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Ⅰ类抗心律失常药物西苯唑啉对人体心房在体不应期和传导的电生理效应

Electrophysiologic effects of a class I antiarrhythmic agent, cibenzoline, on the refractoriness and conduction of the human atrium in vivo.

作者信息

Esato M, Shimizu A, Chun Y H, Tatsuno H, Yamagata T, Matsuzaki M

机构信息

Second Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Japan.

出版信息

J Cardiovasc Pharmacol. 1996 Aug;28(2):321-7. doi: 10.1097/00005344-199608000-00020.

DOI:10.1097/00005344-199608000-00020
PMID:8856490
Abstract

We investigated the effects of a class I antiarrhythmic drug, cibenzoline, on human atrial muscle in vivo. Electrophysiologic measurements were performed in 44 patients (mean age 49 +/- 15 years), before and after an intravenous infusion of cibenzoline 1.4 mg/kg in 5 min. Extrastimuli at a basic cycle length (BCL) of 500 ms were delivered from the right atrial appendage. The effective refractory period of the right atrium (ERP-A), the conduction time from the high right atrium to the coronary sinus, maximum conduction delay (Max. CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were measured. Patients were divided into two groups according to whether repetitive atrial firing (RAF) was induced (group A, n = 18) or not (group B, n = 26). Cibenzoline increased ERP-A from 198 +/- 25 to 214 +/- 26 ms (p < 0.05) and decreased Max. CD from 55 +/- 23 to 43 +/- 19 ms (p < 0.05). There were significant decreases in the RAFZ (10 +/- 17 to 4 +/- 10 ms, p < 0.05), the FAAZ (20 +/- 25 to 12 +/- 18, ms p < 0.05), and the CDZ (41 +/- 21 to 32 +/- 19 ms, p < 0.05). Cibenzoline significantly increased ERP.A (186 +/- 25 to 212 +/- 26 ms, p < 0.05) in group A, but not in group B. There were significant decreases in the RAFZ [25 +/- 19 to 9 +/- 15 ms (p < 0.05) and FAAZ 22 +/- 29 to 11 +/- 21 ms, (p < 0.05)] in group A, but not in group B. The results suggest that cibenzoline can suppress paroxysmal atrial fibrillation by prolongation of ERP-A and may also have preferential effects on the substrate of atrial fibrillation and RAF.

摘要

我们研究了I类抗心律失常药物西苯唑啉对人体心房肌的体内作用。对44例患者(平均年龄49±15岁)在静脉输注1.4 mg/kg西苯唑啉5分钟前后进行电生理测量。从右心耳以500 ms的基础周期长度(BCL)发放期外刺激。测量右心房的有效不应期(ERP-A)、从右心房高位到冠状窦的传导时间、最大传导延迟(Max.CD)、心房重复激动区(RAFZ)、心房碎裂活动区(FAAZ)和传导延迟区(CDZ)。根据是否诱发心房重复激动(RAF)将患者分为两组(A组,n = 18;B组,n = 26)。西苯唑啉使ERP-A从198±25 ms增加到214±26 ms(p < 0.05),并使Max.CD从55±23 ms降低到43±19 ms(p < 0.05)。RAFZ(从10±17 ms到4±10 ms,p < 0.05)、FAAZ(从20±25到12±18 ms,p < 0.05)和CDZ(从41±21 ms到32±19 ms,p < 0.05)均有显著降低。西苯唑啉使A组的ERP.A显著增加(从186±25 ms到212±26 ms,p < 0.05),而B组无变化。A组的RAFZ[从25±19 ms到9±15 ms(p < 0.05)]和FAAZ[从22±29 ms到11±21 ms,(p < 0.05)]有显著降低,而B组无变化。结果表明,西苯唑啉可通过延长ERP-A来抑制阵发性心房颤动,并且可能对心房颤动和RAF的基质有优先作用。

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