Mechanism of Antiarrhythmic Effects of Class Ic Drugs in Paroxysmal Atrial Fibrillation in Man
Mechanism of Antiarrhythmic Effects of Class Ic Drugs in Paroxysmal Atrial Fibrillation in Man
复制标题
Ic类药物治疗人阵发性心房颤动的抗心律失常作用机制
DOI：
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发表时间：
1998
期刊：
影响因子：
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通讯作者：
K. Arakawa
中科院分区：
文献类型：
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作者：
K. Matsuo;K. Kumagai;M. Annoura;M. Ideishi;K. Arakawa
虽然Ic类抗心律失常药物对治疗房颤患者有效，但其作用机制尚不清楚。我们对22例阵发性心房颤动患者在给药前后进行了电生理研究。在两个基本周期长度（600或400 ms）下测量心房不应性、最大房间传导延迟和波长指数。两种药物研究增加心房不应性和波长指数。氟卡尼可降低最大房间传导延迟，而吡西卡尼则无此作用。每种药物以心动过速依赖性方式增加波长指数。Ic类药物可通过增加快速心率期间折返环路的波长来降低心房易损性。
While class Ic antiarrhythmic drugs are effective in treating patients with atrial fibrillation, their mechanism of action is poorly understood. We performed electrophysiological studies before and after their administration to 22 patients with paroxysmal atrial fibrillation. Atrial refractoriness, maximal interatrial conduction delay and the wavelength index were measured at two basic cycle lengths (600 or 400 ms). Both drugs studied increased atrial refractoriness and wavelength index. Flecainide reduced the maximal interatrial conduction delay, but pilsicainide did not. Each drug increased the wavelength index in a tachycardia-dependent manner. Class Ic drugs may reduce atrial vulnerability by increasing the wavelength of the reentrant circuit during periods of rapid heart rate.