Epicardial adipose tissue as a predictor of adverse prognosis

Cardiovascular diseases (CVD) rank as the leading cause of mortality worldwide. Obesity, which is related to metabolic risk factors for CVD, is a common problem globally and in Russia. However, the generally accepted criteria for obesity cannot fully reflect the risk of developing CVD. According to modern concepts, visceral obesity is a more sensitive marker of CVD. The use of epicardial adipose tissue thickness (EAT thickness) is proposed for the determination of visceral obesity. In this regard, the presented review examines studies aimed at determining the threshold values of EAT thickness for more accurate risk prediction of CVD development. Growing interest in the potential influence of epicardial adipose tissue (EAT) on cardiovascular risk has led to an in-depth study of its functions. Genetic, epigenetic, and environmental factors may contribute to a shift toward dysfunctional EAT, characterized by a proinflammatory and profibrotic phenotype. Due to its close anatomical proximity to the coronary arteries, thicker and dysfunctional EAT actively contributes to the development and progression of coronary atherosclerosis. In addition to classical paracrine transmission, EAT can directly release mediators into the vasa vasorum of the coronary artery wall, a mechanism termed “vasocrine.” Similarly, the proinflammatory and profibrotic secretome that characterizes dysfunctional EAT can impair cardiac structure and function, thus contributing to the pathogenesis of a large number of cardiovascular diseases.