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Predictive significance for sudden death of microvolt-level T wave alternans in New York Heart Association class II congestive heart failure patients: a prospective study.

Sudden cardiac death (SDC) is responsible for approximately 60-70% of deaths in New York Heart Association (NYHA) class II congestive heart failure (CHF) patients. Recently, microvolt-level T wave alternans has been proposed as a new noninvasive tool to identify CHF patients at risk for SCD and ventricular tachycardia/fibrillation (VT/VF).</AbstractText>To determine the prognostic value of MTWA in NYHA class II patients.</AbstractText>Among 181 consecutive CHF patients with ischemic and nonischemic cardiomyopathy, 73 patients in NYHA class II with left ventricular ejection fraction &lt;45% were selected and prospectively investigated. MTWA was determined during bicycle exercise testing. The study end point was defined as SCD, documented sustained VT/VF and appropriate implantable cardioverter defibrillator (ICD) shock.</AbstractText>MTWA was positive in 30 (41%) patients, negative in 26(36%) patients and indeterminate in 17 (23%) patients. During an average follow-up of 17.1+/-7.4 months, seven patients had an arrhythmic event in the MTWA positive group, whereas one and no events occurred in the indeterminate and negative group, respectively. From Kaplan-Meier univariate analysis and multivariate Cox analysis, MTWA was a significant arrhythmic risk stratifier (p=0.01 and p=0.03, respectively). Sensitivity, specificity, negative and positive predictive values of MTWA were 100%, 53%, 100% and 24%, respectively.</AbstractText>Our data suggest that MTWA is a promising predictor of arrhythmic events in NYHA class II CHF patients.</AbstractText>

Heart failure after myocardial revascularization: risk markers.

We investigated the prognostic weight of several risk factors for heart failure in patients undergoing CABG. We followed 351 consecutive patients for 18+/-12 months after surgery to assess clinical outcome, presence and degree of heart failure. The risk of developing heart failure &gt;class 2 at 1 year was investigated by logistic regression on the following preoperative variables: sex, age, left ventricular EF, QRS duration, previous MI, history of heart failure, atrial fibrillation (AF), hypertension, hypercholesterolemia, diabetes, previous stroke. Age was 70+/-8 years and EF was 54+/-12% at the time of surgery. Heart failure &gt;class 2 occurred in 95/351 patients (27%) at follow up. Logistic regression identified QRS duration (OR=1.02), a history of stroke (OR=3.94), and diabetes (OR=1.98) as predictors of CHF at follow up. All the other variables were not risk markers for heart failure at logistic regression. Thirty five patients (10%) had QRS&gt; or =140 ms before surgery; 51% of them had CHF at follow up compared to 24% of patients with QRS&lt;140 ms (p&lt;0.05). In the current surgical era, candidates to CABG (50% of patients older than 70 years) have a relevant likelihood of heart failure at follow up, despite myocardial revascularization. Risk stratification may rely upon inexpensive variables as previous stroke, diabetes, and QRS duration. A minority of patients (5%) could benefit from LV-based pacing, which should be considered at the same surgical time via an epicardial implantation.

Diagnosis of unexplained cardiac arrest: role of adrenaline and procainamide infusion.

Cardiac arrest with preserved left ventricular function may be caused by uncommon genetic conditions. Although these may be evident on the ECG, long-term monitoring or provocative testing is often necessary to unmask latent primary electrical disease.</AbstractText>Patients with unexplained cardiac arrest and no evident cardiac disease (normal left ventricular function, coronary arteries, and resting corrected QT) underwent pharmacological challenge with adrenaline and procainamide infusions to unmask subclinical primary electrical disease. Family members underwent noninvasive screening and directed provocative testing on the basis of findings in the proband. Eighteen patients (mean+/-SD age, 41+/-17 years; 11 female) with unexplained cardiac arrest were assessed. The final diagnosis was catecholaminergic ventricular tachycardia (CPVT) in 10 patients (56%), Brugada syndrome in 2 patients (11%), and unexplained (idiopathic ventricular fibrillation) in 6 patients (33%). Of 55 family members (mean+/-SD age, 27+/-17 years; 33 female), 9 additional affected family members were detected from 2 families, with a single Brugada syndrome patient and 8 CPVT patients.</AbstractText>Provocative testing with adrenaline and procainamide infusions is useful in unmasking the etiology of apparent unexplained cardiac arrest. This approach helps to diagnose primary electrical disease, such as CPVT and Brugada syndrome, and provides the opportunity for therapeutic intervention in identified, asymptomatic family members who harbor the same disease.</AbstractText>

An unusual clinical presentation resembling superior vena cava syndrome post heart surgery.

An unusual sequence of post operative events heralded by hemodynamic deterioration followed by dyspnea and rapidly progressive dilatation of superficial neck and facial veins, resembling a superior vena cava syndrome, two days post surgical resection of filamentous aortic valve masses, closure of a patent foramen ovale, and performance of a modified Maze procedure for atrial fibrillation in a patient that presented with transient neurologic findings is presented.</AbstractText>Although both clinical findings and hemodynamic derangements completely resolved following tricuspid valve repair aimed to correct the new onset severe tricuspid regurgitation noted post operatively; a clear mechanism was not readily obvious and diagnostic testing data somewhat conflictive. We present a careful retrospective examination of all clinical data and review possible clinical entities that could have been implicated in this particular case and recognize that transesophageal echocardiographic findings were most useful in identifying the best course of action.</AbstractText>After reviewing all clinical data and despite the inconclusive nature of test results; the retrospective examination of transesophageal echocardiographic findings proved to be most useful in identifying the best course of action. We postulate that in our case, resolution of the suspected pulmonary embolism with anticoagulation and reestablishment of a normal right ventricular geometry with tricuspid valve repair worked in unison in restoring normal hemodynamics and resolving both dyspnea and venous dilatation.</AbstractText>

Radiofrequency catheter septal ablation for hypertrophic obstructive cardiomyopathy in childhood.

Two patients, a 5 year old boy with progressive hypertrophic obstructive cardiomyopathy and increasing symptoms despite appropriate pharmacologic therapy and an 11 year old girl with symptoms of tiredness and peak instantaneous LVOT gradient of 80 and 90 mmHg respectively were considered for radiofrequency catheter septal ablation, to relieve the left ventricular outflow tract obstruction. Via a femoral arterial approach, the His bundle was initially plotted and marked using the LocaLisa navigation system. Subsequently, using a cooled tip catheter a series of lesions was placed in the hypertrophied septum, commencing distally in the ventricle and proceeding towards the aortic valve, taking care to stay away from the His bundle. The procedure was deemed to be completed when the entire extent of the hypertrophied septum had been treated. In the boy the procedure was complicated by two episodes of ventricular fibrillation, requiring DC cardioversion, but without any neurologic sequelae. The peak to peak gradient between left ventricle and aorta was 50 mmHg and 60 mmHg respectively pre-ablation, and remained unchanged immediately after. Both patients were discharged from the hospital 48 hours later. Serial measurement of serum Troponin T and CK-MB isoenzyme confirmed significant myocardial necrosis. Follow-up echocardiography at 7 days and at 6 weeks post-ablation respectively confirmed a beneficial hemodynamic result, with reduction of left ventricular outflow obstruction and relief of symptoms. In young children, in whom alcohol induced septal ablation is not an option, radiofrequency catheter ablation offers an alternative to surgery, with the benefits of repeatability and a lower risk of procedure-related permanent AV block.

[Safety and feasibility of dobutamine-atropine stress echocardiography in octogenarian patients].

To assess the feasibility and safety of dobutamine-atropine stress echocardiography (DASE) in octogenarians.</AbstractText>We evaluated 5,467 DASE which were distributed in two groups: group I (GI) with 203 DASE performed in octogenarians, and group II (GII), the control group, with 5,264 DASE. The mean age of GI and GII was 83 +/- 3 (80-95) and 59 +/- 11 (17-79) years, respectively. DASE parameters that were prospectively collected, were compared and analyzed.</AbstractText>The percentage of patients that achieved maximum heart rate was 63.5% in GI and 41% in GII (p &lt; 0.001), and GI patients required less atropine compared to GII (GI = 47%, GII = 78%, p &lt; 0.001). The presence of chest pain (GI = 13%, GII = 15.6%, p = 0.429) and DASE positive for myocardial ischemia (GI = 20.7%, GII = 16.9%, p = 0.296) were not statistically different between the two groups. However, concomitant positive DASE and absence of chest pain (GI = 17%, GII = 11%, p = 0.029) was higher in GI. The incidence of premature beats in GI was higher than in GII (GI = 47.8%, GII = 27.6%, p &lt; 0.001), and there were more supraventricular tachyarrhythmias (ST) in GI than in GII (GI = 5.9%, GII = 1.9%, p = 0.001). Out of 11 ST that happened in GI, 9 reverted spontaneously. There weren't either deaths or acute myocardial infarction. Ventricular fibrillation only happened in GII (2 cases, 0.03%).</AbstractText>In the present study, octogenarians achieved maximum heart rate more frequently despite the lesser amount of atropine that they required for DASE completion. Moreover, in this elderly population, there was a higher correlation between positive DASE and absence of chest pain. Although octogenarians did present more heart rhythm disturbs, they usually resolved spontaneously. In our study, DASE proved to be feasible and safe in octogenarians.</AbstractText>

[Calcium channel antagonists and arrhythmias].

Ca channel antagonists (CCA) including verapamil and diltiazem work as antiarrhythmic drugs. Because CCA suppresses conduction through atrio-ventricular (AV) node, it is effective on both AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). It is also useful to reduce ventricular response during atrial fibrillation/flutter. Idiopathic left ventricular tachycardia (VT) with a right bundle-branch block configuration and superior axis is sensitive to verapamil, and thus called as verapamil-sensitive VT. A caution should be needed to prevent adverse effects based on cardio-depressive effects of CCA.

Arrhythmic complications of acute coronary syndromes.

Cardiac arrhythmias routinely manifest during or following an acute coronary syndrome (ACS). Although the incidence of arrhythmia is directly related to the type of ACS the patient is experiencing, the clinician needs to be cautious with all patients in these categories. As an example, nearly 90% of patients who experience acute myocardial infarction (AMI) develop some cardiac rhythm abnormality and 25% have a cardiac conduction disturbance within 24 hours of infarct onset. In this patient population, the incidence of serious arrhythmias, such as ventricular fibrillation (4.5%) ,is greatest in the first hour of an AMI and declines rapidly thereafter. This article addresses the identification and treatment of arrhythmias and conduction disturbances that complicate the course of patients who have ACS, particularly AMI and thrombolysis. Emphasis is placed on mechanisms and therapeutic strategies.

Rapid cardiac ultrasound of inpatients suffering PEA arrest performed by nonexpert sonographers.

Cardiac arrest presenting as pulseless electrical activity (PEA) currently has a very low survival rate. Many of the conditions underlying PEA (cardiac tamponade, hypovolemia, and pulmonary embolus) are associated with specific cardiac ultrasound findings. The aim of this study was to evaluate a rapid cardiac ultrasound assessment performed by trained nonexpert sonographers integrated into the ACLS response system at a major medical center.</AbstractText>An emergency sonography system was created and deployed to each inpatient cardiac arrest occurring at Dartmouth Hitchcock Medical Center between November 1, 2003 and April 30, 2004. Thirteen internal medicine house officers received training to perform a limited subcostal cardiac ultrasound examination designed to diagnose cardiac tamponade, pulmonary embolus, severe hypovolemia, and lack of cardiac motion. Time from arrest alert to sonographic result, and correlation with over-reading by blinded echocardiography physicians were assessed.</AbstractText>A complete emergency ultrasound examination was performed in five PEA arrests. The average time from arrest alert to interpretation was 7.75 min. (95% CI 2.8-18.3 min). Three of these examinations (60%, 95% CI 14.7-94.7%) were adequate for interpretation. Agreement between the nonexpert sonographer and echocardiography physician occurred in four of five (kappa=0.706) cases.</AbstractText>Rapid cardiac sonography can be successfully integrated in the ACLS response. Nonexpert sonographers may be able to provide useful interpretive information when sufficiently trained.</AbstractText>

Incidence of EMS-treated out-of-hospital cardiac arrest in Europe.

The potential impact of efforts in Europe to improve survival from out-of-hospital cardiac arrest is unclear, in part, because estimates of incidence and survival are uncertain. The aim of the investigation was to determine a representative European incidence and survival from cardiac arrest in all-rhythms and in ventricular fibrillation treated by the emergency medical services (EMS).</AbstractText>We used Medline to identify peer-reviewed articles published between 1 January 1980 and 30 June 2004 that reported a European community's EMS cardiac arrest experience. Inclusion criteria required the study to include at least 25 cases, report of the total number of all-rhythm and/or ventricular fibrillation arrests, and information about population size and study duration. The incidence was computed by dividing the total number of events by the product of the community's population and the study duration. Reports from 37 communities met the inclusion criteria. A total of 18,105 all-rhythm EMS-treated cardiac arrests occurred during 48 million person-years of observation, resulting in an overall incidence for all-rhythm arrests of 37.72 per 100,000 person-years. Incidence of ventricular fibrillation arrest was 16.84 per 100,000 person-years. Survival was 10.7% for all-rhythm and 21.2% for ventricular fibrillation cardiac arrest. Applying these results to the European population, approximately, 275,000 persons would experience, all-rhythm cardiac arrest treated by the EMS with 29,000 persons surviving to hospital discharge.</AbstractText>The results provide a framework to assess opportunities and limitations of EMS care with regard to the public health burden of cardiac arrest in Europe.</AbstractText>

Pediatric defibrillation doses often fail to terminate prolonged out-of-hospital ventricular fibrillation in children.

The recommended dose for pediatric defibrillation is 2 J/kg, based on animal studies of brief duration ventricular fibrillation (VF) and a single pediatric study of short duration in-hospital VF. In a piglet model of out-of-hospital (prolonged) cardiac arrest, this recommended dose was usually ineffective at terminating VF. We, therefore, hypothesized that pediatric dose defibrillation may be less effective for prolonged out-of-hospital pediatric VF.</AbstractText>We evaluated retrospectively all cardiac arrests in children less than 13 years old in Tucson from November 1998 to April 2003, with special attention to all children in ventricular fibrillation. We determined the rate of ventricular fibrillation termination after pediatric dose shocks in this cohort, and compared this rate with a published historical pediatric in-hospital defibrillation control group. A pediatric dose shock was defined as 2 J/kg (+/-10 J). All shocks in both groups were provided as monophasic damped sinusoidal waveforms.</AbstractText>Thirteen of 151 (9%) children with out-of-hospital cardiac arrest had documented VF. Eleven children received a total of 14 pediatric dose shocks. The median minimum untreated dispatch-to-shock time in unwitnessed arrest or collapse-to-shock in witnessed arrest for those 11 children was 11 min (interquartile range 25-75%; 9-15.5 min). Seven of the 14 pediatric dose shocks terminated the VF (six to asystole, one to pulseless electrical activity). Nine children (68%) died in the emergency department and four (31%) in the pediatric intensive care unit; none survived to hospital discharge. Failure to terminate VF after a pediatric dose shock in this study group with prolonged out-of-hospital ventricular fibrillation was substantially more common than the previously reported in-hospital data (7/14 versus 5/57; OR 10.4; 95% CI 2.6-42; P=0.001).</AbstractText>Termination of VF after a pediatric defibrillation dose is substantially worse for prolonged pediatric out-of-hospital VF cardiac arrest compared with in-hospital (short duration) ventricular fibrillation. The optimal pediatric defibrillation dose for prolonged VF is not known.</AbstractText>

Enlarged left atrial volume in hypertrophic cardiomyopathy: a marker for disease severity.

Patients with hypertrophic cardiomyopathy and left atrial (LA) enlargement have increased morbidity and mortality. We analyzed the clinical and echocardiographic factors related to LA enlargement, particularly the degree of left ventricular (LV) hypertrophy and diastolic function.</AbstractText>A total of 104 patients with hypertrophic cardiomyopathy (age 53 +/- 15 years, 64% men) were divided into two groups based on the indexed LA volume (LAVI) (mL/m2) measured by echocardiography: group A (or smaller LAVI group, n = 43) was defined as LAVI &lt; or = 34 mL/m2; and group B (or larger LAVI group, n = 61) as LAVI &gt; 34 mL/m2. Detailed clinical and echocardiographic data were obtained. LV wall thickness was measured at 15 sites at 3 levels (base, mid, and apex). Diastolic function was assessed from mitral and pulmonary venous inflow velocities and Doppler tissue imaging.</AbstractText>Both groups were similar in terms of sex, functional class (1.6 +/- 0.8 vs 1.5 +/- 0.8, group B vs A, P = .64), and incidence of atrial fibrillation (13% vs 5%, P = .19). However, patients of group B had a significantly higher incidence of serious cardiovascular events (16.4% vs 2.3%, group B vs A, P = .024). Both groups had a similar degree of resting LV outflow tract obstruction (19 +/- 30 vs 12 +/- 13 mm Hg, group B vs A, P = .06). However, those in group B had a higher incidence of at least moderate mitral regurgitation (25% vs 5%, group B vs A, P = .007), more LV hypertrophy at 6 LV nonapical wall segments (P &lt; .05-P &lt; .001), and a higher hypertrophy (Wigle) score (6.2 +/- 2.2 vs 4.5 +/- 2.1, group B vs A, P &lt; .001). In addition, patients of group B had a higher incidence of abnormal diastolic filling (57% vs 28%, group B vs A, P = .003), a higher early diastolic velocity/early diastolic mitral annular velocity (10.2 +/- 4.9 vs 7.5 +/- 2.9, group B vs A, P = .003), and a higher calculated LA pressure (14.8 +/- 6.5 vs 11.1 +/- 3.4 mm Hg, group B vs A, P = .0011).</AbstractText>Patients with hypertrophic cardiomyopathy and LA enlargement had more serious cardiovascular events and demonstrated greater LV hypertrophy, more diastolic dysfunction, and higher filling pressures.</AbstractText>

Gender-related differences in rhythm control treatment in persistent atrial fibrillation: data of the Rate Control Versus Electrical Cardioversion (RACE) study.

