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三磷酸腺苷对宽QRS波心动过速的影响。18例患者的分析。

Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients.

作者信息

Hina K, Kusachi S, Takaishi A, Yamasaki S, Sakuragi S, Murakami T, Kita T

机构信息

Cardiovascular Center, Sakakibara Hospital, Japan.

出版信息

Jpn Heart J. 1996 Jul;37(4):463-70. doi: 10.1536/ihj.37.463.

Abstract

A few studies have indicated that adenosine terminated triggered-activity idiopathic ventricular tachycardia, but all involved a small number of cases. The effects of adenosine triphosphate (ATP) on wide QRS tachycardia have thus not yet been completely clarified. This retrospective study was performed to evaluate the therapeutic and diagnostic utility of ATP in wide QRS tachycardia. A total of 18 patients with wide QRS tachycardia (QRS width > 120 msec, rate > or = 150 beats/min) were evaluated. ATP, 20-40 mg, was administered intravenously. An electrophysiological study and treadmill stress test were performed in all patients to elucidate the mechanism of the tachycardia. ATP terminated tachycardia or induced atrio-ventricular block in all 6 patients who had supraventricular tachycardia, but it had no effect on preexcited atrial fibrillation or pre-excited atrial flutter. Ventricular tachycardia was terminated by ATP in 5 of the 10 patients. In 4 of these 5 patients, the focus of the tachycardia was the right ventricular outflow tract. No entrainment phenomenon was demonstrated by electrophysiological study with induction of the tachycardia by stress test or isoproterenol infusion, suggesting the contribution of triggered activity to the tachycardia. In the remaining patient with complete right bundle branch block type tachycardia with right axis deviation, the mechanism of ventricular tachycardia could not be determined. In the 5 patients in whom ATP failed to terminate ventricular tachycardia, the reentry mechanism was suggested by the presence of entrainment phenomenon depicted on electrophysiological study. In summary, this study suggests that ATP terminates supraventricular wide QRS tachycardia and ventricular tachycardia due to triggered-activity, but that it has no effect on pre-excited atrial fibrillation or flutter or on ventricular tachycardia due to a reentry mechanism. These findings add to the mounting evidence regarding the therapeutic and diagnostic utility of ATP in wide QRS tachycardia.

摘要

一些研究表明,腺苷可终止触发活动所致的特发性室性心动过速,但所有研究涉及的病例数均较少。因此,三磷酸腺苷(ATP)对宽QRS波心动过速的影响尚未完全阐明。本回顾性研究旨在评估ATP在宽QRS波心动过速中的治疗和诊断效用。共评估了18例宽QRS波心动过速患者(QRS波宽度>120毫秒,心率≥150次/分钟)。静脉注射20 - 40毫克ATP。对所有患者进行电生理研究和平板运动试验以阐明心动过速的机制。ATP使所有6例室上性心动过速患者的心动过速终止或诱发房室传导阻滞,但对预激性心房颤动或预激性心房扑动无效。10例患者中有5例的室性心动过速被ATP终止。在这5例患者中的4例,心动过速起源于右心室流出道。通过运动试验或异丙肾上腺素输注诱发心动过速进行电生理研究时,未发现拖带现象,提示触发活动是心动过速的原因。在其余1例完全性右束支传导阻滞型伴电轴右偏的心动过速患者中,室性心动过速的机制无法确定。在ATP未能终止室性心动过速的5例患者中,电生理研究显示的拖带现象提示为折返机制。总之,本研究表明,ATP可终止室上性宽QRS波心动过速以及由触发活动所致的室性心动过速,但对预激性心房颤动或心房扑动以及由折返机制所致的室性心动过速无效。这些发现进一步证明了ATP在宽QRS波心动过速中的治疗和诊断效用。

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