Task Force on Sudden Cardiac Death, European Society of Cardiology.

The European Society of Cardiology has convened a Task Force on Sudden Cardiac Death in order to provide a comprehensive, educational document on this important topic. The main document has been published in the European Heart Journal in August 2001. The Task Force has now summarized the most important clinical issues on sudden cardiac death and provided tables with recommendations for risk stratification and for prophylaxis of sudden cardiac death. The present recommendations are specifically intended to encourage the development and revision of national guidelines on prevention of sudden cardiac death. The common challenge for cardiologists, physicians of other medical specialties and health professionals throughout Europe is to realize the potential for sudden cardiac death prevention and to contribute to public health efforts to reduce its burden.

Relationship between rehospitalization and future death in patients treated for potentially lethal arrhythmia.

INTRODUCTION: It is generally considered that death is the only appropriate endpoint to evaluate interventions for preventing death; however, this belief may be based on the previous use of inappropriate or inadequate surrogates for death. The aim of this study was to evaluate whether rehospitalization following implementation of an intervention is a reasonable surrogate for death. METHODS AND RESULTS: The time from discharge following intervention to rehospitalization was evaluated for 997 patients discharged after baseline hospitalization in the Antiarrhythmics Versus Implantable Defibrillators Trial. The relationship between rehospitalization for various reasons and subsequent death was compared in the two treatment arms to assess the adequacy of rehospitalization as a surrogate for death. Included were rehospitalization for: any reason, a cardiac problem, a noncardiac problem, new or worsened congestive heart failure (CHF), an acute coronary syndrome, and a cardiac procedure. For all of the reasons except cardiac procedure, rehospitalization was associated with a substantially increased hazard for subsequent death. Rehospitalization for new or worsened CHF was most closely (that is, temporally) related to subsequent death and was the only reason for rehospitalization, which fully explained the treatment effect of implantable cardiac defibrillators compared with antiarrhythmic drugs on death. CONCLUSION: Rehospitalization is a significant risk factor for subsequent death. However, only rehospitalization for new or worsened CHF appears to be a potential surrogate for death in the setting of antiarrhythmic interventions.

Mechanisms underlying the reentrant circuit of atrioventricular nodal reentrant tachycardia in isolated canine atrioventricular nodal preparation using optical mapping.

The reentrant pathways underlying different types of atrioventricular (AV) nodal reentrant tachycardia have not yet been elucidated. This study was performed to optically map Koch's triangle and surrounding atrial tissue in an isolated canine AV nodal preparation. Multiple preferential AV nodal input pathways were observed in all preparations (n=22) with continuous (73%, n=16) and discontinuous (27%, n=6) AV nodal function curves (AVNFCs). AV nodal echo beats (EBs) were induced in 54% (12/22) of preparations. The reentrant circuit of the slow/fast EB (36%, n=8) started as a block in fast pathway (FP) and a delay in slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP through the atrial tissue located at the base of Koch's triangle. The reentrant circuit of the fast/slow EB (9%, n=2) was in an opposite direction. In the slow/slow EB (9%, n=2), anterograde conduction was over the intermediate pathway (IP) and retrograde conduction was over the SP. Unidirectional conduction block occurred at the junction between the AV node and its input pathways. Conduction over the IP smoothed the transition from the FP to the SP, resulting in a continuous AVNFC. A "jump" in AH interval resulted from shifting of anterograde conduction from the FP to the SP (n=4) or abrupt conduction delay within the AV node through the FP (n=2). These findings indicate that (1) multiple AV nodal anterograde pathways exist in all normal hearts; (2) atrial tissue is involved in reentrant circuits; (3) unidirectional block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask the existence of FP and SP, producing continuous AVNFCs.

Central clinical research issues in electrophysiology: report of the NASPE Committee.

This article contains the results of an attempt by appointed members of the North American Society of Pacing and Electrophysiology to define the research frontier in electrophysiology and suggest areas of study as an aid in setting the research agenda.

Sudden cardiac death, genes, and arrhythmogenesis : consideration of new population and mechanistic approaches from a national heart, lung, and blood institute workshop, part I.

Malignant ventricular arrhythmias are the leading mechanism of death in patients with acute and chronic cardiac pathologies. The extent to which inherited mutations and polymorphic variation in genes determining arrhythmogenic mechanisms affect these patients remains unknown, but based on recent population studies, this risk appears significant, deserving much greater investigation. This report summarizes a National Heart, Lung, and Blood Institute workshop that considered sources of genetic variation that may contribute to sudden cardiac death in common cardiac diseases. Evidence on arrhythmogenic mechanisms in recent population studies suggests a significant portion of the risk of sudden cardiac death in such broad populations may be unrelated to traditional risk factors for predisposing conditions such as atherosclerosis, hypertension, and diabetes and instead may involve unrecognized genetic and environmental interactions that influence arrhythmic susceptibility more directly. Additional population and genetic studies directed at discovering the sources of inherited molecular risk that are most directly linked to arrhythmia initiation and propagation, in addition to studies on previously well-described risk factors, would appear to have considerable potential for reducing premature cardiovascular mortality.

Transmural reentry during acute global ischemia and reperfusion in canine ventricular muscle.

Coronary occlusion and reperfusion produce tachyarrhythmias. We tested the hypothesis that variations in transmural activation after global ischemia and reperfusion were responsible for arrhythmias. We arterially perfused 36 isolated transmural wedges from canine left ventricular free walls. After > or =100 min of stabilization, the artery was occluded for 25 min, followed by reperfusion at various flow rates. We recorded 256 channels of fluorescent action potentials on transmural surfaces from preocclusion to >15 min after reperfusion. During endocardial pacing at 300 ms, ischemia of > or =570 +/- 165 s (n = 34) produced 1:1 endocardial conduction and then 2:1 and 4:1 block as the wave fronts conducted toward epicardium. Transmural reentry appeared after 535 +/- 146 s of ischemia (n = 31). Further ischemia caused epicardial inactivation and eliminated reentry (n = 24). During reperfusion, tissues progressed through sequences of epicardial inactivation and reappearance of activation with 1:1, 2:1, and 4:1 conduction; both sustained and nonsustained reentry occurred. We conclude that heterogeneous activation responses to endocardial pacing during acute ischemia provide the substrate for initiating reentry, suppressed reentry during further ischemia, and caused reentry during reperfusion.