This study sought to compare whether gender affects the outcome of rate versus rhythm control treatment in patients with persistent atrial fibrillation (AF).</AbstractText>Large trials have shown that rate control is an acceptable alternative to rhythm control. However, the effects of treatment may differ between male and female patients.</AbstractText>In the Rate Control versus Electrical Cardioversion (RACE) study, 522 patients (192 female) were included and randomized to rate or rhythm control. The occurrence of cardiovascular end points and quality of life (QoL) were compared between female and male patients.</AbstractText>At baseline, female patients differed from male patients with regard to age, underlying heart disease, diabetes mellitus, and left ventricular function. Female patients had more AF-related complaints, and QoL was significantly lower. After a mean follow-up of 2.3 +/- 0.6 years, cardiovascular morbidity and mortality was equally distributed between female (21%) and male patients (19%). However, in contrast to male patients, female patients randomized to rhythm control developed more end points (adjusted hazard ratio was 3.1 [95% confidence interval 1.5 to 6.3], p = 0.002), mainly heart failure, thromboembolic complications, and adverse effects of antiarrhythmic drugs, compared with rate control randomized female patients. During follow-up, QoL in female patients remained worse compared with that for male patients. Randomized strategy did not influence QoL in female patients.</AbstractText>In female patients with persistent AF, a rhythm control approach leads to more cardiovascular morbidity and mortality. Because treatment strategy did not influence QoL in female patients, a rate control approach may be considered in these patients.</AbstractText>

Malignant entity of idiopathic ventricular fibrillation and polymorphic ventricular tachycardia initiated by premature extrasystoles originating from the right ventricular outflow tract.

The aim of this study was to assess the clinical characteristics and the efficacy of radiofrequency catheter ablation (RFCA) for idiopathic ventricular fibrillation (VF) and/or polymorphic ventricular tachycardia initiated by ventricular extrasystoles originating from the right ventricular outflow tract (RVOT).</AbstractText>Ventricular fibrillation and/or polymorphic ventricular tachycardia are occasionally initiated by ventricular extrasystoles originating from the RVOT in patients without structural heart disease.</AbstractText>Among 101 patients without structural heart disease in whom RFCA was conducted for idiopathic ventricular tachyarrhythmias arising from the RVOT, we examined the clinical characteristics and the efficacy of RFCA in 16 patients with spontaneous VF and/or polymorphic ventricular tachycardia initiated by the ventricular extrasystoles originating from the RVOT.</AbstractText>Among 16 patients, spontaneous episodes of VF were documented in 5 patients, and 11 patients had prior episodes of syncope. Holter recordings showed frequent isolated ventricular extrasystoles with the same morphology as that of initiating ventricular extrasystoles, and non-sustained polymorphic ventricular tachycardia with short cycle length (mean of 245 +/- 28 ms) in all 16 patients. Radiofrequency catheter ablation by targeting the initiating ventricular extrasystoles eliminated episodes of syncope, VF, and cardiac arrest in all patients during follow-up periods of 54 +/- 39 months.</AbstractText>Our data suggest that the malignant entity of idiopathic VF and/or polymorphic ventricular tachycardia was occasionally present in patients with idiopathic ventricular arrhythmias arising from the RVOT. Radiofrequency catheter ablation was effective as a treatment option for this entity.</AbstractText>

Prognostic value of the QRS duration in patients with heart failure: a subgroup analysis from 24 centers of Val-HeFT.

This study investigated whether QRS duration (QRS D) is a prognostic indicator in patients with heart failure (New York Heart Association [NYHA] classes II-IV).</AbstractText>This subgroup analysis included 248 patients with heart failure recruited in the German centers of the Valsartan Heart Failure Trial (Val-HeFT). Mean age was 60 years, mean NYHA class was 2.3, and mean left ventricular ejection fraction (EF) was 27.9%. Electrocardiograms were recorded and analyzed at the beginning of the study, at 2 weeks, 4 months, 1 year, and 2 years. The mean observation period for mortality was 25 months. Patients &gt; or = 65 years and patients with an EF &lt;20% had a significantly longer QRS D (P = .02; P = .0005). NYHA class, etiology of heart failure, therapy with angiotensin-converting enzyme inhibitors, amiodarone or beta-blockers, implanted defibrillator, and atrial fibrillation had no significant influence on QRS D. Total mortality was 9%: 14 patients died suddenly, 7 from heart failure, 2 from noncardiac causes. Kaplan-Meier plots show significantly different survival rates for patients with QRS D &lt;120 ms, QRS D 120-159 ms, or QRS D &gt; or = 160 ms (P = .0085). Multivariate analysis showed that QRS D was the only independent risk factor for all-cause mortality (P = .008). NYHA class, EF, atrial fibrillation, age, and gender failed to qualify as independent prognostic factors.</AbstractText>QRS duration in the surface electrocardiogram is an easily obtainable parameter with a significant prognostic impact in patients with congestive heart failure and a reduced EF. In this German subgroup of Val-HeFT patients, it was an independent predictor of all-cause mortality.</AbstractText>

Silent strokes in patients with heart failure.

The prevalence of asymptomatic strokes detected by brain imaging in a large cohort of patients with congestive heart failure (CHF) and reduced ejection fraction (EF) is unknown.</AbstractText>The present study was conducted to assess the prevalence of cerebrovascular accidents (CVA) diagnosed by routine brain imaging in neurologically asymptomatic patients with CHF who were being evaluated for heart transplantation. A comprehensive review of clinical data in a consecutive case series of 168 adult patients being evaluated was conducted. Patients at a high risk of having cerebral infarction (ie, history of transient ischemic attack or stroke, paroxysmal or chronic atrial fibrillation, intracardiac thrombi, and prosthetic valves) were excluded. Brain imaging was performed as part of a routine pre-heart transplant evaluation protocol. The prevalence of silent ischemic strokes was 34%. Multiple logistic regression analysis revealed a 2.3 (95% CI 1.05-5.03) times increased risk of silent strokes if a patient was African American. Traditional risk factors such as age, gender, hypertension, and diabetes mellitus were not predictive of CVA in this population.</AbstractText>Patients with CHF and a left ventricular EF less than 20% being evaluated for heart transplantation have a high prevalence of ischemic CVA. The role of anticoagulation in this high-risk group of patients should be further explored.</AbstractText>

Predictors of arrhythmic events during second day monitoring in patients with normal first day Holter recordings.

The diagnostic yield of Holter monitoring in patients with syncope is variably reported to be between 6%-20%. This study was done to define predictors of arrhythmic events during the second day of Holter monitoring in patients whose first day Holter recording was normal.</AbstractText>Two serial 24-hour Holter recordings were obtained in a consecutive series of 100 patients (49 patients with unexplained syncope and/or pre-syncope and 51 patients with palpitation). The age of patients was 53.4 +/- 16.9 years and 51 were men. Seventy-six patients had underlying heart disease. Main electrocardiographic findings were found in 40 (40%) patients including non-sustained ventricular tachycardia in 19, sinus pause in 13, symptomatic bradycardia in 5, paroxysmal atrial fibrillation in 4, sustained supraventricular tachycardia in 2, and Mobitz type II second-degree atrioventricular block in 3 patients. Twenty-seven (27%) patients had 33 main electrocardiographic findings during the first day and 13 out of the remaining 73 patients (17.8%) had it during the second day of Holter recording. Presenting symptom (syncope/pre-syncope), age &gt; 65 years, and male gender were significantly associated with increased likelihood of main electrocardiographic findings during the second day of Holter monitoring (p = 006, 0.023, and 0.024, respectively). The risk of main electrocardiographic findings ranged from 5% in patients with one or no predictor to 35% in those with &gt; or = 2 predictors (OR = 9.95, 95% CI = 2.01-49.2, p = 0.002).</AbstractText>Presenting symptom (syncope/pre-syncope), age &gt; 65 years, and male gender increased the likelihood of main electrocardiographic findings during the second day of Holter monitoring.</AbstractText>

Pathophysiologic targets in the early phase of acute heart failure syndromes.

An episode of acute heart failure syndromes (AHFS) can be defined as a rapid or gradual onset of signs and symptoms of heart failure (HF) in hospital admission and can arise from a variety of pathophysiologic mechanisms. This article reviews our current understanding of the pathophysiology of AHFS in order to identify potential therapeutic targets. Most patients with AHFS present with either normal systolic blood pressure or elevated blood pressure. Patients who present with elevated systolic blood pressure usually have pulmonary congestion and a relatively preserved left ventricular ejection fraction (LVEF), and have symptoms that typically develop abruptly, these patients often are elderly women. Patients with normal systolic blood pressure presenting with systemic congestion and reduced LVEF are usually younger, with a history of chronic HF, and have symptoms that develop gradually over days or weeks. Accordingly, most episodes of AHFS can be classified as either "vascular" failure or "cardiac" failure. In addition to the abnormal hemodynamics (increase in pulmonary capillary wedge pressure and/or decrease in cardiac output) that characterize patients with AHFS, myocardial injury--which may be related to a decrease in coronary perfusion and/or further activation of neurohormones and renal dysfunction (ie, the cardiorenal syndrome)--probably contributes to short-term and post-discharge cardiac events. Patients with AHFS also have significant cardiac and non-cardiac underlying conditions that contribute to the pathogenesis of AHFS, including coronary artery disease (ischemia, hibernating myocardium, and endothelial dysfunction), hypertension, atrial fibrillation, and type 2 diabetes mellitus. The goals of therapy for AHFS should be not only to improve symptoms and hemodynamics, but also to preserve or improve renal function and prevent myocardial damage.

Expanding cardiac resynchronization for systolic heart failure to patients with mechanical dyssynchrony and atrial fibrillation.

Despite progress in the management of heart failure (HF) using pharmacotherapy, the mortality and morbidity associated with this condition remain unacceptably high. Cardiac resynchronization therapy (CRT), a left-sided pacing therapy for drug-refractory and highly symptomatic HF patients with ventricular conduction delay, has been shown to improve left ventricular (LV) systolic function, myocardial oxygen consumption, and New York Heart Association functional class and to inhibit or reverse LV chamber dilation and remodeling. Atrial fibrillation is common in patients with HF and is associated with significant worsening of HF and myocardial function. Only recently have trials been designed to specifically study CRT in patients with HF and chronic atrial fibrillation. These studies have shown that CRT with biventricular or univentricular LV pacing in patients with atrial fibrillation corrects mechanical dyssynchrony and results in significant and sustained improvement in functional capacity, LV ejection fraction, quality of life, and QRS duration.

Emergency treatment with nifekalant, a novel class III anti-arrhythmic agent, for life-threatening refractory ventricular tachyarrhythmias: post-marketing special investigation.

Because class I anti-arrhythmic drugs sometimes suppress cardiac function caused by their negative inotropic effects, they are not adequate for use in patients with severe heart failure, even as emergency treatment for life-threatening ventricular tachyarrhythmias (ventricular tachycardia (VT)/ventricular fibrillation (VF)).</AbstractText>An objective evaluation committee re-evaluated the effect of nifekalant in 191 patients with refractory VT/VF. The attack termination was achieved in 45 out of 93 patients (48.4%). Nifekalant was administered to 39 patients with direct-current (DC) shock-resistant VT/VF and directly terminated VT/VF in 9 patients. In 15 of the remaining 29 patients (51.7%), VT/VF was successfully cardioverted by additional DC shock after nifekalant administration. Prevention of recurrence was achieved in 60 out of 99 patients (60.6%). Corrected QT interval (QTc) was significantly prolonged after initial administration of nifekalant (0.463+/-0.056 to 0.504 +/-0.072), and during maintenance infusion (0.470 +/-0.056 to 0.547+/-0.070). As an adverse reaction, excess prolongation of QTc was noted in 11 patients including 3 patients with torsades de pointes. Hemodynamic parameters tended to improve after maintenance infusion of nifekalant.</AbstractText>Nifekalant is effective and useful for life-threatening refractory ventricular tachyarrhythmias, although careful observation of the QT interval is required.</AbstractText>

Longitudinal study of acute myocardial infarction in the southeast Osaka district from 1988 to 2002.

Data on clinical characteristics, long-term mortality rates, and factors influencing outcome of acute myocardial infarction (AMI) based on an unselected cohort in the percutaneous coronary intervention (PCI) era are still limited in Japan.</AbstractText>In the present study 415 consecutive patients with AMI who were admitted to hospital within 24 h of symptom onset between January 1988 and December 2002 were studied. There was a marked seasonal variation of AMI with a minimum in summer and a maximum in winter, as well as a marked circadian variation with a significant morning peak. Overall, 45.8% of patients were treated with primary PCI. Increased age and female sex were negatively associated with the probability of undergoing PCI. During the follow-up period (mean duration, 4.01+/-3.41 years), the unadjusted long-term all-cause mortality rate was 21.4%. Multivariate Cox regression analysis showed that age, prior cerebrovascular disease, renal failure, Killip &gt; or =2, and ventricular tachycardia/fibrillation were independent predictors of worse long-term mortality after AMI. Furthermore, the use of PCI was independently associated with favorable long-term survival after AMI.</AbstractText>Although PCI was associated with a favorable long-term mortality, it remains underused in subsets of patients and increased use may further reduce the long-term mortality rate in Japanese AMI patients.</AbstractText>

Incidence of ventricular fibrillation in patients with out-of-hospital cardiac arrest in Japan: survey of survivors after out-of-hospital cardiac arrest in Kanto area (SOS-KANTO).

Although there is a close connection between emergency medical services (EMS) system and the outcome of out-of-hospital ventricular fibrillation (VF), few data are available regarding the situation in Japan.</AbstractText>A prospective multicenter study of out-of-hospital cardiac arrest was conducted according to the Utstein guidelines. A total of 4,383 patients who were given cardiopulmonary resuscitation (CPR) by EMS personnel for out-of-hospital cardiac arrest were enrolled. The proportion of VF or pulseless ventricular tachycardia (VT) as the first cardiac rhythm after cardiac arrest was 16.2% with a mean call-to-initial-recorded-electrocardiogram (ECG) interval of 11.1 min. In a subgroup of patients with witnessed collapse, the predicted incidence of VF or pulseless VT was 62.7% at the time of cardiac arrest, and the decline accelerated with every minute that the collapse-to-initial ECG interval was delayed. Multivariate analysis showed that the odds ratio for VF or pulseless VT after collapse-to-initial ECG interval was 0.91 (95% confidence interval (CI), 0.89-0.94, p&lt;0.001), and 1.54 (95%CI, 1.24-1.97, p&lt;0.001) after bystander CPR.</AbstractText>In Japan, VF occurred in 63% of cases at the time of cardiac arrest and the performance of bystander CPR appeared to prolong VF.</AbstractText>

Interrelationships between the autonomic nervous system and atrial fibrillation.

Mechanisms responsible for atrial fibrillation are not completely understood but the autonomic nervous system is a potentially potent modulator of the initiation, maintenance, termination and ventricular rate determination of atrial fibrillation. Complex interactions exist between the parasympathetic and sympathetic nervous systems on the central, ganglionic, peripheral, tissue, cellular and subcellular levels that could be responsible for alterations in conduction and refractoriness properties of the heart as well as the presence and type of triggered activity, all of which could contribute to atrial fibrillation. These dynamic inter-relationships may also be altered dependent upon other neurohumoral modulators and cardiac mechanical effects from ventricular dysfunction and congestive heart failure. The clinical implications regarding the effects of the autonomic nervous system in atrial fibrillation are widespread. The effects of modulating ganglionic input into the atria may alter the presence or absence of atrial fibrillation as has been highlighted from ablation investigations. This article reviews what is known regarding the inter-relationships between the autonomic nervous system and atrial fibrillation and provides state of the art information at all levels of autonomic interactions.

Mechanisms of atrial fibrillation: lessons from animal models.

Studies in animal models have provided extremely important insights about atrial fibrillation (AF). The classic mechanisms that still form the framework for our understanding of AF (focal activity, single-circuit or "mother wave" reentry, and multiple circuit reentry) were established based on animal studies almost 100 years ago. The past 10 years have witnessed a tremendous acceleration of animal work in this area, including the development of a range of AF models in clinically relevant pathological substrates (eg, atrial tachycardia remodeling, congestive heart failure, pericarditis, ischemic heart disease, mitral valve disease, volume overload states, respiratory failure) and the establishment of an increasing number of genetically defined transgenic mouse models. This article reviews the contribution of animal models to our knowledge about AF mechanisms and to clinical management, dealing with such issues as the theory of reentry; the specific applications of various animal models and their contribution to our understanding of electrophysiologic, ionic, and molecular mechanisms; the role of the autonomic nervous system and regional factors; and the development of novel therapeutic approaches. The complementary nature of animal research and clinical investigation is emphasized and the clinical relevance of findings in experimental models is highlighted.

[A comparative study of the effects of antiarrhythmic class III drugs cardiocyclide and sotalol on the atrioventricular fibrillation caused by vagus nerve excitation in narcotized dogs].

The new class III antiarrhythmic agent cardiocyclide effectively prevents the atrioventricular fibrillations caused by the vagus nerve excitation in narcotized dogs. The electrophysiological effect of cardiocyclide was studied by method of programmed electric stimulation of myocardium on the background of excitation of a peripheral segment of the right vagus nerve by current pulses of increasing frequency. On this background, cardiocyclide exhibited characteristic effects manifested primarily by elongation of the QT and QTc intervals (corrected in accordance with the heart rate) and the effective refractory periods of both atrium and ventricles. The ability of cardiocyclide to increase the effective refractory period was retained irrespective of the drive signal frequency. A specific feature of the cardiocyclide effect on the model of vagus nerve excitation is a greater increase in the effective refractory auricular period as compared to that observed under normal conditions. Sotalol is less effective than cardiocyclide in the case of vagotonic atrial stimulation and does not prevent the bradycardia induced by the vagus nerve excitation. However, sotalol still retains its effects on the repolarization, the effective refractory auricular and ventricular periods, and the AV node under these conditions.

Do different atrial flutter types carry the same thromboembolic risk?

