迷走神经去神经支配与心房颤动诱发性:心外膜脂肪垫消融无长期影响。
Vagal denervation and atrial fibrillation inducibility: epicardial fat pad ablation does not have long-term effects.
作者信息
Oh Seil, Zhang Youhua, Bibevski Steve, Marrouche Nassir F, Natale Andrea, Mazgalev Todor N
机构信息
Section of Pacing and Electrophysiology, Department of Cardiovascular Medicine, Cleveland Clinic, Ohio 44195, USA.
出版信息
Heart Rhythm. 2006 Jun;3(6):701-8. doi: 10.1016/j.hrthm.2006.02.020. Epub 2006 Mar 6.
BACKGROUND
Major epicardial fat pads contain cardiac ganglionated plexi of the autonomic, predominantly vagal nerves. Vagal denervation may improve the success rate of atrial fibrillation (AF) treatment.
OBJECTIVES
The purpose of this study was to elucidate the long-term effects of fat pad ablation on the electrophysiologic characteristics of the atrium and AF inducibility.
METHODS
Six mongrel dogs were studied. Cervical vagal stimulation was applied to determine effects on the sinus node, AV node, atrial effective refractory period (AERP), and AF inducibility. AERP and AF inducibility were evaluated at both the right atrial and left atrial appendages and at the right atrial and left atrial free walls. Radiofrequency energy was delivered epicardially to the entire areas of two major fat pads: right pulmonary vein fat pad and inferior vena cava-left atrium fat pad. Cervical vagal stimulation then was applied to confirm the acute effects of fat pad ablation. The same evaluation was repeated 4 weeks later.
RESULTS
The effects of vagal stimulation on the sinus node, AV node, and AERP were significantly eliminated immediately after fat pad ablation. However, these denervation effects disappeared after 4 weeks. At baseline, AF inducibility was increased by vagal stimulation (right atrial appendage: 72% +/- 31% vs 4.8% +/- 12%; right atrial free wall: 75% +/- 31% vs 0.0% +/- 0.0%; left atrial appendage: 60% +/- 29% vs 0.0% +/- 0.0%; left atrial free wall: 65% +/- 42% vs 0.0% +/- 0.0%). Fat pad ablation significantly reduced this vagal stimulation effect (8.3% +/- 20%, 10% +/- 22%, 17% +/- 29%, and 25% +/- 29%, respectively). However, similar to baseline, AF inducibility was strongly augmented by vagal stimulation 4 weeks after fat pad ablation (96% +/- 10%, 100% +/- 0.0%, 100% +/- 0.0%, and 95% +/- 11%, respectively).
CONCLUSION
Radiofrequency fat pad ablation may not achieve long-term suppression of AF induction in this canine model.
背景
主要的心外膜脂肪垫包含自主神经(主要是迷走神经)的心脏神经节丛。迷走神经去神经支配可能提高心房颤动(AF)治疗的成功率。
目的
本研究的目的是阐明脂肪垫消融对心房电生理特性和房颤诱发率的长期影响。
方法
对6只杂种犬进行研究。应用颈迷走神经刺激来确定对窦房结、房室结、心房有效不应期(AERP)和房颤诱发率的影响。在右心耳和左心耳以及右心房游离壁和左心房游离壁评估AERP和房颤诱发率。将射频能量经心外膜传递至两个主要脂肪垫的整个区域:右肺静脉脂肪垫和下腔静脉-左心房脂肪垫。然后应用颈迷走神经刺激来确认脂肪垫消融的急性效应。4周后重复相同评估。
结果
脂肪垫消融后,迷走神经刺激对窦房结、房室结和AERP的影响立即显著消除。然而,这些去神经支配效应在4周后消失。在基线时,迷走神经刺激增加房颤诱发率(右心耳:72%±31%对4.8%±12%;右心房游离壁:75%±31%对0.0%±0.0%;左心耳:60%±29%对0.0%±0.0%;左心房游离壁:65%±42%对0.0%±0.0%)。脂肪垫消融显著降低这种迷走神经刺激效应(分别为8.3%±20%、10%±22%、17%±29%和25%±29%)。然而,与基线相似,脂肪垫消融4周后,迷走神经刺激强烈增加房颤诱发率(分别为96%±10%、100%±0.0%、100%±0.0%和95%±11%)。
结论
在该犬模型中,射频脂肪垫消融可能无法实现对房颤诱发的长期抑制。