Holman W L, Ikeshita M, Lease J G, Ferguson T B, Lofland G K, Cox J L
J Thorac Cardiovasc Surg. 1984 Jul;88(1):67-75.
Paroxysmal supraventricular tachycardia due to atrioventricular nodal reentry is a common arrhythmia that usually responds to medical therapy. When atrioventricular nodal reentry tachycardia is refractory to medical therapy, surgical cryoablation or endocardial catheter ablation of the His bundle has been employed to protect the ventricles from the tachycardia. However, these techniques necessitate implantation of a permanent ventricular pacemaker. The purpose of the present study was to develop a cryosurgical procedure capable of ablating the anatomic-electrophysiological substrate of atrioventricular nodal reentry by modifying, rather than ablating, atrioventricular conduction. Thirty-three adult mongrel dogs underwent either the cryosurgical procedure (n = 23) or a sham operation (n = 10). All animals were restudied immediately postoperatively (acute cryosurgery group [n = 12) and sham group [n = 10]), and 11 animals (chronic cryosurgery group) subjected to cryosurgery were studied 14 weeks postoperatively. Decremental atrial pacing and programmed premature atrial stimulation protocols were utilized to determine atrioventricular nodal conduction time, atrioventricular nodal refractory period, and the Wenckebach point before and after operation in all animals. No electrophysiological alterations were noted in the sham-operated group. In the cryosurgery groups, atrioventricular nodal conduction time, functional refractory period of the atrioventricular node, and the Wenckebach point were all significantly prolonged in the immediate postoperative period, but only atrioventricular nodal conduction time remained prolonged 14 weeks postoperatively. The potential application of the new cryosurgical procedure for the treatment of atrioventricular nodal reentry tachycardia was demonstrated in three animals that exhibited dual atrioventricular nodal conduction preoperatively but had monophasic atrioventricular conduction curves postoperatively. The results in these animals documented that the cryosurgical procedure is capable of ablating the anatomic-electrophysiological substrate necessary for atrioventricular nodal reentry tachycardia.
房室结折返性阵发性室上性心动过速是一种常见的心律失常，通常对药物治疗有反应。当房室结折返性心动过速对药物治疗无效时，已采用手术冷冻消融或希氏束心内膜导管消融来保护心室免受心动过速影响。然而，这些技术需要植入永久性心室起搏器。本研究的目的是开发一种冷冻手术程序，通过改变而非消融房室传导来消融房室结折返的解剖 - 电生理基质。33只成年杂种犬接受了冷冻手术程序（n = 23）或假手术（n = 10）。所有动物在术后立即进行复查（急性冷冻手术组[n =
12]和假手术组[n = 10]），接受冷冻手术的11只动物（慢性冷冻手术组）在术后14周进行研究。采用递减心房起搏和程控房性早搏刺激方案来确定所有动物术前和术后的房室结传导时间、房室结不应期和文氏点。假手术组未观察到电生理改变。在冷冻手术组中，术后即刻房室结传导时间、房室结功能不应期和文氏点均显著延长，但术后14周仅房室结传导时间仍延长。在三只术前表现为房室结双径传导但术后为单相房室传导曲线的动物中，证明了这种新的冷冻手术程序在治疗房室结折返性心动过速方面的潜在应用。这些动物的结果表明，冷冻手术程序能够消融房室结折返性心动过速所需的解剖 - 电生理基质。