Thromboembolic risk of atrial flutter (AFl) types has not been elucidated sufficiently in previous reports. The authors classified the patients according to surface electrocardiogram and electrophysiologic characteristics as those with typical AFl (37 patients, 78.4% male, mean age 59.8 +/-9.5 years) and atypical AFl (13 patients, 69.2% male, mean age 60.9 +/-6.9 years) and compared them regarding some clinical, echocardiographic, and hematologic parameters. An age- and gender-matched control group composed of 20 individuals without any organic heart disease in sinus rhythm was chosen (80% male, mean age 60.3 +/-7.9 years). Clinical features such as age, gender, organic heart disease, hypertension, diabetes mellitus, AFl duration, and the prevalence of paroxysmal atrial fibrillation were similar in both AFl groups. Echocardiographic parameters such as left ventricular ejection fraction, left atrial (LA) diameter, LA spontaneous echo contrast, and LA appendage emptying velocities were similar in both AFl groups. Fibrinogen, fibrin D-dimer, and thrombin-antithrombin III levels reflecting coagulation system activity were found to be increased in the patients with atypical AFl when compared with those with typical AFl and the control group (p &lt; 0.001). In Pearson's correlation analysis, significant correlation between these hematologic markers and clinical and echocardiographic parameters were not found (p &gt; 0.05). The coagulation system activity was found to be increased in patients with atypical AFl. Thus, anticoagulation due to the increased thromboembolic risk should be considered in patients with atypical AFl.

Modification of ventricular fibrillation activation patterns induced by local stretching.

We hypothesize that local modifications in electrophysiological properties, when confined to zones of limited extent, induce few changes in the global activation process during ventricular fibrillation (VF). To test this hypothesis, we produced local electrophysiological modifications by stretching a circumscribed zone of the left ventricular wall in an experimental model of VF.</AbstractText>In 23 Langendorff-perfused rabbit hearts frequency, time-frequency and time-domain techniques were used to analyze the VF recordings obtained with two epicardial multiple electrodes before, during, and after local stretching produced with a left intraventricular device. Acute local stretching accelerated VF in the stretched zone reversibly and to a variable degree, depending on the magnitude of stretch and the time elapsed from its application. In the half time (5 minutes) of the analyzed period, a longitudinal lengthening of 12.1 +/- 4.5% (vertical axis) and 11.8 +/- 6.2% (horizontal axis) in the stretched zone produced an increase in the dominant frequency (DFr) (15.2 +/- 1.9 versus 18.8 +/- 2.5 Hz, P &lt; 0.0001), a decrease in mean VV interval (63 +/- 8 versus 53 +/- 6 msec, P &lt; 0.001), and an increase in the complexity of the activation maps-with more areas of conduction block and more breakthrough patterns (23% versus 37%, P &lt; 0.01), without significant changes in the percentages of complete reentry patterns (9% versus 9%, ns). Simultaneously, in the nonstretched zone, no variations were observed in the DFr (15.2 +/- 2.1 versus 15.3 +/- 2.5 Hz, ns), mean VV intervals (66 +/- 8 versus 65 +/- 8 msec, ns), or types and percentages of maps with breakthrough (25% versus 20%, ns) or reentry patterns (12% versus 8%, ns). No significant correlation was observed between the DFr in the two zones (R = 0.24, P = 0.40).</AbstractText>Local stretching increases the electrophysiological heterogeneity of myocardium and accelerates and increases the complexity of VF in the stretched area, without significantly modifying the occurrences of the types of VF activation patterns in the nonstretched zone.</AbstractText>

Determinants of recurrent ventricular arrhythmia or death in 300 consecutive patients with ischemic heart disease who experienced aborted sudden death: data from the Leiden out-of-hospital cardiac arrest study.

Evaluation of the relation between clinical characteristics and incidence of recurrent ventricular arrhythmias (VAs) or death during long-term follow-up in a cohort of 300 consecutive ischemic heart disease (IHD) patients who had survived an episode of sudden cardiac arrest (SCA).</AbstractText>Survivors of life-threatening VA are at high risk for recurrent events.</AbstractText>A total of 300 consecutive survivors of SCA with IHD were included in a standardized screening and evaluation protocol. Multivariable Cox regression analysis was performed to determine the relation between clinical variables at baseline and the incidence of recurrent VA, all-cause mortality and the composite of both (composite endpoint).</AbstractText>The presenting arrhythmia was VT in 156 (52%) patients and VF in 144 (48%) patients. Revascularization was performed in 78 (26%) patients and an ICD was implanted in 216 (72%) patients. During follow-up (mean 30 +/- 21 months) 37 (12%) patients died and 88 (29%) patients experienced a recurrence. Advanced age (adjusted hazard ratio (HR) 2.0; 1.2-3.3), history of heart failure (HR 1.8; 1.2-2.6), and amiodarone use (HR 3.1; 2.1-4.6) were independent predictors for the composite endpoint. VT as presenting arrhythmia was an independent predictor for all-cause mortality only (HR 2.4; 1.2-4.8). A decreased risk of recurrences was determined by beta-blocker use (HR 0.5; 0.4-0.8) and coronary revascularization (HR 0.3; 0.2-0.6).</AbstractText>In a cohort of 300 consecutive survivors of SCA the incidence of recurrent VA and death is dependent on patient age, history of heart failure, and use of amiodarone. In contrast, use of beta-blockers and aggressive coronary revascularization improve the outcome.</AbstractText>

Pronounced unexplained preoperative tachycardia heralding serious cardiac events: a series of three cases.

Pronounced, unexplained preoperative tachycardia can be a formidable challenge for the anesthesiologist. Whereas the relationship between persistent intraoperative tachycardia and perioperative morbidity is indisputable, there is a lack of available data on unexplained preoperative tachycardia. The main objective of this case series is to stimulate research and discussion on this topic, so that guidelines can be developed to aid in management.</AbstractText>We present three patients with pronounced (&gt; or = 130 beats x min(-1)) unexplained preoperative tachycardia who suffered adverse perioperative events that were garnered from quality improvement records at two teaching hospitals. In the first case, a 38-yr-old woman with a lumbar spinal tumour went into ventricular fibrillation after induction of anesthesia and was found on subsequent evaluation to have an abnormal cardiac re-entrant pathway. In the second case, an otherwise healthy middle-aged man developed a wide complex tachycardia with hypotension during foot surgery, with the subsequent cardiac evaluation being negative. In the third case, a young, healthy woman scheduled for a melanoma incision developed crushing, substernal chest pain accompanied by nausea and shortness of valve prolapse with regurgitation. Before rescheduling the procedures, therapeutic interventions were undertaken that facilitated successful completion of the surgeries.</AbstractText>There are currently no data regarding the prevalence of unexplained preoperative tachycardia, and no guidelines to direct management. More research is needed on this important topic, including epidemiological data and management algorithm(s).</AbstractText>

Brugada syndrome, manifested by propafenone induced ST segment elevation.

We report a case of a 43 year old man who was diagnosed with Brugada syndrome after propafenone administration for chemical cardioversion of new onset atrial fibrillation. Brugada syndrome has been described in the medical literature and is thought to be responsible for the majority of sudden cardiac deaths in patients without ischaemic heart disease. This syndrome has not yet been extensively discussed in the emergency medicine literature despite its importance. Emergency physicians should consider Brugada syndrome in patients who present to the emergency department with right bundle branch block and ST segment elevation in the right precordial leads, which is the classic electrocardiographic pattern of this syndrome.

Intrathecal clonidine reduces the incidence of ischemia-provoked ventricular arrhythmias in a canine postinfarction heart failure model.

Intrathecal clonidine (ITC) is used clinically to manage neuropathic pain but frequently causes hypotension and bradycardia due to centrally mediated sympatholytic effects.</AbstractText>The purpose of this study was to evaluate the cardiac electrophysiologic effects of thoracic ITC and its effects on ischemia-provoked ventricular arrhythmias.</AbstractText>Twelve mongrel dogs with healed myocardial infarctions and heart failure were evaluated. ITC was delivered locally via catheter to the T2-T4 spinal segments and was dosed to reduce heart rate (HR) by &gt;20% to 25%. Electrophysiologic testing was performed before and after ITC. Transient (4-minute) myocardial ischemia was induced via left circumflex coronary artery occlusion on two separate occasions to provoke ventricular arrhythmias (ventricular tachycardia [VT]/ventricular fibrillation [VF]). Ischemic episodes were separated by 1 to 2 days, and dogs were randomly assigned to receive ITC or intrathecal saline flush (control) prior to the first or the second ischemic episode.</AbstractText>ITC produced significant decrease in HR (31%) and increases in PR interval (22%), Wenckebach cycle length (122%), and atrial and ventricular effective refractory periods (19% and 9%, respectively) but had no significant effect on systemic blood pressure. The occurrence of VT/VF was reduced from 9 of 12 to 3 of 12 dogs when ITC was administered prior to transient myocardial ischemia (P = .04). ITC also blunted ischemia-induced HR increase by 74%.</AbstractText>ITC reduced ischemia-induced VT/VF in a canine model of healed myocardial infarction with superimposed heart failure and acute ischemia. Results from electrophysiologic testing were consistent with a clonidine-induced reduction in cardiac sympathetic activity from the spinal cord. These data suggest that ITC administration may be a novel approach to treating ventricular arrhythmias.</AbstractText>

Internal defibrillation with minimal skeletal muscle activation: a new paradigm toward painless defibrillation.

Shock-induced pain produces substantial morbidity in recipients of implantable cardioverter-defibrillators (ICDs). This pain likely derives from activation of skeletal muscle and associated nerves in the chest and abdomen. In an effort to develop a painless defibrillation system, we designed an electrode arrangement that incorporates a conductive sock placed around the heart to confine the electric shock field to cardiac tissue.</AbstractText>The purpose of this study was to test whether cardiac defibrillation could be achieved without skeletal muscle activation using a novel electrode system.</AbstractText>Eight adult mongrel dogs were studied. Force of skeletal muscle contraction was measured by strain gauges attached to the forelimbs during delivery of internal shocks ranging in energy from 0.1 to 31 J. Biphasic shocks were delivered (1) between a right ventricular coil and a subcutaneous dummy can (standard configuration), and (2) between a left ventricular coil and an epicardial electrode sock. Internal and external defibrillation thresholds (DFTs) were determined for each electrode configuration.</AbstractText>Shock-induced muscle contraction force was significantly lower using the sock electrode than with standard ICD electrodes at every shock energy level tested (P &lt; .0001). Internal DFT was similar between electrode configurations (sock electrode: 8.6 +/- 4.2 J; standard: 11.0 +/- 6.3 J, P = .4), but muscle contraction force at DFT was greatly reduced with the new electrode system (1.8 +/- 2.0 kg vs 10.6 +/- 2.1 kg, P &lt; .0001). The sock electrode rendered external defibrillation impossible, however, even at 360 J.</AbstractText>Skeletal muscle activation induced by ICD shocks can be greatly reduced using an electrode system that confines the electric shock field to the heart. Refinement of this strategy may allow for delivery of painless shocks by ICDs. Further development is needed to overcome implant complexity and the higher external DFT with this type of electrode system.</AbstractText>

Spectrum and prevalence of cardiac ryanodine receptor (RyR2) mutations in a cohort of unrelated patients referred explicitly for long QT syndrome genetic testing.

Mutations in the RyR2-encoded cardiac ryanodine receptor/calcium release channel cause type 1 catecholaminergic polymorphic ventricular tachycardia (CPVT1).</AbstractText>Because CPVT and concealed long QT syndrome (LQTS) phenotypically mimic one other, we sought to determine the spectrum and prevalence of RyR2 mutations in a cohort of unrelated patients who were referred specifically for LQTS genetic testing.</AbstractText>Using denaturing high-performance liquid chromatography and direct DNA sequencing, targeted mutational analysis of 23 RyR2 exons previously implicated in CPVT1 was performed on genomic DNA from 269 unrelated patients (180 females, average age at diagnosis 24 +/- 17 years) who were referred to Mayo Clinic's Sudden Death Genomics Laboratory for LQTS genetic testing. Previously, comprehensive mutational analysis of the five LQTS-associated cardiac channel genes proved negative for this entire subset of patients now designated as "genotype-negative" LQTS referrals.</AbstractText>Fifteen distinct RyR2 mutations (14 missense, 1 duplication/insertion, 12 novel) were found in 17 (6.3%) of 269 patients. None of these mutations were present in 400 reference alleles. Two mutations localized to the calstabin-2 (FKBP12.6) binding domain. Upon review of the clinical records, the referral diagnosis for all 17 patients was "atypical" or "borderline" LQTS.</AbstractText>Putative pathogenic CPVT1-causing mutations in RyR2 were detected in 6% of unrelated, genotype-negative LQTS referrals. These findings suggest that CPVT may be underrecognized among physicians referring patients because of a suspected channelopathy. A diagnosis of "atypical LQTS" may warrant consideration of CPVT and analysis of RyR2 if the standard cardiac channel gene screen for LQTS is negative.</AbstractText>

Effect of cardiac resynchronization therapy on the incidence of ventricular arrhythmias in patients with an implantable cardioverter-defibrillator.

Cardiac resynchronization therapy (CRT) reduces mortality in selected patients with heart failure. However, this result may not be entirely related to the beneficial hemodynamic effects of CRT.</AbstractText>The purpose of this study was to assess retrospectively the effect of CRT on the incidence of appropriate therapy in patients with an implantable cardioverter-defibrillator (ICD).</AbstractText>Sixty-five patients (48 men and 17 women; mean age 58 +/- 13 years) with an ICD (31 biventricular, 34 dual-chamber) were included in the study. Clinical, ECG, and ICD stored data and electrograms were collected.</AbstractText>Biventricular and dual-chamber ICDs were implanted in 31 and 34 patients, respectively, who had either ischemic (n = 36) or dilated cardiomyopathy (n = 29). Thirty-two (49%) patients received &gt; or =1 appropriate ICD therapy during follow-up of 11 +/- 8 months. Thirty-five percent and 62% of patients with biventricular (n = 11) and dual-chamber ICDs (n = 21), respectively, received appropriate ICD therapy during the follow-up period (odds ratio = 0.340, P = .048). Stratifying the patients according to underlying heart disease and ejection fraction resulted in an adjusted odds ratio = 0.239 (P = .029). Comparing the rate of &gt; or =1 appropriate ICD therapy between the two groups by Kaplan-Meier analysis and the log rank test resulted in P = .027.</AbstractText>In this retrospective analysis, biventricular pacing was associated with a decreased incidence of sustained ventricular arrhythmias requiring ICD therapy. The antiarrhythmic effect of biventricular pacing could contribute to the reduction in mortality reported in recent large-scale clinical trials on CRT. However, further prospective studies are warranted to clarify this issue.</AbstractText>

Pacemaker utilization during permanent atrial fibrillation in patients who received pacemaker implantation for sinus node dysfunction.

Patients who have pacemakers and sinus node dysfunction frequently have atrial fibrillation (AF). The need for continued pacemaker therapy after conversion to permanent AF remains uncertain. This study showed that, among 174 patients who received pacemaker implantation for sinus node dysfunction, 38% (n = 62) had the minimum intrinsic ventricular rate of &gt;60 beats/min after conversion to AF. The pacemaker memory showed that 30 patients (18%) never used ventricular pacing during permanent AF. The study results suggest that patients who have a stable intrinsic ventricular rate during permanent AF by serial assessment may no longer need continued pacemaker therapy.

Rate versus rhythm control in the management of patients with atrial fibrillation.

The management of patients with atrial fibrillation involves three main areas: anticoagulation, rate control and rhythm control. Importantly, these are not mutually exclusive of each other. Anticoagulation is necessary for patients who are at a high risk of stroke; for example, those who are older than 75 years, or those who have hypertension, severe left ventricular dysfunction, previous cerebrovascular events, or diabetes. It is now clear that patients who are at a high risk of stroke require long-term anticoagulation with warfarin regardless of whether a rate-control or rhythm-control strategy is chosen. One possible exception might be patients who are apparently cured with catheter ablation. Several published trials comparing rate-control and rhythm-control strategies for the treatment of patients with atrial fibrillation have shown no difference in mortality between these approaches. The patients enrolled in these studies were typically over 65 years of age. Data comparing rate and rhythm strategies in patients who are younger than 60 years of age are limited. For more elderly patients, it seems reasonable to consider rate control as a primary treatment option and to reserve rhythm control for those who do not respond to rate control. For younger patients, we prefer to start with a rhythm-control approach and to reserve rate-control approaches for patients in whom antiarrhythmic drugs, ablation, or both, do not ameliorate the symptoms.

Stabilisation of calstabin2--a new approach in sudden cardiac death.

Calstablin2 stabilises the ryanodine receptor (RyR2), preventing aberrant activation of the channels during the resting phase of the cardiac muscle. Loss of this stabilisation may be associated with cardiac arrhythmias, the sudden death occasionally observed in people with structurally normal hearts, as well as the atrial fibrillation in heart failure. Calstabin2-deficient mice have structurally normal hearts but exhibit exercise-induced cardiac ventricular arrhythmias that cause sudden death. In arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2-/- mice, but reduced the arrhythmias in calstabin2+/- mice, illustrating the antiarrhythmic potential of stabilising calstablin2. Familial polymorphic ventricular tachycardia in humans has been linked to missense mutants in the hRyR2 gene. In HEK293 cells, these RyR2 mutants showed less binding of 35S-calstabin2 than the wild type, indicating a reduced binding affinity. In human atrial fibrillation and heart failure, where there is excessive disassociation of calstabin2 from the RyR2 receptor in vitro, JTV519 is able to reverse this. In conclusion, calstabin2 is an important new target in sudden cardiac death associated with structurally normal hearts, and in the treatment of atrial fibrillation and heart failure.

Comparison of defibrillation efficacy using implantable cardioverter-defibrillator with single- or dual-coil defibrillation leads and active can.

The reduction of defibrillation threshold (DFT) in patients treated with an implantable cardioverter-defibrillator increases patients' safety and prolongs ICD battery life.</AbstractText>To evaluate the possibility of reducing the defibrillation threshold in ICDs with an active can and an additional atrial defibrillation coil instead of the typical intracardiac single-coil lead.</AbstractText>This study involved 138 patients (36 F and 102 M, mean age 54+/-15 years) including 62 subjects with dual-coil defibrillation lead (group A) and 76 ones with single-coil defibrillation lead (group B). No statistically significant differences with respect to age, left ventricular function, main disease or exacerbation of heart failure according to the NYHA functional class were observed between groups. The defibrillation threshold was measured using the DFT+ protocol.</AbstractText>No significant differences between groups were identified with respect to pacing and sensing parameters. The comparison of DFT values between the two studied groups revealed significant improvement (by 14% mean) of defibrillation efficacy in group A. In group A, the mean DFT was 9.8+/-4.6 J (3-20 J) and mean defibrillation resistance - 45+/-7 W (32-73 W), whereas in group B: 11.45+/-5.25 J (3-28 J) and 72+/-12.8 W (38-106 W), respectively. In 93% of patients from group A, DFT was below 15 J, in comparison to 81% of patients from group B (p=0.046). The odds ratio of a higher defibrillation threshold (&#x142;15 J) in group A vs. group B was 0.3 (95% confidence interval: 0.09-0.98). The DFT reduction associated with modified ICD system use was independent of following clinical parameters: patient age, gender, main disease, end-diastolic left ventricular diameter, left ventricular ejection fraction, NYHA functional class and concomitant treatment with antiarrhythmic agents.</AbstractText>Modification of the electric field during defibrillation, achieved with the use of active-can ICDs with dual-coil defibrillation leads, allows a reduction of DFT by 14%. At the same time, it reduces the risk of a higher (&gt; or =15 J) DFT by three times compared to patients with a standard single-coil defibrillation lead.</AbstractText>

Circulatory arrest as a model for studies of global ischemic injury and neuroprotection.

