin, sometimes improved by calcium channel blockers and not improved by (and sometimes decreased by) beta-blockers. Information about quality of life with different rate control regimens is sparse.</AbstractText>Rate control in atrial fibrillation provides important benefits to patients in terms of symptoms, quality of life and prevention of late consequences of uncontrolled rate (such as tachycardia induced cardiomyopathy). Restricting treatment objectives to achievement of a specific heart rate range on resting or exercise electrocardiogram may result in lack of patient benefit or worsened symptoms. Understanding the nuances of rate control when treating individual patients and interpreting existing evidence allows patients to experience the most benefit from this treatment strategy.</AbstractText> |
9,864 | Pacing delivered rate and rhythm control for atrial fibrillation. | Device therapy for atrial fibrillation remains contentious despite the recognized benefit of atrial pacing in sinus node dysfunction. There are various new specialized pacing algorithms that aim to provide rhythm or rate control in atrial fibrillation. We review the various options for device therapy and the evidence available concerning their effectiveness.</AbstractText>Randomized trials on preventative algorithms for atrial fibrillation have not shown consistent benefit. Anti-tachycardia pacing for atrial fibrillation has inherent problems illustrated in this review and has failed to demonstrate objective improvement except in the case of atrial flutter. Several large randomized trials have demonstrated an adverse outcome with right ventricular apical pacing. These studies have shown an increase in atrial fibrillation with ventricular pacing. Recent studies have emphasised the importance of right ventricular apical pacing in burden of atrial fibrillation and therefore we discuss the likely confounding effect on previous trials and speculate on future directions.</AbstractText>The use of a device with atrial fibrillation prevention algorithms in a patient with a bradycardia indication for pacing is not unreasonable but there is no hard evidence of benefit. Patients with sinus node dysfunction should be paced in the atrium alone. There is no indication for use of a device for atrial fibrillation without a conventional indication for pacing.</AbstractText> |
9,865 | Defibrillation of the heart: insights into mechanisms from modelling studies. | Despite its critical role in restoring cardiac rhythm and thus in saving human life, cardiac defibrillation remains poorly understood. Further mechanistic inquiry is hampered by the inability of presently available experimental techniques to resolve, with sufficient accuracy, electrical behaviour confined to the depth of the ventricles. The objective of this review article is to demonstrate that realistic 3-D simulations of the ventricular defibrillation process in close conjunction with experimental observations are capable of bringing a new level of understanding of the electrical events that ensue from the interaction between fibrillating myocardium and applied shock. The article does this by reviewing the results of two studies, one on vulnerability to electric shocks and another on defibrillation. An overview of the modelling tools used in these studies is also provided. |
9,866 | Heart diseases and stroke. | A heterogeneous group of heart diseases, varying by cardiac anatomy and physiology, are responsible for a variety of embolic materials that result in cerebral and systemic embolism. Atrial fibrillation accounts for nearly half of all cardioembolic stroke, particularly in the elderly, but in the young congenital septal abnormalities such as patent foramen ovale play a more important role. Therapeutic strategies include stabilization or treatment of the underlying heart disease and prevention of embolism. Oral anticoagulant therapy is indicated for many but decision making on balancing the benefits versus risks can be difficult. New endovascular therapies and devices have become available and await clinical trials that allow them to be compared with existing medical therapies. |
9,867 | Ventricular fibrillation due to severe hypokalemia induced by steroid treatment in a patient with thyrotoxic periodic paralysis. | We report a 25-year-old Japanese man with ventricular fibrillation associated with severe hypokalemia. He developed arm and leg paralysis. He had received 2 g of methylprednisolone because thoracic epidural hematoma had been suspected in another hospital. His serum potassium was 0.8 mEq/l on arrival at our hospital. Half an hour after arrival ventricular fibrillation occurred. Treatment with electric defibrillation 8 times was successful. Afterward Graves' disease was diagnosed, therefore, his clinical symptom was diagnosed as thyrotoxic periodic paralysis. We considered that the unusual condition of hyperthyroid-related hypokalemia worsened by steroid therapy induced the ventricular fibrillation. |
9,868 | The role of vasopressin in cardiorespiratory arrest and pulmonary hypertension. | Vasopressin is a peptide synthesized in the hypothalamus whose primary role is in fluid homeostasis. It has recently gained interest as a potential agent in the treatment of cardiorespiratory arrest. Initial human studies have shown benefits with vasopressin in patients with out of hospital ventricular fibrillation and asystolic cardiac arrest. One subgroup of patients not included in these trials is patients with pulmonary hypertension, who have a five-year mortality rate of 50%. Animal studies have shown vasopressin to be a vasodilator in the pulmonary vascular system of rats, under normoxic and hypoxic conditions, with conflicting results in canines. Human studies have shown conflicting results with increases, decreases and no changes seen in pulmonary artery pressures of patients with a variety of clinical conditions. Research needs to be done in patients with pulmonary hypertension regarding the potential role of vasopressin during cardiac arrest in this subgroup. |
9,869 | Multiple types of cardiac arrhythmias in a child with head injury and raised intracranial pressure. | Arrhythmias occur as a life-threatening complication in adults with severe head injuries. A wide spectrum of brady- and tachyarrhythmias and different pathogenetic mechanisms have been described. We report an 8-year-old boy with traumatic brain injury who developed a variety of independent types of arrhythmias during the course of his illness, including supraventricular and ventricular extrasystoles, prolonged QT duration and ventricular fibrillation, accelerated junctional rhythm, and reentry tachycardia. Each arrhythmia may have had a distinct pathogenic pathway, and not all were associated with raised intracranial pressure. |
