Arrhythmias remain a major cause of late mortality following myocardial infarction. They arise due to fibrosis within the infarct, which creates the conditions of slow conduction necessary for re-entry. In individual patients who have already manifested a malignant arrhythmia, antiarrhythmic drug therapy, guided by invasive electrophysiological testing, is of proven benefit in prolonging survival. By contrast, when used on a population basis, antiarrhythmic drug therapy has proved singularly ineffective. This is illustrated by the recent Cardiac Arrhythmia Suppression Trial (CAST) study--far from improving survival, antiarrhythmic therapy increased mortality. The use of antiarrhythmic drugs on a population basis is therefore fundamentally flawed. Hemodynamic intervention provides an alternative strategy in arrhythmia prevention. Hemodynamic changes may influence electrophysiological parameters and arrhythmogenesis in a number of ways. First, myocardial stretch may contribute to arrhythmogenesis through contraction-excitation feedback. Second, hemodynamic changes can influence ventricular remodeling following infarction, which may be an important determinant of subsequent arrhythmogenesis. Hemodynamic intervention, therefore, represents a promising new approach to arrhythmia prevention following myocardial infarction.