Despite many programs aimed at better immediate care of cardiac arrest victims, the subsequent mortality rate is high, with myocardial and central nervous system (CNS) injuries as the most common causes of death. Preclinical research is badly needed to produce a sound base for future clinical trials and possible improvements in clinical outcome. In our laboratory, we use piglets weighing approximately 25 kg. Ventricular fibrillation is produced by an AC current and left without treatment for 8-12 min, after which cardiopulmonary resuscitation according to current human guidelines is undertaken. The heart is then defibrillated and restoration of spontaneous circulation induced. During the procedure, blood pressure and flow measurements are obtained in the systemic, pulmonary, and cerebral circulation. Peroxidation and inflammation are monitored by systemic and cerebral venous plasma concentrations of isoprostane (8-iso-PGF(2alpha)), an indicator of oxidative damage, and prostaglandin F(2alpha) metabolite (15-keto-dihydro-PGF(2alpha)), an indicator of cyclooxygenase-2 activity, respectively. Neurocellular damage is monitored by the jugular plasma concentration of protein S-100beta. Neurological outcome is assessed at &gt;24 h after the incident. Our results show that plasma concentrations of 8-iso-PGF(2alpha) are greater after more extended periods of ischemia. PBN (alpha-phenyl-N-tert-butyl nitrone), a so-called spin-trap scavenger, has a neuroprotective effect since neurological outcome is enhanced, and the 8-iso-PGF(2alpha) concentration is decreased during reperfusion. Use of water-soluble sulfonated PBN (S-PBN) results in better autoregulation of cerebral cortical blood flow and less peroxidation of CNS lipids during reperfusion. These observations suggest that our model can be used to explore neuroprotective effects of potential therapeutic agents.

Latent arterial hypertension in apparently lone atrial fibrillation.

Longitudinal studies on lone AF are rare and the incidence of hypertension in this population unknown. This study aimed at investigating the incidence of arterial hypertension in patients with apparently lone atrial fibrillation (AF).</AbstractText>Out of 292 consecutive patients presented with permanent or paroxysmal AF, 32 patients were diagnosed as having lone AF according to strict criteria. Three patients were subjected to ablation of the ligament of Marshall, 14 patients to pulmonary vein isolation, and the remainder were treated with beta blockade. Patients were followed-up for a 1-3 year period. During follow-up, 14 patients were diagnosed as having arterial hypertension. Thirteen of them had recurrent AF despite ligament of Marshall ablation (1 patient), pulmonary vein isolation (4 patients) and beta blockade (8 patients). Cox regression analysis revealed that the only significant predictor of development of hypertension was complete or partial response to antiarrhythmic therapy (beta=3.82, S.E.=1.22, exp(b)=45.63, 95% C.I.=4.17-499.2, p=0.001), independent of age (beta=-0.01, p=0.74), sex (beta=-0.91, p=0.28), left ventricular ejection fraction (beta=0.06, p=0.52), left atrial size (beta=0.58, p=0.7) and kind of antiarrhythmic therapy (ablation or drug therapy) (beta=1.36, p=0.09). In patients with lone AF that did not respond at all to antiarrhythmic therapy, there was a 45.6 times higher risk of diagnosing hypertension during the next 3 years as compared to responders.</AbstractText>Approximately 44% of patients with an initial diagnosis of lone AF may represent occult cases of arterial hypertension. In these patients hypertension may affect AF recurrence and treatment outcomes, regardless of the mode of antiarrhythmic therapy used.</AbstractText>

Hypothermia during reperfusion does not reduce myocardial infarct size in pigs.

We previously described a method for regional myocardial cooling that reaches the target temperature within 4 min. The present study evaluated whether this method for regional myocardial cooling during reperfusion reduces myocardial infarct size (IS) in 75-kg pigs. Myocardial infarction was induced by inflation of an angioplasty balloon in the left anterior descendent artery for 45 min followed by 3 h reperfusion. First, 15 pigs were randomized to regional myocardial cooling during reperfusion (n = 8) or control (n = 7). As further control experiments, systemic hypothermia was induced prior to ischemia (n = 3) and during reperfusion (n = 3). IS and area at risk (AAR) were evaluated in vivo by single photon emission cardiac tomography (SPECT) and by standard histochemical staining. Regional cooling during reperfusion did not reduce IS/AAR as assessed by histochemistry (cooling: 0.71 +/- 0.8; control: 0.68 +/- 0.10; p = ns) and SPECT (cooling: 0.90 +/- 0.20; control: 0.88 +/- 0.32; p = ns). Systemic hypothermia during ischemia reduced IS/AAR (histochemistry: 0.09 +/- 0.11; SPECT: 0.25 +/- 0.22; p &lt; 0.001 and p = 0.01 vs control, respectively). Induction of systemic hypothermia during reperfusion had no significant effect on IS/AAR (histochemistry: 0.63 +/- 0.07; SPECT: 0.74 +/- 0.09; p = ns vs control for both comparisons). In conclusion, hypothermia during ischemia is strongly myocardioprotective while hypothermia during reperfusion does not reduce myocardial infarct size in human-sized pigs.

Atrial fibrillation and heart failure comorbidity.

Atrial fibrillation and heart failure have in common that they mainly occur in older patients and the patients have similar underlying heart diseases. The prevalence of atrial fibrillation in heart failure patients varies from 10% to 30%. There are conflicting data whether the presence of atrial fibrillation is an independent predictor for an increased mortality in heart failure. Optimal medical heart failure therapy can improve outcome and may influence the relationship between atrial fibrillation and survival. Keystones for the management of atrial fibrillation in heart failure patients are the optimal treatment of heart failure, the use of oral anticoagulation, the case-adjusted decision of rhythm or rate control, and the primary prevention of sudden cardiac death. Heart failure patients with atrial fibrillation should receive long-term oral anticoagulation. The two options to treat atrial fibrillation are rhythm control and rate control. Given the findings of randomised trials, rhythm control of atrial fibrillation with the aim to improve survival is not justified in heart failure patients because of uncertainty about the role of atrial fibrillation as a predictor of worse outcomes and the safety of antiarrhythmic drugs. Rhythm control can be attempted, if rate control is chosen and symptoms persist. The indications for rhythm control are to control symptoms, including a deterioration of heart failure related to a loss of atrial contraction. Amiodarone seems to be the drug of choice to maintain sinus rhythm in patients with paroxysmal atrial fibrillation as well as in patients who returned to sinus rhythm after cardioversion. New non pharmacologic approaches for rhythm control such as catheter-based techniques seem to be highly effective. Rate control to prevent rapid atrial fibrillation is an acceptable approach in otherwise asymptomatic heart failure patients. Slowing of the ventricular rate often leads to a moderate improvement in left ventricular function in many patients. Standard therapy for rate control in heart failure patients consists of partial atrioventricular (AV) node blockade with digoxin and a beta-blocker. Amiodarone is also highly effective to reduce ventricular rate in patients with atrial fibrillation. When rate control remains refractory to medical therapy, rate control is achieved with AV node ablation and subsequent pacemaker implantation. Non pharmacological treatments for the primary prevention of sudden cardiac death are the implantation of a defibrillator.

Pharmacological treatment of chronic heart failure according to the 2005 guidelines of the European Society of Cardiology.

Recently, the updated guidelines for the diagnosis and treatment of chronic heart failure were published. This review focuses on the pharmacological treatment. Basically, all patients with chronic heart failure and left ventricular systolic dysfunction should be treated with diuretics, ACE-inhibitors and beta-blockers, unless contra-indicated or not tolerated. It is important to uptitrate ACE-inhibitors and beta-blockers to the high recommended doses that were used in the randomised clinical trials. If an ACE-inhibitor is not tolerated or contra-indicated, it is recommended to start an angiotensin receptor blocker (ARB). Dose and choice of diuretics (loop acting or thiazides or combination) depends on volume status, renal function, and severity of heart failure. If patients remain symptomatic (NYHA class II), an ARB can be added, mainly to reduce worsening of heart failure and related hospitalisation. If patients remain severely symptomatic (NYHA class III), it is recommended to either add an aldosterone blocker, an ARB or both. The choice between an aldosterone blocker and an ARB depends on volume status, other specific patient characteristics, side effects, and personal preference. If all other therapies fail, one might consider nitrates, hydralazine and/or digoxin, while digoxin is always recommended in chronic heart failure patients with atrial fibrillation. Therefore, treatment of chronic heart failure is relatively simple. Although individual patient characteristics should always be taken into account, the current recommendations apply to all patients with chronic heart failure, irrespective its underlying cause.

Efficacy and safety of ibutilide for cardioversion of atrial flutter and fibrillation in patients receiving amiodarone or propafenone.

The effectiveness and safety of ibutilide (IB) use in patients receiving amiodarone or propafenone for atrial flutter (AFL) and atrial fibrillation (AF) were compared to IB alone.</AbstractText>In 104 consecutive patients with AF (65%) or AFL (35%), receiving amiodarone (n = 46), propafenone (n = 30), or no specific antiarrhythmic drug (n = 28), IB was given for cardioversion. Fifteen patients in amiodarone group were loaded with 1.2 g intravenously before IB administration. The mean duration of arrhythmia episode was 23 +/- 65 days, while 85% of patients had structural heart disease. The left ventricle ejection fraction was 57 +/- 10% and the left atrium size was 4.2 +/- 0.6 cm. The conversion efficacy did not differ among groups (62% for amiodarone vs 55% for propafenone vs 64% for IB alone). The QTc intervals were significantly prolonged, at 10 minutes and 30 minutes after IB administration, in amiodarone group (from 449 +/- 88 to 496 +/- 92 ms, 508 +/- 52 ms; P = 0.001) and in the group where IB was used alone (from 434 +/- 45 to 517 +/- 74 ms, 492 +/- 65 ms; P &lt; 0.001), while it remained unchanged in propafenone group (from 464 +/- 52 to 471 +/- 80 ms, 489 +/- 93 ms; P = 0.536). The only predictor of conversion was the presence of AFL (P = 0.009). Five patients developed ventricular tachycardias after IB administration (two in propafenone, one in amiodarone, and two in IB group).</AbstractText>The use of IB in patients receiving amiodarone or propafenone for AFL or AF is equally effective and safe as the use of IB alone. The presence of AFL is the stronger predictor factor for cardioversion.</AbstractText>

Significance of inducible ventricular flutter-fibrillation after myocardial infarction.

The purpose of this study was to determine the factors associated with the induction of ventricular flutter/fibrillation (VFl/VF)and its prognostic significance in post-myocardial infarction.</AbstractText>Programmed ventricular stimulation was performed after myocardial infarction (MI) for syncope (n = 232) or systematically (n = 755); 230 patients had an induced VFl/VF and were followed during 4 +/- 2 years.</AbstractText>VFl/VF was induced in 49/232 patients (21%) with syncope versus 181/755 asymptomatic patients (24%) (NS) and 94/410 patients (23%) with left ventricular ejection fraction (LVEF) &lt;40% versus 136/577 patients (22.5%) with LVEF &gt;40% (NS). Cardiac mortality was 9%; LVEF was 33 +/- 15% in patients who died, 43 +/- 13% in alive patients (P &lt; 0.004). In patients with LVEF &lt;40%, induced VFl/VF, mortality rate was 31% in those with syncope, 10% in asymptomatic patients (P &lt; 0.001), because of an increase of deaths by heart failure; patients with LVEF &gt;40% with or without syncope had a low mortality (5% and 3%). After linear logistic regression, VFl/VF and LVEF were predictors of total cardiac mortality, but only LVEF &lt;40% predicted sudden death.</AbstractText>Syncope and the level of LVEF did not increase the incidence of VFl/VF induction after MI, but modified the cardiac mortality: induced VF increased total cardiac mortality in patients with syncope and LVEF &lt;40%, but did not increase sudden death. In patients with LVEF &gt;40%, induced VFl/VF has no significance neither in asymptomatic patients nor in those with syncope.</AbstractText>

Multiple cellular electrophysiological effects of a novel antiarrhythmic furoquinoline derivative HA-7 [N-benzyl-7-methoxy-2,3,4,9-tetrahydrofuro[2,3-b]quinoline-3,4-dione] in guinea pig cardiac preparations.

We studied the electrophysiological and antiarrhythmic actions of HA-7 [N-benzyl-7-methoxy-2,3,4,9-tetrahydrofuro[2,3-b]quinoline-3,4-dione], a furoquinoline alkaloid derivative, in guinea pig heart preparations. In the perfused whole heart model, HA-7 caused a prolongation in the basic cycle length, ventricular repolarization time, and the atrioventricular (AV) nodal Wenckebach cycle length and prolonged the refractory period of the atrium, AV node, and His-Purkinje system. The atrioventricular conduction interval was also prolonged in a frequency-dependent manner. In isolated hearts, HA-7 significantly raised the threshold for experimental atrial fibrillation and reduced the occurrence of reperfusion-induced ventricular fibrillation. Conventional microelectrode-recording study shows that HA-7, but not d-sotalol, prolonged the action potential duration (APD) and decreased the maximum rate of depolarization in isolated atrial strips. In ventricular papillary muscles, higher concentrations of HA-7 caused a prolongation of APD(90) in a frequency-independent manner, whereas d-sotalol exerted a reverse frequency-dependent action on this parameter. Whole-cell patch clamp results on ventricular myocytes indicate that HA-7 decreased both the slow (I(Ks)) (IC(50) = 4.8 muM) and fast component (I(Kr)) (IC(50) = 1.1 muM) of the delayed rectifier K(+) currents. Similar results could also be observed in atrial myocytes. The inward rectifier K(+) current (I(K1)) was also reduced somewhat by HA-7. HA-7 also suppressed the Na(+) inward current (I(Na)) (IC(50) = 2.9 muM) and inhibited the L-type Ca(2+) current (I(Ca)) (IC(50) = 4.0 muM, maximal inhibition = 69%) to a lesser extent. We conclude that HA-7 blocks multiple ionic currents and that these changes affect the electrophysiological properties of the conduction system as well as the myocardial tissues and may contribute to its antiarrhythmic efficacy.

Role of microscopic tissue structure in shock-induced activation assessed by optical mapping in myocyte cultures.

Termination of ventricular fibrillation by electric shocks is believed to be due to the direct activation of large tissue mass that may be caused by microscopic virtual electrodes formed at discontinuities in tissue structure. Here, microscopic shock-induced activation was measured optically in myocyte cultures; spatially averaged microscopic Vm measurements were compared with macroscopic measurements from left ventricular (LV) tissue.</AbstractText>Experiments were performed in linear cell strands of different width (approximately 0.1 and 0.8 mm) and isolated porcine LV preparations. Uniform field shocks were applied across strands or LV preparations during diastole and action potential (AP) plateau. Depending on shock strength, three different types of activation were observed in cell strands. Weakest shocks produced "delayed make" activation that started on the cathodal strand side after long latency and rapidly spread to the anodal side. Stronger shocks caused "make" activation with short latency and rapid spread across strands. Strongest shocks caused nonuniform "make-break" activation where the cathodal side was activated with a short latency but activation of the anodal side was delayed until after the shock end due to a large negative shock-induced polarization. Spatial averaging of Vm responses across 0.1-mm (but not 0.8-mm) strands resulted in AP upstrokes and plateau polarizations that closely resembled the Vm responses measured in LV myocardium. The shock strength for the transition between fast and delayed activation in 0.1-mm cell strands and LV myocardium was similar as well.</AbstractText>These data provide evidence that microscopic tissue structures with dimensions of approximately hundred microns are responsible for shock-induced activation of ventricular tissue.</AbstractText>

Atrial fibrillation in patients with a dual defibrillator: characteristics of spontaneous and induced episodes and effect of ventricular tachyarrhythmia induction.

The pattern of FF intervals during atrial fibrillation (AF) has been analyzed in induced and spontaneous AF episodes, after the induction of ventricular fibrillation (VF) and after atrial shock, in order to suggest practical considerations for AF management in patients implanted with antitachycardia devices.</AbstractText>In 13 patients implanted with a dual-chamber defibrillator, FF intervals were analyzed during two separate induced AF episodes, before and after VF induction over AF, as well as during spontaneous AF episodes and after unsuccessful atrial shocks. The following parameters were considered: mean atrial cycle length (CL), atrial CL stability, and standard deviation of the atrial cycle.</AbstractText>The AF pattern had comparable characteristics considering two separate inductions of AF, as well as spontaneous AF episodes. Ventricular tachyarrhythmia induction resulted in a shortening of atrial CL (P &lt; 0.02) and in a less organized AF pattern (P &lt; 0.005). Changes in the FF interval after ineffective shock therapy showed a shortening of AF cycles after shocks with energies far below the defibrillation threshold.</AbstractText>(a) The AF pattern is reproducible in separate inductions of sustained AF and in spontaneous episodes, (b) dynamic changes involving a shortening of the AF cycle and an evolution to a less homogeneous pattern occur after VF induction, revealing a complex interplay between AF and VF, and (c) FF interval analysis after ineffective shock delivery may allow the relationship between delivered shock energy and effective defibrillation energy to be estimated, thereby providing practical suggestions for step-up protocols in atrial cardioversion.</AbstractText>

Functional roles of Cav1.3(alpha1D) calcium channels in atria: insights gained from gene-targeted null mutant mice.

