Fujiki A, Mizumaki K, Tani M, Yoshida S, Sasayama S
Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
J Cardiovasc Pharmacol. 1992 Sep;20(3):375-9. doi: 10.1097/00005344-199209000-00006.
Electrophysiologic effects of intravenous (i.v.) cibenzoline were evaluated in 18 patients with accessory pathways or dual atrioventricular (AV) nodal pathways (12 men and 6 women with a mean age of 44 +/- 18 years). Twelve patients had accessory AV pathways, including 6 patients with a manifest accessory pathway. Six patients had AV nodal reentrant tachycardia (AVNRT). Electrophysiologic studies were performed before and after cibenzoline (1.4 mg/kg i.v.) infusion for 5 min. Sinus cycle length did not change significantly after cibenzoline administration. Cibenzoline increased both the AH (85 +/- 20 vs. 91 +/- 21 ms, p less than 0.05) and HV intervals (41 +/- 10 ms vs. 53 +/- 11 ms, p less than 0.001). Neither the atrial nor ventricular effective refractory period (ERP) was altered by cibenzoline. Complete block in the accessory pathway occurred antegradely in 4 patients and retrogradely in 1 patient. Cibenzoline prevented induction of AV reentrant tachycardia (AVRT) in 3 of 8 patients with sustained orthodromic AVRT by abolishing retrograde accessory pathway conduction or prolonging the retrograde accessory pathway ERP. Of 5 patients who continued to have inducible AVRT before and after cibenzoline administration, the tachycardia cycle length was increased in 3, mainly due to the increase in retrograde accessory pathway conduction time. Cibenzoline prevented induction of sustained AVNRT in 4 of 5 patients by prolonging the minimum pacing cycle length, maintaining 1:1 ventriculoatrial (VA) conduction through the retrograde fast AVN pathway or shortening the antegrade fast AVN pathway ERP equal to the slow AVN pathway. In one patient who had an uncommon type of AVNRT, sustained tachycardia was induced by cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)
在18例有旁路或房室（AV）结双径路的患者（12例男性和6例女性，平均年龄44±18岁）中评估了静脉注射西苯唑啉的电生理效应。12例患者有房室旁路，其中6例有显性旁路。6例患者有房室结折返性心动过速（AVNRT）。在静脉输注西苯唑啉（1.4mg/kg）5分钟前后进行电生理研究。给予西苯唑啉后窦性周期长度无显著变化。西苯唑啉使AH间期（85±20对91±21毫秒，p<0.05）和HV间期（41±10毫秒对53±11毫秒，p<0.001）均增加。西苯唑啉未改变心房或心室有效不应期（ERP）。4例患者的旁路出现前向完全阻滞，1例出现逆向完全阻滞。西苯唑啉通过消除逆向旁路传导或延长逆向旁路ERP，在8例持续性顺向性房室折返性心动过速（AVRT）患者中的3例中预防了AVRT的诱发。在5例西苯唑啉给药前后仍可诱发AVRT的患者中，3例的心动过速周期长度增加，主要是由于逆向旁路传导时间增加。西苯唑啉通过延长最小起搏周期长度、维持通过逆向快AV结径路的1:1室房（VA）传导或使前向快AV结径路ERP缩短至与慢AV结径路相等，在5例患者中的4例中预防了持续性AVNRT的诱发。在1例有不常见类型AVNRT的患者中，西苯唑啉诱发了持续性心动过速。（摘要截短于250字）
