Epicardial adipocytes in the pathogenesis of atrial fibrillation: An update on basic and translational studies

Abstract

Epicardial adipose tissue (EAT) is an endocrine organ containing a host of cell types and undoubtedly serving a multitude of important physiologic functions. Aging and obesity cause hypertrophy of EAT. There is great interest in the possible connection between EAT and cardiovascular disease, in particular, atrial fibrillation (AF). Increased EAT is independently associated with AF and adverse events after AF ablation (e.g., recurrence of AF, and stroke). In general, the amount of EAT correlates with BMI or visceral adiposity. Yet on a molecular level, there are similarities and differences between epicardial and abdominal visceral adipocytes. In comparison to subcutaneous adipose tissue, both depots are enriched in inflammatory cells and chemokines, even in normal conditions. On the other hand, in comparison to visceral fat, epicardial adipocytes have an increased rate of fatty acid release, decreased size, and increased vascularity. Several studies have described an association between fibrosis of EAT and fibrosis of the underlying atrial myocardium. Others have discovered paracrine factors released from EAT that could possibly mediate this association. In addition to the adjacent atrial cardiomyocytes, EAT contains a robust stromal-vascular fraction and surrounds the ganglionic plexi of the cardiac autonomic nervous system (cANS). The importance of the cANS in the pathogenesis of atrial fibrillation is well known, and it is quite likely that there is feedback between EAT and the cANS. This complex interplay may be crucial to the maintenance of normal sinus rhythm or the development of atrial fibrillation. The extent the adipocyte is a microcosm of metabolic health in the individual patient may determine which is the predominant rhythm.