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Mechanism of idiopathic ventricular tachycardia of the left ventricular origin and the effect of antiarrhythmic agents on it. A study using an entrainment phenomenon.

左心室起源的特发性室性心动过速的机制及抗心律失常药物的作用。

基本信息

批准号：
63570405
负责人：
OKUMURA Ken
金额：
$ 1.34万
依托单位：
Kumamoto University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至 1989
项目状态：
已结题

项目摘要

The mechanism of idiopathic ventricular tachycardia of the left ventricular origin was studied using a tachycardia entrainment phenomenon. In 4 patients with the tachycardia, rapid ventricular pacing at rates 5-25 beats/minute faster than the tachycardia rate was performed from the right ventricular outflow tract during the tachycardia and resulted in constant fusion beats except for the last captured beat. Moreover, progressive fusion was observed with the increment of the pacing rate. Thus, the mechanism of this type of ventricular tachycardia was best explained by reentry with an excitable gap. During entrainment of the tachycardia, the conduction intervals from the pacing site (right ventricular outflow tract) to the earliest activation site during the tachycardia and to the right ventricular apex were measured: The former interval was 395-430 msec and increased with the increment of the pacing rate, while the latter one was 70-90 msec and was constant even with the increment of th … More e pacing rate. Therefore, an area of slow conduction with a property of decremental conduction was strongly suggested to be present within the reentry circuit of the tachycardia.To examine the effect of verapamil which has been shown to be effective in interrupting the tachycardia, a small dose (1.0 mg) of the drug was administered during the tachycardia, which resulted in slowing the tachycardia rate, and entrainment study was repeated. After administration of verapamil, although the conduction interval from the pacing site to the right ventricular apex remained unchanged, that from the pacing site to the earliest activation site during the tachycardia (i.e., conduction via an area of slow conduction) was increased in al patients. This indicates that verapamil selectively suppressed the conduction through an area of slow conduction and thereby slowed the rate of the tachycardia. Tachycardia entrainment is useful to examine a selective effect of antiarrhythmic agents within the reentry circuit. Less

本文利用心动过速夹带现象对起源于左室的特发性室性心动过速的机制进行了研究。在4例心动过速患者中，在心动过速期间从右心室流出道以比心动过速速率快5-25次/分钟的速率进行快速心室起搏，导致除最后一次捕获搏动外的恒定融合搏动。随着起搏频率的增加，融合逐渐增强。因此，这种类型的室性心动过速的机制是最好的解释与兴奋间隙折返。记录了心动过速时起搏点（右室流出道）至心动过速时最早激动点及右室心尖部的传导间期：前者为395-430 msec，随起搏频率的增加而增加;后者为70-90 msec，随起搏频率的增加而增加。 ...更多信息 e起搏频率。因此，强烈建议在心动过速的折返回路内存在具有递减传导特性的慢传导区域，为了检查已被证明能有效中断心动过速的维拉帕米的效果，在心动过速期间给予小剂量（1.0 mg）的药物，这导致心动过速速率减慢，并重复了夹带研究。服用维拉帕米后，起搏点至右室心尖部的传导间期虽然保持不变，但起搏点至心动过速时最早激动点的传导间期（即，通过慢传导区域的传导）在AL患者中增加。这表明维拉帕米选择性地抑制了通过慢传导区域的传导，从而减慢了心动过速的速率。心动过速夹带是有用的，以检查抗心律失常药物的选择性影响内折返电路。少