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

Robert J. Myerburg, MD; Kenneth M. Kessler, MD; and Agustin Castellanos, MD
[+] Article, Author, and Disclosure Information

From the University of Miami School of Medicine and the Veterans Affairs Medical Center, Miami, Florida. Requests for Reprints: Robert J. Myerburg, MD, Division of Cardiology (D-39), University of Miami School of Medicine, P.O. Box 016960, Miami, FL 33101. Grant Support: In part by grants HL21735 and HL28130 from the National Heart, Lung, and Blood Institute and by a grant-in-aid from the American Heart Association, Florida Affiliate, 91GIA/740.

Copyright 2004 by the American College of Physicians

Ann Intern Med. 1993;119(12):1187-1197. doi:10.7326/0003-4819-119-12-199312150-00006
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Purpose: To integrate information from the various disciplines that contribute to the understanding of the cause and prevention of sudden cardiac death: identification of new approaches from applied clinical epidemiology; identification and control of transient risk factors; and evaluation of the results of interventions.

Data Sources: A broad range of research reports and interpretations of data from English-language journal articles and reviews, published primarily between 1970 and 1993. The fields of study included epidemiology, experimental electrophysiology, clinical observations, and interventions.

Study Selection: Continuous literature surveys, done in relation to ongoing clinical and experimental research on sudden cardiac death since 1972.

Data Extraction: Included on the basis of relevance to the topics discussed and with confirmation of data and concepts by more than one investigator when available.

Data Synthesis: Information from several disciplines was integrated by the authors to synthesize new ways to view the problem of sudden cardiac death. Quantitative information was used primarily to derive qualitative statements about new perspectives on sudden cardiac death.

Conclusions: 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.


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Figure 2.
Time-dependence of risk after cardiovascular events. Top.[5]Middle.[13]Bottom.[14][5]

Survival curves for hypothetical patients with known cardiovascular disease free of a major index event (curve A) and for patients surviving major cardiovascular events (curve C). Attrition is accelerated during the initial 6 to 24 months after the event. Curve B shows the dynamics of risk over time in low-risk patients with an interposed major event that is normalized to a time point (for example, 18 months). The subsequent attrition is accelerated for 6 to 24 months. (Reproduced from with permission of the American Heart Association.) Kaplan-Meier estimates representing 3 years of follow-up after acute myocardial infarction. Both the frequency of ventricular premature depolarizations (VPD) and depressed ejection fractions (EF) contribute to increasing mortality rates. As risk increases based on the presence of neither (curve A), one (curves B and C), or both (curve D) of these predictors, increasing risk is expressed preferentially within the first year (curves C and D). (Modified from ; reproduced with permission of the American Journal of Cardiology). Survival curve showing time-dependence of risk for recurrence among survivors of cardiac arrest. The risk was highest during the first 6 months. (Modified from ; reproduced from with permission of the American Heart Association.).

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Figure 3.
Structure, function, and the pathogenesis of sudden cardiac death.[35]

Four categories of the conditioning risk factors (structural abnormalities) predisposing to sudden cardiac death interact with one or more inciting influences (functional perturbations) to cause transient destabilization. This interaction may convert premature ventricular complexes (PVCs), which are pathophysiologically innocuous, into triggering events for ventricular tachycardia or fibrillation (VT/VF). See text for details. (Modified from Myerburg RJ, et al ; reproduced with permission of the American Journal of Cardiology).

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Figure 1.
Sudden cardiac deaths among population subgroups.[5]

Estimates of incidence (percent per year) and total number of sudden cardiac deaths per year are shown for the overall adult population in the United States and for higher-risk subgroups. The overall estimated incidence is 0.1% to 0.2% per year, totaling more than 300 000 deaths per year. Within subgroups identified by increasingly powerful risk factors, the increasing incidence is accompanied by progressively decreasing total numbers. Practical interventions for the larger subgroups will require identification of higher-risk clusters within the groups. EF = ejection fraction; MI = myocardial infarction; VT/VF = ventricular tachycardia-ventricular fibrillation. The horizontal axis for the incidence figures is nonlinear; see text for details. (From Myerburg, et al ; reproduced with permission of the American Heart Association.).

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Figure 4.
Antiarrhythmic-proarrhythmic equilibrium.Figure 1Figure 1(right panel)

The risk for sudden death, as shown in , is used to provide examples of antiarrhythmia-proarrhythmia equilibrium. The untreated risks in the same six groups shown in are indicated by the open bars. Patients with previous coronary events and cardiac arrest survivors are estimated to have the antiarrhythmic benefit (residual risk) indicated by the superimposed black bars. When the risk for proarrhythmia is added in patients with a previous coronary event, based on data from CAST, the residual risk plus the added proarrhythmic risk exceeds untreated risk and results in a net adverse outcome. Among survivors of cardiac arrest, a 10% residual risk with antiarrhythmic therapy based on reported data, plus a 5% added risk for fatal proarrhythmic events, yields an equilibrium that is lower than the estimated untreated risk, resulting in a net benefit. See text for further details.

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