Reiter M J, Higgins S L, Payne A G, Mann D E
Am J Cardiol. 1986 Sep 1;58(6):512-6. doi: 10.1016/0002-9149(86)90025-1.
Eighteen patients were given quinidine and procainamide separately to evaluate whether prolongation of the QT interval by type Ia antiarrhythmic agents is a drug-specific phenomenon. Doses were titrated to achieve standard trough therapeutic levels of quinidine (2 to 5 micrograms/ml) and procainamide (4 to 12 micrograms/ml). In 16 of the 18 patients, the increase in corrected QT interval (QTc) was greater with quinidine than with procainamide, averaging 78 +/- 10 ms (+/- standard error of the mean) with quinidine and 39 +/- 7 ms with procainamide (p less than 0.001). The greater degree of QTc prolongation with quinidine than with procainamide was not due to differences in sinus cycle length, QRS duration, serum potassium level or concomitant drug therapy. Differences in relative drug level did not appear to account for the greater effect of quinidine. Thus, at frequently used plasma levels, quinidine prolongs QTc to a greater degree than does procainamide. This effect does not appear to be due to the comparison of "nonequivalent" drug levels.
18名患者分别接受奎尼丁和普鲁卡因胺治疗,以评估Ia类抗心律失常药物导致的QT间期延长是否是一种药物特异性现象。调整剂量以达到奎尼丁(2至5微克/毫升)和普鲁卡因胺(4至12微克/毫升)的标准谷治疗水平。18名患者中有16名,奎尼丁导致的校正QT间期(QTc)增加幅度大于普鲁卡因胺,奎尼丁平均增加78±10毫秒(±平均标准误差),普鲁卡因胺平均增加39±7毫秒(p<0.001)。奎尼丁导致的QTc延长程度大于普鲁卡因胺,这并非由于窦性周期长度、QRS时限、血清钾水平或联合药物治疗的差异。相对药物水平的差异似乎无法解释奎尼丁的更大效应。因此,在常用血浆水平下,奎尼丁比普鲁卡因胺更能延长QTc。这种效应似乎并非由于“非等效”药物水平的比较。