目的:心房纤维化和自主神经重构是心房颤动(AF)的病理生理机制。评估了它们对传导速度(CV)动力学和波前传播的影响。
结果:本地激活时间(LAT),电压,和几何数据来自持续房颤消融术患者。在窦性心律(SR)中以三个起搏间隔(PI)获得LAT。LAT用于确定CV动态及其与局部电压幅度的关系。自主调节的影响-药理学和神经节丛(GP)刺激,在CV动力学上,波前传播,并在SR中确定枢轴点(波前传播变化≥90°)。包括54名患者。电压影响CV动态,在非低电压区(LVZs)(≥0.5mV),CV恢复曲线更陡[0.03±0.03m/sΔCVPI600-400ms(PI1),0.54±0.09m/sΔCVPI400-250ms(PI2)],在LVZ(0.2-0.49mV)(0.17±0.09m/sΔCVPI1,0.25±0.11m/sΔCVPI2)处更宽,并且在非常LVZ(<0.2mV)(0.03±0.01m/sΔCVPI1,0.04±0.02m/sΔCVPI2)下平坦。阿托品没有改变CV动力学,而异丙肾上腺素和GP刺激导致更大的CV随速率减慢。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,即速率依赖性CV(RDCV)减慢位点。大多数枢轴点位于RDCV减速站点(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)也增加了确定的枢轴点的数量。
结论:心房CV动力学受纤维化负荷和自主神经调节的影响,自主神经调节增强CV异质性和支点分布。这项研究提供了对自主神经重塑在AF中的影响的进一步见解。
OBJECTIVE: 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.
RESULTS: 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.
CONCLUSIONS: 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.