Hasin Y, Kriwisky M, Gotsman M S
Cardiology. 1984;71(4):199-206. doi: 10.1159/000173665.
We compared the effects of verapamil to high dose procainamide on the rate of inducible and spontaneously occurring ventricular tachycardia (VT) in 10 patients. Verapamil induced a significant increase in the rate of tachycardia (R-R interval decreased from 278 +/- 54 to 233 +/- 32 ms, mean +/- SD; p less than 0.025 by paired t test) while procainamide slowed the tachycardia (mean R-R interval was 328 +/- 72 ms, p less than 0.02). Verapamil prevented the induction of sustained VT and was effective as chronic oral antiarrhythmic therapy in 2 patients. The accelerated VT culminated in ventricular fibrillation in 1 patient. It is assumed that verapamil may have either increased conduction velocity or shortened the reentrant cycle. This may be related either to a primary effect of the drug or secondary to increased catecholamine stimulation due to a vasodilatory effect.
我们比较了维拉帕米与高剂量普鲁卡因胺对10例患者可诱导及自发发生的室性心动过速（VT）发生率的影响。维拉帕米使心动过速发生率显著增加（R-R间期从278±54毫秒降至233±32毫秒，均值±标准差；配对t检验p<0.025），而普鲁卡因胺使心动过速减慢（平均R-R间期为328±72毫秒，p<0.02）。维拉帕米可预防持续性VT的诱发，且对2例患者作为慢性口服抗心律失常治疗有效。1例患者加速性VT最终发展为心室颤动。推测维拉帕米可能增加了传导速度或缩短了折返周期。这可能与药物的直接作用有关，也可能是由于血管舒张作用导致儿茶酚胺刺激增加的继发结果。
