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Fever-Induced Brugada Syndrome in Patients with Malaria Plasmodium Falciparum Ervan Zuhri1,2 1 Department of Emergency, Fak Fak Hospital, West Papua, Indonesia 2 Faculty of Medicine, University of Indonesia Brugada syndrome (BS) is reported to be responsible for about 4% of all sudden deaths and about 20% of all sudden deaths in people without structural heart disease. BS is characterized by a coved-type ST-segment elevation ≥2 mm in the right precordial leads (BS type I) and a tendency to develop malignant polymorphic ventricular arythmias that may lead to syncope or cardiac arrest. BS is caused by mutations in the SCN5A gene encoding the α-subunit of the voltage-gated sodium channel Nav1.5. Several experimental studies reported that dysfunction of the mutated sodium channel can be temperature sensitive. Fever can unmask or exacerbate the typical BS electrocardiogram (ECG) pattern and trigger ventricular tachycardia or ventricular fibrillation. Molecular mechanism underlying fever-induced ventricular arrhythmias leading syncope or cardiac arrest in patients with BS are not well understood, but some mechanism were proposed. Fever-induced BS are tought involving the effect of high temperature to reduce sodium current, accelerated inactivation of sodium channels, and the loss of sodium channels function augmented by higher temperatures. Other studies proposed that a high temperature could alter functional expression of other genetic mutations. Here, we presented the case report of a 49-year-old non-obese man with chief complaint fever for 1 day, athralgia-myalgia, headache, and nausea. There was no chest pain or dyspnea. There was no history of syncope, diabetes mellitus, hypertension, dyslipidemia, or coronary artery disease. He was a smoker and alcoholic man. The patient’s vital sign was normal, except his body temperature (38,5oC). An ECG at the time of admission revealed ST-segment elevation of >2 mm in lead V1 and V2 with T-wave inversion and saddleback-shaped ST-T-segment in lead V3. Plasmodium falciparum was found in his blood examination. In emergency department, the patient get syncope, and the doctor did precordial thump. At day 3, after the patient get antipyretic, anti-malaria drugs, and other supportive treatments, his ECG pattern was normal. Figure 1. Patient’s electrocardiogram at the time of admission in emergency department