Chen S A, Tsang W P, Yeh H I, Wang T C, Hsia C P, Ting C T, Kong C W, Wang S P, Chiang B N, Chang M S
Department of Medicine, National Yang-Ming Medical College, Taipei, Taiwan, ROC.
Int J Cardiol. 1992 Oct;37(1):51-60. doi: 10.1016/0167-5273(92)90131-l.
A modified catheter ablation technique was studied prospectively in 29 patients with atrioventricular (AV) nodal reentrant tachycardia. A His bundle electrode catheter was used for mapping and ablation. Cathodic electroshocks (100-250 J) were delivered from the distal two electrodes (connected in common) of the His bundle catheter to the site selected for ablation. The optimal ablation site recorded the earliest retrograde atrial depolarization, simultaneous or earlier than the QRS complex, with absence of a His bundle deflection during AV nodal reentrant tachycardia. One additional electrical shock was delivered if complete abolition of retrograde VA conduction persisted for more than 30 min and AV nodal reentrant tachycardia was not inducible during isoproterenol and/or atropine administration. With a cumulative energy of 323 +/- 27 J and a mean of 2.3 +/- 0.5 shocks interruption or impairment of retrograde nodal conduction was achieved. Antegrade conduction, although modified, was preserved in 27 patients, with persistence of complete AV block in 2 patients. Two of the 27 patients still need antiarrhythmic agents to control tachycardia, the other 25 patients were free of tachycardia within a mean follow-up period of 13 +/- 2 months (range 7 to 20 months). Twenty-three patients received late follow-up electrophysiological studies (3-6 months after the ablation procedures), and the AV nodal function curves were classified into 4 types. The majority of the patients (15/23) had loss of retrograde conduction. Among the 8 patients with prolongation of retrograde conduction, 4 patients still had antegrade dual AV nodal property but all without inducible tachycardia. In conclusion, preferential interruption or impairment of retrograde conduction was the major, but not the sole, mechanism of electrical cure of AV nodal reentrant tachycardia.
对29例房室结折返性心动过速患者前瞻性地研究了一种改良的导管消融技术。使用希氏束电极导管进行标测和消融。阴极电休克（100 - 250焦耳）从希氏束导管远端的两个共同连接的电极传递至选定的消融部位。最佳消融部位记录到最早的逆行心房去极化，与QRS波群同时或早于QRS波群，且在房室结折返性心动过速时无希氏束波。如果逆行VA传导完全消失持续超过30分钟，且在给予异丙肾上腺素和/或阿托品期间不能诱发房室结折返性心动过速，则再给予一次电击。累积能量为323±27焦耳，平均电击2.3±0.5次，实现了逆行结传导的中断或损害。27例患者的前向传导虽有改变但得以保留，2例患者出现完全性房室传导阻滞。27例患者中有2例仍需抗心律失常药物控制心动过速，其余25例患者在平均13±2个月（7至20个月）的随访期内心动过速未再发作。23例患者接受了后期随访电生理研究（消融术后3 - 6个月），房室结功能曲线分为4种类型。大多数患者（15/23）逆行传导消失。在8例逆行传导延长的患者中，4例仍有前向双房室结特性，但均不能诱发心动过速。总之，可以优先中断或损害逆行传导是房室结折返性心动过速电治愈的主要但非唯一机制。
