Sudden death, a major cause of mortality in the Western world, usually results from electrophysiologic phenomena in chronically damaged hearts with advanced coronary atherosclerosis. The exact pathophysiologic mechanisms are not known, but there is reasonable circumstantial evidence to implicate myocardial ischemia--clinically manifest or silent--as one of probably multiple factors of pathogenetic significance. This may be on the basis of coronary artery spasm, platelet aggregation, left ventricular dysfunction perpetuating a vicious circle of hypoperfusion and ventricular vulnerability to electrical instability. The increasing use and quality of continuous ambulatory electrocardiographic (Holter) monitoring have allowed improved detection of ST-segment changes and arrhythmias. The majority of sudden deaths result from ventricular tachyarrhythmias degenerating into ventricular fibrillation, and a more significant proportion of these than had been previously thought may be ischemically mediated. Importantly, as many as 20 to 25 per cent of the approximately 450,000 yearly terminal events represent bradyarrhythmias that may be preceded or accompanied by silent myocardial ischemia. Research is still required to determine the incidence, role, and mechanisms of silent myocardial ischemia in sudden death, with the hope that this common catastrophic event can be better prevented.