Sudden Cardiac Death: Interface Between Pathophysiology and Epidemiology

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Key points

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    Sudden cardiac death (SCD) accounts for 50% of all cardiovascular deaths; approximately 50% of all SCDs are first cardiac events; sudden cardiac arrest (SCA) accounts for up to 50% of heart disease–related years of productive life lost.

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    Measures of risk of SCA and SCD can be substrate based or expression based.

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    The pathophysiologic cascade for SCA includes modules of atherogenesis, plaque destabilization, onset of ischemia, and arrhythmia.

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    Mechanisms of tachyarrhythmias leading to SCA differ for

Incidence of sudden cardiac arrest

The incidence of SCD has long been estimated to be in the range of 1 per 1000 population per year for the middle-aged and older population.9 Although the age at which an SCD occurs has shifted to an older age group over years, likely resulting from a combination of coronary risk factor control strategies and interventions for acute coronary syndromes, the cumulative population burden, measured as total number of SCDs, has not changed substantially but has shifted to an older age group. At the

Causes and mechanisms of cardiac arrest

It has long been established that coronary atherosclerosis is the most common cause of SCA and SCD in Western societies, with an increasing dominance in other areas as the world becomes more uniformly developed. The general estimates cite coronary artery disease as the cause in up to 80% of the SCDs in the United States among patients more than 35 years of age.9 The cardiomyopathies as a group are second, accounting for approximately 10% to 20% of all SCDs, and various other disorders, such as

Mechanistic targets derived from epidemiologic subdivisions

Preventive strategies targeting risk for SCA and SCD can be divided into 4 epidemiologic targets (Box 3). The most commonly used model from a general population perspective is conventional preventive epidemiology, targeted to primary or secondary prevention of structural heart disease and in some cases to mechanisms of expression, such as hypertension. A second model focuses on transient risk factors as an epidemiologic category incorporating the triggering mechanisms. A commonly appreciated

Mechanisms and pathophysiology of sudden cardiac arrest in coronary heart disease

SCDs caused by coronary heart disease, lethal tachyarrhythmias, or asystolic or PEA mechanisms are all the consequences of pathophysiologic cascades resulting from complex interactions between coronary vascular events, myocardial injury, variations in autonomic tone, and the metabolic and electrolyte state of the myocardium.18, 19 The general cascade, most easily viewed in the context of SCD associated with coronary heart disease, incorporates a series of modules ranging from atherogenesis,

Transition from myocardial instability to lethal tachyarrhythmias

A triggering event interacting with susceptible myocardium is a primary mechanism leading to the initiation of lethal arrhythmias (see Figs. 2 and 3). The triggering event for ventricular tachycardia (VT) or VF, or persisting risk for recurrence, can be electrophysiologic, ischemic, metabolic, or hemodynamic. For VF, the end point of these interactions is disorganization of patterns of myocardial activation into multiple uncoordinated reentrant pathways. Clinical, experimental, and

Asystolic arrest

The basic electrophysiologic mechanism in this form of arrest is failure of normal subordinate automatic activity to assume mechanical activation of the ventricular myocardium, caused by the absence of the electrical stimulus. Asystolic arrest is more common in severely diseased hearts and in patients with several end-stage disorders, both cardiac and noncardiac. These mechanisms may result, in part, from diffuse involvement of subendocardial Purkinje fibers in advanced heart disease.

Pulseless electrical activity

PEA is separated into primary and secondary forms. No single unifying definition for PEA, mechanistically or clinically, is generally accepted. The common denominator is the presence of organized cardiac electrical activity in the absence of effective mechanical function.25 The absence of rapid ROSC is important in that it excludes transient losses of cerebral blood flow, such as the various patterns of vasovagal reflex syncope, which have different clinical implications than the meaning

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      A novel hypothesis has recently been advanced linking SIDS to CO2 retention [106]. SCD includes deaths due to nonarrhythmic, mechanical causes, such as ruptured AMI, and deaths due to fatal ventricular arrhythmia, i.e., SAD and sudden arrhythmic death syndrome (SADS) [107,108]. Dysfunctions of the cardiac conduction and autonomic nervous systems are known to contribute to SCD pathogenesis, as are ventricular arrhythmias triggered by ectopic foci in hypertrophied hearts and those with acute ischemia [4,8].

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    Disclosures: None.

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