Contribution of epicardial adipose tissue and fatty liver disease to the development of atrial fibrillation

Obesity is a proven risk factor for cardiovascular diseases, including atrial fibrillation (AF). Adipose tissue is metabolically and hormonally active. In recent years, there has been a lot of discussion about whether ectopic adipose tissue, particularly excessive accumulation of fat in the epicardium and liver, can be a marker of cardiovascular diseases, particularly AF. Purpose of the publication - systematization and analysis of publications on the pro-inflammatory and hormonal role of ectopic adipose tissue (epicardial fat, liver) in the development of atrial fibrillation. Results. Epicardial fat, located in close proximity to the heart, is involved in structural remodeling and the progression of atrial fibrosis. Due to its close anatomical connection and shared blood supply with the heart, epicardial fat tissue directly affects its function. Pro-inflammatory cytokines and free fatty acids, when they enter the heart muscle, alter its electrical properties, contributing to atrial remodeling (fibrosis), a key mechanism in AF. The presence of non-alcoholic fatty liver disease (NAFLD) is associated with systemic inflammation and high levels of oxidative stress, which further worsens the metabolic condition of the myocardium. Moreover, the liver is a source of atherogenic lipid fractions, which exacerbates cardiovascular risk. Thus, epicardial fat and NAFLD represent an important intermediate link between metabolic disorders and AF. In order to prevent AF in patients with ectopic fat depots, it is necessary to identify and correct these risk factors in a timely manner.