Mechanistic inquiry into the role of tissue remodeling in fibrotic lesions in human atrial fibrillation.

ABSTRACT: Atrial fibrillation (AF), the most common arrhythmia in humans, is initiated when triggered activity from the pulmonary veins propagates into atrial tissue and degrades into reentrant activity. Although experimental and clinical findings show a correlation between atrial fibrosis and AF, the causal relationship between the two remains elusive. This study used an array of 3D computational models with different representations of fibrosis based on a patient-specific atrial geometry with accurate fibrotic distribution to determine the mechanisms by which fibrosis underlies the degradation of a pulmonary vein ectopic beat into AF. Fibrotic lesions in models were represented with combinations of: gap junction remodeling; collagen deposition; and myofibroblast proliferation with electrotonic or

SUBMITTER: McDowell KS 

PROVIDER: S-EPMC3686346 | biostudies-literature | 2013 Jun

REPOSITORIES: biostudies-literature