Intracellular overloading by calcium ions may play an important role in the development of ischemic ventricular fibrillation, as shown by experimental data. Mechanisms are those that develop secondary to the rise in cytosolic calcium thought to occur in ischemia. After-depolarizations are stressed as a possible cause of automaticity and triggered arrhythmias in ventricular tissue. The ideal calcium antagonist should be able to inhibit such afterdepolarizations in ischemic tissue without having a negative inotropic effect on nonischemic tissue. Hence, it might be possible to extend the beneficial results of verapamil found in a recent postinfarct trial to show even better postinfarct protection by a calcium antagonist with these specific properties. On the other hand, a highly vascular-selective calcium antagonist, by avoiding any effect on the myocardium, could also be desirable in postinfarct patients with heart failure. Future trials should compare these two types of calcium antagonists. If the adverse effect of calcium antagonists on heart failure could be avoided, then the calcium antagonists would stand along-side the beta-blockers as agents able to prevent postinfarct sudden death. Furthermore, the combination of calcium antagonists and beta-blockade could then become attractive as potentially powerful postinfarct protection.