首页> 外文期刊>Japanese circulation journal >Dynamic effects of intravenous procainamide infusion on the electrophysiological properties during atrial fibrillation.
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Dynamic effects of intravenous procainamide infusion on the electrophysiological properties during atrial fibrillation.

机译:静脉注射普鲁卡因酰胺对心房颤动期间电生理特性的动态影响。

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Although the mechanism of atrial fibrillation (AF) is still controversial, multiple wandering reentry is considered the primary mechanism in most AF. It has been suggested that prolongation of the wavelength would make it impossible for the reentry to continue and would lead to the termination of the AF. In the present study a dynamic fluctuation in the electrophysiological properties was observed with procainamide infusion during AF. In 12 patients, both the local electrogram and monophasic action potentials (MAP) during AF were recorded from the right atrium before, during and after infusion of procainamide (10 mg/kg). The minimum AF cyclelength (CLmin), MAP duration at 90% repolarization (MAPD90) and widths of the intraatrial potentials (WAP) were measured with custom-made computer software. The conduction velocity index (CVI) was determined from the WAP. The wavelength index (WLI=CVIxCLmin) and postrepolarization refractoriness (PRR= CLmin-MAPD90) were calculated. In 6 patients, AF was terminated by procainamide infusion (group A), but not in the other 6 patients (group B). Group A patients showed a biphasic change in the parameters following procainamide infusion. In phase I, the CLmin, MAPD90 and PRR increased, while the CVI decreased, and the WLI remained unchanged. In phase II, the PRR, CVI and WLI increased and the AF was terminated. No restoration of the CVI nor increase in the WLI were observed in group B. The biphasic fluctuation in the CVI and the remarkable increase of the PRR and WLI were observed before termination of AF by procainamide infusion.
机译:尽管房颤(AF)的机制仍存在争议,但在大多数AF中,多次游荡折返被认为是主要机制。已经提出,波长的延长将使得再入不可能继续并且将导致AF的终止。在本研究中,在房颤期间用普鲁卡因酰胺输注观察到电生理特性的动态波动。在12例患者中,在注射普鲁卡因酰胺(10 mg / kg)之前,期间和之后,从右心房记录了AF期间的局部电描记图和单相动作电位(MAP)。使用定制的计算机软件测量最小AF周期长度(CLmin),90%复极化时的MAP持续时间(MAPD90)和房内电位的宽度(WAP)。根据WAP确定传导速度指数(CVI)。计算波长指数(WLI = CVIxCLmin)和复偏后的耐火度(PRR = CLmin-MAPD90)。在6例患者中,普鲁卡因胺输注终止了AF(A组),而其他6例患者(B组)则没有。普鲁卡因胺输注后,A组患者的参数出现双相变化。在第一阶段,CLmin,MAPD90和PRR增加,而CVI减少,WLI保持不变。在第二阶段,PRR,CVI和WLI增加,AF终止。在B组中未观察到CVI的恢复或WLI的增加。在通过普鲁卡因胺输注终止AF之前,未观察到CVI的双相波动以及PRR和WLI的显着增加。

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