9,870 | Are implantable cardioverter defibrillator shocks a surrogate for sudden cardiac death in patients with nonischemic cardiomyopathy? | Ventricular tachyarrhythmias long enough to cause implantable cardioverter defibrillator (ICD) shocks are generally thought to progress to cardiac arrest. In previous ICD trials, shocks have been considered an appropriate surrogate for sudden cardiac death (SCD) because the number of shocks has been thought to be equivalent to the mortality excess in patients without ICDs. The practice of equating ICD shocks with mortality is controversial and has not been validated critically.</AbstractText>The Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial was a prospective, randomized, multicenter trial of ICD therapy in 458 patients with nonischemic cardiomyopathy. Patients were randomized to receive standard medical therapy (STD) or STD plus an ICD. Shock electrograms were reviewed, and the cause of death was evaluated by a separate blinded events committee. There were 15 SCD or cardiac arrests in the STD group and only 3 in the ICD arm. In contrast, of the 229 patients randomized to an ICD, 33 received 70 appropriate ICD shocks. Patients in the ICD arm were more likely to have an arrhythmic event (ICD shock plus SCD) than patients in the STD arm (hazard ratio 2.12, 95% CI 1.153 to 3.893, P=0.013). The number of arrhythmic events when one includes syncope as a potential arrhythmic event was similar in both groups (hazard ratio 1.20, 95% CI 0.774 to 1.865, P=0.414). Approximately the same number of total events was noted in each arm when we compared syncope plus SCD/cardiac arrest in the STD arm with SCD plus ICD shocks plus syncope in the ICD arm.</AbstractText>Appropriate ICD shocks occur more frequently than SCD in patients with nonischemic cardiomyopathy. This suggests that episodes of nonsustained ventricular tachycardia frequently terminate spontaneously in such patients.</AbstractText> |
9,871 | Cardiovascular complications of severe acute respiratory syndrome. | Severe acute respiratory syndrome (SARS) is a virulent viral infection that affects a number of organs and systems. This study examined if SARS may result in cardiovascular complications.</AbstractText>121 patients (37.5 (SD13.2) years, 36% male) diagnosed to have SARS were assessed continuously for blood pressure, pulse, and temperature during their stay in hospital. Hypotension occurred in 61 (50.4%) patients in hospital, and was found in 28.1%, 21.5%, and 14.8% of patients during the first, second, and third week, respectively. Only one patient who had transient echocardiographic evidence of impaired left ventricular systolic function required temporary inotropic support. Tachycardia was present in 87 (71.9%) patients, and was found in 62.8%, 45.4%, and 35.5% of patients from the first to third week. It occurred independent of hypotension, and could not be explained by the presence of fever. Tachycardia was also present in 38.8% of patients at follow up. Bradycardia only occurred in 18 (14.9%) patients as a transient event. Reversible cardiomegaly was reported in 13 (10.7%) patients, but without clinical evidence of heart failure. Transient atrial fibrillation was present in one patient. Corticosteroid therapy was weakly associated with tachycardia during the second (chi(2) = 3.99, p = 0.046) and third week (chi(2) = 6.53, p = 0.01), although it could not explain tachycardia during follow up.</AbstractText>In patients with SARS, cardiovascular complications including hypotension and tachycardia were common but usually self limiting. Bradycardia and cardiomegaly were less common, while cardiac arrhythmia was rare. However, only tachycardia persisted even when corticosteroid therapy was withdrawn.</AbstractText> |
9,872 | Modern management of arrhythmias. | The specialist management of arrhythmias has changed significantly over the past decade. This article outlines current management strategies for atrial flutter and atrial fibrillation, with particular emphasis on curative strategies with catheter ablation and the recent data on rhythm compared with rate control strategies. The expanding role of catheter ablation in the treatment of a wide variety of supraventricular and ventricular arrhythmias is discussed. The current evidence for implantable cardioverter defibrillators in the prevention of sudden cardiac death is summarised. The article also highlights the increasing recognition of a number of inherited syndromes that predispose to sudden cardiac death (for example, Brugada and long QT syndromes). |
9,873 | Selective induction of matrix metalloproteinases and tissue inhibitor of metalloproteinases in atrial and ventricular myocardium in patients with atrial fibrillation. | Atrial fibrillation (AF) produces changes in atrial structure and extracellular matrix composition, which is regulated by matrix metalloproteinases (MMPs). Moreover, AF often occurs in the setting of congestive heart failure (CHF), which also affects MMPs. Whether changes in MMPs or the tissue inhibitors of metalloproteinases (TIMPs) within atrial and ventricular myocardium are differentially regulated with AF remains unclear. Myocardium from the walls of the right atrium, right ventricle, left atrium, and left ventricle was obtained from the explanted hearts of 43 patients with end-stage CHF. AF was present in 23 patients (duration 1 to 84 months). The remaining 20 patients served as non-AF controls. The groups were well matched clinically, but left atrial (LA) size was increased in the AF cohort (5.5 +/- 0.8 vs 4.9 +/- 0.7 cm, p <0.05). Myocardial collagen content and levels of MMP-1, -2, -8, -9, -13, and -14, and TIMP-1, -2, -3, and TIMP-4 were determined. With AF, collagen content was greater within the atrial myocardium but less in the ventricular myocardium. There were chamber-specific differences in MMPs and TIMPs with AF. For example, MMP-1 in the right atrium and MMP-9 in the left atrium were greater with AF. TIMP-3 levels were greater in the right ventricle, left atrium, and left ventricle. Although total LA collagen was positively correlated with AF duration (r = 0.49, p <0.03), there was an inverse relation between soluble collagen I and AF duration (n = 6, r = -0.84, p <0.04). In conclusion, AF is associated with chamber-specific alterations in myocardial collagen content and MMP and TIMP levels, indicative of differential remodeling and altered collagen metabolism. Differences in MMP and TIMP profiles may provide diagnostic and mechanistic insights into the pathogenesis of AF with CHF. |
