Yamada S, Kuga K, Yamaguchi I
Cardiovascular Division, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan.
Jpn Circ J. 2001 Mar;65(3):236-8. doi: 10.1253/jcj.65.236.
A 70-year-old woman with dilated cardiomyopathy and ventricular tachyarrhythmia was initially treated in 1990 with intravenous amiodarone (240 mg). She developed a junctional escape rhythm (48 beats/min) with QT prolongation (QT: 0.68 s) and 8 h later developed torsade de pointes (TdP). Because other antiarrhythmic drugs did not suppress the arrhythmia, oral amiodarone (100 mg/day) was started in 1995, 7 weeks before she presented with congestive heart failure. The QT prolongation (QTc: 0.64) increased after administration of dopamine, and TdP again developed. This case suggests that amiodarone induces proarrhythmias by different mechanisms when administered intravenously or orally.
一名患有扩张型心肌病和室性快速心律失常的70岁女性于1990年最初接受静脉注射胺碘酮(240毫克)治疗。她出现了交界性逸搏心律(48次/分钟),QT间期延长(QT:0.68秒),8小时后发生了尖端扭转型室速(TdP)。由于其他抗心律失常药物未能抑制心律失常,1995年在她出现充血性心力衰竭前7周开始口服胺碘酮(100毫克/天)。服用多巴胺后QT间期延长(QTc:0.64)加重,TdP再次发生。该病例表明,静脉注射或口服胺碘酮时,其通过不同机制诱发心律失常。