Ghias Muhammad, Scherlag Benjamin J, Lu Zhibing, Niu Guodong, Moers Annerie, Jackman Warren M, Lazzara Ralph, Po Sunny S
Heart Rhythm Institute, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.
J Am Coll Cardiol. 2009 Nov 24;54(22):2075-83. doi: 10.1016/j.jacc.2009.09.014.
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.
An increasing number of clinical reports have associated sleep apnea and AF, and many possible mechanisms responsible for this relationship have been proposed.
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 radiofrequency 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.
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).
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.
本研究旨在通过实验模型模拟睡眠呼吸暂停诱发的心房颤动（房颤），并确定神经消融是否能预防房颤。
越来越多的临床报告将睡眠呼吸暂停与房颤联系起来，并且已经提出了许多可能导致这种关系的机制。
30只戊巴比妥钠麻醉的犬通过正压呼吸器通气。方案1（n = 14）：右胸切开术后，以2倍和4倍阈值进行心房和肺静脉程控刺激，确定最短心房不应期。在呼气末关闭呼吸器2分钟诱导阻塞性呼吸暂停。在呼吸暂停期间，以比心房不应期早5至10毫秒的S1-S2进行程控刺激。从右肺静脉附近的神经节丛（GP）监测神经活动。方案2（n = 16）：通过电刺激确定右肺动脉（RPA）处的GP。在呼吸暂停2分钟期间，再次在低于心房不应期的情况下进行程控刺激。在对RPA GP进行射频消融后，在呼吸暂停2分钟期间再次重复连续程控刺激。在5只犬中，在基线和呼吸暂停2分钟时测定血气。
方案1：在呼吸暂停期间，S1-S2在85±38秒内诱发房颤（10只中的9只）。在1例中，房颤在呼吸暂停1分36秒时自发发生。记录到的GP神经活动在房颤发作前逐渐增加。房颤前收缩压显著升高，但舒张压未升高（149±26毫米汞柱至193±38毫米汞柱，p<0.05）。在4只犬中，自主神经阻滞可预防呼吸暂停诱发的房颤。方案2：在神经消融前，11只犬中有8只在呼吸暂停的2分钟内由起搏诱发房颤。消融后，6只犬中有0只在呼吸暂停2分钟期间出现房颤（p = 0.009）。
这种呼吸暂停实验模型显示房颤的发生率具有可重复性。在对RPA GP进行神经消融或自主神经阻滞后，房颤的诱发能力显著受到抑制。
