Sudden death in coronary artery disease: acute ischemia versus myocardial substrate.

Abstract

Sudden cardiac death accounts for ≈50% of the estimated 500 000 cardiovascular deaths that occur annually in the United States, and a vast majority are the result of coronary artery disease.1-4 Although in some subjects there is a history of angina pectoris, myocardial infarction, or previous cardiac arrest, a significant proportion of events occur in subjects without any history of cardiac disease.1,5 Advanced therapies such as thrombolytic agents and implantable cardioverter/defibrillators are of no value to the thousands of victims who do not survive to receive medical attention. Because so many instances of sudden cardiac death cannot be predicted, any intervention directed toward the general community would have to be applied to an estimated 1000 persons for every 1 person in whom sudden death might be prevented.6 Ventricular tachyarrhythmias are responsible for most cases of sudden cardiac death, although there is more than one mechanism for these arrhythmias. Some victims die from ventricular fibrillation, which can result from acute coronary ischemic thrombosis in an otherwise normal heart,7-9 whereas others die from tachyarrhythmias arising from chronic scar.9 The relative incidence of the two mechanisms is uncertain due to (1) the lack of a consistent definition of sudden cardiac death, especially in terms of the timing between the onset of symptoms and death, and (2) the frequent overlap of the two mechanisms. Most authors define sudden death as that which occurs within 1 hour of the onset or abrupt change of symptoms.1 Some earlier series used more liberal criteria and included subjects who died up to 24 hours after symptom onset.10 However, there are important pathophysiological differences between deaths that occur instantaneously and those that occur hours after the onset of symptoms, as noted by Friedman et al11 more than 2 decades ago. Most …