Correlation between functional and ultrastructural substrate in Brugada syndrome

Brugada syndrome (BS) was reported for the first time in 1992 and is associated with an ST-segment elevation in the right precordial leads in the absence of any demonstrable structural heart disease, as well as with sudden cardiac death due to ventricular fibrillation (VF).1 A patent type 1 electrocardiogram (ECG) is diagnostic of BS and is characterized by a coved ST-segment elevation of ≥2 mm followed by a negative T wave in >1 right precordial lead (V1 to V3) in the presence or absence of a sodium channel–blocking agent, and in conjunction with 1 of the following: documented VF, polymorphic ventricular tachycardia (VT), a family history of sudden cardiac death at