Queen Mary University of London, London, UK.
Electrophysiology Department, Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.
Europace. 2024 Aug 30;26(9). doi: 10.1093/europace/euae219.
Atrial fibrosis and autonomic remodelling are proposed pathophysiological mechanisms in atrial fibrillation (AF). Their impact on conduction velocity (CV) dynamics and wavefront propagation was evaluated.
Local activation times (LATs), voltage, and geometry data were obtained from patients undergoing ablation for persistent AF. LATs were obtained at three pacing intervals (PIs) in sinus rhythm (SR). LATs were used to determine CV dynamics and their relationship to local voltage amplitude. The impact of autonomic modulation- pharmacologically and with ganglionated plexi (GP) stimulation, on CV dynamics, wavefront propagation, and pivot points (change in wavefront propagation of ≥90°) was determined in SR. Fifty-four patients were included. Voltage impacted CV dynamics whereby at non-low voltage zones (LVZs) (≥0.5 mV) the CV restitution curves are steeper [0.03 ± 0.03 m/s ΔCV PI 600-400 ms (PI1), 0.54 ± 0.09 m/s ΔCV PI 400-250 ms (PI2)], broader at LVZ (0.2-0.49 mV) (0.17 ± 0.09 m/s ΔCV PI1, 0.25 ± 0.11 m/s ΔCV PI2), and flat at very LVZ (<0.2 mV) (0.03 ± 0.01 m/s ΔCV PI1, 0.04 ± 0.02 m/s ΔCV PI2). Atropine did not change CV dynamics, while isoprenaline and GP stimulation resulted in greater CV slowing with rate. Isoprenaline (2.7 ± 1.1 increase/patient) and GP stimulation (2.8 ± 1.3 increase/patient) promoted CV heterogeneity, i.e. rate-dependent CV (RDCV) slowing sites. Most pivot points co-located to RDCV slowing sites (80.2%). Isoprenaline (1.3 ± 1.1 pivot increase/patient) and GP stimulation (1.5 ± 1.1 increase/patient) also enhanced the number of pivot points identified.
Atrial CV dynamics is affected by fibrosis burden and influenced by autonomic modulation which enhances CV heterogeneity and distribution of pivot points. This study provides further insight into the impact of autonomic remodelling in AF.
心房纤维化和自主神经重构被认为是心房颤动（AF）的病理生理机制。本研究旨在评估它们对传导速度（CV）动力学和波前传播的影响。
本研究纳入了因持续性 AF 接受消融治疗的患者。在窦性节律（SR）下，使用三个起搏间期（PIs）获取局部激活时间（LAT）、电压和几何数据。使用 LAT 确定 CV 动力学及其与局部电压幅度的关系。在 SR 下，通过药理学和神经节丛（GP）刺激评估自主神经调节对 CV 动力学、波前传播和枢轴点（波前传播改变≥90°）的影响。共纳入 54 例患者。电压影响 CV 动力学，在非低电压区（LVZ）（≥0.5 mV），CV 复极曲线更陡峭[0.03±0.03 m/s ΔCV PI 600-400 ms（PI1），0.54±0.09 m/s ΔCV PI 400-250 ms（PI2）]，在 LVZ 更宽（0.2-0.49 mV）[0.17±0.09 m/s ΔCV PI1，0.25±0.11 m/s ΔCV PI2]，在极低 LVZ（<0.2 mV）更平坦[0.03±0.01 m/s ΔCV PI1，0.04±0.02 m/s ΔCV PI2]。阿托品不改变 CV 动力学，而异丙肾上腺素和 GP 刺激可导致 CV 随心率减慢。异丙肾上腺素（2.7±1.1 增加/患者）和 GP 刺激（2.8±1.3 增加/患者）促进 CV 异质性，即心率依赖性 CV（RDCV）减慢部位。大多数枢轴点与 RDCV 减慢部位重合（80.2%）。异丙肾上腺素（1.3±1.1 枢轴增加/患者）和 GP 刺激（1.5±1.1 增加/患者）也增加了枢轴点的数量。
心房 CV 动力学受纤维化负荷的影响，并受自主神经调节的影响，后者增强了 CV 的异质性和枢轴点的分布。本研究进一步深入探讨了自主神经重构对 AF 的影响。
