Huemer Martin, Sarganas Giselle, Bronder Elisabeth, Klimpel Andreas, Garbe Edeltraut, Haverkamp Wilhelm
Department of Cardiology, Division for Rhythmology and Electrophysiology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Clinical Pharmacology and Toxicology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Pharmacotherapy. 2015 May;35(5):e61-5. doi: 10.1002/phar.1573. Epub 2015 Mar 30.
Dronedarone is a promising, relatively new antiarrhythmic agent characterized by structural similarities to amiodarone but without amiodarone's severe organ toxicity. The proarrhythmic potential of dronedarone, however, is of increasing concern. We describe a 76-year-old woman who had been receiving dronedarone 400 mg twice/day to prevent recurrent atrial tachycardia with rapid ventricular response. Several months later, she came to the emergency department with decompensated congestive heart failure and episodes of atrial tachycardia; digoxin 0.5 mg and furosemide 40 mg were administered intravenously. Thereafter nonsustained torsade de pointes (TdP) tachycardia occurred. She was transferred to the intensive care unit where a dose of amiodarone 150 mg was administered intravenously by mistake. Thereafter, the patient showed sustained TdP necessitating cardiac resuscitation. Dronedarone was discontinued, and digoxin and amiodarone were not administered again. Under dronedarone a relevant QT prolongation was documented that was additionally augmented after concomitant treatment with digoxin and amiodarone. Use of the Naranjo adverse drug reaction probability scale indicated a probable adverse drug reaction to dronedarone (score of 7). To our knowledge, this is the first case report of a patient who experienced TdP tachycardias while receiving dronedarone therapy in connection with a worsening of heart failure and possible drug interactions with digoxin and amiodarone. Clinicians should be aware of this potential adverse drug reaction and perform repeated heart rate-corrected QT (QTc) interval measurements as well as screening for congestive heart failure in patients receiving dronedarone therapy.
决奈达隆是一种有前景的、相对较新的抗心律失常药物，其结构与胺碘酮相似，但没有胺碘酮严重的器官毒性。然而，决奈达隆的促心律失常潜力日益受到关注。我们描述了一名76岁女性，她一直每天两次服用400毫克决奈达隆以预防复发性房性心动过速伴快速心室反应。几个月后，她因失代偿性充血性心力衰竭和房性心动过速发作来到急诊科；静脉注射了0.5毫克地高辛和40毫克呋塞米。此后发生了非持续性尖端扭转型室性心动过速（TdP）。她被转入重症监护病房，在那里错误地静脉注射了150毫克胺碘酮。此后，患者出现持续性TdP，需要进行心脏复苏。停用决奈达隆，不再使用地高辛和胺碘酮。在服用决奈达隆期间记录到相关的QT延长，在与地高辛和胺碘酮联合治疗后进一步延长。使用Naranjo药物不良反应概率量表显示对决奈达隆可能存在药物不良反应（评分为7分）。据我们所知，这是首例关于患者在接受决奈达隆治疗时发生TdP室性心动过速，同时伴有心力衰竭恶化以及可能与地高辛和胺碘酮发生药物相互作用的病例报告。临床医生应意识到这种潜在的药物不良反应，并对接受决奈达隆治疗的患者进行反复的心率校正QT（QTc）间期测量以及充血性心力衰竭筛查。
