Left ventricular endocardial pacing is less arrhythmogenic than conventional epicardial pacing when pacing in proximity to scar.

Background: Epicardial pacing increases risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when pacing in proximity to scar. Endocardial pacing may be less arrhythmogenic as it preserves the physiological sequences of activation and repolarization.

Objective: The purpose of this study was to determine the relative arrhythmogenic risk of endocardial compared to epicardial pacing, and the role of the transmural gradient of action potential duration (APD) and pacing location relative to scar on arrhythmogenic risk during endocardial pacing.

Methods: Computational models of ICM patients (n = 24) were used to simulate left ventricular (LV) epicardial and endocardial pacing 0.2-3.5 cm from a scar. Mechanisms were investigated in idealized models of the ventricular wall and scar. Simulations were run with/without a 20-ms transmural APD gradient in the physiological direction and with the gradient inverted. Dispersion of repolarization was computed as a surrogate of VT risk.

Results: Patient-specific models with a physiological APD gradient predict that endocardial pacing decreases VT risk (34%; P <.05) compared to epicardial pacing when pacing in proximity to scar (0.2 cm). Endocardial pacing location does not significantly affect VT risk, but epicardial pacing at 0.2 cm compared to 3.5 cm from scar increases it (P <.05). Inverting the transmural APD gradient reverses this trend. Idealized models predict that propagation in the direction opposite to APD gradient decreases VT risk.

Conclusion: Endocardial pacing is less arrhythmogenic than epicardial pacing when pacing proximal to scar and is less susceptible to pacing location relative to scar. The physiological repolarization sequence during endocardial pacing mechanistically explains reduced VT risk compared to epicardial pacing.