ELECTROPHYSIOLOGICAL MECHANISMS FOR POSTCARDIOPLEGIA REPERFUSION VENTRICULAR-FIBRILLATION

Background Reperfusion arrhythmias that follow regional ischemia at no rmothermia have been studied extensively and are considered to be a ma nifestation of ischemia-reperfusion injury. In contrast, reperfusion a rrhythmias that occur following hypothermic cardioplegic arrest have r eceived little attention from investigators. This study defines the el ectrophysiological mechanisms for postcardioplegia reperfusion ventric ular fibrillation (RVF). Methods and Results The electrophysiology of postcardioplegia RVF was examined by using in situ porcine hearts. Com plete heart block was created by using cryoablation before cardioplegi c arrest so that isolated ventricular electrical activity could be obs erved for a prolonged time after reperfusion. Electrophysiological dat a were collected from limb leads, right atrial electrodes, and left ve ntricular electrodes in all 12 pigs. In 5 pigs, right and left ventric ular endocardial electrograms were also recorded. A total of 103 episo des of RVF were analyzed. In 90 instances, an accelerating automatic v entricular focus initiated RVF. In five animals, RVF occurred after ve ntricular pacing (ie, purely re-entrant RVF). The mechanism for RVF wa s indeterminant in 8 instances. The origin of RVF was mapped in 44 ins tances. RVF usually originated in the left ventricle (25 instances) or septum (16 instances). Conclusions Enhanced automaticity and re-entry are the mechanisms for postcardioplegia and regional ischemia-reperfu sion arrhythmias. This finding supports the use of postcardioplegia RV F 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 re perfusion arrhythmias and ischemia-reperfusion injury.