Epicardial adipose tissue and atrial fibrillation: pathophysiological mechanisms, clinical implications and potential therapies.

Epicardial adipose tissue and atrial fibrillation: pathophysiological mechanisms, clinical implications and potential therapies. Curr Med Res Opin. 2018 Apr 06;:1-26 Authors: Goudis CA, Vasileiadis IE, Liu T Abstract Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Epicardial adipose tissue (EAT) serves as a biologically active organ with important endocrine and inflammatory function. An accumulating body of evidence suggests that EAT is associated with the initiation, perpetuation and recurrence of AF, but the precise role of EAT in AF pathogenesis is not completely elucidated. Pathophysiological mechanisms involve adipocyte infiltration, profibrotic and pro-inflammatory paracrine effects, oxidative stress, neural mechanisms and genetic factors. Notably, EAT accumulation seems to be associated with stroke and adverse cardiovascular outcomes in AF. Weight loss, specific medications and ablation of ganglionated plexi (GP) seem to be potential therapies in this setting. PMID: 29625530 [PubMed - as supplied by publisher]
Source: Current Medical Research and Opinion - Category: Research Tags: Curr Med Res Opin Source Type: research