Abstract
BACKGROUND: Electrolyte depletion during alcohol withdrawal can cause acquired long QT syndrome (LQTS), leading to torsades de pointes (TdP) and ventricular fibrillation (VF) CASE SUMMARY: A 64-year-old man with a history of heavy alcohol use presented with syncope. Evaluation revealed a prolonged QTc interval of 511 ms, along with hypokalemia (K(+) level: 3.09 mmol/L) and hypomagnesemia (Mg(2+) level: 0.70 mmol/L). Telemetry documented TdP and VF during an in-hospital syncopal episode. Genetic test results for congenital LQTS were negative. Aggressive potassium and magnesium repletion stabilized his rhythm, shortening the QTc interval to 460 ms. DISCUSSION: Alcohol withdrawal can cause marked QTc prolongation via electrolyte disturbances, precipitating TdP and VF. This under-recognized complication highlights the need for vigilant monitoring and prompt electrolyte correction to prevent fatal arrhythmias. TAKE-HOME MESSAGES: In acute alcohol withdrawal syndrome , severe hypokalemia and hypomagnesemia can induce acquired LQTS, resulting in TdP and VF. Management includes defibrillation, magnesium and potassium repletion, and avoiding QT-prolonging drugs. Implantable cardioverter-defibrillator placement is not indicated once electrolyte abnormalities are corrected.