9,874 | A percutaneous swine model of myocardial infarction. | The aim of this study was to develop a percutaneous, low risk, and reproducible technique of MI that simulates human disease.</AbstractText>MI was induced in 44 swine (32.8+/-7.2 kg) by percutaneous embolization coil deployment in the left anterior descending coronary artery. Hemodynamic measurements, left heart catheterization, and echocardiography were performed pre, post, and 30 days after MI. 3D NOGA viability mapping was performed at baseline and 30 days. Excised hearts were examined histologically.</AbstractText>Pre-MI mortality was 6.8% and 24 h mortality was 13.6%. All pigs that survived 24 h after MI remained alive at 30 days. The mean left ventricular ejection fraction decreased from 58.4% to 42.1% (p<0.001) at 30 days. The average thrombolysis in myocardial infarction score was 3, 0, and 1.5 at baseline, post-MI, and 30 days, respectively. At 30 days, the end diastolic diameter, end diastolic volume, end systolic volume, and wall motion index increased from 3.76 to 3.89 cm, 32.5 to 50.0 ml, 14.9 to 27.0 ml, and 1.01 to 1.38, respectively (all p<0.05), while the ejection fraction decreased from 56.5% to 49.4% (p<0.01). Additionally, at 30 days, statistically significant reductions in both unipolar and bipolar voltage in the mid and apical regions of the left ventricle were observed. Postmortem pathology showed a transmural scar in the apical anteroseptal regions with fibrosis in the MI region, which accounted for 14.8% and 14.2% of the total left and right ventricular myocardial area and volume, respectively.</AbstractText>This model of MI is reliable, reproducible, has a pathophysiology similar to humans, and a lower mortality and ventricular fibrillation rates compared to other models. This model may be used to evaluate the effects of pharmacologics, gene therapy, and stem cell transplantation for the treatment of cardiovascular disease as well as studying mechanisms of cardiac remodeling.</AbstractText> |
9,875 | The effects of pre-arrest heparin administration dose for cardiac arrest model using extracorporeal lung and a heart assist (ECLHA) in dogs. | Clinical and experimental studies have shown that marked activation of blood coagulation occurs in cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Extracorporeal lung and heart assist (ECLHA) is applied in CA patients who cannot be rescued using conventional therapies. We hypothesized that the dose of heparin administered during the pre-arrest period would influence the outcome in a canine model of CA induced by 15 min of normothermia followed by ECLHA, which consists of heparin coating membrane lung and tubing. We therefore investigated the effects of two dose regimes of the pre-arrest heparin for this model.</AbstractText>Twelve mongrel female dogs were divided into two groups: a group given 200 U/kg heparin (H200, n=6) and a group given 700 U/kg heparin (H700, n=6), group during pre-arrest period. Normothermic ventricular fibrillation (VF) was induced in all dogs for 15 min, followed by 24h of ECLHA with rapidly induced mild hypothermia (33 degrees C) and 120 h of intensive care. Outcome evaluations included: (1) activated coagulation time (ACT); (2) catecholamine dose; (3) hematocrit (Hct) and platelet count; (4) survival rate; (5) neurological deficit scores (NDS); (6) postmortal macroscopic examination with the exception of the brain.</AbstractText>In the H200 group, four dogs died of cardiogenic shock within 28 h. The autopsy revealed extensive patchy hemorrhages in the heart and intestine. In the H700 group, the amount of dopamine was significantly lower (6+/-10mg versus 75+/-41 mg, p<0.05) and the survival rate was significantly higher (100% versus 17%, p<0.05) than in the H200 group. The NDS at 120 h in the H700 group was 18+/-8% and the autopsy revealed an almost normal external appearance of the vital organs. There were no significant differences between groups in either the Hct and platelet count during the 24h of resuscitation, and no bleeding complications were observed.</AbstractText>The use of ECLHA to resuscitate animals in prolonged CA may require a large dose of systemic heparin during the pre-arrest period even if ECLHA circuit was coated with heparin.</AbstractText> |
9,876 | The characteristics of postcountershock pulseless electrical activity may indicate the outcome of CPR. | When ventricular fibrillation is cardioverted to pulseless electrical activity (PEA), PEA has been regarded as a non-resuscitatable rhythm. Yet, recent reports and our earlier observations suggested otherwise. We therefore investigated outcomes after postcountershock PEA, and aimed to develop a scoring system for outcome classification at the onset of initial postcountershock PEA.</AbstractText>Data from 215 domestic pigs were retrospectively reviewed. VF was induced and untreated for 7 min. Defibrillation was attempted with up to three 150 J biphasic shocks. Failing to restore spontaneous circulation (ROSC), 1 min of CPR preceded subsequent sequences of shocks until animals were resuscitated or for a total of 15 min. Fifty-nine instances of PEA followed defibrillation, including 29 animals that attained ROSC.</AbstractText>ROSC animals required a shorter interval between the first shock and the initial postcountershock PEA, fewer shocks prior to onset of initial postcountershock PEA, demonstrated a greater VF wavelet amplitude prior to onset of initial PEA, smaller QRS intervals, and higher heart rates. Using Fisher's linear discriminant analysis, 79.3% of the ROSC and 63.3% of non-ROSC cases were predicted correctly. A total of 71.2% of all cases were classified correctly.</AbstractText>Animals in which postcountershock PEA was converted to ROSC required shorter intervals from first shock to initial postcountershock PEA, fewer shocks prior to onset of initial postcountershock PEA, had greater VF wavelet amplitude prior to initial postcountershock PEA, small QRS intervals, and higher heart rates. Fisher's discriminant analysis is helpful in predicting the likelihood of ROSC for an individual animal presenting with postcountershock PEA.</AbstractText> |
9,877 | Postoperative white blood cell count predicts atrial fibrillation after cardiac surgery. | Postoperative atrial fibrillation (AF) occurs in as many as 50% of cardiac surgery patients and represents the most common postoperative rhythm complication. The cause of AF after cardiac surgery is incompletely understood, and its prevention remains suboptimal. Currently the role of inflammation and oxidative stress on electrical remodeling is under investigation, and recent studies have demonstrated that C-reactive protein levels are elevated in AF. The purpose of the present study was to investigate the correlation between the postoperative white blood cell (WBC) count as a marker of inflammation and the development of postoperative AF after cardiac surgery.