Previous data suggest that L-type Ca2+ channels containing the Cav1.3(alpha(1D)) subunit are expressed mainly in neurons and neuroendocrine cells, whereas those containing the Cav1.2(alpha1C) subunit are found in the brain, vascular smooth muscle, and cardiac tissue. However, our previous report as well as others have shown that Cav1.3 Ca2+ channel-deficient mice (Cav1.3(-/-)) demonstrate sinus bradycardia with a prolonged PR interval. In the present study, we extended our study to examine the role of the Cav1.3(alpha1D) Ca2+ channel in the atria of Cav1.3(-/-) mice.</AbstractText>We obtained new evidence to demonstrate that there is significant expression of Cav1.3 Ca2+ channels predominantly in the atria compared with ventricular tissues. Whole-cell L-type Ca2+ currents (I(Ca,L)) recorded from single, isolated atrial myocytes from Cav1.3(-/-) mice showed a significant depolarizing shift in voltage-dependent activation. In contrast, there were no significant differences in the I(Ca,L) recorded from ventricular myocytes from wild-type and null mutant mice. We previously documented the hyperpolarizing shift in the voltage-dependent activation of Cav1.3 compared with Cav1.2 Ca2+ channel subunits in a heterologous expression system. The lack of Cav1.3 Ca2+ channels in null mutant mice would result in a depolarizing shift in the voltage-dependent activation of I(Ca,L) in atrial myocytes. In addition, the Cav1.3-null mutant mice showed evidence of atrial arrhythmias, with inducible atrial flutter and fibrillation. We further confirmed the isoform-specific differential expression of Cav1.3 versus Cav1.2 by in situ hybridization and immunofluorescence confocal microscopy.</AbstractText>Using gene-targeted deletion of the Cav1.3 Ca2+ channel, we established the differential distribution of Cav1.3 Ca2+ channels in atrial myocytes compared with ventricles. Our data represent the first report demonstrating important functional roles for Cav1.3 Ca2+ channel in atrial tissues.</AbstractText>

Coronary occlusion and reperfusion promote early afterdepolarizations and ventricular tachycardia in a canine tissue model of type 3 long QT syndrome.

Although long QT syndrome (LQTS) and coronary occlusion-reperfusion (O/R) are arrhythmogenic, they affect ventricular action potential duration (APD) differently. In contrast to the prolonged APD in LQTS, ischemia abbreviates APD after a transient prolongation. Thus we hypothesized that the dynamic interactive effects of ischemia and LQTS on APD and its dispersion would affect ventricular arrhythmogenicity. We mapped transmural distribution of action potentials in 6 groups of 10 isolated wedges of canine ventricular walls: LQTS-O/R, LQTS only, and O/R only, with separate groups for pacing cycle lengths (PCL) of 1,000 and 2,000 ms. We created type 3 LQTS with anemone toxin (ATX) II followed &gt;30 min later by arterial occlusion (40 min) and reperfusion (&gt;100 min). Arterial occlusion initially (first 4 min) prolonged and then shortened APD. Early afterdepolarizations (EADs) occurred during the initial 4 min of occlusion in 4 of the 10 LQTS-O/R wedges at PCL of 2,000 ms but not in the other groups. Reperfusion restored APD in the O/R-only groups but caused APD to overshoot its original duration, indicating depressed repolarization reserve, in the LQTS-O/R group. Reperfusion increased the dispersion of APDs and initiated ventricular tachycardia-fibrillation in 7 of 10 and 6 of 10 LQTS-O/R wedges and in 2 of 10 and 1 of 10 O/R-only wedges at PCLs of 1,000 and 2,000 ms, respectively. The LQTS-only wedges exhibited neither EADs nor ventricular tachycardia. We conclude that coronary O/R increased the arrhythmogenicity of LQTS via cumulative prolongation of APD, increase in repolarization dispersion, and suppression of repolarization reserve.

Ischemic ventricular arrhythmias during heart failure: a canine model to replicate clinical events.

Development of experimental animal models has played an invaluable role in understanding the mechanisms of ventricular arrhythmias.</AbstractText>The purpose of this study was to evaluate a new canine model of myocardial infarction (MI), heart failure, and ischemic ventricular arrhythmias in an attempt to replicate clinical conditions.</AbstractText>Thirty-six mongrel dogs underwent placement of a permanent ventricular pacemaker and induction of an anterior MI by percutaneous transcatheter embolization of polyvinyl foam particles into the left anterior descending coronary artery (just distal to the first septal branch). After a 2-week recovery period, heart failure was induced by continuous rapid ventricular pacing at 200 to 240 ppm for 3 weeks. Transient (4-minute) myocardial ischemia was induced via balloon occlusion of the proximal left circumflex coronary artery. Echocardiographic and electrophysiologic testing was performed before MI creation and repeated prior to acute ischemia induction.</AbstractText>Seven dogs (19%) died within several hours of MI creation. All surviving dogs developed severe left ventricular systolic dysfunction. Significant increases in the intraatrial and intraventricular conduction intervals were observed following MI creation and heart failure induction compared with baseline values, as evidenced by increases in the duration of the P wave and QRS complex. Significant increases in corrected QT interval and ventricular refractoriness were observed. Acute transient ischemia induced sustained ventricular tachycardia or ventricular fibrillation in 21 of 29 dogs (72%).</AbstractText>This canine model can serve as a useful tool for studying ventricular arrhythmias during the interactions of healed infarction, heart failure, increased sympathetic tone, and myocardial ischemia.</AbstractText>

Potential proarrhythmic effect of biventricular pacing: fact or myth?

Hemodynamic improvement from biventricular pacing is well documented; however, its electrophysiologic effects have not been systematically studied. Sporadic case reports suggest a proarrhythmic effect of biventricular pacing resulting primarily in polymorphic ventricular tachycardia/ventricular fibrillation (VT/VF).</AbstractText>The purpose of this study was to report a series of patients in whom implantation of a biventricular system resulted in VT/VF storm with predominance of monomorphic VT.</AbstractText>In a retrospective analysis of all biventricular implants over a 4-year period at a single medical center, we identified 5 of 145 patients (3.4%) who developed VT/VF after they were upgraded to a biventricular system. All patients were male, age 71 +/- 8 years, with ejection fraction of 0.25 +/- 0.1. Four of five patients had ischemic cardiomyopathy.</AbstractText>All patients developed incessant VT/VF within 1 week of implantation. Monomorphic VT of single morphology was noted in 3 of 5 patients, monomorphic VT of multiple morphologies in 1, and polymorphic VT/VF in 1. VT was managed by temporary discontinuation of biventricular pacing in all patients, amiodarone in 3 of 5, sotalol in 1, and beta-blocker in 1. During 11 +/- 7 months of follow-up, 4 of 5 patients remain alive and are arrhythmia-free.</AbstractText>Biventricular pacing may result in precipitation of VT/VF storm in a minority of patients with prior history of VT/VF. This may be the first case series reporting both monomorphic and polymorphic VT after an upgrade to a system with biventricular pacing capabilities. The arrhythmias can be managed by conventional therapy and may require temporary discontinuation of left ventricular pacing. This observation is relevant to patients receiving a biventricular pacemaker without an implantable cardioverter-defibrillator backup.</AbstractText>

Impedance monitoring during catheter ablation of atrial fibrillation.

Delivery of radiofrequency energy in proximity of a pulmonary vein can cause vein stenosis. A sudden decrease in impedance as the catheter is moved from the vein into the left atrium (LA) has been used to define the pulmonary vein-LA transition during ablation procedures.</AbstractText>The purpose of this study was to define the variables affecting impedance measurement.</AbstractText>In vitro analysis of impedance was performed in a saline bath using sheaths and a plastic stereolithographic model of the LA. Impedance was continuously monitored during a calibrated pullback from the pulmonary vein into the LA in 37 veins of 10 patients referred for catheter ablation. Location of the catheter was confirmed by the following imaging modalities: intracardiac echocardiography, contrast venography, electroanatomic mapping, and computed tomography/magnetic resonance imaging (offline) in all patients.</AbstractText>Larger cross-sectional areas containing the catheter correlated with lower impedance in an exponential manner both with respect to sheath size (R(2) = 0.99) and in the stereolithographic model (R(2) = 0.91). In vivo, the impedance in the pulmonary veins decreased in an exponential manner as the catheter was pulled back into the LA. However, impedance at the vein orifice was not significantly higher than the LA. A defined cutoff value for defining the pulmonary vein-LA transition could not be identified.</AbstractText>The primary determinant of impedance is the cross-sectional area of the space containing the catheter. Impedance monitoring alone does not guarantee a catheter tip position outside the pulmonary vein. Intraprocedural imaging confirmation should be considered to avoid radiofrequency application within pulmonary veins.</AbstractText>

Cardiac arrest in a 17-year-old boy--a case report.

Cardiac arrest (CA) refers to abrupt cessation of cardiac pump function. Most sudden deaths in young people are of cardiac origin, at the same time most patients have unrecognised prior heart disease. We report a case of a 17-year-old boy with cardiac arrest induced by ventricular fibrillation. Sinus rhythm was restored after one hour's resuscitation. Based upon elevated necrotic markers, ECG changes and echocardiographic examinations the diagnosis of anterolateral myocardial infarction was established. Coronary angiography revealed only a small myocardial bridge. The patient in a poor general and unconscious state was transferred to the Coronary Care Unit of the Department of Coronary Disease. The patient improved after treatment and without neurological deficit or circulatory insufficiency continued cardiac rehabilitation in a spa hospital. The paper reviews differential diagnosis of cardiac arrest, treatment modalities and describes the course of hospitalisation.

[Causes of atrial fibrillation early after coronary artery bypass grafting].

The aim of the study was to define the frequency of atrial fibrillation early after coronary artery bypass grafting (CABG) and clinical risk factors for the development of atrial fibrillation in the post-operative course. The study population consisted of 1578 patients (1283 men and 295 women ranging in age from 25 to 85 years, mean age 59.373 +/- 8.686 years) undergoing isolated coronary artery bypass grafting in extracorporeal circulation between 1.01.1998 and 21.12.1999. The patients were divided into two groups: group 1 with atrial fibrillation after CABG (193 patients, mean age 62.399 +/- 7.097 years) and group 2 without atrial fibrillation in the postoperative course (1385 patients, mean age 58.952 +/- 9.009 years). Both groups were compared with respect to pre-, intra- and postoperative parameters. Additionally in group 1 the following aspects were taken into account: timing of atrial fibrillation and its relapses in relation to the surgical procedure, serum potassium level, type and efficacy of antiarrhythmic treatment.</AbstractText>Postoperative atrial fibrillation developed in 193 patients i.e. 12.23% of the CABG population. The complication occurred most frequently on the third day after the procedure and it recurred in about 60% of the patients. Analysis of clinical pre, intra- and postoperative factors identified those affecting the occurrence of atrial fibrillation in the postoperative course as follows: age, paroxysmal atrial fibrillation occurring before the operation, previous inferior myocardial infarction, type 2 diabetes mellitus, arterial hypertension, left ventricular ejection fraction, left atrial size, volume of cardioplegia used during the procedure, volume of blood lost during the procedure, postoperative ischaemia, timing of postoperative ischaemia, perioperative withdrawal of beta adrenolytics, prolonged intubation after the procedure, low cardiac output syndrome, prolonged administration of pressor amines after CABG, and Intraaortic balloon counterpulsation, especially during the procedure.</AbstractText>(1) Atrial fibrillation is an important clinical problem early after coronary artery bypass grafting. It is poorly tolerated and shows a tendency to recur. (2) Atrial fibrillation after CABG is most strongly correlated with age over 60 years, arterial hypertension and perioperative withdrawal of beta adrenolytics.</AbstractText>

High-dose streptokinase in the treatment of acute massive pulmonary embolism complicated with cardiogenic shock, respiratory arrest and ventricular fibrillation.

Despite advances in prophylaxis, diagnostic modalities, and therapeutic options, pulmonary embolism remains a commonly undiagnosed entity with lethal outcome. Clinically, pulmonary embolism ranges from massive thromboembolism with cardiogenic shock to asymptomatic, microebolism with anatomically small emboli without hemodynamic, respiratory or other disturbances.</AbstractText>A patient with massive pulmonary embolism complicated with ventricular fibrillation, respiratory arrest and cardiogenic shock was treated with a total dose of 3 750 000 IU of intravenous streptokinase in the 8-hour time period. After successful cardiopulmonary resuscitation, and thrombolytic therapy, the patient regained hemodynamic stability six hours after admission; all clinical and electrocardiographic signs of the right ventricle insufficiency disappeared.</AbstractText>This case report suggested that treatment with the high-dose of streptokinase could be beneficial in the patients with massive pulmonary embolism complicated with cardiogenic shock, which must be confirmed by further randomized trials.</AbstractText>

[Arrhythmogenic right ventricular cardiomyopathy].

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary myocardial disorder that is characterized by localized or diffuse atrophy of predominantly right ventricular myocardium with subsequent replacement by fatty and fibrous tissue. Arrhythmias of right ventricular origin are the main clinical manifestation. Affected patients present with ventricular premature beats and nonsustained or sustained ventricular tachycardia demonstrating a left bundle branch block pattern. However, since ventricular tachycardia may also degenerate into ventricular fibrillation, sudden death may be the first manifestation of ARVC.In recent years, ARVC has been more and more recognized as an important and frequent cause of ventricular tachyarrhythmias and sudden cardiac death, particularly in young patients and athletes, with apparently normal hearts. Evidence of the disease is found in 30-50% of family members. ARVC is a genetically heterogeneous disease. The diagnosis is based on electrocardiographic abnormalities and the identification of regional or global right ventricular dysfunction and fibrolipomatosis. Although several potentially causative genes have been identified, currently, genetic testing is not part of the routine diagnostic work-up.An implantable cardioverter-defibrillator is indicated in selected high-risk patients with ARVC (i. e., patients with life-threatening ventricular tachycardia or survivors of sudden cardiac death). The clinical course of the disease is often characterized by progression. In individual patients heart transplantation may become necessary.

Prevalence and clinical significance of cardiac arrhythmia in Anderson-Fabry disease.

Anderson-Fabry disease (AFD) is an X-linked lysosomal storage disorder caused by a deficiency in the enzyme alpha-galactosidase A. More than 60% of patients with AFD have evidence for cardiac involvement; the prevalence and clinical significance of arrhythmia in AFD are unknown. Seventy-eight consecutive patients (mean age 43.5 +/- 15.0 years, range 13.0 to 83.0; 43 men) with AFD were studied for 1.9 years (range 0.25 to 10). All patients underwent clinical evaluation, 12-lead electrocardiography, and echocardiography. Sixty patients (76.9%) underwent 24-hour ambulatory electrocardiographic monitoring. Persistent atrial fibrillation (AF) was present in 3 of 78 patients (3.9%); 8 (13.3%) had paroxysmal AF, and 5 (8.3%) had nonsustained ventricular tachycardia (VT). Patients with nonsustained VT were all men, with a maximal left ventricular (LV) wall thickness &gt;20 mm. Age (p &lt;0.001), left atrial diameter (p = 0.001), maximal LV wall thickness (p = 0.003), LV mass index (p = 0.009), and angina (p = 0.02) were univariate predictors of AF or paroxysmal AF. Using these predictors in a stepwise logistic regression analysis model, age was the only independent predictor of AF or paroxysmal AF (odds ratio 1.2, 95% confidence interval 1.1 to 1.3, p = 0.001). During follow-up, there was 1 sudden cardiac death, 4 patients received pacemakers for bradyarrhythmia, and 1 received a biventricular pacemaker and an internal cardioverter defibrillator. In conclusion, arrhythmias are common in older patients with AFD. The high incidence of pacemaker implantation and sudden cardiac death suggests that arrhythmia has a significant impact on the natural history of AFD.

Outcome of ventricular fibrillation developing during percutaneous coronary interventions in 19,497 patients without cardiogenic shock.

Ventricular fibrillation (VF) developing out of hospital or even in hospital has a reported prognosis for survival that is &lt;50%. We examined the prognosis for VF in 19,497 patients undergoing percutaneous coronary intervention and identified 164 who had VF (0.84%). The time to defibrillation was &lt;1 minute and was successful in all without sequelae. Thus, VF developing in the catheterization laboratory is unique in terms of prognosis.

Isolated heart function during ischemia and reperfusion in sucrose-fed rats: effect of insulin infusion.

In myocardial damage due to ischemia-reperfusion, the administration of insulin together with glucose and potassium may be protective, although in some patients and animal models, it is ineffective. In a rat model (HTG) with characteristics of the metabolic syndrome, induced by sucrose feeding, ischemia-reperfusion of the isolated heart evidences a less favorable outcome than in control animals, particularly males. We investigated the effect of insulin infusion during the reperfusion period in isolated hearts from control and HTG male and female rats. Weanling Wistar rats were given commercial rat chow and tap water (C rats) or 30% sucrose solution (HTG rats) for 8 months. They developed moderate hypertension and hyperinsulinemia, central adiposity, nephropathy, and hypertriglyceridemia. Cardiac function was recorded in a Langendorff preparation subjected to 25 min ischemia and 15 min reperfusion. The handicapped functionality of HTG hearts is more apparent under conditions of stress. Insulin administration improved particularly mechanical work and +dp/dt max variables. The effect of sex was observed on the type of arrhythmias developed during reperfusion: Only the males showed lethal ventricular fibrillation, which disappeared after insulin administration. Females had lower levels of cardiac enzymes creatine kinase (CKMB) and lactic dehydrogenase (LDH), but their performance was not hindered, probably on account of protective factors such as estrogens. Summing up, the pathological features of the HTG model did not prevent insulin from exerting some of its beneficial effects in HTG hearts. Sex differences in the outcome were more apparent in the type of arrhythmias after reperfusion; they were lethal in HTG males only, but insulin prevented their onset.

Global endocardial electrical restitution in human right and left ventricles determined by noncontact mapping.

