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维拉帕米和磷酸丙吡胺对阵发性室上性心动过速的终止、再诱发及长期预防作用

[Effects of verapamil and disopyramide phosphate on the termination, reinduction and long-term prevention of paroxysmal supraventricular tachycardia].

作者信息

Tsuchioka Y, Nakagawa H, Yamagata T, Sakura E, Hashimoto M, Okamoto M, Matsuura H, Kajiyama G

机构信息

1st Department of Internal Medicine, Hiroshima University School of Medicine.

出版信息

Kokyu To Junkan. 1990 Mar;38(3):243-8.

PMID:2109870
Abstract

The efficacy of verapamil and disopyramide phosphate for the termination and prevention of paroxysmal supraventricular tachycardia (PSVT) were studied electrophysiologically in 32 patients with inducible sustained PSVT (17 patients received verapamil, 15 patients received disopyramide). Twelve patients had atrioventricular nodal tachycardia, 7 had concealed and 13 had overt Wolff-Parkinson-White syndrome. Intravenous verapamil (0.15 mg/kg) terminated the sustained PSVT in 15 of the 17 patients (88%) by production of AV block in 13 patients, VA block in one, and a ventricular premature beat in one. PSVT could not be induced in any of these 15 patients after they had received verapamil. In the remaining 2 patients, PSVT could not be terminated by the use of verapamil, but the cycle lengths of PSVT were lengthened. Long-term oral dosages of verapamil of 120-240 mg/day were administered in 13 of the 17 patients. All patients except two, whose PSVT was unable to be effected by intravenous verapamil, were well controlled: PSVT disappeared in 7 patients and decreased in 4. Intravenous disopyramide (1.5 mg/kg) terminated induced PSVT in 10 of the 15 patients (67%) by production of VA block. Although PSVT could not be reinitiated in 5 of these 10 patients, non-sustained PSVT was induced in 2 and sustained PSVT was induced in 3 after having received disopyramide. PSVT was induced in all of the 5 patients who failed to respond to disopyramide. The cycle lengths of PSVT after administration of disopyramide remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在32例可诱发出持续性阵发性室上性心动过速(PSVT)的患者中,通过电生理研究了维拉帕米和磷酸丙吡胺终止及预防PSVT的疗效(17例患者接受维拉帕米,15例患者接受丙吡胺)。12例患者为房室结折返性心动过速,7例为隐匿性及13例为显性预激综合征。静脉注射维拉帕米(0.15mg/kg)使17例患者中的15例(88%)的持续性PSVT终止,其中13例产生房室传导阻滞,1例产生室房传导阻滞,1例出现室性早搏。这15例患者在接受维拉帕米后均不能再诱发出PSVT。其余2例患者,维拉帕米未能终止PSVT,但PSVT的周长延长。17例患者中的13例接受了120 - 240mg/天的维拉帕米长期口服治疗。除2例静脉注射维拉帕米无效的患者外,所有患者病情均得到良好控制:7例患者PSVT消失,4例患者PSVT发作减少。静脉注射丙吡胺(1.5mg/kg)使15例患者中的10例(67%)诱发出的PSVT终止,通过产生室房传导阻滞。虽然这10例患者中的5例不能再诱发PSVT,但2例患者在接受丙吡胺后诱发了非持续性PSVT,3例患者诱发了持续性PSVT。5例对丙吡胺无反应的患者均能诱发出PSVT。给予丙吡胺后PSVT的周长无变化。(摘要截短于250字)

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