{"title":"Idiosyncratic Amiodarone-Induced Torsades de Pointes: A Case Report","authors":"","doi":"10.1007/s42399-024-01677-3","DOIUrl":null,"url":null,"abstract":"<h3>Abstract</h3> <p>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.</p>","PeriodicalId":21944,"journal":{"name":"SN Comprehensive Clinical Medicine","volume":"66 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"SN Comprehensive Clinical Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s42399-024-01677-3","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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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.
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