Iesaka Y, Aonuma K, Nitta J, Tokunaga T, Fujiwara H, Hiraoka M
Department of Cardiology, Tsuchiura Kyodo Hospital, Ibaraki, Japan.
Jpn Circ J. 1988 Mar;52(3):262-71. doi: 10.1253/jcj.52.262.
The effects of procainamide and lidocaine, representative of class IA and IB antiarrhythmic agents, on electrically inducible ventricular tachycardia (VT) were studied using programmed ventricular stimulation in 47 post myocardial infarction patients at an average of 1.5 months after the onset. The mean doses of administered procainamide and lidocaine were 1050 mg and 161 mg, and their mean plasma concentrations were 7.5 micrograms/ml and 3.1 micrograms/ml respectively. The induction of sustained VT was suppressed in 15 of 29 patients (52%) by procainamide, but in none by lidocaine. The induction of nonsustained VT was suppressed in 6 of 18 patients (33%) by procainamide, and in 1 of 8 patients (13%) by lidocaine. The efficacy rate of procainamide was significantly higher than that of lidocaine in suppression of VT induction (21/47 vs 1/14 p less than 0.01). Procainamide significantly prolonged the effective refractory period of the right ventricle as well as the HV and QRS interval, however lidocaine did not affect them significantly. On the other hand, the worsening effect which changed nonsustained VT inducible in the baseline into sustained VT inducible post drug administration was demonstrated in 8 of 18 procainamide cases (44%), and in 3 of 8 lidocaine cases (38%). Between the procainamide effective and ineffective or worsening patients, there were no differences found in the electrophysiologic variables either in the baseline or post procainamide administration. We concluded that procainamide was more effective than lidocaine for the prevention of potential life-threatening VT induction in post myocardial infarction patients, although its efficacy was considerably limited, and to confirm the effectiveness and exclude the worsening effects of the class IA and IB antiarrhythmic agents, drug testing using programmed ventricular stimulation appeared to be valuable.
在47例心肌梗死后平均发病1.5个月的患者中，使用程控心室刺激研究了ⅠA类和ⅠB类抗心律失常药物的代表药物普鲁卡因胺和利多卡因对电诱导性室性心动过速（VT）的影响。普鲁卡因胺和利多卡因的平均给药剂量分别为1050mg和161mg，其平均血浆浓度分别为7.5μg/ml和3.1μg/ml。29例患者中有15例（52%）的持续性VT诱导被普鲁卡因胺抑制，但利多卡因对其无抑制作用。18例患者中有6例（33%）的非持续性VT诱导被普鲁卡因胺抑制，8例患者中有1例（13%）被利多卡因抑制。在抑制VT诱导方面，普鲁卡因胺的有效率显著高于利多卡因（21/47 vs 1/14，p＜0.01）。普鲁卡因胺显著延长了右心室的有效不应期以及HV和QRS间期，然而利多卡因对它们无显著影响。另一方面，在18例普鲁卡因胺病例中有8例（44%）出现了将基线时可诱导的非持续性VT转变为给药后可诱导的持续性VT的恶化效应，在8例利多卡因病例中有3例（38%）出现了这种情况。在普鲁卡因胺有效、无效或恶化的患者之间，无论是在基线还是在给予普鲁卡因胺后，电生理变量均未发现差异。我们得出结论，在预防心肌梗死后患者潜在的危及生命的VT诱导方面，普鲁卡因胺比利多卡因更有效，尽管其疗效相当有限，并且为了证实ⅠA类和ⅠB类抗心律失常药物的有效性并排除其恶化效应，使用程控心室刺激进行药物测试似乎是有价值的。
