Epicardial Adipose Tissue as an Independent Cardiometabolic Risk Factor for Coronary Artery Disease.

During the last decades, visceral adiposity has been at the forefront of scientific research because of its complex role in the pathogenesis of cardiovascular diseases. Epicardial adipose tissue (EAT) is the visceral lipid compartment between the myocardium and the visceral pericardium. Due to their unobstructed anatomic vicinity, epicardial fat and myocardium are nourished by the same microcirculation. It is widely known that EAT serves as an energy lipid source and thermoregulator for the human heart. In addition to this, epicardial fat exerts highly protective effects since it releases a great variety of anti-inflammatory molecules to the adjacent cardiac muscle. Taking into account the unique properties of human EAT, it is undoubtedly a key factor in cardiac physiology since it facilitates complex heart functions. Under pathological circumstances, however, epicardial fat promotes coronary atherosclerosis in a variety of ways. Therefore, the accurate estimation of epicardial fat thickness and volume could be utilized as an early detecting method and future medication target for coronary artery disease (CAD) elimination. Throughout the years, several therapeutic approaches for dysfunctional human EAT have been proposed. A balanced healthy diet, aerobic and anaerobic physical activity, bariatric surgery, and pharmacological treatment with either traditional or novel antidiabetic and antilipidemic drugs are some of the established medical approaches. In the present article, we review the current knowledge regarding the anatomic and physiological characteristics of epicardial fat. In addition to this, we describe the pathogenic mechanisms which refer to the crosstalk between epicardial fat alteration and coronary arterial atherosclerosis development. Lastly, we present both lifestyle and pharmacological methods as possible treatment options for EAT dysfunction.