</AbstractText>Patients undergoing elective cardiac surgery in the absence of significant left ventricular dysfunction (n = 253; average age, 65 +/- 11 years) were recruited to the present prospective study. Atrial fibrillation developed during the postoperative period in 99 patients (39.1%) of the total study population. The WBC count was prospectively assessed in all patients to determine the predictive value of baseline and postoperative WBC count on development of postoperative AF. Baseline WBC count was 6.8 +/- 1.9 x 10(9)/L and 6.8 +/- 2.2 x 10(9)/L (p = 0.95), respectively, in patients with and without postoperative AF; and postoperative peak WBC count was 16.3 +/- 6.5 x 10(9)/L and 15 +/- 4.2 x 10(9)/L (p = 0.048), respectively, in patients without postoperative AF. However, neither baseline nor peak monocyte count differed significantly among patients with and without postoperative AF: 0.43 +/- 0.15 x 10(9)/L and 0.46 +/- 0.46 x 10(9)/L (p = 0.5), and 0.91 +/- 0.3 x 10(9)/L and 0.93 +/- 0.4 x 10(9)/L (p = 0.8), respectively. In addition to a more pronounced increase in peak WBC count (above v below median; odds ratio [OR], 1.8; 95% confidence interval [CI], 1.1-2.7; p < 0.05), increasing age (above v below median; OR, 2.6; CI, 1.2-3.9; p < 0.01), surgery for valvular heart disease versus coronary artery bypass grafting (OR, 2.8; CI, 1.1-3.5; p < 0.01), development of postoperative complications, such as stroke, infections, or unstable hemodynamics (OR, 1.9; CI, 1.0-7.5; p < 0.05), and perioperative nonuse of beta-adrenergic blockers (OR, 1.7; CI, 1.1-4.9; p < 0.05) were identified as independent predictors of postoperative AF by multivariate logistic regression analysis.</AbstractText>Cardiac surgery is associated with an elevated postoperative WBC count that represents a common marker of inflammation. A more pronounced increase in postoperative WBC count independently predicts development of postoperative AF. These data provide additional evidence to support the association between the inflammatory response and postoperative AF.</AbstractText> |
9,878 | A new device producing manual sternal compression with thoracic constraint for cardiopulmonary resuscitation. | Blood flow during conventional cardiopulmonary resuscitation (CPR) is usually less than adequate to sustain vital organ perfusion. A new chest compression device (LifeBelt) which compresses both the sternum and the lateral thoraces (compression and thoracic constraint) has been developed. The device is light weight, portable, manually powered and mechanically advantaged to minimize user fatigue. The purpose of this study was to evaluate the mechanism of blood flow with the device, determine the optimal compression force and compare the device to standard manual CPR in a swine arrest model.</AbstractText>Following anesthesia and instrumentation, intravascular contrast injections were performed in four animals and the performance characteristics of the device were evaluated in eight animals. In a comparative outcome study, 42 anesthetized and instrumented swine were randomized to receive LifeBelt or manual CPR. Ventricular fibrillation (VF) was induced electrically and was untreated for 7.5 min. After 7.5 min, countershocks were administered and chest compressions initiated. Pulseless electrical activity (PEA) was observed after one to three shocks in all animals. CPR was continued until restoration of spontaneous circulation (ROSC) or for 10 min after the first shock. If ROSC had not occurred within 5 min of beginning CPR, 0.01 mg/kg of epinephrine (adrenaline) was administered. During CPR, peak systolic aortic pressure (Ao), diastolic coronary perfusion pressure (CPP-diastolic aortic minus diastolic right pressure) and end-tidal CO(2) were measured.</AbstractText>Angiographic studies demonstrated cardiac compression as the mechanism of blood flow. Optimal performance, determined by coronary perfusion pressure, was observed at a sternal force of 100-130 lb (45-59 kg). In the comparative trial, significant differences in the measured CPP were observed between LifeBelt and manual CPR both at 1 min (15+/-8 mmHg versus 10+/-6 mmHg, p<0.05) and 5 min (17+/-4 mmHg versus 13+/-7 mmHg, p<0.02) of chest compression. A greater (p<0.05) ETCO(2), a marker of cardiac output and systemic perfusion, was observed with LifeBelt CPR (20+/-7 mmHg) than with manual CPR (15+/-5 mmHg) at 1 min. Peak Ao pressures were not different between methods. With the device, 86% of animals were resuscitated compared to 76% in the manual group.</AbstractText>Blood flow with the LifeBelt device is primarily the result of cardiac compression. At a sternal force of 100-130 lb (45-59 kg), the device produces greater CPP than well-performed manual CPR during resuscitation from prolonged VF.</AbstractText> |
9,879 | Leukoaraiosis is associated with functional impairment in older patients with Alzheimer's disease but not vascular dementia. | Leukoaraiosis (LA) is a common finding in older persons, and might be associated with reduced cognitive performance, gait abnormalities, and functional impairment. Although LA is more frequent in persons affected by dementia, scant data are available about its clinical consequences in this group of patients.</AbstractText>To study the association between presence of LA and functional performance in basic activities of daily living in a sample of older persons affected by dementia.</AbstractText>We conducted a cross-sectional study on 214 patients; 77 affected by late onset Alzheimer's disease (LOAD), and 137 by vascular dementia (VD). Functional status was assessed using Barthel Index (BI). LA was assessed using computed tomography.</AbstractText>In LOAD patients, LA (OR: 7.87; 1.26-48.94), and MMSE score (OR: 0.83; 0.71-0.98) were associated with the risk of severe disability, independent of age, gender, diabetes, hypertension, coronary heart disease, left ventricular hypertrophy, atrial fibrillation, and brain atrophy. In VD patients, MMSE score (OR: 0.77; 0.64-0.93), and CHD (OR: 7.41; 1.09-50.21), but not LA (OR: 2.07; 0.45-9.45) were associated with a severe functional impairment after multivariate adjustment.</AbstractText>Our study suggests that LA might be associated with a worse functional status in basic activities of daily living in patients affected by LOAD but not VD. LA might act synergistically with cognitive and behavioural disturbances to the onset and progression of disability of these patients.</AbstractText> |
9,880 | Correlation of alpha-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in rats. | We have analysed alterations of alpha-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of alpha-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of alpha-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in alpha-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. |