This study was aimed at evaluating global characteristics of electrical restitution in the human ventricle using noncontact mapping.</AbstractText>Steep action potential restitution (slope &gt;1) and conduction velocity (CV) restitution have been linked with propensity to ventricular fibrillation, but clinical measurement of global electrical restitution had not been feasible.</AbstractText>Activation-recovery interval (ARI) and CV restitution curves were simultaneously constructed from 16 regional segments of the left and right ventricles in 8 patients (6 male, 2 female, age 42 +/- 17 years) following successful ablation of idiopathic ventricular tachycardia in the absence of structural disease guided by the Ensite 3000 system (Endocardial Solutions Inc., St. Paul, Minnesota). The ARIs were determined from reconstructed unipolar electrograms as validated with monophasic action potential recordings. The ARI restitution slopes were determined using the overlapping least-squares linear segments.</AbstractText>Global electrical restitution curves were heterogeneous in shape and distribution. ARI restitution slope was &gt;1 at 25% of 128 sites. The overall mean slope was 0.79 and was greater in the left than the right ventricle (0.93 +/- 0.49 vs. 0.65 +/- 0.26, p &lt; 0.001). Dispersion of ARI restitution slopes increased with decreasing diastolic intervals. The CV restitution operated over a narrower range of diastolic intervals compared with ARI restitution, reaching a plateau (10 +/- 6 ms vs. 38 +/- 13 ms, p &lt; 0.001) after refractoriness. The magnitude of CV restitution was also greater (steeper) than ARI restitution (25 +/- 10% vs. 18 +/- 9%, p &lt; 0.001).</AbstractText>Noncontact mapping can be used to examine global electrical restitution in the human ventricle. The ARI restitution is heterogeneous, with a slope &gt;1 at 25% of all sites. The heterogeneity of ARI and CV restitution may be important in determining myocardial electrical stability.</AbstractText>

Pharmacologic control of ventricular rate: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery.

While there is a deficiency in the number of randomized control studies dealing with the pharmacologic control of the ventricular response to atrial fibrillation (AF) or atrial flutter (AFL) after cardiac surgery, evidence-based recommendations are presented from those studies that are available. Because of the hyperadrenergic state after surgery, beta-blockers are recommended as the first line of therapy for patients with AF or AFL who do not require urgent cardioversion. Calcium channel blockers are recommended as second-line therapeutic agents. Digoxin has little efficacy because of the heightened adrenergic tone that is present postoperatively. Agents that are proarrhythmic, such as dofetilide, or agents that are contraindicated in patients with coronary artery disease, such as flecainide and propafenone, are not recommended.

Pharmacologic control of rhythm: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery.

Of the 128 articles evaluated on the overall topic of atrial fibrillation (AF) after cardiac surgery, only 19 studies dealing with pharmacologic heart rhythm control were relevant for inclusion in this analysis, indicating the relative paucity of evidence-based studies addressing this topic. We found limited data on guiding treatment for the rhythm control of AF following cardiac surgery in patients who do not require urgent cardioversion; therefore, the choice of an antiarrhythmic drug needs to be guided by patient characteristics. Based on limited available evidence, amiodarone is recommended for pharmacologic conversion of postoperative AF and AFL in patients with depressed left ventricular function who do not need urgent electrical cardioversion. This recommendation is made largely because of the effectiveness of amiodarone and also because of its relatively favorable side-effects profile. Sotalol and class 1A antiarrhythmic drugs are reasonable choices for patients with coronary artery disease who do not have congestive heart failure. There are currently no definitive data to guide the decision about the duration of antiarrhythmic drug therapy for patients with AF following cardiac surgery. Most protocols continue therapy with the antiarrhythmic drug for 4 to 6 weeks following surgery, but evidence from randomized studies is lacking.

Epidemiology, mechanisms, and risks: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery.

Atrial fibrillation (AF) is one of the most frequent complications of cardiac surgery, affecting more than one third of patients. The mechanism of this arrhythmia is believed to be reentry. The electrophysiologic substrate may be preexisting or may develop due to heterogeneity of refractoriness after surgery. Multiple perioperative factors have been proposed to contribute to the latter, including operative trauma, inflammation, elevations in atrial pressure (including that due to left ventricular diastolic dysfunction), autonomic nervous system imbalance, metabolic and electrolyte imbalances, or myocardial ischemic damage incurred during the operation. Whether ectopic beats originating in the pulmonary veins explain at least some episodes of postoperative AF, as has been shown for nonsurgical patients with the arrhythmia, is of current interest as such sites could easily be isolated at the time of surgery. The development of postoperative AF is associated with a higher risk of operative morbidity, prolonged hospitalization, and increased hospital cost compared with that in patients remaining in sinus rhythm. Many factors have been identified as being associated with postoperative AF, but the most consistent variable across studies is increasing patient age. It is speculated that age-related pathologic changes in the atrium contribute to arrhythmia susceptibility. An important modifiable risk factor for postoperative AF is the failure to resume therapy with beta-adrenergic receptor blockers after surgery. The stratification of patients who are at higher risk for AF would focus preventative strategies on patients who are most likely to benefit from such therapy. Nonetheless, since postoperative AF often develops in patients with comorbidities who are predisposed to other complications and prolonged hospitalization, it is presently unclear whether the prevention of postoperative AF will result in improved patient outcomes, particularly shorter hospitalizations.

Introduction: American College of Chest Physicians guidelines for the prevention and management of postoperative atrial fibrillation after cardiac surgery.

Atrial fibrillation (AF) and atrial flutter (AFL) are arrhythmias that commonly occur following cardiac surgery. The precipitating events are not always obvious, although predisposing factors including age have been defined. Postoperative AF and AFL add significantly to both the cost and morbidity of cardiac surgery. This guideline report, which was created under the auspices of the American College of Chest Physicians (ACCP), critically reviews evidence-based literature defining optimal treatment and prophylaxis for postoperative AF. Specific issues addressed include the following: (1) controlling the ventricular response rate in the patient with postoperative AF and AFL; (2) preventing thromboembolism in the setting of AF and AFL including the appropriate role of anticoagulation therapy; (3) pharmacologic approaches to converting AF or AFL to normal sinus rhythm, and maintaining normal sinus rhythm postoperatively; and (4) pharmacologic and surgical prophylaxis against postoperative AF and AFL. The resulting clinical practice guidelines represent the best-supported treatments, based on a rational scientific approach formulated from randomized clinical trials and systematic reviews. The panel convened by the Health and Sciences Policy Committee of the ACCP reviewed the currently available evidence to provide a basis for making specific recommendations for patient care.

A national programme for on-site defibrillation by lay people in selected high risk areas: initial results.

To report on the effectiveness of an initiative to reduce deaths from sudden cardiac arrest occurring in busy public places.</AbstractText>110 such places identified from ambulance service data as high risk sites.</AbstractText>172 members of the public who developed cardiac arrest at these sites between April 2000 and March 2004. 20,592 defibrillator months' use is reported, representing one automated external defibrillator (AED) use every 120 months.</AbstractText>681 AEDs were installed; staff present at the sites were trained in basic life support and to use AEDs.</AbstractText>Initial rhythm detected by AED, restoration of spontaneous circulation, survival to hospital discharge.</AbstractText>172 cases of cardiac arrest were treated by trained lay staff working at the site before the arrival of the emergency services during the period. A shockable rhythm was detected in 135 (78%), shocks being administered in 134 an estimated 3-5 minutes after collapse; 38 (28.3%) patients subsequently survived to hospital discharge. Spontaneous circulation was restored in five additional patients who received shocks but died later in hospital. In 37 cases no shock was initially indicated; one patient survived after subsequent treatment by paramedics, cardiopulmonary resuscitation having been given soon after collapse. Overall, irrespective of the initial rhythm, 39 patients (22.7%), were discharged alive from hospital. For witnessed arrests of presumed cardiac cause in ventricular fibrillation (an international Utstein comparator) survival was 37 of 124 (29.8%).</AbstractText>The use of AEDs by lay people at sites where cardiac arrest commonly occurs is an effective strategy to reduce deaths at these sites.</AbstractText>

Cardiac resynchronisation therapy in chronic atrial fibrillation: impact on left atrial size and reversal to sinus rhythm.

To evaluate the impact of long term cardiac resynchronisation therapy (CRT) on left atrial and left ventricular (LV) reverse remodelling and reversal to sinus rhythm (SR) in patients with heart failure with atrial fibrillation (AF).</AbstractText>74 consecutive patients (age 68 (8) years; 67 men) with advanced heart failure and AF (20 persistent and 54 permanent) were implanted with a CRT device.</AbstractText>Patients were evaluated clinically (New York Heart Association (NYHA) class, quality of life, six minute walk test) and echocardiographically (LV ejection fraction, LV diameters, and left atrial diameters) before and after six months of CRT. Additionally, restoration of SR was evaluated after six months of CRT.</AbstractText>NYHA class, quality of life score, six minute walk test, and LV ejection fraction had improved significantly after six months of CRT. In addition, left atrial and LV end diastolic and end systolic diameters had decreased from 59 (9) to 55 (9) mm, from 72 (10) to 67 (10) mm, and from 61 (11) to 56 (11) mm, respectively (all p &lt; 0.01). During implantation 18 of 20 (90%) patients with persistent AF were cardioverted to SR. At follow up 13 of 18 (72%) patients had returned to AF and none had spontaneously reverted to SR; thus, only 5 of 74 (7%) were in SR.</AbstractText>Six months of CRT resulted in significant clinical benefit with significant left atrial and LV reverse remodelling. Despite these beneficial effects, 93% of patients had not reverted to SR.</AbstractText>

Treatment of out-of-hospital cardiac arrest with LUCAS, a new device for automatic mechanical compression and active decompression resuscitation.

Lund University Cardiopulmonary Assist System (LUCAS) is a new gas-driven CPR device providing automatic chest compression and active decompression. This is a report of the first 100 consecutive cases treated with LUCAS due to out-of-hospital cardiac arrest (58% asystole, 42% ventricular fibrillation (VF)). Safety aspects were also investigated and it was found that LUCAS can be used safely regarding noise levels and oxygen concentrations within the ambulance. A crash test (10G) showed no displacement of the device from the manikin. Of the 71 patients with witnessed cardiac arrest, 39% received bystander CPR. In those 28 patients where LUCAS-CPR was initiated more than 15 min after the ambulance alarm and in the 29 unwitnessed cases, none survived for 30 days. Of the 43 witnessed cases treated with LUCAS within 15 min, 24 had VF and 15 (63%) of these cases achieved a stable return of spontaneous circulation (ROSC) and 6 (25%) of them survived with a good neurological recovery after 30 days; 5 (26%) of the 19 patients with asystole achieved ROSC and 1 (5%) survived for over 30 days. One patient where ROSC could not be achieved was transported with on-going LUCAS-CPR to the catheter laboratory and after PCI for an occluded LAD a stable ROSC occurred, but the patient never regained consciousness and died 15 days later. To conclude, establishment of an adequate cerebral circulation as quickly as possible after cardiac arrest is mandatory for a good outcome. In this report patients with a witnessed cardiac arrest receiving LUCAS-CPR within 15 min from the ambulance call had a 30-day survival of 25% in VF and 5% in asystole, but if the interval was more than 15 min, there were no 30-day survivors.

[Predictive factors of maintenance of sinus rhythm after direct current (DC) cardioversion of atrial fibrillation/atrial flutter].

Our aim was to determine the immediate and long-term outcome of direct current (DC) electrical cardioversion in patients with atrial fibrillation or flutter, and to determine factors predicting clinical outcome.</AbstractText>A retrospective one-year follow-up study of 220 patients with atrial fibrillation or flutter undergoing electrical cardioversion between September 1998 and April 2001 was done.</AbstractText>Electrical cardioversion was successful in 82% of the patients. Multivariate analysis revealed that female gender was associated with successful cardioversion (p=0.008). Only 29% remained in sinus rhythm after the one-year follow-up. Maintenance of sinus rhythm was associated with anti-arrhythmic drug treatment (p=0.042). Relapse of atrial fibrillation was associated with reduced left ventricular ejection fraction (p=0.002). Complications occurred in 7.7% of the electrical cardioversions; of these, 1.2% were thromboembolic events.</AbstractText>Less than one third of the patients remained in sinus rhythm after the one-year follow-up despite the use of anti-arrhythmic drugs. Electrical cardioversion is not without risk. Thorough consideration of choice of treatment in patients with atrial fibrillation or flutter is therefore important. According to Danish and international guidelines, electrical cardioversion should be considered primarily when symptoms of AF are unacceptable despite optimal frequency regulation or in patients with AF detected for the first time.</AbstractText>

Ventricular fibrillation refractory to ICD therapy.

A 14-year-old boy was admitted for the evaluation of recurrent syncope. His ECG on admission revealed a sinus rhythm with an undetermined QRS axis, T wave inversion at leads V3, V4 and abnormal q at leads I, aVL, V5 and V6. However, no underlying disease could be detected by any morphological examination. Programmed ventricular stimulation also induced no ventricular tachycardia or fibrillation (VF). Only signal-averaged ECG showed ventricular late potential and the cause of syncope was not clarified. As his brother with a similar ECG had died suddenly, he was prophylactically treated with an ICD. However, 14 months later he died suddenly after playing a video game. The ICD recorded VF, which was not converted despite 6 cardioversion attempts by the ICD. Progression of myocardial damages and/or elevation of defibrillation threshold may have been the cause of unsuccessful cardioversion.

Efficacy of nifekalant hydrochloride in the treatment of fatal ventricular arrhythmia in patients with ischemic heart disease.

Ventricular tachycardia (VT), which causes hemodynamic instability, and ventricular fibrillation (VF) sometimes occur in patients with severe underlying cardiovascular disease such as myocardial ischemia or infarction, and are associated with high mortality. This report presents the efficacy of nifekalant hydrochloride (nifekalant), a pure class III antiarrhythmic agent, in treating life-threatening ventricular arrhythmia in such patients. From June 2000, when nifekalant became commercially available in Japan, to May 2003, 30 ischemic heart disease (IHD) patients with VT/VF resistant to direct-current (DC) countershock received nifekalant in our hospital. These 30 patients served as the nifekalant group in this study. As a control group, we also included 33 IHD patients with VT/VF that had been resistant to DC countershock upon or during hospitalization between January 1996 and May 2000 before nifekalant became commercially available. No significant differences were observed in patient background factors and treatments between the two groups. The rates of death within 48 hours of occurrence of VT/VF were significantly lower in the nifekalant group (7%, 2/30) than in the control group (27%, 9/33; P &lt; 0.03). The rates of cardiac death during hospitalization were also significantly lower in the nifekalant group (40%, 12/30) than in the control group (67%, 22/33; P &lt; 0.03). The rates of survival until hospital discharge were significantly higher in the nifekalant group (57%, 17/30) than in the control group (30%, 10/33; P &lt; 0.03). Multivariate analysis of all 63 patients revealed nifekalant administration was the factor that significantly improved the mortality (odds ratio for cardiac death, 0.26; 95% confidence interval (CI), 0.07 to 0.95; P = 0.041). Nifekalant improves the prognosis for life-threatening ventricular arrhythmia in IHD patients.

Electrophysiological characteristics and catheter ablation in patients with paroxysmal right atrial fibrillation.

Catheter ablation of the right atrial (RA) substrate has had variable efficacy in curing paroxysmal atrial fibrillation (PAF), suggesting that RA substrate ablation can play an important role in the treatment of atrial fibrillation (AF) in some patients. The aim of this study was to investigate the electrophysiological characteristics and ablation strategy and its results in a specific group of patients with paroxysmal RA-AF.</AbstractText>The study population consisted of 13 patients (8 men; age, 64+/-15 years) with drug-refractory (2+/-1 drugs), frequent episodes of PAF. Provocation maneuvers did not reveal any ectopic beat-initiating AF. However, rapid atrial pacing easily induced AF. Activation mapping during sinus rhythm, atrial pacing, and AF was visualized by using a noncontact mapping system. Noncontact mapping revealed RA reentry (6 patients with single-loop circuits and 7 with double-loop circuits) with conduction through channels between lines of block, crista terminalis gaps, and the cavotricuspid isthmus, which could be identified during sinus rhythm and atrial pacing, resulting in fibrillatory conduction in other parts of the RA. The consistency of wavefront activation was confirmed by frequency analysis from equally distributed mapping sites in the RA. Short lines of ablation lesions were aimed at the conduction channels between the lines of block, crista terminalis gaps, and the cavotricuspid isthmus, resulting in bidirectional block. AF was eliminated in 11 (85%) of 13 patients, and those 11 patients with acute success were free of AF without any antiarrhythmic drugs during the long-term follow-up period (16+/-6 months).</AbstractText>RA ablation still can cure selected patients with PAF. Linear ablation of the RA substrate guided by the electrophysiological characteristics of RA-AF is an effective approach for treating this specific group of patients with AF.</AbstractText>

Torsade de pointes in a patient with complex medical and psychiatric conditions receiving low-dose quetiapine.

Describe potential cardiac complications of low-dose quetiapine and other atypical antipsychotic drugs.</AbstractText>We present a case report of a 45-year-old Black woman with multiple medical and psychiatric problems taking low-dose quetiapine.</AbstractText>Coincident with a generalized seizure, the patient developed 'ventricular fibrillation'. She was countershocked with restoration of normal sinus rhythm. The initial electrocardiogram showed QT interval prolongation. Shortly thereafter, classical torsade de pointes appeared, lasted 10 min, and resolved spontaneously. Hypomagnesemia was present. A cardiac electrophysiologist was concerned that the very slow shortening of the prolonged QTc interval after magnesium replacement implicated quetiapine as a risk factor for QTc interval prolongation and torsade de pointes. A psychosomatic medicine consultant asserted that the fragmented medical and psychiatric care almost certainly contributed to the patient's medical problems. We discuss other cases of QT interval prolongation by newer antipsychotic drugs and previous reports by our group concerning the association of psychotropic drugs, QT interval prolongation, and torsade de pointes.</AbstractText>Atypical antipsychotic drug administration, when accompanied by risk factors, may contribute to cardiac arrhythmias including torsade de pointes.</AbstractText>

Denaturing high-performance liquid chromatography screening of the long QT syndrome-related cardiac sodium and potassium channel genes and identification of novel mutations and single nucleotide polymorphisms.

Mutations in cardiac potassium and sodium channel genes are responsible for several hereditary cardiac arrhythmia syndromes. We established a denaturing high-performance liquid chromatography (DHPLC) protocol for rapid mutation screening of these genes, and reported mutations and variations identified by this method. We included 28 patients with Brugada syndrome, 4 with congenital long QT syndrome (LQTS), 11 with drug-induced LQTS, 4 with idiopathic ventricular fibrillation, and 50 normal volunteers. Polymerase chain reactions were performed to amplify the entire coding region of these genes. DHPLC was used to screen for heteroduplexes then DNA sequencing was performed. With this method, we identified the mutation(s) in all four patients with congenital LQTS (KCNQ1 A341V, KCNH2 N633D, KCNH2 2768Cdel and KCNE1 K70 N Y81C double mutations). We also identified the SCN5A A551T mutation in 1 of the 28 patients with Brugada syndrome. All the above-mentioned mutations were novel except KCNQ1 A341V. No mutations were identified in patients with drug-induced LQTS or idiopathic ventricular fibrillation. In total, 25 single nucleotide polymorphisms were identified, 10 of which were novel. In conclusion, DHPLC is a sensitive and rapid method for detection of cardiac sodium and potassium channel gene mutations.

