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.