Sudden Cardiac Death: Epidemiology, Transient Risk, and Intervention Assessment

Abstract

Progress in the prevention of sudden death will require development of new approaches, including epidemiologic techniques to address risk characteristics specific to the problem; characterization of triggering events and identification of specific persons at risk for responding adversely to these events; and methods of evaluating outcomes appropriate to the nature of sudden cardiac death.

Arrhythmogenic right ventricular cardiomyopathy/dysplasia: a not so rare “disease of the desmosome” with multiple clinical presentations

“…The histological findings described above mirror the electrical reentrant phenomena and late potentials probably generated in the strands of cardiomyocytes within the fibrofatty tissue. However, environmental factors are important in the triggering of a life threatening arrhythmia 20 . The histological analysis of the right ventricle showing massive fibrofatty replacement of the myocardium remains a hallmark of ARVC/D.…”

Indications for an Implantable Cardioverter Defibrillator (ICD)

“…One had been treated with septal myotomy and a pacemaker. At electrophysiologic study, induced hypotensive VT or VF could be terminated by the automatic defibrillator and thereafter, 3 patients underwent implantation (1).…”

The Search for Novel Antiarrhythmic Strategies

“…92 The clinical observation that patients with an obvious structural substrate (eg, scar) have episodic post myocardial infarction arrhythmias suggests a role for intermittent triggers in the setting of chronic maladaptation. 93 Clinically, several triggering events have been suggested 94,95 : (1) transient ischemia; (2) fluctuations in the activity of the autonomic nervous system; (3) changes in general body homeostasis (eg, electrolytes, circulating hormones); (4) drugs that prolong the QT interval; and (5) regional sympathetic denervation induced by infarction. 96 While some of these triggers are relatively non-specific and are encountered in other arrhythmias, some appear to be specific in that they result from the interaction between the chronic, compromised substrate and a superimposed acute event.…”

“…Assuming equal levels of efficacy (% reduction in events), a trial in patient-groups with many events will be smaller than in groups with relatively few events. 95 In general, it is desirable to carry out initial studies in high-risk groups to establish "proof of principle" in the smallest reasonable population. However, less high-risk patients may not respond similarly, and the largest populations (eg, the general population) with the lowest event rates may, because they are so numerous, contain the highest absolute numbers of events (Fig 3), accompanied by the greatest potential for doing harm.…”

“…95 While secondary endpoints such as arrhythmic mortality and arrhythmia event rates provide useful therapeutic insights, they are difficult to measure and do not necessarily reflect the net mortality benefit. 5 Finally, comparisons of active therapies limit interpretation of benefit; a true concurrent placebocontrolled design (if ethically defensible) is the most reliable measure of mortality benefit.…”