Statins, ventricular arrhythmias and heart rate variability in patients with implantable cardioverter defibrillators and coronary heart disease.

The aim of this study was to evaluate whether the incidence of ventricular arrhythmias and heart rate variability were influenced by statin treatment and lipid levels in patients treated with an implantable cardioverter defibrillator (ICD). Heart rate variability measurements were performed in 86 patients with coronary heart disease and an ICD implant. The number of events with ventricular fibrillation and ventricular tachycardia were recorded during a 12-month period. This study lends little support for an antiarrhythmic effect of statins or any relation between plasma lipids and lipoproteins and malignant ventricular arrhythmias in patients with an ICD.

Independent evaluation of a defibrillation outcome predictor for out-of-hospital cardiac arrested patients.

We evaluated the ability of a previously derived outcome predictor to discriminate between ECG segments corresponding to return of spontaneous circulation (ROSC) or not in validation data from 136 patients with cardiac arrest. The new data used for validation were totally independent from the predictor derivation data used in the original study. Features corresponding to those used in the development of the original outcome predictor, centroid frequency, peak power frequency, spectral flatness and energy, were computed following which a second decorrelated feature set was generated. The outcome predictor was applied to the new data with good correspondence in performance (testing) to what was expected (training) with receiver operator characteristics (ROC) areas of 0.80 and 0.79, respectively. Outcome predictor performance was reproducible. As in the present study, future testing should be performed on totally independent data not included in the design of the outcome predictor to get a reliable impression of expected performance.

Reducing no flow times during automated external defibrillation.

There has recently been an increased attention focused on the importance of reducing time without blood flow from chest compressions (no flow time, NFT) during cardiopulmonary resuscitation (CPR). In this study we have analyzed and quantified the NFTs during external automatic defibrillation in 105 cardiac arrest patients. We found that for around half of the time (about 10 min), these patients were not perfused. We have proposed methods to reduce NFT in connection with analyses and shocks. The key factors were rhythm analysis during ongoing CPR, capacitor charging during analysis, 1 min of CPR immediately after a shock (with rhythm analysis during CPR at the end of the 1 min), and distinguishing between asystole and organized rhythm in analyses to skip pulse check if asystole. The potential reduction in NFT using these methods was calculated theoretically and we found a reduction in the total NFT of about 4.5 and 1 min, respectively, in the subgroups of patients having at least one shock and patients having received no shocks. In the present study, the median NFT ratio could theoretically be reduced from 51% to 34% or 49% to 39% depending on if the patient would have a shockable rhythm or not. By introducing the proposed methods into an AED, the NFT would be significantly reduced, hopefully increasing the survival.

Doppler tissue evaluation of intra-atrial and interatrial electromechanical delay and comparison with P-wave dispersion in patients with mitral stenosis.

The aim of our study was to: (1) measure atrial electromechanical delay in patients with mitral stenosis (MS) and in a control group; (2) find the echocardiographic parameters that affect atrial electromechanical delay; and (3) examine the correlation between atrial electromechanical delay and P-wave dispersion (PWD).</AbstractText>A total of 25 patients with pure MS (age 43 +/- 10 years; 18 women, 7 men) and 16 control subjects (age 41 +/- 8 years; 9 women, 7 men) were studied. Interatrial and intra-atrial electromechanical delay was measured with Doppler tissue echocardiography. From the 12-lead electrocardiograms, PWD was calculated.</AbstractText>Interatrial electromechanical delay was 71.2 +/- 33 in the MS group and 40.5 +/- 21.0 in the control group (P = .01). In the MS group, PWD was 50 +/- 7 and in the control group it was 29 +/- 5 (P = .03). A positive correlation was detected between interatrial electromechanical delay and PWD (r = 0.6, P = .03).</AbstractText>This study shows that interatrial electromechanical delay gets longer in MS and is correlated with PWD. Atrial electromechanical delay is related with left atrial size but not with severity of MS.</AbstractText>

Left atrial appendage function analyzed by tissue Doppler imaging in mitral stenosis: effect of afterload reduction after mitral valve commissurotomy.

This study sought to investigate the relative load dependence of left atrial appendage (LAA) tissue Doppler velocities in patients with mitral stenosis after percutaneous mechanical mitral commissurotomy (PMMC).</AbstractText>LAA tissue Doppler velocities were obtained in 34 patients with mitral stenosis (20 with sinus rhythm and 14 with atrial fibrillation) before and after PMMC by transesophageal echocardiography. Standard ultrasound studies were also performed for mitral valve orifice area, transmitral pressure gradient, and LAA blood flow velocity measurements.</AbstractText>PMMC resulted in a significant increase in mitral valve area (P &lt; .001) and decrease in mean transmitral pressure gradient (P &lt; .001). LAA tissue Doppler velocities consisted of a triphasic velocity profile: SLAA and ELAA occurring during left ventricular contraction and relaxation, respectively, and ALAA occurring after the atrial contraction. After PMMC, ELAA and ALAA velocities consistently increased (4.8 +/- 1.2 to 7.9 +/- 2.6 cm/sec [P &lt; .001] and 6.6 +/- 2.9 to 8.1 +/- 4.2 cm/sec [P &lt; .05], respectively). The mean transmitral pressure gradient was significantly correlated with ALAA before and after PMMC (r = .65).</AbstractText>In mitral stenosis, tissue Doppler velocities illustrated improvement of regional LA function after PMMC, in relation to decreased transmitral pressure gradient.</AbstractText>

Refinement on single-beat determination of left ventricular systolic function in patients with atrial fibrillation.

Single-beat determination of left ventricular systolic function at a beat with equal subsequent cardiac cycles has been proposed as an accurate method in atrial fibrillation. However, there has still been substantial variability between the values calculated from beats with equal subsequent cycles. Therefore, some refinement on the single-beat method is needed. In 100 patients with atrial fibrillation, Doppler aortic flow time-velocity integral was determined for at least 20 consecutive cardiac cycles. The values at beats with equal subsequent cardiac cycles were chosen and compared with the average values over all cardiac cycles. The values at beats with cycle lengths shorter than 500 milliseconds were usually far below the average values over all cardiac cycles. Bland-Altman agreement analysis revealed improved accuracy by gradually narrowing the range of the limits of agreement when 2 or 3 beats with equal subsequent cycles and cycle lengths longer than 500 milliseconds were used for evaluation.

Risk factors of postoperative atrial fibrillation after cardiac surgery.

Postoperative atrial fibrillation (AF) occurs in up to 50% of cardiac surgery patients and represents the most common postoperative arrhythmic complication. The etiology of AF after open-heart surgery is incompletely understood and its prevention remains suboptimal. Identification of patients vulnerable for postoperative AF would allow targeting of those most likely to benefit from aggressive prophylactic intervention. The aim of the present study was to evaluate clinical predictors of postoperative AF.</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. Ninety-nine patients (39.1%) of the total study population developed AF during the postoperative period. The median age for patients with postoperative AF was 69 years compared with 64 years for patients without (p &lt; 0.001). In addition to advanced age, AF patients were more likely to have surgery for valvular heart disease and less likely to have preoperative beta-adrenergic blockers than patients without AF. Multivariate logistic regression analysis (odds ratio, +/-95% CI, p value) was used to identify the following independent clinical predictors of postoperative AF: increasing age (above vs. below median [OR = 2.6; CI, 1.2 to 3.9; p &lt; 0.01]), and surgery for valvular heart disease (vs. coronary artery bypass grafting [OR 2.8; CI, 1.1 to 3.5; p &lt; 0.01)]). Additionally, postoperative complications (stroke, infections, unstable hemodynamics [OR = 1.9; CI, 1.0 to 7.5; p &lt; 0.05]), and preoperative nonuse of beta-adrenergic blockers (OR = 1.7; CI, 1.1 to 4.9; p &lt; 0.05) were associated with increased risk for postoperative AF. Both, patients with and without AF had similar body mass index, preoperative heart rate, preoperative blood pressure, and duration of surgery. Male sex did not identify patients at high risk for development of AF after cardiac surgery.</AbstractText>Postoperative AF remains the most common complication after cardiac surgery. A combination of advanced age and type of surgery identifies patients at high risk for development of AF after cardiac surgery.</AbstractText>

Autologous stem cell transplantation in acute myocardial infarction: The ASTAMI randomized controlled trial. Intracoronary transplantation of autologous mononuclear bone marrow cells, study design and safety aspects.

Intracoronary transplantation of different cell populations has been used in acute myocardial infarction (AMI) with promising results. The primary objective of the Autologous Stem cell Transplantation in Acute Myocardial Infarction (ASTAMI) study is to test whether intracoronary transplantation of autologous mononuclear bone marrow cells (mBMC) improves left ventricular ejection fraction (LVEF) after anterior wall AMI.</AbstractText>The ASTAMI study is a randomized, controlled, prospective study. One hundred patients with acute anterior wall ST-elevation myocardial infarction (STEMI) treated with acute percutaneous coronary intervention (PCI) are randomized in a 1:1 way to either intracoronary transplantation of autologous mBMC 5-8 d after PCI or to control. Left ventricular function, exercise capacity, biochemical status, functional class, quality of life and complications are validated at baseline and during a 12-month follow-up.</AbstractText>By August 2004, out of 1004 patients with STEMI, 49 patients have been included in the study. Twenty-four patients have been randomized to intracoronary mBMC transplantation. Twenty patients had chest pain and 16 patients had ischemic ECG changes during the mBMC transplantation procedure. One patient had ventricular fibrillation 24 h after transplantation.</AbstractText>Intracoronary transplantation of autologous mBMC in the acute phase after AMI is feasible and seems safe in the short term.</AbstractText>

Anorexia nervosa and ventricular fibrillation.<Pagination><StartPage>629</StartPage><EndPage>632</EndPage><MedlinePgn>629-32</MedlinePgn></Pagination><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lindblade</LastName><ForeName>Christopher L</ForeName><Initials>CL</Initials><AffiliationInfo><Affiliation>James Whitcomb Riley Hospital for Children, Indianapolis, IN 46202, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hubbard</LastName><ForeName>Joyce E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Miller</LastName><ForeName>John M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Batra</LastName><ForeName>Anjan S</ForeName><Initials>AS</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Pediatr (Phila)</MedlineTA><NlmUniqueID>0372606</NlmUniqueID><ISSNLinking>0009-9228</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000856" MajorTopicYN="N">Anorexia Nervosa</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014883" MajorTopicYN="N">Water-Electrolyte Imbalance</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000523" MajorTopicYN="Y">psychology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>9</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>1</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>9</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16151570</ArticleId><ArticleId IdType="doi">10.1177/000992280504400712</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16148376</PMID><DateCompleted><Year>2006</Year><Month>01</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>124-125</Issue><PubDate><Year>2005</Year><Season>Jul-Aug</Season></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal>[Optimal approach to the treatment of atrial fibrillation in patients with chronic heart failure].

Atrial fibrillation (AF) is one of the most frequently seen arrhythmia. Optimal strategy of its treatment still remains a serious problem. The goal of the investigation was the evaluation of the efficacy of combined treatment of AF with Cordaron and ACE inhibitor Diroton (lizinopril) (D) in patients with chronic heart failure (CHF). 29 patients (32-78 years old) with persistive AF and CHF (II - III class NYHA) were under observation. The treatment with C 200 - 300 mg/day and D 5 -10mg/day for 12 weeks resulted in improvement of clinical status of the patients, improvement in functional class of CHF, decrease in frequency of recurrences of AF in comparison with patients who were not given ACE inhibitor. Ultrasound study showed that combined therapy increases myocardial contractility corrects left ventricular remodeling, maintains the sinus rhythm and improve prognoses in this category of the patients. The use of ACE inhibitior D in antiarrhythmic (antirecurrent) therapy together with C is optimal in patients with persistive AF CHF.

Trends in treated ventricular fibrillation in out-of-hospital cardiac arrest: ischemic compared to non-ischemic heart disease.

The incidence of ventricular fibrillation (VF) out-of-hospital cardiac arrest (OHCA) treated by first responders has declined over the past decade. Since VF OHCA occurs primarily in the setting of severe coronary artery disease, primary and secondary prevention strategies may in part account for the decline. However, such strategies may not have a similar impact on non-ischemic arrest.</AbstractText>All Rochester Minnesota residents who presented with a VF OHCA from 1991 to 2004, treated by emergency medical services (EMS), were included in the study. Incidence rates were calculated based on the population for Rochester during the time period. Changes over time were tested using Poisson regression models. The significance of the trends was estimated according to the Mantel-Haenszel test for association, and two-tailed p-values reported.</AbstractText>The overall incidence of EMS-treated VF OHCA in Rochester during the study period was 10.6 per 100,000 (95% CI 9.1-11.8). The incidence decreased significantly (p&lt;0.001) over the study period [1991-1994: 18.2/100,000 (95% CI 13.4-21.9); 1995-1999: 11.8/100,000 (95% CI 10.4-17.9); 2000-2004: 8.7/100,000 (95% CI 6.0-13.0)]. The incidence of VF OHCA with ischemic heart disease also declined [1991-1994: 13.4/100,000 (95% CI 8.9-16.9); 1995-1999: 11.1/100,000 (95% CI 8.2-15.9); 2000-2004: 5.5/100,000 (95% CI 3.8-8.2), p&lt;0.001]. In contrast, the incidence VF OHCA with non-ischemic heart disease increased [1991-1994: 2.1/100,000 (95% CI 1.13-3.1); 1995-1999: 2.3/100,000 (95% CI 1.9-3.7); 2000-2004: 2.9/100,000 (95% CI 2.0-3.4), p&lt;0.001].</AbstractText>The incidence of VF OHCA is declining. The decline is attributable to the reduction of VF cardiac arrest with ischemic heart disease; suggesting an impact of treatment strategies targeted at coronary artery disease. The relative increasing incidence of non-ischemic VF OHCA suggests that more efforts are required to minimize mortality in this cohort population.</AbstractText>

Cardiac arrest in the early stage of cardiosurgical procedure.

Cardiosurgical operations remain one of the most demanding and complicated surgical procedures. Cardiac arrest before extra corporeal circulation (ECC) is one of severe intraoperative complications which can occur in any moment of operation. We have tried to evaluate possible risk factors of intraoperative, pre-ECC cardiac arrest in cardiac surgical patients and also have tried to estimate, if such an incident itself can be a risk factor for further post-operative complications. Pre-ECC intraoperative cardiac arrest (ICA) has occurred in 28 (aged 34-9) of 1,288 cardiac surgical patients operated on in our institution between July 1998 and December 2001. In 20 of these patients (71%) CABG was a planned procedure and in the remaining eight heart valve prostheses implantation were planned. In all 28 cases ventricular fibrillation was a cause of ICA and all patients required indirect and/or direct cardiac massage up to the moment of ECC start. In the subgroup with coronary artery disease (CAD) eight patients (35%) had left main stenosis, 13 (46.4%) had myocardial infarction in medical history. In the group of valve patients mitro-aortis valve disease was diagnosed in three cases and mitro-aorto-tricuspid valve disease with CAD or mitral valve disease or aortic valve disease in single patients. ICA was the most frequent during sternotomy (eight cases), pericardium opening (seven cases) and harvesting of left internal mammary artery (LIMA). In 16 cases prolonged reperfusion was necessary after declamping of the aorta, and in two of these cases ECC re-entry was needed. Eight patients (28.6%) have died, in 14 cases (50%) low output syndrome has been diagnosed, in five cases (18%) myocardial infarction has occurred and, in nine cases (32%) different neurological complications have been found postoperatively and five patients required resternotomy. All these complications were significantly more frequent in the investigated group than in the whole population of patients. We conclude that pre-ECC ICA contributes to noticeable post-operative complications rate increase. Sternotomy and opening of pericardium are the most frequent moments when pre-ECC ICA appears. We have not found any significant preoperative risk factors for pre-ECC ICA.

Predictors of quality of life in patients with implantable cardioverter defibrillators.

Few studies have prospectively examined characteristics of implantable cardioverter defibrillator (ICD) patients as predictors of postimplant outcome. In this study the authors considered the association between preimplant psychological characteristics, ICD shocks, and postimplant quality of life at short- and long-term follow-ups, controlling for age and ejection fraction (N=88). Hierarchical regression analyses revealed that history of depression, trait anxiety, optimism, social support, and ICD shocks accounted for 41.8% to 64.5% of the variance in quality of life indices at 8- and 14-month follow-ups, depending on the outcome assessed. Further, psychological variables were as strong as, or stronger than, age, ejection fraction, and ICD shocks in predicting quality of life outcomes.

Mechanisms of ventricular fibrillation in canine models of congestive heart failure and ischemia assessed by in vivo noncontact mapping.

Much of the research performed studying the mechanism of ventricular fibrillation (VF) has been in normal ventricles rather than under a pathological condition predisposing to VF. We hypothesized that different ventricular substrates would alter the mechanism and characteristics of VF.</AbstractText>Three groups of dogs were studied: (1) control (n=8), (2) pacing-induced congestive heart failure (n=7), and (3) acute ischemia produced by 30 minutes of mid left anterior descending artery ligation (n=5). A noncontact mapping catheter (Ensite 3000, ESI) was placed via transseptal into the left ventricle (LV), along with an electrophysiology catheter. A multielectrode basket catheter (EP Technologies) was placed in the right ventricle, along with an electrophysiology catheter. Several episodes of VF were recorded in each animal. In addition to constructing isopotential and isochronal maps of the VF episodes, signals underwent frequency domain analysis as a fast Fourier transform was performed over a 2-second window every 1 second. From the fast Fourier transform, the dominant frequency was determined, and the organization was calculated. In control dogs, meandering, reentrant spiral wave activity was the main feature of the VF. The congestive heart failure group showed evidence of a stable rotor (n=3), evidence of a focal source (n=3), or no evidence of a driver in the LV (n=1). The ischemic group showed evidence of an initial focal mechanism that transitioned into reentry. In the control and ischemic groups, the LV always had higher dominant frequencies than the right ventricle.</AbstractText>Different ventricular substrates produced by the different animal models altered the characteristics of VF. Thus, different mechanisms of VF may be present in the LV, depending on the animal model.</AbstractText>

Amiodarone prophylaxis reduces major cardiovascular morbidity and length of stay after cardiac surgery: a meta-analysis.

