Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

To gain insight into the mechanisms of reperfusion arrhythmias, we studied ventricular automaticity and conduction characteristics in 35 dogs during 10 minutes of left anterior descending coronary artery (LAD) occlusion and subsequent reperfusion. The frequency of ectopic activity reached a maximum within the first 6-8 minutes after LAD occlusion and then declined, leading to an ectopia-free quiescent period. The arrhythmias after occlusion were marked by prolonged ischemic zone conduction times as measured from local bipolar plunge electrodes while marked fractionation of electrical activity was recorded from specially constructed composite epicardial electrodes. The quiescent period was characterized by a loss of marked fractionation of electrical activity from composite recordings and a progressive decrease or complete loss of electrogram amplitude from plunge electrodes. Reperfusion was characterized by a rapid improvement in both the ischemia-induced conduction delay and amplitude on the local bipolar electrogram. However, the composite electrode recorded a return of the marked fractionation of electrical activity associated with a return of arrhythmias. Ventricular automaticity druing reperfusion (50.6 ± 6.0 beats/min) was assessed in five dogs with complete atrioventricular block and was not significantly different from control preocclusive automaticity (47.6 ± 5.8 beats/min). In addition, reperfusion at a heart rate of 220 beats/min was associated with increased frequency and severity of arrhythmias compared with those at a heart rate of 150 beats/min. We conclude that the early ischemic arrhythmias result from conduction slowing through the ischemic zone establishing reentrant pathways, while the quiescent period is a manifestation of further conduction suppression so that reentrant pathways become blocked. Reperfusion of this electrically unresponsive tissue results in