143: Brugada Syndrome and Polymorphic Vt Following Flecainide Reinitiation After Lung Transplantation

Introduction: Drug-induced Brugada syndrome is extremely rare, with an estimated annual risk of sudden death of just 0.08%. Only a handful of cases have been documented in the medical literature. We describe a case in which reinitiation of flecainide, a Class IC antiarrhythmic, following surgery resulted in Brugada syndrome and subsequent polymorphic ventricular tachycardia. Description: A 67-year-old male with chronic atrial fibrillation underwent bilateral orthotopic lung transplantation for end-stage interstitial lung disease. On postoperative day (POD) 2, the patient was found to be in atrial fibrillation, and his home medications, flecainide and extended-release diltiazem, were reinitiated. On POD 10, he developed KDIGO stage II non-oliguric acute kidney injury, with an estimated glomerular filtration rate (eGFR) of < 50 mL/min. A preoperative electrocardiogram (ECG) showed an intraventricular conduction delay without a Brugada pattern. ECGs on days 1–3 after flecainide reinitiation showed no change from baseline. However, two weeks after restarting flecainide, an ECG demonstrated QRS prolongation from 110 ms to 160 ms and a new type 1 Brugada pattern, with characteristic coved ST-segment in leads V1–V3. He had no symptoms or signs of myocardial ischemia. Given the concerning ECG findings and suspected flecainide cardiotoxicity, the flecainide was discontinued. That evening, the patient experienced non-sustained polymorphic ventricular tachycardia with associated presyncope, but without loss of consciousness. The arrhythmia self-terminated after 10 seconds, and he was treated with 4 mg of magnesium sulfate and 50 mEq of sodium bicarbonate. The serum flecainide level was 1.1 mcg/mL (therapeutic range: 0.2-1.0 mcg/mL). Cardiology recommended avoiding all sodium channel–blocking antiarrhythmics. The ECG normalized within 48 hours of flecainide discontinuation. Discussion: This case underscores the importance of cautious reinitiation of home medications during hospitalization. We describe how Brugada syndrome developed due to excessive cardiac sodium channel blockade from accumulating flecainide in the setting of reduced renal clearance. Close monitoring of plasma flecainide levels and serial ECGs should be used to monitor for drug toxicity when hepatic or renal dysfunction is suspected.