Moro C, Romero J, Corres Peiretti M A
Int J Cardiol. 1986 Dec;13(3):365-8. doi: 10.1016/0167-5273(86)90121-x.
We describe the appearance of long QT interval and polymorphous ventricular tachycardia in a patient treated with amiodarone who presented with hypokalemia secondary to chronic diuretic therapy. Ventricular pacing was initiated upon admission. The hypokalemia was corrected and amiodarone was discontinued. After three days the patient showed a normal QT interval and was free of ventricular tachyarrhythmias. Although hypokalemia could itself have been the arrhythmogenic factor in this particular patient, the additional toxic effect of amiodarone cannot be ruled out. It seems reasonable to consider the combination of both as dangerous when we take into account that the majority of patients cited as having amiodarone-induced torsade de pointes had also potassium depletion.
我们描述了一名接受胺碘酮治疗的患者出现长QT间期和多形性室性心动过速的情况，该患者因慢性利尿治疗继发低钾血症。入院时开始进行心室起搏。低钾血症得到纠正，胺碘酮停用。三天后，患者QT间期正常，无室性快速心律失常。虽然低钾血症本身可能是该特定患者的致心律失常因素，但不能排除胺碘酮的额外毒性作用。考虑到大多数被认为有胺碘酮诱发尖端扭转型室速的患者也有钾缺乏，将两者结合起来视为危险似乎是合理的。
