“…In particular, an increase in epicardial collagen, fibrosis and fatty infiltration, a reduction in connexin43 expression and altered gap junction communication, particularly in the RVOT, were detected [ 12 , 89 , 107 ]. These alterations are typically associated with cardiomyopathies, and an overlap in clinical as well as molecular features between BrS, arrhythmogenic cardiomyopathy (ACM/ARVC), hypertrophic cardiomyopathy, and laminopathies are emerging [ 108 , 109 , 110 ]. As in dilated cardiomyopathies, RVOT dilation reduced RV ejection fraction and RV wall motion impairment, in addition to age-related fibrosclerotic degeneration in the RV myocardium, which can also take place in BrS over decades [ 103 , 111 ].…”