Dependence of epicardial T-wave on local activation voltage in Brugada syndrome

Brugada syndrome (BrS) manifests as a spontaneous variability of the electrocardiographic marker suggesting a dynamic variability of the electrical substrate. A “coved J-ST” aspect can be explained by mechanisms primarily affecting repolarization, or secondary to defective activation.1 Animal models using pharmacological agents produce J-ST elevation through repolarization gradients, while in patients, evidence points to a slow-conductive structural substrate in the right ventricular outflow tract (RVOT) epicardium.