The Importance of the Assessment of Epicardial Adipose Tissue in Scientific Research

Abstract

Epicardial adipose tissue (EAT) exhibits morphological similarities with pericardial adipose tissue, however, it has different embryological origin and vascularization. EAT is a metabolically active organ and a major source of anti-inflammatory and proinflammatory adipokines, which have a significant impact on cardiac function and morphology. Moreover, it can regulate vascular tone by releasing various molecules. The relationship between EAT and cardiovascular disease and diseases of other organ systems is now considered a common discussion subject. The present clinical review article summarizes the epidemiological findings based on imaging techniques in studies conducted so far. In conclusion, evaluation of the epicardial adipose tissue constitutes a helpful scientific parameter, which can be assessed by means of different diagnostic imaging examinations.

Exploring the role of epicardial adipose-tissue-derived extracellular vesicles in cardiovascular diseases

“… 14 EAT accumulates within the interventricular and atrioventricular grooves and is present along the coronary vessels, the right edge of the wall of the right ventricle, on the anterior wall, and around the apex of the heart. 15 According to its specific anatomical distribution, the EAT located directly around or on the coronary artery adventitia is known as “pericoronary EAT”; “myocardial EAT” is the fat depot covering the myocardium, whereas periatrial and periventricular EAT is distributed within and around the atria and ventricles, respectively. Although the externally located pericardial adipose tissue receives its blood supply from branches of the internal thoracic artery, 16 EAT receives its blood supply from branches of the coronary arteries, given their close vicinity.…”

Epicardial Adipose Tissue Thickness and Preserved Ejection Fraction Heart Failure

“…Lying between the myocardium and visceral pericardium, EAT covers most of the right ventricle (RV) and part the left ventricle (LV) with an EAT-myocardium ratio of 0.48 for the RV and 0.15 for the LV [22] (Fig. 1).…”

“…Semaglutide reduced CRP levels by 44, 39, and 48% in the Semaglutide Treatment Effect in People with Obesity (STEP) 1, 2 and 3 trials, and caloric reduction-induced weight loss increased peak oxygen uptake by 1.8 ml/min/kg in patients with HFpEF [76,77]. Inclusion of epicardial adiposity as an endpoint in obesity therapeutic trials may help uncover how anti-obesity medication or procedures benefit elevated BMI patients with HFpEF besides a straight weight loss [22,[78][79][80].…”