LAUSR

Biventricular pacing (BiVP) has become a well-established therapy for diverse conditions including cardiomyopathy, reduced left ventricular ejection fraction, and left bundle branch block.1,2 Despite the demonstrated utility of this approach, conceptual and practical concerns persist. Specifically, BiVP achieves cardiac resynchronization via nonphysiologic fusion of paced wavefronts, which traverse the heart through slow cell-to-cell conduction from the right ventricular endocardium and left ventricular epicardium.1 This disruption in excitation of the heart can set the stage for reentrant arrhythmias and potentially for risk of sudden cardiac death. This article is protected by copyright. All rights reserved.