Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.
Authors: D K Murdock, J M Loeb, D E Euler, W C Randall
Journal: Circulation (1980)

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 frac- tionation of electrical activity from composite recordings and a progressive decrease or complete loss of elec- trogram 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 suppres- sion so that reentrant pathways become blocked.Reperfusion of this electrically unresponsive tissue results in a nonhomogenuous improvement in conduction that transiently restores the conditions necessary for reentry.IN 1943 Harris and Rojas' first demonstrated a specific time course for ventricular arrhythmias during acute ischemia.After coronary occlusion, they noted a progressive increase in the frequency of ectopic ac- tivity that reached maximal intensity within 6-10 minutes and then abated, resulting in a relatively ectopia-free quiescent period.Ventricular fibrillation, when present, was limited to the early arrhythmic period.These investigators also demonstrated that reperfusion of acutely ischemic myocardium also gave rise to a rapid increase in ectopic activity, leading frequently to ventricular fibrillation.The malignant potential of coronary reperfusion has since been demonstrated by several investigators.2`9Several studies using both specially constructed composite electrodes'0 "1 and bipolar electrodes'2 13 have demonstrated a close relationship between the extent of desynchronization of electrical activity dur- ing acute ischemia and ventricular arrhythmias.The desynchronization of electrical activity is believed to represent marked slowing and inhomogeneity of con- duction through the ischemic zone.This finding, coupled with the failure to demonstrate enhanced