Aizawa Y, Chinushi M, Kitazawa H, Washizuka T, Abe A, Shibata A, Kodama I
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Heart. 1996 Mar;75(3):281-6. doi: 10.1136/hrt.75.3.281.
Monomorphic sustained ventricular tachycardia (VT) can often be entrained and interrupted at a critical paced cycle length. The aim was to evaluate a possible determinant of this phenomenon by observing the action of mexiletine on the critical paced cycle length and other variables.
Nine consecutive patients with symptomatic VT were studied. After induction of VT, the area of slow conduction was mapped as the earliest site of the activation or the site with mid-diastolic potential during the tachycardia. Rapid pacing was performed at a site distant from the tachycardia circuit to entrain the tachycardia, starting at a cycle length 10-20 ms shorter than the VT cycle length, and repeated after a decrement of the cycle length in steps of 10 ms to obtain the longest paced cycle length that interrupted the tachycardia: the block cycle length. The effective refractory period (ERP) was measured at the pacing site at which the myocardium was presumed to be normal and also in the area of slow conduction. The effects of mexiletine on the cycle length of VT, the block cycle length, and the ERP at two sites were obtained before and after mexiletine administration. The relation between the cycle length of VT and block cycle length and their changes were also analysed.
11 VTs with the same morphology were induced before and after mexiletine administration. The VT cycle length was prolonged by mexiletine from 309 (SD 53) to 361 (47) ms, and it was interrupted at block cycle lengths of 247 (37) and 307 (41) ms, respectively, the changes being 18 (12)% and 23 (8)% (both P < 0.001). All VTs were entrained, and during pacing at the block cycle length there was abrupt loss of fusion and change in the presystolic electrogram, always associated with interruption of VT on cessation of rapid pacing. A good correlation was observed between the VT cycle length and the block cycle length (r = 0.77 to 0.80). The ERP at the pacing site (normal myocardium) and in the area of slow conduction showed no significant change: 241 (21) v 240 (22) ms and 262 (9) v 252 (9) ms, respectively. The block cycle length was longer than the ERP after mexiletine administration: 362 (55) v 252 (9) ms (P < 0.02).
Mexiletine prolonged the cycle length of VT and the VT-interrupting critical cycle length but not the ERP. The prolongation of the VT cycle length and the block cycle length by mexiletine seemed to be unrelated to the action potential duration, but related to depressed intercellular conduction.
单形性持续性室性心动过速（VT）通常可在临界起搏周期长度时被拖带并终止。本研究旨在通过观察美西律对临界起搏周期长度及其他变量的作用，评估这一现象的可能决定因素。
对9例有症状的VT患者进行连续研究。诱发VT后，将缓慢传导区域定位为心动过速时最早激动部位或舒张中期电位所在部位。在远离心动过速环路的部位进行快速起搏以拖带心动过速，起始周期长度比VT周期长度短10 - 20 ms，然后以10 ms的步长递减周期长度重复操作，以获得终止心动过速的最长起搏周期长度：阻滞周期长度。在假定心肌正常的起搏部位以及缓慢传导区域测量有效不应期（ERP）。在给予美西律前后，观察美西律对VT周期长度、阻滞周期长度以及两个部位ERP的影响。同时分析VT周期长度与阻滞周期长度之间的关系及其变化。
在给予美西律前后分别诱发了11次形态相同的VT。美西律使VT周期长度从309（标准差53）ms延长至361（47）ms，其分别在247（37）ms和307（41）ms的阻滞周期长度时被终止，变化分别为18（12）%和23（8）%（均P < 0.001）。所有VT均被拖带，在以阻滞周期长度起搏时，融合突然消失且收缩前期心电图发生改变，总是与快速起搏停止时VT终止相关。观察到VT周期长度与阻滞周期长度之间有良好的相关性（r = 0.77至0.80）。起搏部位（正常心肌）和缓慢传导区域的ERP无显著变化：分别为241（21）ms对240（22）ms和262（9）ms对252（9）ms。给予美西律后，阻滞周期长度长于ERP：362（55）ms对252（9）ms（P < 0.02）。
美西律延长了VT周期长度和终止VT的临界周期长度，但未改变ERP。美西律对VT周期长度和阻滞周期长度的延长似乎与动作电位持续时间无关，而与细胞间传导减慢有关。
