Heart Rhythm Institute and Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Heart Rhythm. 2009 Dec;6(12 Suppl):S26-34. doi: 10.1016/j.hrthm.2009.07.029. Epub 2009 Oct 24.
The intrinsic cardiac autonomic nervous system (ganglionated plexuses [GP]) plays a significant role in the initiation and maintenance of atrial fibrillation (AF) in both experimental models and AF patients. Left atrial GP, located in epicardial fat pads and the ligament of Marshall, contain afferent neurons from the atrial myocardium and the central autonomic nervous system, efferent neurons (cholinergic and adrenergic neurons), and interconnecting neurons, which allow communication between GP. Stimulation of the GP produces both parasympathetic stimulation (markedly shortens action potential duration) and sympathetic stimulation (increases calcium transient) in the pulmonary vein (PV) myocardium and atrial myocardium. In a canine model, GP stimulation resulted in early afterdepolarizations, and calcium transient triggered firing in the adjacent PV and initiated AF. Fractionated atrial potentials (FAP) were consistently located in the left atrium close to the stimulated GP. Ablation of the stimulated GP eliminated the FAP surrounding the GP. In patients with paroxysmal AF, epicardial and endocardial high-frequency stimulation produced a positive vagal response (transient AV block during AF and hypotension), allowing the identification and localization of five major left atrial GP (superior left GP, inferior left GP, Marshall tract GP, anterior right GP, inferior right GP). High-density electroanatomic maps of the left atrium and PVs obtained during AF showed the FAP are located in four main left atrial areas (left atrial appendage ridge FAP area, superior-left FAP area, inferoposterior FAP area, anterior-right FAP area). All five GP are located within one of the four FAP areas. In 63 patients with paroxysmal AF, GP ablation alone (before PV antrum isolation) significantly decreased the occurrence of PV firing (47/63 patients before ablation vs 9/63 patients after ablation, P <.01). GP ablation also decreased the inducibility of sustained AF (43/63 patients vs 23/63 patients, P <.01) and markedly reduced or eliminated the left atrial FAP areas.
内在心脏自主神经系统(神经节丛[GP])在实验模型和房颤(AF)患者中对心房颤动(AF)的起始和维持起着重要作用。左心房 GP 位于心外膜脂肪垫和 Marshall 韧带中,包含来自心房心肌和中枢自主神经系统的传入神经元、传出神经元(胆碱能和肾上腺素能神经元)和连接神经元,这些神经元允许 GP 之间进行通信。GP 的刺激在肺静脉(PV)心肌和心房心肌中产生副交感神经刺激(明显缩短动作电位持续时间)和交感神经刺激(增加钙瞬变)。在犬模型中,GP 刺激导致早期后除极,钙瞬变触发相邻 PV 的发射,并引发 AF。分裂的心房电位(FAP)始终位于靠近刺激 GP 的左心房内。刺激 GP 的消融消除了围绕 GP 的 FAP。在阵发性 AF 患者中,心外膜和心内膜高频刺激产生阳性迷走神经反应(AF 期间短暂的 AV 阻滞和低血压),允许识别和定位五个主要的左心房 GP(左上 GP、左下 GP、Marshall 束 GP、前右 GP、右下 GP)。在 AF 期间获得的左心房和 PV 的高密度电解剖图显示,FAP 位于四个主要的左心房区域(左心房心耳嵴 FAP 区域、左上 FAP 区域、后下 FAP 区域、前右 FAP 区域)。所有五个 GP 都位于四个 FAP 区域之一内。在 63 例阵发性 AF 患者中,GP 消融(在 PV 窦隔离之前)单独显著降低了 PV 触发的发生率(消融前 47/63 例 vs 消融后 9/63 例,P <.01)。GP 消融还降低了持续性 AF 的可诱导性(43/63 例 vs 23/63 例,P <.01),并显著减少或消除了左心房 FAP 区域。