Role of Epicardial Adipose Tissue in Health and Disease: A Matter of Fat?

Abstract

Epicardial adipose tissue (EAT) is a small but very biologically active ectopic fat depot that surrounds the heart. Given its rapid metabolism, thermogenic capacity, unique transcriptome, secretory profile, and simply measurability, epicardial fat has drawn increasing attention among researchers attempting to elucidate its putative role in health and cardiovascular diseases. The cellular crosstalk between epicardial adipocytes and cells of the vascular wall or myocytes is high and suggests a local role for this tissue. The balance between protective and proinflammatory/profibrotic cytokines, chemokines, and adipokines released by EAT seem to be a key element in atherogenesis and could represent a future therapeutic target. EAT amount has been found to predict clinical coronary outcomes. EAT can also modulate cardiac structure and function. Its amount has been associated with atrial fibrillation, coronary artery disease, and sleep apnea syndrome. Conversely, a beiging fat profile of EAT has been identified. In this review, we describe the current state of knowledge regarding the anatomy, physiology and pathophysiological role of EAT, and the factors more globally leading to ectopic fat development. We will also highlight the most recent findings on the origin of this ectopic tissue, and its association with cardiac diseases. © 2017 American Physiological Society. Compr Physiol 7:1051-1082, 2017.

Relationship between epicardial and perivascular fatty tissue and adipokine-cytokine level in coronary artery disease patients

“…Some researchers believe that an increase in the thickness of epicardial fat reflects the presence of visceral obesity in the body and serves as a prognostic marker of coronary heart disease and its associated complications [21]. The results obtained in this study show that EAT thickness is directly dependent on the value of the PVAT; this concurs with the results of previous studies [22,23]. Our findings also show that the presence of a direct connection between an increase in EAT thickness and LV hypertrophy, as well as insulin resistance.…”

Non-Systematic Review of Diet and Nutritional Risk Factors of Cardiovascular Disease in Obesity

“…EAT is located between the myocardium and visceral layer of the pericardium and interacts directly with the myocardium due to its proximity [43]. It acts mainly locally and produces a variety of bioactive molecules (e.g., proinflammatory cytokines; profibrotic factors; adipokines; and chemokines) that may have both harmful and protective effects on cardiac function and morphology [44,45]. Environmental factors including excessive caloric intake and an unhealthy lifestyle may drive the development of ectopic fat in the heart [44].…”

“…It acts mainly locally and produces a variety of bioactive molecules (e.g., proinflammatory cytokines; profibrotic factors; adipokines; and chemokines) that may have both harmful and protective effects on cardiac function and morphology [44,45]. Environmental factors including excessive caloric intake and an unhealthy lifestyle may drive the development of ectopic fat in the heart [44]. EAT affects cardiac function by increasing the left ventricular chamber (LV) mass and atypical right ventricular chamber (RV) geometry [44].…”

“…Environmental factors including excessive caloric intake and an unhealthy lifestyle may drive the development of ectopic fat in the heart [44]. EAT affects cardiac function by increasing the left ventricular chamber (LV) mass and atypical right ventricular chamber (RV) geometry [44]. Due to the profibrotic, proinflammatory, and oxidative stress mechanisms it is also associated with severity and prevalence of the most prevalent cardiac arrythmia-atrial fibrillation (AF) [4,46].…”

Expression Profile of Circular RNAs in Epicardial Adipose Tissue in Heart Failure

“…EAT produces multiple bioactive molecules, including adipokines and cytokines 5,6 , as well as microparticles carrying proteins, lipids and ribonucleic acids (RNAs) 7 . In addition, EAT is correlated with heart failure(HF), without regard to metabolic status or coronary artery disease (CAD) [8][9][10] .Meanwhile, EAT releases molecules with vasocrine and paracrine impacts on the myocardium 11,12 .…”