Sakurai M, Nishiono T, Yoshida I, Kato N, Yasuda H
Department of Cardiovascular Medicine, Hokkaido University School of Medicine; Sapporo, Japan.
Jpn Circ J. 1988 Mar;52(3):272-9. doi: 10.1253/jcj.52.272.
In 24 patients with idiopathic ventricular tachycardia (VT), mechanisms of VT and the effects of antiarrhythmic drugs after induction were studied electrophysiologically, and by exercise testing. VT was induced electrophysiologically in 14 patients. Class 1 antiarrhythmic drugs were effective in 7 of them, which implied that one of the mechanisms of idiopathic VT was reentry related to the depressed channel dependent slow conduction. In 6 of the 14 patients, the QRS morphology of VT showed a complete RBBB with axis deviation pattern and the tachycardia was responsive to verapamil. In 2 of them, induction of VT was facilitated at low plasma verapamil concentrations. In the other 2 patients, left ventricular mapping showed that a notched potential preceding each QRS complex and the retrograde His bundle deflection with a short interval were recorded during VT. These findings suggested that the mechanism of this type of VT was reentry, mediated by Ca dependent slow conduction and located within the left bundle branch network. Exercise testing provoked VT in eight. Beta-blockers and Ca-antagonists were effective in 6 and in 4, respectively. These findings indicate the possibility that in addition to enhanced automaticity or reentry, triggered activity could play a role in the genesis of exercise related VT.
对24例特发性室性心动过速（VT）患者，通过电生理检查及运动试验研究了VT的机制及诱发后抗心律失常药物的效果。14例患者通过电生理方法诱发出VT。Ⅰ类抗心律失常药物对其中7例有效，这提示特发性VT的机制之一是与通道依赖性缓慢传导受抑制相关的折返。14例患者中有6例，VT的QRS形态呈完全性右束支传导阻滞伴电轴偏移图形，且心动过速对维拉帕米有反应。其中2例在低血浆维拉帕米浓度时易于诱发出VT。另外2例患者，左心室标测显示在VT发作时，每个QRS波群之前有一个切迹电位，且逆行希氏束波间期较短。这些发现提示这种类型VT的机制是折返，由钙依赖性缓慢传导介导，位于左束支网络内。运动试验诱发出8例VT。β受体阻滞剂和钙拮抗剂分别对6例和4例有效。这些发现表明，除了自律性增强或折返外，触发活动可能在运动相关VT的发生中起作用。
