The immediate cause of cardiac sudden death in the majority of cases, is ventricular fibrillation (VF); VF is precipitated by ventricular premature beats (VPBs) which are early enough to interrupt the T wave. The basis for ventricular vulnerability is inhomogeneous excitability of the ventricle in its relative refractoriness. The premature impulse initiated during the vulnerable period is forced to propagate along irregular wave fronts and this will predispose the ventricle to multiple reentrant activity and subsequent fractionation of the wave fronts into many irregular wavelets. Ventricular fibrillation is more likely to be induced by early VPBs in the presence of clinical and electrocardiographic evidence of myocardial infarction, long ventricular cycle lengths, Q-T prolongation, and increase in the T wave amplitude. These changes are associated with increased inhomogeneity of excitability in ventricular myocardium.