LAUSR

Introduction Epicardial mapping revealed the existence of abnormal potentials on the right ventricular outflow tract (RVOT) in patients with Brugada syndrome. It is reported that tissues of the RVOT epicardium from open-chest biopsy and autopsy showed the existence of fibrosis and fatty infiltration associated with increased interstitial collagen and decreased connexin 43. Although the abnormal potentials can be explained by repolarization abnormality of delayed upstroke of the action potential dome and concealed phase 2 reentry, these abnormal potentials are associated with epicardial tissue fibrosis and include the mechanism of delayed conduction. We experienced a case of Brugada syndrome and frequent ventricular fibrillation (VF) episodes. The patient had abnormal epicardial delayed potentials that have been reported previously and also an unusual isolated very delayed potential (IVDP) that was reproducibly recorded 400–500 ms after the last ventricular activation on the epicardium of the RVOT.