Table 3. Factors supporting the Brugada syndrome as a repolarization abnormality.

Bradycardia- or Pause-dependent augmentation of the Brugada wave or bradycardia or pause promotes transition from type II or III Brugada wave to type I Brugada wave

VF always initiated by a short-coupled premature ventricular beat on T wave that is not seen in known depolarization abnormalities

Quinidine, a sodium channel blocker with a feature of blocking Ito, can abolish the Brugada wave and prevent VF in the BrS. In contrast, other sodium channel blockers with the feature of blocking Ito potentiate the Brugada wave and promote VF

Similar to that in depolarization currents (INa and ICa-L), gene mutation in the repolarization currents like Ito and IK-ATP can also result in the Brugada syndrome