9,881 | Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study. | Steep action potential duration (APD) restitution has been shown to facilitate wavebreak and ventricular fibrillation. The global APD restitution properties in cardiac patients are unknown. We report a combined clinical electrophysiology and computer modelling study to: (1) determine global APD restitution properties in cardiac patients; and (2) examine the interaction of the observed APD restitution with known arrhythmia mechanisms. In 14 patients aged 52-85 years undergoing routine cardiac surgery, 256 electrode epicardial mapping was performed. Activation-recovery intervals (ARI; a surrogate for APD) were recorded over the entire ventricular surface. Mono-exponential restitution curves were constructed for each electrode site using a standard S1-S2 pacing protocol. The median maximum restitution slope was 0.91, with 27% of all electrode sites with slopes<0.5, 29% between 0.5 and 1.0, and 20% between 1.0 and 1.5. Eleven per cent of restitution curves maintained slope>1 over a range of diastolic intervals of at least 30 ms; and 0.3% for at least 50 ms. Activation-recovery interval restitution was spatially heterogeneous, showing regional organization with multiple discrete areas of steep and shallow slope. We used a simplified computer model of 2-D cardiac tissue to investigate how heterogeneous APD restitution can influence vulnerability to, and stability of re-entry. Our model showed that heterogeneity of restitution can act as a potent arrhythmogenic substrate, as well as influencing the stability of re-entrant arrhythmias. Global epicardial mapping in humans showed that APD restitution slopes were organized into regions of shallow and steep slopes. This heterogeneous organization of restitution may provide a substrate for arrhythmia. |
9,882 | Onset and progression of fatal coronary dissection during angiography. | Coronary angiography was performed in a 43-year-old man admitted to hospital for chest pain. The first frames after the injection of contrast medium showed plaque in the left main coronary artery and subtotal stenosis of the mid-left anterior descending coronary artery. Dissection of the left main coronary artery appeared, with intimal flaps at the proximal segment of the main trunk and the origin of the left anterior descending artery. Dissection rapidly progressed into the circumflex artery and left anterior descending coronary artery. Although two stents were deployed in the left main coronary artery, the patient died of ventricular fibrillation.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Porzionato</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Environmental Medicine and Publlic Health, University of Padova, Padova, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zancaner</LastName><ForeName>Silvano</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ramondo</LastName><ForeName>Angelo</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Ferrara</LastName><ForeName>Santo D</ForeName><Initials>SD</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Can J Cardiol</MedlineTA><NlmUniqueID>8510280</NlmUniqueID><ISSNLinking>0828-282X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000784" MajorTopicYN="N">Aortic Dissection</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003323" MajorTopicYN="N">Coronary Aneurysm</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017023" MajorTopicYN="N">Coronary Angiography</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D023921" MajorTopicYN="N">Coronary Stenosis</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017809" MajorTopicYN="N">Fatal Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre">Une coronarographie a été exécutée chez une femme de 43 ans hospitalisée pour des douleurs thoraciques. Les premières images après l’injection du produit de contraste ont révélé la présence de plaque dans le tronc de l’artère coronaire gauche et d’une sténose partielle de l’interventriculaire antérieure proximale. Une dissection du tronc de l’artère coronaire gauche s’est manifestée, avec des lambeaux intimaux au segment proximal du tronc et à l’origine de l’interventriculaire antérieure. La dissection a rapidement progressé dans l’artère auriculoventriculaire et l’interventriculaire antérieure. Bien que deux endoprothèses aient été installées dans le tronc de l’artère coronaire gauche, la patiente est décédée d’une fibrillation ventriculaire. |
9,883 | Tissue Doppler-derived index of left ventricular filling pressure, E/E', predicts survival of patients with non-valvular atrial fibrillation. | To investigate whether the ratio of early transmitral flow velocity (E) to early diastolic mitral annular velocity (E') predict prognosis in patients with non-valvular atrial fibrillation.</AbstractText>230 patients with non-valvular atrial fibrillation were enrolled and studied. According to E/E' value, patients were divided into groups with lower (group A with E/E' <or= 15) and higher (group B with E/E' > 15) E/E'.</AbstractText>During follow up (average 245 days), 21 (9.1%) deaths were documented. All cause death (15/90 (16.7%) v 6/140 (4.3%)), cardiac death (10 (11.1%) v 2 (1.4%)) and congestive heart failure (16 (17.8%) v 8 (5.7%)) were more common in group B than in group A (all p < 0.01). A Kaplan-Meier survival curve showed that the cumulative survival rate was significantly lower in group B than in group A (log rank p = 0.0013). By multivariate logistic regression analysis, E/E' (chi(2) = 4.47, odds ratio (OR) 1.05, 95% confidence interval (CI) 1.01 to 1.11, p = 0.03) and age (chi(2) = 6.45, OR 1.06, 95% CI 1.01 to 1.11, p = 0.02) were independent predictors of mortality.</AbstractText>The Doppler-derived index of left ventricular filling pressure, E/E', is a powerful predictor of the clinical outcome of patients with non-valvular atrial fibrillation.</AbstractText> |
9,884 | [Atrial fibrillation, heart failure and QT interval prolongation -- diastolic and therapeutic difficulties]. | A case of a 51-year old female with persistent atrial fibrillation, decompensated heart failure and polymorphic ventricular tachycardia due to acquired long QT syndrome is presented. Difficulties in monitoring QT interval and factors associated with torsades de points are discussed. |
9,885 | The relationship between T-wave polarity and clinical as well as angiographic findings in the early stage of acute myocardial infarction. | Restoration of a positive T-wave in the chronic stage of myocardial infarction (MI) is usually seen in patients with a non-Q-wave (non-transmural) MI, where a viable tissue is present. The causes and significance of a positive T-wave in the early phase of acute MI are not clear.</AbstractText>To investigate angiographic and clinical characteristics of patients with a positive T-wave in the early stage of acute MI.</AbstractText>We evaluated the clinical and angiographic data in relation to T-wave polarity in 188 patients with acute MI. Coronary risk factors, pre-infarction angina, CK-MB level, left ventricular ejection fraction and angiographic findings were analysed. Death, cardiogenic shock, ventricular tachycardia/fibrillation and high-degree atrioventricular block were regarded as in-hospital complications. All electrocardiograms were divided into two groups, according to the shape of the T-wave, as exhibiting a positive T-wave or negative T-wave.</AbstractText>A positive T-wave was present in 30 (15.9%) patients. None of the patients with a positive T-wave had three-vessel disease compared with 21.5% of patients with a negative T-wave (p <0.04). In-hospital complication rates were similar in both groups.</AbstractText>Patients with a positive T-wave in the early phase of acute MI have significantly less frequently three-vessel disease than patients with a negative T-wave.</AbstractText> |
