The Role of Ganglionated Plexi in Apnea-Related Atrial Fibrillation
The Role of Ganglionated Plexi in Apnea-Related Atrial Fibrillation
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DOI：
10.1016/j.jacc.2009.09.014
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发表时间：
2009-11-24
影响因子：
24
通讯作者：
Po, Sunny S.
中科院分区：
文献类型：
--
作者：
Ghias, Muhammad;Scherlag, Benjamin J.;Po, Sunny S.
目的 本研究旨在在实验模型中模拟睡眠呼吸暂停诱发的心房颤动 (AF)，并确定神经消融是否会预防 AF。 背景 越来越多的临床报告将睡眠呼吸暂停与 AF 联系起来，并提出了造成这种关系的许多可能机制。 方法 用戊巴比妥钠麻醉的 30 只狗通过正压呼吸器进行通气。方案 1 (n = 14)：右胸廓切开术后，心房和肺静脉以 2x 和 4x 阈值编程起搏，确定最短心房不应期。通过在呼气末关闭呼吸器 2 分钟来诱发阻塞性呼吸暂停。呼吸暂停期间，程序化起搏的执行时间为 S1-S2 = 比心房不应期早 5 至 10 毫秒。通过邻近右肺静脉的神经节丛（GP）监测神经活动。方案 2 (n = 16)：电刺激识别右肺动脉 (RPA) 处的 GP。在呼吸暂停 2 分钟期间，在心房不应期以下再次开始程序化起搏。 RPA GP 射频消融后，在 2 分钟呼吸暂停期间再次重复连续程序起搏。在 5 只狗中，在基线和呼吸暂停 2 分钟时测定血气。 结果方案 1：在呼吸暂停期间，S1-S2 在 85 +/- 38 秒内诱发 AF（10 秒中的 9 秒）。 1 例患者在呼吸暂停 1 分 36 秒时自发发生房颤。记录的 GP 神经活动在 AF 发生前逐渐增加。 AF 前收缩压而非舒张压显着升高（149 +/- 26 mm Hg 至 193 +/- 38 mm Hg，p < 0.05）。在 4 只狗中，自主神经阻滞预防了呼吸暂停诱发的房颤。方案 2：在神经消融之前，11 只狗中有 8 只在呼吸暂停 2 分钟内发生由起搏引起的 AF。消融后，6 例中的 0 例在 2 分钟呼吸暂停期间出现 AF（p = 0.009）。 结论 该呼吸暂停实验模型显示 AF 发生率可重复。 RPA GP 神经消融或自主神经阻滞后，AF 诱导能力显着受到抑制。 （J Am Coll Cardiol 2009；54：2075-83）(C) 2009 年，美国心脏病学会基金会
Objectives This study was conducted to simulate sleep apnea-induced atrial fibrillation (AF) in an experimental model and to determine whether neural ablation will prevent AF.Background An increasing number of clinical reports have associated sleep apnea and AF, and many possible mechanisms responsible for this relationship have been proposed.Methods Thirty dogs anesthetized with Na-pentobarbital were ventilated by a positive pressure respirator. Protocol 1 (n = 14): After a right thoracotomy, atrial and pulmonary vein programmed pacing at 2x and 4x threshold determined the shortest atrial refractory period. Obstructive apnea was induced by turning off the respirator during end expiration for 2 min. During apnea, programmed pacing was performed with S1-S2 = 5 to 10 ms earlier than the atrial refractory period. Neural activity was monitored from the ganglionated plexi (GP) adjacent to the right pulmonary veins. Protocol 2 (n = 16): Electrical stimulation identified the GP at the right pulmonary artery (RPA). Programmed pacing was again instituted, below atrial refractory period, during 2 min of apnea. After radio-frequency ablation of the RPA GP, continuous programmed pacing was again repeated during 2 min of apnea. In 5 dogs, blood gases were determined at baseline and at 2 min of apnea.Results Protocol 1: During apnea, S1-S2 induced AF within 85 +/- 38 s (9 of 10). In 1 case, AF occurred spontaneously at 1 min 36 s of apnea. Recorded GP neural activity progressively increased before AF onset. Systolic but not diastolic blood pressure rose significantly before AF (149 +/- 26 mm Hg to 193 +/- 38 mm Hg, p < 0.05). In 4 dogs, autonomic blockade prevented apnea-induced AF. Protocol 2: AF induced by pacing occurred in 8 of 11 dogs within the 2-min period of apnea, before neural ablation. After ablation, 0 of 6 showed AF during 2 min of apnea (p = 0.009).Conclusions This experimental model of apnea shows a reproducible incidence of AF. After neural ablation of the RPA GP or autonomic blockade, AF inducibility was significantly inhibited. (J Am Coll Cardiol 2009; 54: 2075-83) (C) 2009 by the American College of Cardiology Foundation