Lee W K, Strong J M, Kehoe R F, Dutcher J S, Atkinson A J
Clin Pharmacol Ther. 1976 May;19(5 Pt 1):508-14. doi: 10.1002/cpt1976195part1508.
Oral administration of a 1.5-gm dose of N-acetylprocainamide (NAPA) to 9 patients with premature ventricular contractions (PVCs) confirmed previous indirect evidence that this metabolite of procainamide has antiarrhythmic efficacy and potency comparable to those of procainamide. Although the mechanism by which NAPA acts as an antiarrhythmic drug is not known, it was found that the 6 patients with coupled PVCs responded to NAPA therapy and that the 3 patients without coupled PVCs failed to respond. Coupling interval prolongation also occurred during NAPA therapy in 4 of the 6 responding patients. These observations suggest that NAPA may terminate coupled PVCs by slowing and then interrupting conduction of re-entrant impulses, as has been proposed for procainamide. NAPA plasma concentrations of 7.4-17.2 mug/ml were well tolerated by the patients and produced an average fall of 3 mm Hg in mean arterial pressure and a 7.6% mean increase in corrected QT interval.
给9名室性早搏（PVCs）患者口服1.5克剂量的N - 乙酰普鲁卡因胺（NAPA），证实了先前的间接证据，即普鲁卡因胺的这种代谢物具有与普鲁卡因胺相当的抗心律失常疗效和效力。虽然NAPA作为抗心律失常药物的作用机制尚不清楚，但发现6名伴有联律性室性早搏的患者对NAPA治疗有反应，而3名无联律性室性早搏的患者无反应。在6名有反应的患者中，有4名在NAPA治疗期间也出现了联律间期延长。这些观察结果表明，NAPA可能通过减慢然后中断折返冲动的传导来终止联律性室性早搏，正如对普鲁卡因胺所提出的那样。患者对7.4 - 17.2微克/毫升的NAPA血浆浓度耐受性良好，平均动脉压平均下降3毫米汞柱，校正QT间期平均增加7.6%。