9,886 | Does p-wave dispersion predict the atrial fibrillation occurrence after direct-current shock therapy? | Supraventricular tachycardia attacks, including atrial fibrillation (AF), occur after both external and internal cardioversions. These attacks of atrial fibrillation after direct-current (DC) shock may be related to hemodynamic impairment, thromboembolic events, or enhanced electrical instability of the ventricular and atrial myocardium, especially in predisposed patients. In this study, the authors aimed to show the importance of P-wave dispersion (PWD), which lead the atrium to fibrillate, in predicting post-DC shock AF after external cardioversion. Thus physicians may be able to choose the patients with high risk for AF occurrence and apply some other therapeutic modalities to those patients. The authors identified 18 patients in whom an AF attack was induced by urgent or elective cardioversion for a ventricular tachycardia attack and compared these patients with a control group composed of 40 patients without AF in regard to some clinical, echocardiographic, and electrocardiographic parameters. Left atrial diameters were greater (4.3+/-0.3 vs 3.5+/-0.5 cm, p = 0.001), left ventricular ejection fractions (LVEF) were lower (45.2+/-8.2 vs 54.9+/-7.5, p = 0.001), the energy needed for successful cardioversion was higher (166.6+/-59.4 vs 80.8+/-51.6 J, p = 0.001), and P max (135.2+/-7.4 vs 118.7+/-10.5 ms, p = 0.001) and PWD (53.8+/-12.2 vs 23.8+/-9.5 ms, p = 0.001) values were higher in patients with AF when compared to those without AF. Thus, the patients with higher PWD values had a greater risk for development of AF after a DC shock. |
9,887 | Development and testing of an algorithm to detect implantable cardioverter-defibrillator lead failure. | Implantable cardioverter-defibrillator (ICD) lead failures often present as inappropriate shock therapy. An algorithm that can reliably discriminate between ventricular tachyarrhythmias and noise due to lead failure may prevent patient discomfort and anxiety and avoid device-induced proarrhythmia by preventing inappropriate ICD shocks.</AbstractText>The goal of this analysis was to test an ICD tachycardia detection algorithm that differentiates noise due to lead failure from ventricular tachyarrhythmias.</AbstractText>We tested an algorithm that uses a measure of the ventricular intracardiac electrogram baseline to discriminate the sinus rhythm isoelectric line from the right ventricular coil-can (i.e., far-field) electrogram during oversensing of noise caused by a lead failure. The baseline measure was defined as the product of the sum (mV) and standard deviation (mV) of the voltage samples for a 188-ms window centered on each sensed electrogram. If the minimum baseline measure of the last 12 beats was <0.35 mV-mV, then the detected rhythm was considered noise due to a lead failure. The first ICD-detected episode of lead failure and inappropriate detection from 24 ICD patients with a pace/sense lead failure and all ventricular arrhythmias from 56 ICD patients without a lead failure were selected. The stored data were analyzed to determine the sensitivity and specificity of the algorithm to detect lead failures.</AbstractText>The minimum baseline measure for the 24 lead failure episodes (0.28 +/- 0.34 mV-mV) was smaller than the 135 ventricular tachycardia (40.8 +/- 43.0 mV-mV, P <.0001) and 55 ventricular fibrillation episodes (19.1 +/- 22.8 mV-mV, P <.05). A minimum baseline <0.35 mV-mV threshold had a sensitivity of 83% (20/24) with a 100% (190/190) specificity.</AbstractText>A baseline measure of the far-field electrogram had a high sensitivity and specificity to detect lead failure noise compared with ventricular tachycardia or fibrillation.</AbstractText> |
9,888 | Survival in biopsy-proven myocarditis: a long-term retrospective analysis of the histopathologic, clinical, and hemodynamic predictors. | We hypothesized that histopathology predicts survival without cardiac transplantation in patients with biopsy-proven myocarditis.</AbstractText>The role of endomyocardial biopsy in diagnosing myocarditis remains controversial. Histopathology has been integrated with clinical and hemodynamic features to predict prognosis. However, the influence of histopathology on survival > 5 years has not been explored.</AbstractText>We retrospectively identified 112 consecutive patients with histopathologic confirmation of myocarditis. We examined these patients' clinical presentation, hemodynamic assessment, hospital course, and treatment. We selected 14 variables that might influence survival without cardiac transplantation.</AbstractText>A total of 62 (55%) of 112 patients had lymphocytic myocarditis; 88 (79%) and 63 (56%) were alive without cardiac transplantation at 1 and 5 years, respectively. Median follow-up was a mean 95.5 months and median 74.5 months. Among the 55 with complete data of the 14 candidate predictor variables, age, sex, and clinical presentation with congestive heart failure and ventricular (ventricular tachycardia or fibrillation) or atrial arrhythmias (atrial fibrillation or flutter) did not predict the study end point of death or need for transplantation. In univariate analysis, pulmonary capillary wedge pressure > or = 15 mm Hg significantly predicted the study end point. In multivariate analysis, pulmonary capillary wedge pressure > or = 15 mm Hg and histopathology of lymphocytic, granulomatous, or giant cell myocarditis each significantly predicted mortality or transplant (P = .047, P = .013, and P = .054, respectively) on cumulative survival without cardiac transplantation.</AbstractText>Histopathology predicts long-term survival in patients with myocarditis. Clinical presentation, including presentation with congestive heart failure, ventricular tachycardia/ventricular fibrillation, or atrial fibrillation/atrial flutter, does not predict survival without transplantation. Endomyocardial biopsy can play a role in predicting transplant-free survival in patients with myocarditis.</AbstractText> |
