Sager P T, Perlmutter R A, Rosenfeld L E, Batsford W P
Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
Am Heart J. 1992 Apr;123(4 Pt 1):926-33. doi: 10.1016/0002-8703(92)90698-u.
Most studies examining antiarrhythmic drug exacerbation of ventricular arrhythmias have been performed in patients in whom clinical proarrhythmia developed. The clinical significance and predictors of antiarrhythmic drug exacerbation of inducible ventricular arrhythmias during electrophysiologic study have received less attention. Accordingly, a consecutive number of patients undergoing electrophysiologic study for evaluation of ventricular arrhythmias (but who had no history of clinical proarrhythmia) were prospectively examined. Drug-induced exacerbation was defined as no inducible ventricular tachycardia in the baseline drug-free state that increased to inducible nonsustained or sustained ventricular tachycardia, or inducible nonsustained ventricular tachycardia at baseline that increased to inducible sustained ventricular tachycardia. After administration of primarily type IA antiarrhythmic agents (procainamide and quinidine in 97% of the patients), patients were considered drug test negative (n = 80) when they had no increase in inducible ventricular tachycardia, and patients were considered drug test positive (n = 16) when they had exacerbation of inducible arrhythmias. The drug test-positive group's clinical characteristics differed markedly from those of the drug test-negative group. Compared with the drug test-negative group, the drug test-positive group had reduced (less than 40%) left ventricular ejection fractions (80% vs 39%, p = 0.005) and higher prevalences of myocardial infarctions (81% vs 35%, p = 0.027), left ventricular aneurysms (27% vs 5%, p = 0.026), and bundle branch blocks (53% vs 16%, p = 0.005). Thus exacerbation of ventricular tachycardia induction after antiarrhythmic agent administration was most common in patients with significant organic heart disease. The drug test-positive group was more frequently treated with antiarrhythmic therapy than was the drug test-negative group.(ABSTRACT TRUNCATED AT 250 WORDS)
大多数关于抗心律失常药物加重室性心律失常的研究是在发生临床致心律失常作用的患者中进行的。抗心律失常药物在电生理研究期间加重可诱发室性心律失常的临床意义和预测因素较少受到关注。因此，我们对连续一系列因评估室性心律失常而接受电生理研究（但无临床致心律失常病史）的患者进行了前瞻性检查。药物诱发加重被定义为在基线无药物状态下不能诱发室性心动过速，而在用药后可诱发非持续性或持续性室性心动过速，或基线时可诱发非持续性室性心动过速在用药后加重为可诱发持续性室性心动过速。在主要给予IA类抗心律失常药物（97%的患者使用普鲁卡因胺和奎尼丁）后，未出现可诱发室性心动过速增加的患者被视为药物试验阴性（n = 80），出现可诱发心律失常加重的患者被视为药物试验阳性（n = 16）。药物试验阳性组的临床特征与药物试验阴性组明显不同。与药物试验阴性组相比，药物试验阳性组左心室射血分数降低（低于40%）（80%对39%，p = 0.005），心肌梗死患病率更高（81%对35%，p = 0.027），左心室室壁瘤患病率更高（27%对5%，p = 0.026），束支传导阻滞患病率更高（53%对16%，p = 0.005）。因此，抗心律失常药物给药后室性心动过速诱发加重在有严重器质性心脏病的患者中最为常见。药物试验阳性组比药物试验阴性组更频繁地接受抗心律失常治疗。（摘要截断于250字）
