Anderson J L
Am J Cardiol. 1984 Jul 30;54(2):7A-13A. doi: 10.1016/0002-9149(84)90811-7.
The concept of antifibrillatory action distinct from antiarrhythmic effect has recently been recognized. An antiarrhythmic (antiectopic) action leads to a decrease in the frequency of ventricular ectopic beats. In contrast, an antifibrillatory drug action increases myocardial electric stability, decreasing the propensity for ventricular fibrillation. Agents with predominant antiarrhythmic action (designated class I) include lidocaine, quinidine, procainamide and disopyramide. Bretylium is an agent with predominant antifibrillatory action (class III). Amiodarone and sotalol are experimental class III drugs. The beta-blockers (class II) also possess antifibrillatory action, particularly in ischemic heart disease. The rationale for the use of agents with antiarrhythmic (antiectopic) effects is the reduction of triggering events for more complex ventricular tachyarrhythmias. These agents act by slowing conduction, decreasing abnormal automaticity and affecting phase IV depolarization. In contrast, agents with antifibrillatory action may exert little effect on cardiac conduction and automaticity. However, they raise the energy threshold required for premature electrical discharge to initiate ventricular fibrillation (ventricular fibrillation threshold). The inhomogeneity of electrophysiologic properties and adrenergic tone in different portions of the heart may be reduced or eliminated. Direct electrophysiologic effects of agents such as bretylium include a general lengthening of the refractory period and the action potential duration in the heart and a diminution in the disparity of their durations between normal and abnormal myocardium. Clinical studies are incomplete, but they support the concept of antifibrillatory therapy. In postmyocardial infarction patients at intermediate risk of sudden death, the broad use of oral antiarrhythmic agents has not decreased the incidence of sudden death, whereas high-dose beta-blocker therapy, which exerts experimental antifibrillatory effects, may reduce sudden death by 30 to 70%.(ABSTRACT TRUNCATED AT 250 WORDS)
与抗心律失常作用不同的抗颤动作用这一概念最近已得到认可。抗心律失常（抗异位）作用会导致室性早搏频率降低。相比之下，抗颤动药物作用可增强心肌电稳定性，降低心室颤动倾向。具有主要抗心律失常作用的药物（归类为I类）包括利多卡因、奎尼丁、普鲁卡因胺和丙吡胺。溴苄铵是具有主要抗颤动作用的药物（III类）。胺碘酮和索他洛尔是实验性III类药物。β受体阻滞剂（II类）也具有抗颤动作用，尤其是在缺血性心脏病中。使用具有抗心律失常（抗异位）作用药物的基本原理是减少引发更复杂室性心律失常的触发事件。这些药物通过减慢传导、降低异常自律性和影响4期去极化发挥作用。相比之下，具有抗颤动作用的药物可能对心脏传导和自律性影响很小。然而，它们会提高过早放电引发心室颤动所需的能量阈值（心室颤动阈值）。心脏不同部位电生理特性和肾上腺素能张力的不均一性可能会降低或消除。溴苄铵等药物的直接电生理效应包括普遍延长心脏的不应期和动作电位持续时间，并减少正常心肌和异常心肌之间动作电位持续时间的差异。临床研究尚不完整，但它们支持抗颤动治疗的概念。在有中度猝死风险的心肌梗死后患者中，广泛使用口服抗心律失常药物并未降低猝死发生率，而具有实验性抗颤动作用的大剂量β受体阻滞剂治疗可能会使猝死率降低30%至70%。（摘要截选至250词）
