Lindsay B D, Chung M K, Gamache M C, Luke R A, Schechtman K B, Osborn J L, Cain M E
Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri 63110.
J Am Coll Cardiol. 1993 Sep;22(3):733-40. doi: 10.1016/0735-1097(93)90184-3.
The purpose of this prospective study was to test the hypothesis that the elimination of inducible repetitive atrioventricular (AV) node reentry despite the persistence of slow AV pathway conduction is a valid end point for radiofrequency catheter ablation procedures in patients with supraventricular tachycardia due to AV node reentry.
Although modification of AV node physiology by radiofrequency current can eliminate AV node reentrant tachycardia, therapeutic end points that are definitive of a satisfactory result in patients undergoing modification of the slow AV pathway have not been established. Applications of radiofrequency current at selected sites may eliminate all evidence of slow pathway conduction or sufficiently modify the refractory properties of the slow pathway to preclude sustained arrhythmias. Accordingly, total abolition of dual AV node physiology may not be necessary to prevent arrhythmia recurrence.
Radiofrequency catheter ablation of the slow AV pathway was attempted in 59 patients with typical AV node reentry. Tissue ablation was performed with a continuous wave of 500-kHz radiofrequency current. Twenty-five to 35 W was applied for 60 s at the site selected for tissue destruction.
Dual AV node physiology was eliminated completely in 35 patients (59%), persisted without inducible AV node reentry in 13 patients (22%) and persisted with inducible single AV reentrant beats in 11 patients (19%). In patients with persistent dual AV node physiology, the maximal difference between the effective refractory period of the fast and slow pathways was reduced from 104 +/- 62 ms before the procedure to 37 +/- 37 ms after AV conduction had been modified (p < 0.001). During a mean follow-up interval of 15 months (range 4 to 28), only one patient (2%) had a recurrence of the tachycardia.
Results demonstrate that when complete elimination of dual AV node physiology is difficult, modification of slow pathway conduction to the extent that repetitive AV node reentry cannot be induced is a definitive end point that portends a good prognosis.
本前瞻性研究的目的是检验以下假设，即对于因房室结折返引起室上性心动过速的患者，尽管慢房室传导通路持续存在，但消除可诱发的反复性房室结折返是射频导管消融术的一个有效终点。
尽管射频电流对房室结生理功能的改变可消除房室结折返性心动过速，但对于接受慢房室传导通路改良的患者，能明确满意治疗结果的治疗终点尚未确立。在选定部位施加射频电流可能会消除慢传导通路传导的所有证据，或充分改变慢传导通路的不应期特性以防止持续性心律失常。因此，完全消除双房室结生理功能对于预防心律失常复发可能并非必要。
对59例典型房室结折返患者尝试进行慢房室传导通路的射频导管消融。使用500kHz的连续射频电流进行组织消融。在选定的组织破坏部位施加25至35W的功率，持续60秒。
35例患者（59%）的双房室结生理功能被完全消除，13例患者（22%）双房室结生理功能持续存在但无诱发的房室结折返，11例患者（19%）双房室结生理功能持续存在且有诱发的单次房室折返搏动。在双房室结生理功能持续存在的患者中，快、慢传导通路有效不应期的最大差值从术前的104±62毫秒降至房室传导改良后的37±37毫秒（p<0.001）。在平均15个月（4至28个月）的随访期间，只有1例患者（2%）出现心动过速复发。
结果表明，当难以完全消除双房室结生理功能时，将慢传导通路传导改变至不能诱发反复性房室结折返的程度是一个预示良好预后的明确终点。
