Arrhythmogenic influence of mutations in a myocyte-based computational model of the pulmonary vein sleeve.

ABSTRACT: In the heart, electrophysiological dysregulation arises from defects at many biological levels (from point mutations in ion channel proteins to gross structural abnormalities). These defects disrupt the normal pattern of electrical activation, producing ectopic activity and reentrant arrhythmia. To interrogate mechanisms that link these primary biological defects to macroscopic electrophysiologic dysregulation most prior computational studies have utilized either (i) detailed models of myocyte ion channel dynamics at limited spatial scales, or (ii) homogenized models of action potential conduction that reproduce arrhythmic activity at tissue and organ levels. Here we apply our recent model (EMI), which integrates electrical activation and propagation across these scales, to study human atr

SUBMITTER: Jæger KH 

PROVIDER: S-EPMC9054808 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature