Calkins H, Sousa J, el-Atassi R, Schmaltz S, Kadish A, Morady F
University of Michigan Medical Center, Department of Internal Medicine, Ann Arbor, Michigan 48109-0022.
J Am Coll Cardiol. 1992 Feb;19(2):347-52. doi: 10.1016/0735-1097(92)90490-e.
Although previous studies have demonstrated that the electrophysiologic effects of many antiarrhythmic agents can be reversed by catecholamines, the susceptibility of amiodarone to such reversal is unknown. The objective of this study was to compare the relative degree of reversal of the electrophysiologic effects of quinidine and amiodarone by epinephrine infusions that result in plasma epinephrine levels similar to those achieved during various physiologic stresses. Twenty-nine patients who had inducible sustained monomorphic ventricular tachycardia and underwent electropharmacologic testing with quinidine and amiodarone were enrolled in the study. The variables measured before and during an epinephrine infusion (25 or 50 ng/kg per min) included the sinus cycle length, mean arterial pressure, QT interval and effective refractory period at drive train cycle lengths of 600 and 400 ms. The effective refractory period measured at a drive train cycle length of 600 ms shortened less during amiodarone therapy (2 +/- 2%) than during quinidine therapy (6 +/- 4%) or than in the baseline state (6 +/- 4%; p less than 0.01). Similar results were obtained during evaluation of the effective refractory period at a cycle length of 400 ms. Epinephrine infusion, at both 25 and 50 ng/kg per min, completely reversed the effects of quinidine and partially reversed the effects of amiodarone on the effective refractory period. The effects of epinephrine on the sinus cycle length and QT interval were similar in the baseline state and in conjunction with quinidine and amiodarone. Twenty-four patients underwent programmed ventricular stimulation during amiodarone therapy alone and in conjunction with either a 25- or a 50-ng/kg per min infusion of epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
尽管先前的研究表明，许多抗心律失常药物的电生理效应可被儿茶酚胺逆转，但胺碘酮对这种逆转的敏感性尚不清楚。本研究的目的是比较静脉输注肾上腺素导致血浆肾上腺素水平与各种生理应激时相似，从而逆转奎尼丁和胺碘酮电生理效应的相对程度。29例有可诱导的持续性单形性室性心动过速且接受了奎尼丁和胺碘酮电药理测试的患者纳入本研究。在静脉输注肾上腺素（25或50 ng/kg每分钟）之前和期间测量的变量包括窦性周期长度、平均动脉压、QT间期以及在驱动周期长度为600和400毫秒时的有效不应期。在胺碘酮治疗期间，驱动周期长度为600毫秒时测量的有效不应期缩短程度（2±2%）低于奎尼丁治疗期间（6±4%）或基线状态（6±4%；P＜0.01）。在评估驱动周期长度为400毫秒时的有效不应期时也得到了类似结果。静脉输注肾上腺素，剂量为25和50 ng/kg每分钟时，完全逆转了奎尼丁的效应，部分逆转了胺碘酮对有效不应期的效应。在基线状态以及与奎尼丁和胺碘酮联合使用时，肾上腺素对窦性周期长度和QT间期的效应相似。24例患者在单独使用胺碘酮治疗期间以及与25或50 ng/kg每分钟的肾上腺素输注联合使用时接受了程控心室刺激。（摘要截断于250字）
