A Study on the mechanism and treatment of verapamil-sensitive idiopathic ventricular tachycardia

维拉帕米敏感的特发性室性心动过速（VT）发生在相对年轻的患者中（平均年龄28岁，15 - 61岁，n = 32）。我们之前的研究表明，这种室速的机制是具有可兴奋间隙的再入（Am J Cardiol. 1988），并且在再入回路中存在钙通道依赖和部分抑制的钠通道依赖的慢传导区（Am J Cardiol. 1996）。我们最近报道，在浦肯野电位（PP）和局部心室电位(V)之前，晚舒张电位（LDP）记录在室间隔中部，LDP记录位点在再入回路上，因为射频能量应用于该部位可以消除VT （Circulation 1999）。在本研究中，LDP的性质相对于再入电路被进一步检查。在夹带过程中，LDP随LDP- pp的延长和V-LDP随起搏速率的增加而恒定而正交捕获。利多卡因（1mg /kg）和维拉帕米（≦1mg）均显著增加VT周期长度和LDP-PP。给药后VT周期长度的增加与LDP-PP的增加显著相关。因此，主要显示钙通道依赖性和部分抑制钠通道依赖性传导的组织被限制在LDP记录部位远端的成分（JACC 2001）。在再入回路的其他部分传导的细胞机制仍有待研究。

Verapamil-sensitive idiopathic ventricular tachycardia (VT) occurs in relatively young patients (mean age, 28 years, ranging from 15 to 61, n = 32). We previously showed that the mechanism of this VT is reentry with an excitable gap (Am J Cardiol. 1988), and there is a calcium channel-dependent, and partly depressed sodium channel-dependent slow conduction zone in the reentry circuit (Am J Cardiol. 1996). We recently reported that late diastolic potential (LDP) preceding Purkinje (PP) and local ventricular potentials (V) is recorded in the middle mterventricular septum, and the LDP recording site is on the reentry circuit since VT can be eliminated by radio frequency energy application to this site (Circulation 1999). In this study, the nature of LDP relative to the reentry circuit was further examined. During entrainment, LDP was orthodromically captured with prolongation of LDP-PP and constant V-LDP with the increase in the pacing rate. Both lidocaine (1 mg/kg) and verapamil (≦1 mg) significantly increased VT cycle length and LDP-PP. The increases in VT cycle length after the drugs significantly correlated with those in LDP-PP. Thus, a tissue showing mainly calcium channel-dependent and partly depressed sodium channel-dependent conduction is confined to the component distal to the LDP recording site (JACC 2001). The cellular mechanism for conduction in the other part of the reentry circuit remains to be investigated.