J-wave syndrome(s)

The hypothesis incorporates the pharmacological provocation of the Brugada ECG pattern by sodium channel blockers [3] and the attenuation of the Brugada ECG pattern and J-point elevation in idiopathic VF victims by quinidine [4,5] and isoproterenol [3,5]. [...]the hypothesis provides a mechanism of initiation of the ventricular arrhythmias. [...]the differential effects of sodium channel blockers contradict the hypothesis that a single repolarization-based mechanism underlies Brugada syndrome and idiopathic VF in the setting of inferolateral J-point elevation.