Barts Heart Centre, St. Bartholomew's Hospital, West Smithfield, London EC1A 7BE, United Kingdom.
William Harvey Research Institute, Charterhouse Square, Queen Mary University of London, London EC1M 6BQ, UK.
Europace. 2023 Feb 16;25(2):536-545. doi: 10.1093/europace/euac224.
Cardiac resynchronization therapy programmed to dynamically fuse pacing with intrinsic conduction using atrioventricular (AV) timing algorithms (e.g. SyncAV) has shown promise; however, mechanistic data are lacking. This study assessed the impact of SyncAV on electrical dyssynchrony across various pacing modalities using non-invasive epicardial electrocardiographic imaging (ECGi).
Twenty-five patients with left bundle-branch block (median QRS duration (QRSd) 162.7 ms) and intact AV conduction (PR interval 174.0 ms) were prospectively enrolled. ECGi was performed acutely during biventricular pacing with fixed nominal AV delays (BiV) and using SyncAV (optimized for the narrowest QRSd) during: BiV + SyncAV, LV-only single-site (LVSS + SyncAV), MultiPoint pacing (MPP + SyncAV), and LV-only MPP (LVMPP + SyncAV). Dyssynchrony was quantified via ECGi (LV activation time, LVAT; RV activation time, RVAT; LV electrical dispersion index, LVEDi; ventricular electrical uncoupling index, VEU; and biventricular total activation time, VVtat). Intrinsic conduction LVAT (124 ms) was significantly reduced by BiV pacing (109 ms) (P = 0.001) and further reduced by LVSS + SyncAV (103 ms), BiV + SyncAV (103 ms), LVMPP + SyncAV (95 ms), and MPP + SyncAV (90 ms). Intrinsic RVAT (93 ms), VVtat (130 ms), LVEDi (36 ms), VEU (50 ms), and QRSd (163 ms) were reduced by SyncAV across all pacing modes. More patients exhibited minimal LVAT, VVtat, LVEDi, and QRSd with MPP + SyncAV than any other modality.
Dynamic AV delay programming targeting fusion with intrinsic conduction significantly reduced dyssynchrony, as quantified by ECGi and QRSd for all evaluated pacing modes. MPP + SyncAV achieved the greatest synchrony overall but not for all patients, highlighting the value of pacing mode individualization during fusion optimization.
使用房室(AV)计时算法(例如 SyncAV)程控心脏再同步治疗,使起搏与固有传导动态融合,显示出良好的前景;然而,缺乏机制数据。本研究使用非侵入性的心外膜心电图成像(ECGi)评估了 SyncAV 对各种起搏模式下电不同步的影响。
前瞻性纳入 25 名左束支传导阻滞患者(中位 QRS 时限(QRSd)为 162.7ms)和完整的 AV 传导(PR 间期为 174.0ms)。在双心室起搏时急性进行 ECGi,使用固定的名义 AV 延迟(BiV),并使用 SyncAV(优化为最窄的 QRSd):BiV+SyncAV、LV 单部位起搏(LVSS+SyncAV)、多点起搏(MPP+SyncAV)和 LV 单部位多点起搏(LVMPP+SyncAV)。通过 ECGi 量化不同步(LV 激活时间(LVAT)、RV 激活时间(RVAT)、LV 电弥散指数(LVEDi)、心室电分离指数(VEU)和双心室总激活时间(VVtat))。BiV 起搏显著降低了固有传导的 LVAT(124ms)(109ms)(P=0.001),LVSS+SyncAV、BiV+SyncAV、LVMPP+SyncAV 和 MPP+SyncAV 进一步降低了固有 RVAT(93ms)、VVtat(130ms)、LVEDi(36ms)、VEU(50ms)和 QRSd(163ms)。与其他任何模式相比,MPP+SyncAV 起搏时更多患者表现出最小的 LVAT、VVtat、LVEDi 和 QRSd。
以固有传导融合为目标的 AV 延迟动态程控显著降低了所有评估的起搏模式的电不同步,通过 ECGi 和 QRSd 来衡量。MPP+SyncAV 起搏总体上实现了最大的同步性,但并非所有患者均如此,这突出了在融合优化期间对起搏模式个体化的价值。