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

点击翻译按钮获取中文摘要

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.