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Although we commend Pieroni et al.(1) for their important work toward understanding BrS and its purported structural basis, we would exercise caution in implicating myocardial inflammation in its pathogenesis based upon these data. Fibrosis alone would explain the areas of low voltage seen in their patients. Indeed, we have reported previously, in the Journal, pathological findings from a series of 12 cases of BrS, 6 diagnosed in vivo and 6 following a sudden death with direct comparison with a control of noncardiac deaths (2). In line with the observations of Pieroni et al., the BrS group showed increased epicardial and interstitial fibrosis, particularly within the RV outflow tract, with quantification of collagen content further supporting the observation. However, there was no evidence of increased myocardial inflammatory cells among the Brugada group compared with controls. This is concordant with our extensive …