首页> 美国卫生研究院文献>British Heart Journal >Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.
【2h】

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

机译:维拉帕米通过程序性电刺激心脏对阵发性折返性室上性心动过速患者的影响。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Atrioventricular (AV) conduction, ventriculoatrial (VA) conduction, and the mechanism of tachycardia, were studied by programmed electrical stimulation before and after the administration of verapamil, in 10 patients with paroxysmal re-entrant supraventricular tachycardia. In 7 patients the tachycardia circuit was confined to the AV node. In 3 patients an accessory pathway conducting only in the ventriculoatrial direction was used during tachycardia. When administered intravenously during tachycardia, verapamil terminated the arrhythmia in 9 patients. Verapamil lengthened the effective and the functional refractory period of the AV node and the AV nodal transmission time in all patients in whom this could be studied. As a result of these changes, it was not possible to initiate tachycardia in 3 patients. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in 5 patients, and increased in 2 patients. In 6 of these 7 patients the tachycardia zone shifted to longer premature beat intervals. Verapamil resulted in slowing of the heart rate during tachycardia. Apart from slowing in heart rate during tachycardia and termination of tachycardia after intravenous verapamil, the 3 patients with an accessory pathway showed no beneficial effect of verapamil on the mechanism of initiation of tachycardia. Five patients were restudied after 2 to 3 weeks of oral administration of verapamil. Though less, effects were similar to those obtained after intravenous administration.
机译:在10例阵发性折返性室上性心动过速患者中,在给予维拉帕米前后,通过程序电刺激研究了房室(AV)传导,心室(VA)传导和心动过速的机制。在7例患者中,心动过速回路仅限于AV节点。在3例患者中,心动过速期间使用了仅在心房方向上进行的辅助通路。在心动过速期间静脉内给药时,维拉帕米可终止9例患者的心律不齐。维拉帕米延长了所有可以进行研究的患者的房室结有效和功能不应期以及房室结的传播时间。这些变化的结果是,有3例患者无法开始心动过速。能够引发心动过速的房性早搏区的宽度(心动过速区)在5例患者中变窄,在2例中增加。在这7例患者中的6例中,心动过速区转移到更长的早搏间隔。维拉帕米导致心动过速期间心率减慢。除心动过速过程中的心律减慢和静脉注射维拉帕米后心动过速的终止外,3例具有辅助途径的患者均未显示维拉帕米对心动过速的发生机制有任何有益作用。口服维拉帕米2至3周后对5例患者进行了研究。尽管效果较小,但效果与静脉内给药后相似。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号