9,889 | Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle-aged and elderly adults: the Strong Heart Study (SHS). | Echocardiographic left atrial (LA) volume has been documented to be an independent predictor of cardiovascular events. Less is known about the predictive ability of anteroposterior LA diameter, a simpler measure of LA size obtained routinely during echocardiographic evaluation.</AbstractText>We investigated the prognostic value of LA diameter for incident cardiovascular events in 2804 American Indians free of clinical cardiovascular disease, valvular disease, and atrial fibrillation. Echocardiographic variables were obtained using standardized methods, and previously derived sex-specific partition values were used to define left ventricular (LV) hypertrophy indexed to height(2.7) (in meters) and LA enlargement (> 4.2 cm in men, > 3.8 cm in women). Cardiovascular events included nonfatal stroke, coronary heart disease, congestive heart failure, and fatal cardiovascular disease based on validated definitions.</AbstractText>During a median follow-up of 7 years, 368 events occurred. LA diameter, both as a continuous and as a categorical variable, was significantly associated with incident cardiovascular events in unadjusted analyses. In multivariable analyses that adjusted for age, sex, body mass index, hypertension, diabetes, total cholesterol-high-density lipoprotein cholesterol, smoking, renal insufficiency, LV hypertrophy, abnormal LV systolic and diastolic function, mitral annular calcification, fibrinogen, and C-reactive protein, both LA diameter (risk ratio 1.04/mm, 95% CI 1.02-1.07, P < .002) and LA enlargement (risk ratio 1.57, 95% CI 1.17-2.10, P = .002) remained independent predictors of first cardiovascular events.</AbstractText>In this population-based cohort, LA diameter independently predicted incident cardiovascular events after adjustment for established clinical, echocardiographic, and inflammatory risk factors. This simple measure of LA dilatation can identify individuals at heightened risk who may warrant more aggressive risk factor modification.</AbstractText> |
9,890 | Prediction of the recurrence of atrial fibrillation after cardioversion in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study. | The early recurrence of atrial fibrillation (AF) after cardioversion and the need for frequent cardioversions to maintain sinus rhythm are important clinical features of AF management.</AbstractText>We evaluated patients in the AFFIRM study whose qualifying episode of AF lasted > or = 48 hours and was terminated by cardioversion. Clinical, electrocardiographic, and echocardiographic risk factors associated with AF recurrence within 2 months of cardioversion and > or = 2 cardioversions during the first year were identified using multivariate analysis in 1293 eligible patients.</AbstractText>The risk factors for the recurrence of AF within 2 months of cardioversion were no coronary artery disease and an electrocardiographic lead II P-wave duration of > 135 milliseconds. In the subset of patients not taking antiarrhythmic drug therapy, the multivariate risk factors were no coronary artery disease, second or greater episode of AF, left ventricular ejection fraction < 0.50, and mitral valve thickening. Significant risk factors for the need for > 2 cardioversions in the first year in patients taking antiarrhythmic medication were left atrial diameter > 4.5 cm and mitral valve thickening. The overall sensitivity and specificity of these parameters for recurrence and repeated cardioversion are low.</AbstractText>There are several risk factors for difficulty maintaining sinus rhythm after cardioversion of persistent AF. The clinical predictive value of these factors is low, and they probably should not be used to justify withholding rhythm control efforts in patients who might benefit from sinus rhythm.</AbstractText> |
9,891 | Strategy for safe performance of magnetic resonance imaging on a patient with implantable cardioverter defibrillator. | Clinically indicated magnetic resonance imaging (MRI) of the brain was safely performed at 1.5 T on a patient with an implantable cardioverter defibrillator (ICD). The ICD was reprogrammed to detection only, and imaging hardware and protocols were modified to minimize radiofrequency power deposition to the ICD system. The integrity of the ICD system was verified immediately post-MRI and after 6 weeks, including an ICD test with induction of ventricular fibrillation. This case demonstrates that in exceptional circumstances, in carefully selected patients, and using special precautions, an MRI exam of the brain may be possible in patients with ICDs. |
9,892 | Catheter ablation for an incessant form of antiarrhythmic drug-resistant ventricular fibrillation after acute coronary syndrome. | A 77-year-old man was admitted with an acute coronary syndrome (ACS), severe heart failure (HF), and repeated ventricular fibrillation (VF) episodes. A single premature ventricular complex (PVC) induced ventricular tachycardia (VT), which degenerated to VF reproducibly. This PVC was eliminated by catheter ablation at the left ventricular posteroseptal region where double Purkinje potentials preceding the ventricular wave had been recorded. The electrical storm disappeared, and programmable stimulation failed to induce any tachyarrhythmias after the ablation. A Purkinje fiber network-related PVC served as a trigger and as a substrate for VT and VF in a case of ACS with HF. |
9,893 | Dyslipidemia is associated with ventricular tachyarrhythmia in patients with acute ST-segment elevation myocardial infarction. | Ventricular tachyarrhythmia developing in the acute stage of myocardial infarction (MI) is an important cause of sudden cardiac death. The aim of this study was to determine whether dyslipidemia is associated with the occurrence of ventricular tachycardia/fibrillation (VT/VF) during the acute stage of ST-segment elevation MI (STEMI).</AbstractText>A total of 58 patients experiencing VT/VF within 24 hours after the onset of MI were selected as the study group. A group of 58 patients with MI but without VT/VF was selected as the control group matched for sex (overall, 104 males), age (overall, 58 +/- 10 years), and the use of thrombolytic therapy (n = 82). The lipid profiles including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride were measured during the first week and at the third month after the index MI. Other coronary risk factors, and clinical, hemodynamic and angiographic characteristics were also included in the assessment.</AbstractText>During the acute stage, patients with VT/VF had higher levels of LDL-C and lower blood pressure on initial arrival at our hospital. At the 3-month follow-up, those patients with VT/VF showed higher levels of TC, LDL-C and triglyceride. Multivariate analysis revealed that LDL-C (p < 0.001) at the 3-month follow-up, mean blood pressure on arrival (p < 0.01), and the difference in triglyceride levels between the first week and the third month (p < 0.05) were independent predictors for the occurrence of VT/VF in the acute stage of MI.</AbstractText>This study suggests that dyslipidemia imposes a higher risk of developing tachyarrhythmia in the acute phase of STEMI.</AbstractText> |
