Abstract

Numerous drugs prolong the QT interval, and drug-induced QT prolongation is a frequently encountered situation in hospital settings. QT prolongation increases the risk of Torsades de Pointes (TdP), which can be life-threatening. A 70-year-old female with a history of atrial flutter post ablation and ischemic heart disease was admitted for shortness of breath and found to be in atrial flutter with variable atrioventricular block. She was treated with intravenous amiodarone, digoxin loading dose, beta-blockers, and diuretics. The patient converted to sinus rhythm but developed QT prolongation and TdP secondary to amiodarone. The drug was discontinued. After ruling out active ischemia, a diagnosis of idiosyncratic amiodarone-induced TdP was made. Although the incidence of TdP due to amiodarone use is rare, idiosyncratic amiodarone-induced TdP can occur secondary to long QT syndrome or polymorphisms. The treatment includes holding the drug, administration of magnesium sulfate, replenishment of all electrolytes, and cardioversion if needed. Although amiodarone is considered a low-risk drug for precipitating TdP, risk factors including older age, female sex, ischemic heart disease, and electrolyte abnormalities are essential considerations. Drug-induced TdP can be life-threatening due to its potential to degenerate into ventricular fibrillation. Prompt recognition, discontinuation of the drug, and empiric administration of magnesium sulfate are essential.

中文翻译：

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特异胺碘酮诱发尖端扭转型室速：病例报告

摘要

许多药物会延长 QT 间期，药物引起的 QT 间期延长是医院环境中经常遇到的情况。 QT 延长会增加尖端扭转型室速 (TdP) 的风险，从而危及生命。一名 70 岁女性，有消融后心房扑动病史和缺血性心脏病史，因呼吸急促入院，发现心房扑动伴可变性房室传导阻滞。她接受静脉注射胺碘酮、地高辛负荷剂量、β-受体阻滞剂和利尿剂治疗。患者转为窦性心律，但出现继发于胺碘酮的 QT 间期延长和 TdP。该药已停药。排除活动性缺血后，诊断为特异质胺碘酮诱发的 TdP。尽管因使用胺碘酮导致的 TdP 发生率很少见，但特异质胺碘酮诱发的 TdP 可能继发于长 QT 综合征或多态性。治疗包括停药、服用硫酸镁、补充所有电解质以及必要时进行心脏复律。尽管胺碘酮被认为是诱发 TdP 的低风险药物，但年龄、女性、缺血性心脏病和电解质异常等危险因素是重要考虑因素。药物引起的 TdP 可能会危及生命，因为它有可能退化为心室颤动。及时识别、停药和经验性施用硫酸镁至关重要。