Left bundle branch area pacing produces more physiological ventricular activation than biventricular pacing in patients with heart failure and LBBB

FUNDING ACKNOWLEDGEMENTS: Type of funding sources: Public grant(s) – EU funding. Main funding source(s): National Institute for Research of Metabolic and Cardiovascular Diseases, Programme EXCELES, Ministry of Health of the Czech Republic, grant number NU21-02-00584. INTRODUCTION: Biventricular pacing (BiV) is an established treatment for patients with heart failure and dyssynchronous ventricular activation. Left bundle branch area pacing (LBBAP) appears to be a promising alternative to BiV-CRT. To date, there is insufficient data regarding their effect on the reduction of ventricular dyssynchrony. PURPOSE: To compare ventricular synchrony during spontaneous rhythm, BiV and LBBAP in patients with heart failure, reduced left ventricular ejection fraction (LVEF), and LBBB using ultra-high-frequency ECG (UHF-ECG). METHODS: This was a retrospective analysis of consecutive patients with indication to CRT from two centers. It included patients with heart failure, QRS of LBBB morphology, and LVEF ≤ 40%, treated by BiV and/or LBBAP-CRT. UHF-ECG data were obtained during spontaneous and paced rhythms. These parameters were calculated: eDYS (time difference between the first and last activation), Vdmean (average of V1-V8 local depolarization durations) and QRSd (measured from pacing artifact). RESULTS: Analyzes were performed on 80 spontaneous rhythms, 39 biventricular captures and 64 LBBAP, obtained from 80 patients. Their mean age was 74±10 years, 61% were men, mean LV ejection fraction was 31±9 %, and 32% had ischemic cardiomyopathy. Both BiV and LBBAP-CRT significantly reduced QRSd compared to the spontaneous rhythm (from 172 ms, 95% CI [168;176] to 146 ms [141;152] during BiV and 143 ms [139;149] during LBBAP). Also, the eDYS and Vdmean were significantly reduced by both BiV and LBBAP-CRT, i.e., the eDYS from 82 ms [76;86] during LBBB to 33 ms [28;37], p<0.001 during biventricular pacing and to 24 ms [20;28], p<0.001, during LBBAP and Vdmean from 71 ms [68;73] to 59 ms [56;61], p<0.001 during BiV and to 53 ms [51;55], p<0.001 during LBBAP. Although the QRSd did not differ between LBBAP and biventricular pacing (143ms [139;148] vs 146ms [141;152], p=NS), LBBAP compared to BiV led to significantly shorter eDYS (24ms [20;28] vs 33ms [28;38]; p<0.008 and Vdmean (53ms [51;55] vs 59ms [56;61], respectively; p<0.003}. CONCLUSIONS: In patients with heart failure, LBBB and reduced LVEF, both BiV and LBBAP CRT significantly reduce ventricular dyssynchrony compared to the spontaneous rhythm. Our results indicate that LBBAP is associated with more physiological ventricular activation than BiV-CRT.