Flow of "injury" current and patterns of excitation during early ventricular arrhythmias in acute regional myocardial ischemia in isolated porcine and canine hearts. Evidence for two different arrhythmogenic mechanisms.

We recorded 60 DC-extracellular electrograms simultaneously from epicardial and intra- mural sites of the left ventricle of isolated perfused porcine and canine hearts during the first 15 minutes after occlusion of the left anterior descending coronary artery. During coronary occlusion, maximal current flow across the ischemic border occurred when normal cells had repolarized and ischemic cells had not. At that moment, maximal current sources at the normal side of the ischemic border were in the order of 2 μA/mm3 and maximal current sinks were -5 μA/mm3. During propagation of a broad wavefront in nonischemic myocardium, current sources in the wake of the wavefront were about twice as large. Ventricular premature beats usually followed deep negative T waves in ischemic myocardium, when “injury” currents were maximal. Earliest activity always occurred at the normal side of the ischemic border, and whenever Purkinje activity was recorded it preceded myocardial activity in both single premature beats and the initial beats of ventricular tachycardia (VT) or ventricular fibrillation (VF). For later beats of VT, circus movements with a diameter of 1-2 cm were responsible for continuation of the arrhythmia. Dimension and position of the reentrant circuit changed from beat to beat. In VF, fragmentation of wavefronts occurred, and multiple wavelets followed tortuous paths. Circus movements were seldom completed; when they were, their diameter was 0.5 cm. It is concluded that two mechanisms are responsible for the very early ischemic arrhythmias: one, a μfocalμ mechanism located at the normal side of the ischemic border, possibly induced by injury currents in normal Purkinje fibers and, two, macro- and micro-reentry in ischemic myocardium. Circ Res 47:151-165, 1980