Makai Attila, Rudas László, Liszkai Gizella, Fazekas Tamás
Szegedi Tudományegyetem, Altalános Orvostudományi Kar, II. Belgyógyászati Klinika és Kardiológiai Centrum, Belgyógyászati Intenzív Osztály, Szeged.
Orv Hetil. 2003 Feb 2;144(5):241-7.
The authors report on the case history of a 61 year old woman with hyperthyroidism induced atrial fibrillation, tachycardiomyopathy and congestive heart failure, in whom life threatening ventricular proarrhythmia (torsades de pointes) developed in response to intravenous amiodarone. The patient in a septic state was resuscitated because of ventricular fibrillation. The atrial fibrillation complicated by a high ventricular frequency was slowed down with intravenous amiodarone; additionally, the iodine-containing antiarrhythmic drug was expected to counter thyrotoxicosis. In response to amiodarone (2 x 300 mg), the sinus rhythm was restored, but the excessive post-cardioversion bradycardia led to the development of extreme QT interval prolongation and torsades de pointes ventricular tachycardias that often degenerated into ventricular fibrillation. In connection with this case, the authors survey those electropharmacological and pathophysiological factors which may have played a role in the emergence of ventricular proarrhythmia based on a lengthening of repolarization through the exhaustion of the repolarization reserve.
作者报告了一名61岁患有甲状腺功能亢进诱发心房颤动、心动过速性心肌病和充血性心力衰竭的女性病例，该患者在静脉注射胺碘酮后出现危及生命的室性心律失常（尖端扭转型室速）。该处于脓毒症状态的患者因室颤而接受复苏。静脉注射胺碘酮使合并高心室率的心房颤动减慢；此外，这种含碘抗心律失常药物预期可对抗甲状腺毒症。静脉注射胺碘酮（2×300mg）后恢复了窦性心律，但复律后过度的心动过缓导致QT间期极度延长和尖端扭转型室性心动过速，后者常恶化为室颤。结合该病例，作者探讨了那些可能通过复极储备耗竭导致复极延长从而在室性心律失常发生中起作用的电药理学和病理生理学因素。
