Ventricular fibrillation is the likely mechanism for sudden death and the leading cause of fatality among patients with coronary heart disease. In this country alone, ventricular fibrillation claims about 450,000 lives per year. Since prolonged survival is possible after resuscitation, the catastrophic arrhythmia seems to represent an electrical accident rather than the culmination of extensive, irreversible structural damage to the heart.¹ Indeed, in most cases of sudden death pathological studies have failed to uncover acute lesions either in the coronary arteries or in the myocardium. How, then, is the heart catapulted into such disorganized electrical activity?

Two related hypotheses directed . . .