McGuire M A, Robotin M, Yip A S, Bourke J P, Johnson D C, Dewsnap B I, Grant P, Uther J B, Ross D L
Cardiology Department, Westmead Hospital, Sydney, New South Wales, Australia.
J Am Coll Cardiol. 1994 Mar 1;23(3):693-701. doi: 10.1016/0735-1097(94)90756-0.
This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node.
Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node.
Atrioventricular node function and electrical excitation of Koch's triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy.
The compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exists from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs.
This procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.
本研究旨在探讨破坏房室（AV）结后入路的影响。
已经开发出手术和导管消融程序来治疗房室结折返性心动过速。其中一些会破坏房室结的后入路。
在18只犬中检查房室结功能以及科赫三角和冠状窦近端的电激动情况。对10只犬进行后房室结连接的解剖，8只犬进行假手术。28至35天后，进行重复电生理和标测研究，以评估房室结功能以及房室和室房（VA）传导途径的变化。然后用光学显微镜检查房室连接。
8例（80%）致密房室结未受损。2例在致密结后缘出现轻度纤维化。所有病例中，位于冠状窦口和三尖瓣环之间的右侧后房室结连接均被瘢痕组织替代，但左侧后连接和前连接保持完整。房室和VA传导间期及不应期未改变。解剖前10只犬存在房室交界性回波，解剖后7只犬存在（p = 0.06）。解剖前7只犬存在房室结后（慢径路）逆行传导，解剖后7只犬仍存在。然而，这7只犬中有4只的逆行心房激动发生改变，使得房室结的出口部位比术前更偏左。术后该结对自主神经阻断药物仍有反应。所有犬均发现类似于慢径路电位的双房电图。
该手术可消融后房室结连接，但很少损伤致密房室结。房室结功能未受损，且该结未去神经支配。房室结折返性心动过速的治愈机制可能是结周心房受损。这表明房室结慢径路的一部分可能位于致密房室结之外。正常犬心脏中存在双房室结出口和双房电图。
