Aizawa Y, Abe A, Ohira K, Furushima H, Chinushi M, Fujita S
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
J Am Coll Cardiol. 1996 Dec;28(7):1759-64. doi: 10.1016/S0735-1097(96)00375-0.
The action of mexiletine on diseased myocardium was assessed in reentrant ventricular tachycardia (VT).
Whether class Ib antiarrhythmic agents exert a preferential action on the central common pathway of reentrant ventricular tachycardia has not yet been studied in humans.
In 10 consecutive patients (7 with a previous myocardial infarction, 3 with nonischemic disease), VT was induced and entrained with rapid pacing. The orthodromic conduction time was measured from stimulus to the entrained electrogram at the exit from the presumed central common pathway (i.e., the earliest site of activation). Mexiletine at 125 to 250 mg was administered intravenously, and when VT with the same configuration was induced, the study was repeated. The action of mexiletine on the central common pathway was assessed from the changes in VT cycle length and orthodromic conduction time. The effects on QRS complex duration, local conduction time between the exit and the pacing site and duration of the local electrogram were compared between normal and diseased myocardium.
Mexiletine prolonged the VT cycle length in all patients, from (mean +/- SD) 316 +/- 30 to 360 +/- 64 ms (mean change 20 +/- 7%, p < 0.001); during entrainment of VT, the orthodromic conduction time was prolonged, from 306 +/- 58 to 367 +/- 89 ms (mean change 18 +/- 9%, p < 0.001). These changes were highly correlated (r = 0.95, p < 0.001). QRS duration changed little (4 +/- 3%), and local conduction time showed no change. The duration of the fragmented electrogram width was prolonged by mexiletine: from 146 +/- 50 to 176 +/- 56 ms (mean change 23 +/- 8% during VT, p < 0.001). Only a slight change occurred in the effective refractory period, both at the pacing site and at the exit.
Mexiletine caused little change in conduction time in normal myocardium but prolonged VT cycle length, orthodromic conduction time and duration of the local electrogram at the earliest site of activation of VT. From these findings, a preferential action of mexiletine on diseased myocardium was suggested but seemed to occur only at higher frequencies during tachycardia.
在折返性室性心动过速（VT）中评估美西律对病变心肌的作用。
I b类抗心律失常药物是否对折返性室性心动过速的中央共同径路具有优先作用尚未在人体中进行研究。
连续纳入10例患者（7例既往有心肌梗死，3例有非缺血性疾病），诱发VT并进行快速起搏拖带。从刺激开始至假定中央共同径路出口处（即最早激动部位）的拖带心电图测量顺向传导时间。静脉注射125至250mg美西律，当诱发相同形态的VT时，重复该研究。根据VT周期长度和顺向传导时间的变化评估美西律对中央共同径路的作用。比较正常心肌和病变心肌中美西律对QRS波群时限、出口与起搏部位之间的局部传导时间以及局部电图时限的影响。
美西律使所有患者的VT周期长度延长，从（均值±标准差）316±30ms延长至360±64ms（平均变化20±7%，p<0.001）；在VT拖带期间，顺向传导时间延长，从306±58ms延长至367±89ms（平均变化18±9%，p<0.001）。这些变化高度相关（r=0.95，p<0.001）。QRS时限变化不大（4±3%）且局部传导时间无变化。美西律使碎裂电图宽度延长：从146±50ms延长至176±56ms（VT期间平均变化23±8%，p<0.001）。起搏部位和出口处的有效不应期仅有轻微变化。
美西律对正常心肌的传导时间影响不大，但延长了VT周期长度、顺向传导时间以及VT最早激动部位的局部电图时限。从这些发现提示美西律对病变心肌有优先作用，但似乎仅在心动过速时较高频率下才会出现。
