Restitution properties during ventricular fibrillation and the effects of cardiac pacing location on ventricular electrophysiology in the rabbit heart

Abstract Sudden cardiac death is a cause of mortality due to malignant arrhythmias such as ventricular fibrillation (VF). Although action potential duration (APD) restitution is a method to assess arrhythmic susceptibility, repolarisation may depend on prior activation history, a phenomenon known as cardiac memory. Cardiac memory describes the persistence of repolarisation effects from previous beats, such that APD reflects not only the immediately preceding diastolic interval (DI) but also earlier activation effects. This may be relevant during VF, where continuously varying activation patterns prevent a steady electrophysiological state. This study investigated how pacing location affects ventricular electrophysiology and whether repolarisation during VF exhibits short‐term cardiac memory. Langendorff‐perfused rabbit hearts were used to record monophasic action potentials from the left ventricular apex and base. Pacing was conducted from five sites. Steady‐state APD was assessed during constant pacing. Effective refractory period (ERP), APD restitution and conduction time restitution (CTR) were assessed using an S 1 –S 2 extra‐stimulus protocol (S 1 , conditioning stimuli; S 2 , premature extra‐stimulus). Additionally, APD–DI and APD–APD relationships were analysed during early VF. Pacing location significantly influenced S 1 and S 2 conduction delays, consistent with site‐dependent activation timing. However, steady‐state APD, ERP and CTR were not significantly affected by pacing location. In contrast, during VF, APD exhibited a significant dependence on preceding DI and preceding APD over approximately the first 30 beats, with these relationships progressively deteriorating thereafter. These findings demonstrate that while pacing location alters activation timing, repolarisation dynamics under stable activation histories are robust. During VF, continuously changing activation patterns unmask short‐term cardiac memory.