Brugada Syndrome

Brugada syndrome is an inherited primary electrical disorder of the heart. The ventricles are usually structurally normal, so routine echocardiography may look reassuring even when the patient carries a substrate for sudden ventricular arrhythmia. The dominant mechanism is reduced inward cardiac sodium current through Nav1.5 channels. This alters conduction and repolarization, particularly across the right ventricular outflow tract (RVOT), creating electrical heterogeneity that can support polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF). The characteristic ECG finding is right-precordial ST-segment elevation, not the diffuse ventricular dysfunction seen in cardiomyopathy. Loss-of-function variants in SCN5A, which encodes Nav1.5, are the most frequently identified genetic finding, occurring in roughly 15–30% of probands. Inheritance is typically autosomal dominant with incomplete penetrance. A pathogenic variant may be present without a diagnostic ECG, and a negative genetic test does not rule out Brugada syndrome. Clinical expression is markedly more common in males, but the syndrome can affect people of any sex. Temperature and medications can expose the substrate. Fever can worsen sodium-channel dysfunction and make the ECG pattern or ventricular arrhythmia more likely. That is why...