Abstract

Introduction: Ventricular fibrillation (VF) in Brugada syndrome (BS) patients are thought to be triggered by vagal nerve activation, which leads to sudden cardiac arrest (SCA) at rest or while asleep. Generally, exercise is not considered as trigger of SCA in BS patients. Aim: To report 2 rare cases of patients with BS phenotype developing exercise-induced ventricular (VF). Case reports: Case 1: 48 year-old male developed SCA during marathon running and was successfully resuscitated with cardiopulmonary resuscitation (CPR). The stored automatic external defibrillator (AED) electrogram (ECG) showed VF. The 12-lead ECG did not show abnormal morphology, however sodium channel blocker challenge test (intravenous injection of pilsicainide, a pure sodium channel blocker 1mg/Kg) unmasked typical type-1 BS ECG. The treadmill stress test induced single premature ventricular contraction by Bruce protocol, and ventricular tachycardia by a flat-out dash without a run-up. Genetic analysis did not show mutation of SCN5A gene. Case 2: 18 year-old male experienced SCA while playing basketball and was successfully resuscitated with CPR. The stored ECG record of AED showed VF. The 12-lead ECG showed normal result, then we performed the drug challenge test. Pilsicainide unmasked typical type-1 BS ECG. He also had exercise-induced atrial fibrillation (AF) and experienced inappropriate shock delivery from implantable cardioverter defibrillator. The treadmill stress test by Bruce protocol did not induce any ventricular arrhythmias. We avoided a flat-out dash protocol because of possibility of exercise-induced AF. Genetic analysis did not show SCN5A mutation. Conclusion: These 2 rare cases of drug-induced BS phenotype developing exercise-induced VF highlight important role of exercise testing as risk stratification tool in certain BS patients.

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