INTRODUCTION:
Brugada syndrome, described in 1992 by brothers Josep and Pedro Brugada, is a genetic arrhythmia syndrome caused due to gene defects involving the sodium, calcium, and potassium channels of the cardiac musculature among others. Around 18-30% of defects can be attributed to SCN5A gene mutation affecting the alpha subunit of the cardiac sodium channel(1). The syndrome is characterized by a typical ECG pattern of >0.2 mV of ST-segment elevation with a coved ST segment and negative T-wave in more than one anterior precordial lead (V1-V3) along with Right bundle branch block in a structurally normal heart(2). This is accompanied by a risk of sudden death due to ventricular fibrillation, or syncope resulting from polymorphic ventricular tachycardia.
Most patients with this syndrome are asymptomatic. Nevertheless, diagnosing the syndrome, which is by its specific ECG pattern, is essential, as the first manifestation of the disease may even be sudden cardiac death. An Implantable cardioverter defibrillator (ICD) is indicated for patients who have had unexplained syncope or have been resuscitated from cardiac arrest(3). Anti-arrhythmic drugs like quinidine and catheter ablation of abnormal regions have been beneficial in suppressing VT. This help to reduce the incidence of sudden death to an extent.
The characteristic ST-elevation crucial for diagnosis may not be present always. It fluctuates with time and is precipitated by various factors(3). Most important among them are acute illnesses and fever. The syndrome can unmask itself in the event of a febrile illness and as a result, the disease may present itself for the first time, during such an episode.
In a region where febrile illnesses, such as dengue; and Brugada syndrome are both prevalent, such as Southeast Asia, case reports such as these become relevant. So the factors responsible for precipitating arrhythmias, such as febrile illnesses like dengue need to be analyzed and their relation needs to be understood.