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Fever-Induced Brugada Syndrome in Patients with Malaria Plasmodium Falciparum
Ervan Zuhri1,2
Department of Emergency, Fak Fak Hospital, West Papua, Indonesia
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