Chiou C W, Eble J N, Zipes D P
Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis 46202-4800, USA.
Circulation. 1997 Jun 3;95(11):2573-84. doi: 10.1161/01.cir.95.11.2573.
The purpose of this study was to investigate the functional pathways of efferent vagal innervation to the atrial myocardium and sinus and atrioventricular (AV) nodes.
Using vagally induced atrial effective refractory period shortening, slowing of spontaneous sinus rate, and prolongation of AV nodal conduction time as end points of vagal effects, we determined the actions of phenol and epicardial radiofrequency catheter ablation (RFCA) applied to different sites at or near the atrial myocardium to inhibit these responses. We found that efferent vagal fibers to the atria are located both subepicardially and intramurally or subendocardially. Most efferent vagal fibers to the atria appear to travel through a newly described fat pad located between the medial superior vena cava and aortic root (SVC-Ao fat pad), superior to the right pulmonary artery, and then project onto two previously noted fat pads at the inferior vena cava-left atrial junction (IVC-LA fat pad) and the right pulmonary vein-atrial junction (RPV fat pad) and to both atria. A few vagal fibers may bypass the SVC-Ao fat pad and go directly to the IVC-LA or RPV fat pad and then innervate the atrial myocardium. Vagal fibers to the sinus and AV nodes also converge at the SVC-Ao fat pad (a few fibers to the sinus node go directly to the RPV fat pad) before projecting to the RPV and IVC-LA fat pads. Long-term vagal denervation of the atria and sinus and AV nodes can be produced by RFCA of these fat pads and results in vagal denervation supersensitivity. Vagal denervation prevents induction of atrial fibrillation in this model.
The newly described SVC-Ao fat pad receives most of the vagal fibers to the atria and sinus and AV nodes. Elimination of the fat pads with RFCA selectively vagally denervated the atria and sinus and AV nodes.
本研究旨在探讨传出迷走神经支配心房肌、窦房结和房室（AV）结的功能通路。
以迷走神经诱导的心房有效不应期缩短、自发窦性心率减慢和房室结传导时间延长作为迷走神经效应的终点，我们确定了将苯酚和心外膜射频导管消融（RFCA）应用于心房肌或其附近不同部位以抑制这些反应的作用。我们发现，支配心房的传出迷走神经纤维位于心外膜下以及壁内或心内膜下。大多数支配心房的传出迷走神经纤维似乎穿过一个新描述的位于上腔静脉内侧和主动脉根部之间的脂肪垫（上腔静脉 - 主动脉脂肪垫），该脂肪垫位于右肺动脉上方，然后投射到下腔静脉 - 左心房交界处的两个先前已提及的脂肪垫（下腔静脉 - 左心房脂肪垫）和右肺静脉 - 心房交界处（右肺静脉脂肪垫）以及两个心房。少数迷走神经纤维可能绕过上腔静脉 - 主动脉脂肪垫，直接到达下腔静脉 - 左心房或右肺静脉脂肪垫，然后支配心房肌。支配窦房结和房室结的迷走神经纤维在投射到右肺静脉和下腔静脉 - 左心房脂肪垫之前也汇聚在上腔静脉 - 主动脉脂肪垫（少数支配窦房结的纤维直接到达右肺静脉脂肪垫）。对这些脂肪垫进行RFCA可导致心房、窦房结和房室结的长期迷走神经去神经支配，并导致迷走神经去神经支配超敏反应。在该模型中，迷走神经去神经支配可防止心房颤动的诱发。
新描述的上腔静脉 - 主动脉脂肪垫接收了大部分支配心房、窦房结和房室结的迷走神经纤维。用RFCA消除这些脂肪垫可选择性地使心房、窦房结和房室结发生迷走神经去神经支配。