9,894 | A case of dextrocardiac ventricular fibrillation arrest. | Successful defibrillation of a patient with dextrocardia using conventional anterolateral paddle positions raises doubts about the necessity to place paddles in the exact recommended positions. Evidence found relates either to volunteers in a laboratory setting or to defibrillation of atrial arrhythmias. The conclusion is that there is no published difference either in transthoracic impedance or in success of defibrillation between anteroposterior and anterolateral paddle positions. In the absence of any evidence for an ideal apical paddle position in the standard anterolateral defibrillation of ventricular arrhythmias, the emphasis in ALS and resuscitation guidelines on "correct" positioning seems misplaced, and, by adding unnecessary information, may hinder learning the skill of defibrillation. Early defibrillation is crucial to successful recovery from cardiac arrest and anything that delays cardioversion should be avoided. The limited evidence suggests that the exact position of the paddles does not matter. The time taken to find the "correct" position is time wasted and it may instead be preferable to teach people merely to place the apical paddle to the left of the nipple in the midaxillary line. |
9,895 | Renal infarction without hematuria: two case reports. | Clinical cases of renal infarction are rarely seen and often either misdiagnosed or initially treated as something else. In most circumstances, renal infarctions are discovered accidentally, not due to a consideration of the diagnosis. A review of the literature reveals that we ought to search for the entity in patients with risk factors such as atrial fibrillation, infarction history or potential, mitral stenosis, infective endocarditis, atrial or ventricular septal defect, hypertension and ischemic heart diseases. In addition, the rise of LDH (lactate dehydrogenase) in serum and the presence of hematuria serves as a good indicator of the malady. We present two cases we encountered early this year in our Emergency Department. In both cases, white blood cell count and LDH showed significant increases, but there was no hematuria present. Both were successfully treated with LMWH (low-molecular-weight heparin). Upon discharge, both patients regained normal renal function. |
9,896 | Measurement of microvolt T-wave alternans, a new arrhythmic risk stratification test, in Type 2 diabetic patients without clinical cardiovascular disease. | Patients with a positive microvolt T-wave alternans (TWA) are at increased risk of ventricular arrhythmias and sudden cardiac death. Although Type 2 diabetes is associated with an increased risk of these events, there is a dearth of available data on measurements of TWA in people with Type 2 diabetes.</AbstractText>We studied 43 Type 2 diabetic volunteers who were free of diagnosed cardiovascular disease (CVD). Microvolt TWA analysis was performed non-invasively using the CH 2000 system during submaximal exercise with the patients sitting on a bicycle ergometer.</AbstractText>TWA analysis was positive in 9 (21%) patients, negative in 32 (74.4%) and indeterminate in 2 (4.6%) subjects. TWA positive patients had significantly higher HbA(1c) levels than those with TWA negativity (8.1 +/- 0.9 vs. 7.2 +/- 0.8%, P < 0.01). Age, sex, BMI, blood pressure, lipids, 24-h heart rate variability, QTc interval duration, smoking history, diabetes duration and treatment, and microvascular complication status did not differ between the groups. In regression logistic analysis, HbA(1c) was the only significant predictor of TWA positivity (odds ratio 5.7, 95% CI 1.3-26, P = 0.023) after controlling for potential confounders.</AbstractText>These results suggest that in Type 2 diabetic patients without clinically manifest CVD, TWA positivity is common (approximately 20%) and is closely correlated with glycaemic control.</AbstractText> |
9,897 | A lethal complication of propofol. | High-dose propofol infusion for sedation of patients in the intensive care unit can result in rhabdomyolysis, acute renal failure, metabolic acidosis, hyperkalemia, ventricular arrhythmia, hyperthermia, and death. The death of a patient with such complications after lung biopsy is reported. Until a safer dosage range has been determined, propofol infusion at rates higher than 5 mg x kg(-1) x h(-1) should be discouraged for long-term sedation (> 48 h). |
9,898 | Cardiocerebral resuscitation for cardiac arrest. | Survival rates from out-of-hospital cardiac arrest continue to be low despite periodic updates in the Guidelines for Emergency Medical Services and periodic improvements such as the addition of automatic external defibrillators (AEDs). The low incidence of bystander cardiopulmonary resuscitation (CPR), substantial time without chest compressions throughout the resuscitation effort, and a lack of response to initial defibrillation after prolonged ventricular fibrillation contribute to these unacceptably poor results. Resuscitation guidelines are only revised every 5 to 7 years and can be difficult to change because of the lack of randomized controlled trials in humans. Such trials are rare because of a number of logistical difficulties, including the problem of obtaining informed consent. An alternative approach to advancing resuscitation science is for evidence-based demonstration projects in areas that have adequate records, so that one may determine whether the new approach improves survival. This is reasonable because the current guidelines make provisions for deviations under certain local circumstances or as directed by the emergency medical services medical director. A wealth of experimental evidence indicates that interruption of chest compressions for any reason in patients with cardiac arrest is deleterious. Accordingly, a new approach to out-of-hospital cardiac arrest called cardiocerebral resuscitation (CCR) was developed that places more emphasis on chest compressions for witnessed cardiac arrest in adults and de-emphasizes ventilation. There is also emphasis on chest compressions before defibrillation in circulatory phase of cardiac arrest. CCR was initiated in Tucson, Arizona, in November 2003, and in two rural Wisconsin counties in early 2004. |
9,899 | [Ventricular fibrillation caused by a misplaced Sengstaken tube]. | Uncontrollable hemorrhage from esophageal varicose veins in portal hypertension and cirrhosis of the liver may be treated with a Sengstaken-Blakemore tube. A case of ventricular fibrillation caused by a misplaced Sengstaken-Blakemore tube is described. Patients with a Sengstaken-Blakemore tube in place should be checked by a trained nurse for early signs of misplacement of the tube. |
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