Abstract
AbstractIntroductionLeft bundle branch pacing (LBBP) can deliver physiological left ventricular activation, but typically at the cost of delayed right ventricular (RV) activation. A proposed solution is to advance RV activation through anodal capture, but there is uncertainty regarding the mechanism by which early RV activation is achieved (capture of right bundle or RV myocardial capture) and it is not known whether this produces hemodynamic benefit.MethodsWe recruited patients with LBBP leads in whom anodal capture eliminated the terminal R wave in lead V1.Ventricular activation pattern, timing and high precision acute hemodynamic response were studied during LBBP with and without anodal capture.ResultsWe recruited 21 patients, mean age 67 years, 14 were males. We measured ECG timings and hemodynamics in all patients and in 15 we also performed non-invasive mapping. Ventricular epicardial propagation maps demonstrated that right ventricular septal myocardial capture, rather than right bundle capture, was the mechanism for earlier RV activation. With anodal capture, QRS duration was shorter (116 ± 12ms versus 129 ± 14ms, p < 0.01), and total ventricular activation time was shorter (83 ± 18ms versus 90 ± 15ms, p = 0.01). This required higher outputs (3.6 ± 1.9V versus 0.6 ± 0.2V, p <0.01) but did not provide additional hemodynamic benefit (mean difference −0.2 ± 3.8 mmHg compared to pacing without anodal capture, p = 0.2).ConclusionLeft bundle pacing with anodal capture advances right ventricular activation as a result of stimulation of the RV septal myocardium. However, this requires higher outputs and did not improve acute hemodynamics. Aiming for anodal capture may therefore not be necessary.
Publisher
Cold Spring Harbor Laboratory