Although evidence supports the prophylactic use of beta-blockade in cardiac surgery, postoperative atrial fibrillation or flutter occurs in 40% to 60% of patients. Trials that assessed whether amiodarone prophylaxis decreases the incidence of postoperative atrial tachyarrhythmias have had mixed results and were not specifically powered to detect changes in cardiovascular morbidity, length of stay, or mortality.</AbstractText>To see whether prophylactic administration of amiodarone decreases the incidence of major cardiovascular events, length of stay, and mortality after cardiac surgery.</AbstractText>English-language and non-English-language publications listed in the MEDLINE, EMBASE, and CINAHL databases and the Cochrane Central Register of Controlled Trials, and bibliographies of published reviews. Sources were searched from the earliest possible dates through February 2005.</AbstractText>Double-blind, randomized studies comparing amiodarone with placebo that reported the incidence of supraventricular arrhythmia, atrial fibrillation, or atrial flutter as the primary end point.</AbstractText>Two investigators independently collected all data. Discrepancies were resolved by consensus.</AbstractText>After DerSimonian-Laird random-effects models were used to combine data from 10 trials involving 1744 patients, amiodarone therapy was found to decrease the incidence of atrial fibrillation or flutter (relative risk, 0.64 [95% CI, 0.55 to 0.75]), ventricular tachycardia and fibrillation (relative risk, 0.42 [CI, 0.28 to 0.63]), stroke (relative risk, 0.39 [CI, 0.21 to 0.76]), and length of stay (weighted mean difference, -0.63 day [CI, -1.03 to -0.23 days]). All studies reported adverse events, but none indicated how these events were assessed. Three studies found significantly more adverse events with amiodarone therapy, including nausea permitting continuation of therapy, bradycardia of unclear clinical significance, and increased intensive care monitoring and support.</AbstractText>Not all studies used beta-blockade, and regimens were not uniform among trials. Few trials met the stringent inclusion criteria, some did not report each type of cardiovascular event, and none reported completeness of follow-up.</AbstractText>Amiodarone prophylaxis decreases the occurrence of atrial fibrillation, ventricular tachyarrhythmias, and stroke and length of stay after cardiac surgery. To further evaluate the potential benefits of concomitant prophylaxis with beta-blockers and amiodarone, a multicenter, randomized, double-blind trial with cardiovascular outcomes that compares amiodarone with placebo in patients already receiving beta-blocker prophylaxis is needed.</AbstractText>

Dynamic changes in right ventricular pressures during haemodialysis recorded with an implantable haemodynamic monitor.

Intermittent and chronic volume overload contributes to the development of cardiovascular disease in patients on maintenance haemodialysis (HD). Continuous monitoring of central haemodynamic parameters may provide valuable information to improve volume control, particularly in patients with left ventricular dysfunction.</AbstractText>Five patients on HD, age 53-76 years, with systolic and/or diastolic dysfunction (EF 20-50%) received an implantable haemodynamic monitor (IHM) (Chronicle model 9520, Medtronic). The IHM consists of a memory device implanted subcutaneously and a transveneous right ventricular (RV) lead carrying a pressure sensor. It continuously records heart rate, RV systolic (RVSP) and diastolic pressures (RVDP), RV dP/dt and an estimate of pulmonary artery diastolic pressure (ePAD). Continuous haemodynamic profiles were recorded in all patients.</AbstractText>During dialysis RVSP and ePAD dropped by a mean of 39 and 50%, respectively. RVDP decreased by 6.6 mmHg. The lowest pressures occurred during the first 90 min of dialysis and were partly restored at the end of the procedure. Long-term haemodynamic monitoring unmasked severe volume overload in one patient, when dry weight was kept stable despite a decrease in lean body mass. In another patient with recurrent dyspnea after dialysis, paroxysmal atrial fibrillation, regularly occurring during dialysis, was identified as the cause of symptoms.</AbstractText>The implanted haemodynamic monitor was a sensitive indicator for changes in volume load. Continuous haemodynamic monitoring may offer a valuable tool to improve volume management in dialysis patients with left ventricular dysfunction.</AbstractText>

[Protection of oxyphenamone on myocardium against ischemia-reperfusion injury in rat heart].

To study the protective effect of oxyphenamone, a novel inodilator against myocardial ischemia-reperfusion injury.</AbstractText>A model of regional myocardial ischemia-reperfusion injury was established by ligating the left anterior desending coronary artery (LAD) in rat heart 10 min followed by reperfusion 15 min in vitro or 30 min in vivo. The protective effects of oxyphenamone were evaluated from the incidence of arrhythmia and the changes of myocardial creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) activities, malondialdehyde (MDA) content, and myocardial ultrastructure.</AbstractText>In preparations of rat Langendorff hearts, infusion of oxyphenamone (1-10 micromol.L(-1)) diminished the incidence of ventricular fibrillation, decreased the activities of CPK and LDH in coronary efflux, and antagonized the increase of MDA content in ischemic myocardium significantly. The ischemia-reperfusion injury in anesthetized rats produced severe ventricular arrhythmia, decrease of CPK in myocardium, increase of CPK in serum, increase both of LDH and MDA both in myocardium and in serum, and severe damage of myocardial ultrastructure. Intravenous injection of oxyphenamone 0.1-1.0 mg.kg(-1) 5 min before ischemia ameliorated dose-dependently ventricular arrhythmia, antagonized the changes of CPK, LDH and MDA in both myocardium and serum induced by ischemia-reperfusion. It even maintained these parameters at normal level. The effects were somewhat similar to that of verapamil 1.0 mg.kg(-1) Intravenous injection of oxyphenamone 0.5 or 1.0 mg.kg(-1) 5 min after ligation of LAD also antagonized the ischemia-reperfusion induced changes in CPK, LDH and MDA in myocardium and serum significantly, and ameliorated the damage of myocardial ultrastructure markedly. The therapeutic effects of oxyphenamone were similar to that of propranolol 2. 0 mg.kg(-1).</AbstractText>From the examination of ECG, myocardial enzymes and ultrastructure, it appears that oxyphenamone can protect myocardium against ischemia-reperfusion injury induced by occlusion of LAD both in vitro and in vivo.</AbstractText>

Left ventricular functional recovery with percutaneous, transvascular direct myocardial delivery of bone marrow-derived cells.

The potential for cellular cardiomyoplasty to provide functional left ventricular recovery in the chronically injured heart remains unclear.</AbstractText>Yorkshire swine (n = 10; 35-50 kg) had anterolateral myocardial infarction (MI) induced by coil embolization of the left anterior descending artery. Approximately 5 weeks post-MI, a composite, intravascular ultrasound-guided catheter system (TransAccess) was used to deliver an autologous, labeled, bone marrow-derived cell sub-population (approximately 3 x 10(8) cells) or saline control (approximately 50 injections/arm) through coronary veins directly into infarct and peri-infarct myocardium. Two months post-transplant, the animals had blinded endocardial and epicardial left ventricular electrical scar mapping and biventricular electrical stimulation. Coronary angiography and quantitative biplane ventriculography were performed at baseline, transplant, and sacrifice time-points.</AbstractText>Robust, viable, predominantly desmin-negative cell grafts were demonstrated post-mortem in all treatment animals. Baseline and pre-transplant global and regional wall motion was similar between groups. The cell treatment group demonstrated functional recovery with a left ventricular ejection fraction of 38.1% at the time of transplant increasing to 48.5% (p = 0.005) at sacrifice, whereas the control arm was unchanged (38.0% vs 34.3%, respectively; p = NS). The regional improvement corresponded with a reduction in percentage of hypokinetic (52.1%-42.9%, p = 0.002) and percentage of akinetic (24.8%-17.7%, p = 0.04) segments in the cell-treated animals. Epicardial scar area was not different (37 cm2 vs 23 cm2, p = 0.37) between groups.</AbstractText>Percutaneous, transvascular, direct intramyocardial bone marrow cell transplantation is safe and feasible in chronically infarcted tissue. In this pilot study, cell therapy improved overall left ventricular systolic function by recruiting previously hypokinetic or akinetic myocardial tissue.</AbstractText>

[Acute hydroxychloroquine poisoning. The danger of rapid or excessive correction of initial hypokalemia].

Toxic effects of hydroxychloroquine, like chloroquine, include membrane stabilization and hypokalemia, which is correlated with the severity of the overdose. Correction of hypokalemia can expose patients to the risk of ventricular arrhythmia.</AbstractText>A 19-year-old woman who had ingested 6 grams of hydroxychloroquine was admitted to intensive care with severe hypokalemia (1.5 mmol/L on admission). Thirty-six hours after correction of the hypokalemia, circulatory arrest followed ventricular fibrillation. Her potassium level at that time was 5.8 mmol/L. Outcome was favorable after it returned to normal.</AbstractText>Because its pathogenesis remains debatable, the hypokalemia following hydroxychloroquine poisoning must be corrected with care, even when severe. This correction is difficult, and extracellular transfer of the excess potassium after elimination of the toxin exposes the patient to the risk of ventricular arrhythmia.</AbstractText>

Spironolactone reduces fibrosis of dilated atria during heart failure in rats with myocardial infarction.

Congestive heart failure (CHF) is associated with severe structural changes of atria, contributing to impaired atrial function and the risk of arrhythmia. This study investigated the effects of CHF treatments on atrial remodelling.</AbstractText>Three months after myocardial infarction (MI), rats were treated for 1 month with spironolactone, lisinopril, or atenolol alone or in combination. Echocardiography-Doppler tissue imaging, haemodynamic measurements, and 24-h Holter monitoring were used to characterize the cardiomyopathy. Atrial fibrosis was quantified with Picrosirius Red staining. Left atrial diameter was increased (5.8+/-0.6 mm in MI vs. 3.6+/-0.3 mm in sham; P&lt;0.0001), as was atrial fibrosis (26.7+/-3.8% in MI vs. 10.5+/-2.2% in sham; P&lt;0.0001), which correlated with left ventricular (LV) dysfunction after 3 months of MI. P-wave duration was also increased and premature atrial beats were frequent on the 24-h electrocardiogram. Similar improvements in LV dysfunction were observed after 1 month of spironolactone, ACE-inhibitor, or beta-blocker therapy alone or in combination. Atrial hyperexcitability was reduced by all the treatments, but only spironolactone attenuated atrial fibrosis and reduced P-wave duration.</AbstractText>Atrial fibrosis caused by chronic CHF is reduced by spironolactone.</AbstractText>

Left atrial volume predicts cardiovascular events in patients originally diagnosed with lone atrial fibrillation: three-decade follow-up.

The objectives of this study were to determine the long-term outcome and the predictors of adverse events in patients originally diagnosed with lone atrial fibrillation (AF).</AbstractText>This population-based historical cohort study comprised 46 residents of Olmsted County, MN, USA, with well-documented, clinically defined lone AF and a complete two-dimensional echocardiographic examination. The original echocardiographic videotape recordings were analysed in a blinded fashion for left atrial volume (LAV) and left ventricular ejection fraction. With 1296 person-years of follow-up, the median duration of AF was 27 (first quartile=24, third quartile=33) years. Twenty-three (50%) patients developed events. Cerebral infarction occurred in seven patients, myocardial infarction in 11, and congestive heart failure in 16. In a multivariable analysis, patients with indexed LAV &gt;or=32 mL/m(2) had a significantly worse event-free survival (adjusted HR, 4.46; 95% CI, 1.56-12.74; P=0.005). All cerebral infarctions occurred in patients with an indexed LAV &gt;32 mL/m(2).</AbstractText>Patients originally diagnosed with benign lone AF follow divergent courses based on LAV. Those originally diagnosed with lone AF and normal sized atria had a benign clinical course throughout the long-term follow-up. Patients with increased LAV at diagnosis or later during the follow-up experienced adverse events.</AbstractText>

Device-based therapies for atrial fibrillation.

Ablation of the atrioventricular conduction system and pacemaker implantation is the preferred procedure for patients with atrial fibrillation (AF) in whom a rate control strategy has been selected but in whom rate-controlling medications are intolerable or ineffective. Selection of standard right ventricular (RV) pacing versus biventricular pacing is individualized, based on the degree and etiology of left ventricular dysfunction. Atrial-based pacing is clearly preferable to ventricular-based pacing in patients with sick sinus syndrome, because it leads to a reduction in the development of AF. Emerging evidence indicates that excess RV pacing is deleterious, increasing AF, heart failure, and possibly mortality. Therefore, physiologic pacing with minimization of RV pacing is desirable. Atrial pacing algorithms that increase the frequency of atrial pacing have shown modest efficacy in the prevention of AF. Use of atrial pacing algorithms is reasonable for patients with a history of AF and standard bradycardia indications for permanent pacing in whom maintenance of sinus rhythm is desirable. Studies assessing novel and multiple site atrial pacing therapies have mixed results, without compelling evidence of clinically important benefit. The exceptions are biatrial and right atrial overdrive pacing immediately after cardiac surgery. Several studies have shown effective suppression of postoperative AF with their use. Device therapy (eg, atrial antitachycardia pacing and defibrillation) for the termination of AF is effective in reducing arrhythmia burden. However, improvement in clinically relevant end points is not established and indications are not clearly defined. If a patient lacks an indication for an implantable cardioverter-defibrillator, we do not offer atrial defibrillation as a treatment option. Atrial arrhythmias may be better prevented by programming to avoid ventricular pacing than by specific atrial interventions.

Mechanisms of ventricular arrhythmias in heart failure.

Congestive heart failure continues to be a leading cause of mortality and morbidity worldwide. In approximately 50% of these patients, the mode of death is sudden. Ventricular tachycardia and fibrillation represent the majority of arrhythmias; the mechanisms responsible are heterogeneous and complex. Myocardial scar, a potent environment for reentry, is likely to contribute to many of the ventricular arrhythmias in ischemic heart failure. Altered calcium handling and changes in potassium currents may contribute to the increase in early and delayed afterdepolarizations seen in the failing heart. In addition, compensatory mechanisms may become deleterious and potentially arrhythmogenic via a variety of mechanisms. This article provides a general overview of the mechanisms thought to be responsible for ventricular arrhythmias in chronic heart failure.

Complications during pharmacological stress echocardiography: a video-case series.

Stress echocardiography is a cost-effective tool for the modern noninvasive diagnosis of coronary artery disease. Several physical and pharmacological stresses are used in combination with echocardiographic imaging, usually exercise, dobutamine and dipyridamole. The safety of a stress is (or should be) a major determinant in the choice of testing. Although large scale single center experiences and multicenter trial information are available for both dobutamine and dipyridamole stress echo testing, complications or side effects still can occur even in the most experienced laboratories with the most skilled operators.</AbstractText>We decided to present a case collection of severe complications during pharmacological stress echo testing, including a ventricular tachycardia, cardiogenic shock, transient ischemic attack, torsade de pointe, fatal ventricular fibrillation, and free wall rupture.</AbstractText>We believe that, in this field, every past complication described is a future complication avoided; what happens in your lab is more true of what you read in journals; and Good Clinical Practice is not "not having complications", but to describe the complications you had.</AbstractText>

Sudden cardiac death and inherited arrhythmia syndromes.

Sudden cardiac death (SCD) at youth is rare and is often caused by inherited cardiac disorders. This review focuses on the genetic background of inherited primary electrical diseases, the so-called "channelopathies." Following a short clinical description of each syndrome, the recent findings in the genetics of long QT syndrome, short QT syndrome, isolated cardiac conduction defect, familial sick sinus syndrome, familial atrial fibrillation, cathecholaminergic polymorphic ventricular tachycardia, familial Wolff-Parkinson-White (WPW) syndrome, and Brugada syndrome are discussed. The currently proposed theoretical model of overlapping phenotypes in SCN5A sodium channel mutations is presented. The recent data indicate that advances in molecular genetics, experimental and clinical electrophysiology shed some light on the genetic background of primary electrical diseases. However, it is also becoming clear that the process from a mutation of a gene to the clinical presentation of a patient is currently only partially understood and extremely complex.

Ventricular tachycardia/ventricular fibrillation ablation in the setting of ischemic heart disease.

Recurrent ventricular tachycardia (VT) in the setting of coronary artery disease is frequently a life-threatening electrophysiologic emergency. Even in patients with an implantable defibrillator, recurrent VT is frequently accompanied by repeated and disabling shock therapy. Catheter ablative therapy offers the ability to provide immediate control of recurrent VT. Long-term elimination of VT should be anticipated in most patients. This article reviews the strategies, tools, techniques, and expected outcome for catheter ablation of stable and unstable ventricular arrhythmias in the setting ischemic heart disease.

Electrophysiological basis and genetics of Brugada syndrome.

Brugada syndrome is a primary arrhythmic syndrome arising in the structurally normal heart. Any proposed mechanism should account for the major features of the syndrome: localization of the ST segment and T-wave changes to the right precordial leads, association of conduction slowing at several levels, precipitation or aggravation of the major ECG changes by sodium channel-blocking drugs and the occurrence of ventricular fibrillation. Heterogeneity of repolarization across the ventricle wall plays a major role. Any agency that shifts the net current gradient during phase I outward would exaggerate the normal heterogeneity of repolarization and result in the ST segment and T-wave changes characteristic of the syndrome. When the outward current shift is marked, premature repolarization may occur in epicardial zone and the resulting gradient may precipitate reentry. The syndrome is inherited as an autosomal dominant. However, 75% of clinically affected individuals are males. In 20% of cases, the syndrome is associated with mutations of the cardiac sodium channel gene SCN5A. The mutations result in a loss-of-function as a result of the synthesis of a non-functional protein, altered protein trafficking, or change in gating. Agencies that reduce the sodium current may precipitate the characteristic ECG changes, for example, sodium channel blockers and membrane depolarization by hyperkalemia. Sympathetic stimulation may reverse the ECG changes and reduce arrhythmia recurrence. By its nonspecific potassium channel blocking action, quinidine may also reduce arrhythmia recurrence. We still do not know the basis for defect in the majority of patients with Brugada syndrome.