Figure 1.

Theories of J-ST elevation and factors influencing Brugada syndrome. (A) The theory positing repolarization abnormality posits that the preservation of deep membrane potentials during phase 2, along with the extension of action potentials in the epicardium compared to those observed in the endocardium, precipitates J-ST elevation coupled with a negatively deflected T-wave. The absence of a prominent dome in epicardial action potentials instigates phase 2 reentry, driven by transmural dispersion, thereby exacerbating the manifestation of a negative T-wave. On the other hand, the theory emphasizing conduction disturbances posits that localized epicardial excitation failure underlies J-ST elevation, and delayed conduction culminates in the appearance of a negatively oriented T-wave, typically exhibiting the coved-type morphology. (B) Gene mutations, frequently affecting SCN5A, or structural cardiac pathologies, often characterized by localized fibrotic alterations in the right ventricular outflow tract and, at times, a combination thereof, serve as the genesis for the distinctive Brugada-type ECG patterns. Perturbations such as isoproterenol administration, vagal tone modulation, or elevated body temperature due to fever can exert influence over J-ST segment levels and the propensity for arrhythmic events.