Electrophysiological mechanisms for postcardioplegia reperfusion ventricular fibrillation

Reperfusion arrhythmias that follow regional ischemia at normothermia have been studied extensively and are considered to be a manifestation of ischemia-reperfusion injury. In contrast, reperfusion arrhythmias that occur following hypothermic cardioplegic arrest have received little attention from investigators. This study defines the electrophysiological mechanisms for postcardioplegia reperfusion ventricular fibrillation (RVF).

The electrophysiology of postcardioplegia RVF was examined by using in situ porcine hearts. Complete heart block was created by using cryoablation before cardioplegic arrest so that isolated ventricular electrical activity could be observed for a prolonged time after reperfusion. Electrophysiological data were collected from limb leads, right atrial electrodes, and left ventricular electrodes in all 12 pigs. In 5 pigs, right and left ventricular endocardial electrograms were also recorded. A total of 103 episodes of RVF were analyzed. In 90 instances, an accelerating automatic ventricular focus initiated RVF. In five animals, RVF occurred after ventricular pacing (ie, purely re-entrant RVF). The mechanism for RVF was indeterminant in 8 instances. The origin of RVF was mapped in 44 instances. RVF usually originated in the left ventricle (25 instances) or septum (16 instances).

Enhanced automaticity and re-entry are the mechanisms for postcardioplegia and regional ischemia-reperfusion arrhythmias. This finding supports the use of postcardioplegia RVF as a variable for comparing strategies for myocardial protection and suggests that information generated by the study of regional ischemia reperfusion arrhythmias can be used to understand postcardioplegia reperfusion arrhythmias and ischemia-reperfusion injury.