The most important ventricular arrhythmias, the ventricular tachycardias (VTs) and ventricular fibrillations (VFs), are thought to underlie the majority of cases of sudden cardiac death. In ischemic heart disease, they can be divided into several pathophysiological entities: (a) arrhythmias occurring during the acute reversible phase of ischemia, (b) arrhythmias taking place during reperfusion of acutely ischemic myocardium, (c) arrhythmias occurring 24-72 h after acute infarction, and (d) arrhythmias associated with chronic infarction. In all three settings, the mechanisms sustaining ventricular arrhythmias need to be distinguished from initiating mechanisms. With the exception of the 24-72-h stage, these arrhythmias are sustained by circus movement with reentry: the electrophysiological determinants of circus movements at a cellular level and, consequently, the appearance of the circulating wave fronts, differ according to the ischemic phase. In acute ischemia, multiple circulating waves, with somewhat large diameters, change their vortexes from beat to beat. In chronic infarction, the location of the stable circuits with elongated central zones of block are closely related to myocardial fiber architecture and probably to scar tissue. These differences indicate that (a) in acute ischemia, the conduction disturbances are mainly determined by the development of inexcitability at the level of cardiac membranes; and (b) in chronic infarction, the site of conduction block and the pivoting points of the wave fronts are determined by impairment of electrical cell-to-cell coupling. In contrast to the mechanisms sustaining VT and VF, the initiating mechanisms are less well defined.(ABSTRACT TRUNCATED AT 250 WORDS)