B-PO02-187 THE DOMINANT MECHANISM OF BIVENTRICULAR PACING IN LEFT BUNDLE BRANCH BLOCK IS SHORTENING OF ATRIOVENTRICULAR DELAY

Abstract

Biventricular pacing (BVP) is thought to improve ventricular function through ventricular resynchronization. BVP also improves filling by shortening atrioventricular delay (AVD). Quantifying the contributions of these two mechanisms requires AVD alteration without resynchronising LBBB. This occurs with His bundle pacing (HBP) at outputs below LBBB correction threshold. To perform HBP with preservation of LBBB to measure the relative contributions of AVD shortening and ventricular resynchronisation to the overall hemodynamic benefit of BVP. Patients with LBBB referred for BVP-CRT were recruited. Using a high precision systolic blood pressure (SBP) protocol, we measured hemodynamic effects of BVP and temporary HBP with LBBB preservation at a full AVD range. We used non-invasive epicardial mapping (ECGI) to assess left ventricular activation time (LVAT). LBBB preservation was defined as <20ms shortening of intrinsic H-endQRS to HBP Stim-endQRS. In 19 patients, HBP with preservation of LBBB produced peak SBP improvement of 4.4mmHg (95% CI: 1.3-7.6, p<0.01) vs AAI pacing. In 16, BVP was performed and produced peak SBP improvement of 7.2mmHg (3.9-10.5, p<0.001) vs AAI. The mean SBP improvement from HBP with LBBB preservation to BVP was 2.8mmHg (-0.3-5.9, p<0.05). Mean SBP improvement with LBBB-preserved HBP was 67% of BVP. Change in LVAT from intrinsic to HBP was 0.1ms (-6.4-6.7). BVP in LBBB improves haemodynamic function through ventricular resynchronization and AVD shortening. The majority of benefit appears to be from AVD shortening. When LBBB is not corrected, HBP may still produce considerable hemodynamic improvement.