Key result
Ventricular pacing site alters conduction delays without affecting action potential duration or restitution dynamics.
Why the study?
Repolarisation may depend on prior activation history (cardiac memory), which is relevant during ventricular fibrillation where continuously varying activation patterns prevent a steady electrophysiological state. How pacing location affects ventricular electrophysiology and whether repolarisation during VF exhibits short-term cardiac memory required investigation.
Does cardiac pacing location alter ventricular repolarisation restitution and conduction properties under stable activation, and does repolarisation during early ventricular fibrillation exhibit short-term beat-to-beat cardiac memory in the rabbit heart?
Does cardiac pacing location alter ventricular repolarisation restitution and conduction properties under stable activation, and does repolarisation during early ventricular fibrillation exhibit short-term beat-to-beat cardiac memory in the rabbit heart?
Demonstrates that under stable pacing conditions, ventricular repolarisation and restitution kinetics are independent of pacing site despite distance-dependent conduction delays, whereas the chaotic activation of early ventricular fibrillation unmasks transient short-term beat-to-beat cardiac memory over the first 30 beats.
Answers are grounded in this paper and cite their sources.
Pacing site alters conduction delays without affecting repolarization in stable rabbit hearts; leaves open whether early VF cardiac memory translates clinically.
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.
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Roper-Jones et al. (2026) studied Ventricular fibrillation and ventricular electrophysiology (n=6). Cardiac pacing at five ventricular sites (RV apex endocardium, RV apex epicardium, RV base epicardium, LV apex epicardium, LV base epicardium) and burst pacing-induced ventricular fibrillation vs. Within-heart comparisons across the five pacing locations and recording sites (LV apex vs LV base) was evaluated on Steady-state action potential duration (MAPD90), maximum slope of action potential duration restitution (APDRmax), S1/S2 conduction delays, and short-term cardiac memory (APD50 vs preceding DI and APD50) during VF (p=≥0.093). Pacing location altered S1/S2 conduction delays (p≤0.05) without affecting steady-state APD (p≥0.093) or restitution slope (p≥0.211), while early VF unmasked short-term cardiac memory for 30 beats.
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