Strickberger S A, Daoud E, Niebauer M, Williamson B D, Man K C, Hummel J D, Morady F
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0022.
J Cardiovasc Electrophysiol. 1994 Aug;5(8):645-9. doi: 10.1111/j.1540-8167.1994.tb01187.x.
The purpose of this study was to prospectively compare the effects of complete and partial ablation of slow pathway function on the fast pathway effective refractory period (ERP).
The subjects were 20 patients (mean age 43 +/- 13 years) with atrioventricular nodal reentrant tachycardia (AVNRT), no structural heart disease, and easily inducible AVNRT. Autonomic blockade was achieved with propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). After elimination of AVNRT and during autonomic blockade, the presence of residual slow pathway function was determined by the presence of a single AV nodal echo and/or dual AV nodal physiology. After autonomic blockade and before ablation, the mean fast pathway ERP was 319 +/- 44 msec and the mean slow pathway ERP was 251 +/- 31 msec. After slow pathway ablation and during autonomic blockade, 7 patients had residual slow pathway function and 13 did not. Complete loss of slow pathway function was associated with a shortening of the fast pathway ERP from 334 +/- 35 msec to 300 +/- 62 msec (P < 0.01), while the fast pathway ERP did not change significantly in patients with residual slow pathway function (291 +/- 29 msec vs 303 +/- 38 msec, respectively; P = 0.08). A shortening of 30 msec or more in the fast pathway ERP was observed in 11 of 13 patients who did not have residual slow pathway function, compared to 0 of 7 patients with residual slow pathway function (P < 0.001).
Shortening of the fast pathway ERP after successful ablation of AVNRT is dependent upon complete loss of slow pathway function. This observation is consistent with electrotonic inhibition of the fast pathway by the slow pathway.
本研究的目的是前瞻性比较慢径路功能完全和部分消融对快径路有效不应期(ERP)的影响。
研究对象为20例房室结折返性心动过速(AVNRT)患者(平均年龄43±13岁),无结构性心脏病,且易于诱发AVNRT。通过普萘洛尔(0.2mg/kg)和阿托品(0.04mg/kg)实现自主神经阻滞。在消除AVNRT后且在自主神经阻滞期间,通过单一房室结回波和/或双房室结生理现象的存在来确定残余慢径路功能。在自主神经阻滞和消融前,平均快径路ERP为319±44毫秒,平均慢径路ERP为251±31毫秒。在慢径路消融后且在自主神经阻滞期间,7例患者有残余慢径路功能,13例没有。慢径路功能完全丧失与快径路ERP从334±35毫秒缩短至300±62毫秒相关(P<0.01),而在有残余慢径路功能的患者中快径路ERP无显著变化(分别为291±29毫秒和303±38毫秒;P = 0.08)。在13例没有残余慢径路功能的患者中有11例观察到快径路ERP缩短30毫秒或更多,相比之下,7例有残余慢径路功能的患者中无1例出现这种情况(P<0.001)。
成功消融AVNRT后快径路ERP的缩短取决于慢径路功能的完全丧失。这一观察结果与慢径路对快径路的电紧张性抑制一致。