Furosemide-Induced Acquired Bartter-Gitelman Phenotype Causing Torsades de Pointes in Acute Coronary Syndrome with HFrEF: A Case Series

Abstract

Background: Patients with acute coronary syndrome (ACS) complicated by heart failure with reduced ejection fraction (HFrEF) are at increased risk for malignant ventricular arrhythmias due to ischemia-related electrical instability and impaired repolarization reserve (Al-Khatib et al., 2018, Wellens et al., 2014). Loop diuretics are frequently required for the management of congestion; however, furosemide-induced renal potassium and magnesium wasting may produce an acquired electrolyte phenotype resembling Bartter or Gitelman syndromes (Seyberth and Schlingmann, 2011, Colussi et al., 1992). In the proarrhythmic milieu of ACS and HFrEF, this disturbance can precipitate QT prolongation and torsades de pointes (TdP) (Al-Khatib et al., 2018, Wellens et al., 2014, Roden, 2004). Case Summary: We report three patients with ACS and HFrEF who developed severe hypokalemia and hypomagnesemia during furosemide therapy, resulting in marked QT prolongation and TdP. All patients were successfully treated with prompt rhythm stabilization, intravenous magnesium, aggressive potassium repletion, withdrawal or modification of precipitating factors, and heart-rate augmentation when required (Al-Khatib et al., 2018, Roden, 2004, Tzivoni et al., 1988). No patient experienced arrhythmia recurrence after correction of electrolyte abnormalities. Conclusion: In patients with ACS and HFrEF, the occurrence of TdP should prompt immediate evaluation for diuretic-induced electrolyte depletion representing a reversible acquired pseudo–Bartter/Gitelman syndrome. Early recognition and targeted correction are lifesaving and may prevent unnecessary long-term device therapy (Al-Khatib et al., 2018, Wellens et al., 2014, Roden, 2004).