Identification and regulation of epicardial adipose tissue biomarkers in atrial fibrillation

Abstract

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It is a multifactorial disease aggravated by a myriad of pathophysiological mechanisms. Among its risk factors, hypertension, heart failure and obesity are the main ones. The local adipose depot most associated with AF is the epicardial adipose tissue (EAT). One of the promoter events of AF is the alteration in the autonomic tone and one of the favouring substrates is inflammation. Our aim was to study the mechanisms of acetylcholine (ACh) in EAT and its relationship with AF. Our results showed the expression of muscarinic receptors in EAT stromal cells and its regulation during adipogenesis. The results of this work elucidate the role of the cholinergic system in the secretory and inflammatory activity of EAT (through IL-6, MCP1 and DEFA3) and a possible mechanism associated with postoperative AF. In addition, Chronic cholinergic imbalance in long-term persistent AF could explain the greater accumulation of fatty acids. Consequently, FABP4 increases in the epicardial stroma. Our results showed that FABP4 induces in hiPSC-derived atrial cardiomyocytes changes in calcium handling.