Diffuse fibrosis and repolarization disorders explain ventricular arrhythmias in Brugada syndrome: a computational study.

ABSTRACT: In this work, we reported a computational study to quantitatively determine the individual contributions of three candidate arrhythmic factors associated with Brugada Syndrome. In particular, we focused our analysis on the role of structural abnormalities, dispersion of repolarization, and size of the diseased region. We developed a human phenomenological model capable of replicating the action potential characteristics both in Brugada Syndrome and in healthy conditions. Inspired by physiological observations, we employed the phenomenological model in a 2D geometry resembling the pathological RVOT coupled with healthy epicardial tissue. We assessed the insurgence of sustained reentry as a function of electrophysiological and structural abnormalities. Our computational study indicates that

SUBMITTER: Biasi N 

PROVIDER: S-EPMC9123016 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature