c t r b ( p Sudden cardiac arrest remains a leading cause of death, the underlying cause typically being ventricular tachycardia or ventricular fibrillation (VT/VF). The mechanism for VT/VF is thought to be reentry in most cases, but our inadequate understanding of how reentry is initiated hampers our ability both to identify those at greatest risk and to design preventive strategies. The theory of repolarization alternans has been proposed as an explanation of how reentry is induced in the absence of identifiable anatomic obstacles. The induction of reentrant VT/VF requires heterogeneous excitability leading to conduction block (“wave break”) of a premature stimulus at an area of temporary refractoriness while conduction persists in adjoining tissue. The resulting wave of depolarization can lead to further wave break and propagation of daughter waves, resulting in meandering, multiwave fibrillation. While Antzelevitch et al have shown that significant transmural gradients of reolarization heterogeneity exist even in normal ventricles, ource-sink mismatch prevents the induction of reentry by ypical premature foci. Under stressful conditions, that is, high stimulation rates, drugs that alter ion channel kinetics, or sympathetic stimulation, spatially differential variability in repolarization may occur transiently, increasing the risk for wave break in the presence of a premature stimulus. When the duration of the action potential alternately shortens and prolongs in a fixed short-long-short-long pattern, repolarization alternans exists. If repolarization alternans occurs in a consistent manner across a region of the ventricular wall, it is considered spatially concordant alternans. If, however, an area of myocardium manifests action potential prolongation and shortening while an adjacent area manifests alternans in the opposite phase, that is, long-short in one area and short-long in another, it is referred to as spatially discordant alternans. Discordant alternans have