Brugada syndrome has been linked to a genetic mutation
located on the SCN5A gene, which codes for the
α sub unit of the cardiomyocyte sodium ion channels.
This mutation leads to either complete loss of channel
function or an accelerated recovery from activation.
This can generate heterogeneity of repolarization
and increase the chance of intramyocardial re-entry
circuits, which may induce ventricular tachyarrhythmias.17,22,23
SCN5A mutations account for 18% to 30%
of cases of Brugada syndrome.24