Singh B N, Feld G, Nademanee K
Angiology. 1986 Dec;37(12 Pt 2):930-8.
In recent years, data has become available to support the concept that a selective lengthening of the cardiac action potential (a Class III antiarrhythmic action) by whatever mechanism with an attendant increase in the effective refractory period constitutes a distinct antiarrhythmic mechanism. Such an action is exemplified clinically by hypocalemia and hypothyroidism and pharmacologically by amiodarone, sotalol and bretylium, all of which have other associated features. The N-acetylation of procainamide leads to the pharmacologically active compound, N-acetylprocainamide (NAPA). The loss of propensity to block depolarization with the preservation of the effect on repolarization in the case of NAPA makes the compound a class III antiarrhythmic agent. The process of N-acetylation has also led to longer elimination half-life and predominantly renal excretion with linear kinetics but with the preservation of the antiarrhythmic properties of the parent compound. The electrophysiologic data are consistent with the results of studies which have demonstrated that NAPA has the potential to suppress premature ventricular contractions and prevent spontaneously occurring as well inducible ventricular tachycardia in patients with heart disease. The effects on atria indicate that the drug has the potential to electively reverse atrial flutter and fibrillation to normal rhythm and maintain stability of sinus rhythm. The overall experimental and clinical data warrant further evaluation of NAPA as an antiarrhythmic agent.
近年来，已有数据支持这样一种概念，即无论通过何种机制使心脏动作电位选择性延长（Ⅲ类抗心律失常作用），并伴随有效不应期延长，都构成一种独特的抗心律失常机制。低钙血症和甲状腺功能减退在临床上体现了这种作用，而胺碘酮、索他洛尔和溴苄铵在药理学上体现了这种作用，它们都有其他相关特征。普鲁卡因胺的N - 乙酰化产生了药理活性化合物N - 乙酰普鲁卡因胺（NAPA）。在NAPA的情况下，失去了阻断去极化的倾向，但保留了对复极化的作用，这使得该化合物成为一种Ⅲ类抗心律失常药物。N - 乙酰化过程还导致消除半衰期延长，主要经肾脏排泄，呈线性动力学，但保留了母体化合物的抗心律失常特性。电生理数据与研究结果一致，这些研究表明NAPA有潜力抑制心脏病患者的室性早搏，并预防自发发生以及诱发性室性心动过速。对心房的作用表明，该药物有潜力选择性地将心房扑动和颤动转为正常心律，并维持窦性心律的稳定性。总体的实验和临床数据值得对NAPA作为一种抗心律失常药物进行进一步评估。
