Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
An in silico guide for ventriculo-ventricular delay programming for left bundle branch-optimized cardiac resynchronization therapy.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Strocchi Marina, Samways Jack W, Naraen Akriti, Ali Nadine, Shun-Shin Matthew J, Gillette Karli, Rinaldi Christopher Aldo, Arnold Ahran D, Plank Gernot, Vigmond Edward J, Whinnett Zachary I, Niederer Steven A
Аннотация
AIMS: Left bundle branch pacing (LBBP)-optimized cardiac resynchronization therapy (LOT-CRT) can improve left ventricular (LV) activation when LBBP alone or conventional biventricular pacing are ineffective. However, the optimal programming settings for ventriculo-ventricular delay (VVD) for LOT-CRT are unknown. We aim to investigate how to optimally program VVD for LOT-CRT in the presence of various LV conduction substrates using computational modelling.
METHODS AND RESULTS: We simulated ventricular activation on 24 anatomies and validated the model against clinical data. Diffuse LV conduction system and intra-myocardial delay were simulated by slowing the conduction velocity of the LV His-Purkinje system and myocardium, respectively, alone or in combination with proximal left bundle branch block (LBBB). We simulated LOT-CRT with selective or myocardial capture (LV septal pacing, LVSP) with VVD ranging between -100 ms (LBBP/LVSP ahead) and +100 ms [LV epicardial lead (LVepiP), ahead]. Response was quantified with 95% LV activation times (LVAT95). In the presence of diffuse LV conduction system delay, the optimal VVD for LOT-CRT was always negative (LBBB: -42.5 ± 6.6 ms; no LBBB: -36.2 ± 5.6 ms), as delivering LBBP ahead of LVepiP compensates for the slow LV His-Purkinje. In the presence of LV intra-myocardial disease, the shortest LVAT95 with LOT-CRT was achieved by pacing the coronary sinus LV first (optimal VVD for LBBB: 23.3 ± 8.5 ms; no LBBB: 79.2 ± 18.0 ms). The type of capture for LOT-CRT affected the optimal VVD, with myocardial capture favouring negative VVDs (LVSP ahead).
CONCLUSION: The optimal VVD for LOT-CRT depends on the mechanism of delayed LV activation and type of capture achieved, highlighting the importance of VVD optimization.
METHODS AND RESULTS: We simulated ventricular activation on 24 anatomies and validated the model against clinical data. Diffuse LV conduction system and intra-myocardial delay were simulated by slowing the conduction velocity of the LV His-Purkinje system and myocardium, respectively, alone or in combination with proximal left bundle branch block (LBBB). We simulated LOT-CRT with selective or myocardial capture (LV septal pacing, LVSP) with VVD ranging between -100 ms (LBBP/LVSP ahead) and +100 ms [LV epicardial lead (LVepiP), ahead]. Response was quantified with 95% LV activation times (LVAT95). In the presence of diffuse LV conduction system delay, the optimal VVD for LOT-CRT was always negative (LBBB: -42.5 ± 6.6 ms; no LBBB: -36.2 ± 5.6 ms), as delivering LBBP ahead of LVepiP compensates for the slow LV His-Purkinje. In the presence of LV intra-myocardial disease, the shortest LVAT95 with LOT-CRT was achieved by pacing the coronary sinus LV first (optimal VVD for LBBB: 23.3 ± 8.5 ms; no LBBB: 79.2 ± 18.0 ms). The type of capture for LOT-CRT affected the optimal VVD, with myocardial capture favouring negative VVDs (LVSP ahead).
CONCLUSION: The optimal VVD for LOT-CRT depends on the mechanism of delayed LV activation and type of capture achieved, highlighting the importance of VVD optimization.