Dynamic AV delay programming (SyncAV) significantly reduced electrical dyssynchrony across all pacing modes, with MultiPoint pacing plus SyncAV reducing intrinsic LVAT from 124 ms to 90 ms.
Observational (n=25)
Does dynamic atrioventricular delay programming (SyncAV) improve electrical synchrony in patients with left bundle branch block and preserved atrioventricular conduction?
Dynamic AV delay programming targeting fusion with intrinsic conduction significantly reduces electrical dyssynchrony across multiple pacing modes in patients with LBBB and preserved AV conduction.
Absolute Event Rate: 109% vs 124%
p-value: p=0.001
AIMS: 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). METHODS AND RESULTS: 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. CONCLUSION: 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.
Waddingham et al. (Thu,) conducted a observational in Left bundle-branch block and intact AV conduction (n=25). SyncAV (dynamic AV delay programming) with various pacing modalities vs. Intrinsic conduction and fixed nominal AV delays (BiV) was evaluated on Left ventricular activation time (LVAT) (p=0.001). Dynamic AV delay programming (SyncAV) significantly reduced electrical dyssynchrony across all pacing modes, with MultiPoint pacing plus SyncAV reducing intrinsic LVAT from 124 ms to 90 ms.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: