Epicardial Adipose Tissue: A Precise Biomarker for Cardiovascular Risk, Metabolic Diseases, and Target for Therapeutic Interventions

Abstract

Epicardial adipose tissue (EAT) is located between the heart muscle and visceral pericardium, where it has direct contact with coronary blood vessels. Elevated thickness of this tissue can induce local inflammation affecting the myocardium and the underlying coronary arteries, contributing to various cardiovascular diseases such as coronary artery disease, atrial fibrillation, or heart failure with preserved ejection fraction. Recent studies have identified EAT thickness as a simple and reliable biomarker for certain cardiovascular outcomes. Examples include the presence of atherosclerosis, incident cardiovascular disease (CVD) in individuals with type 2 diabetes mellitus (T2DM), and the prevalence of atrial fibrillation. Furthermore, EAT measurements can help to identify patients with a higher risk of developing metabolic syndrome. Since the EAT thickness can be easily measured using echocardiography, such examinations could serve as a useful and cost-effective preventive tool for assessing cardiovascular health. This review also summarizes therapeutical interventions aimed at reducing EAT. Reducing EAT thickness has been shown to be possible through pharmacological, surgical, or lifestyle-change interventions. Pharmaceutical therapies, including thiazolidinediones, glucagon-like peptide 1-receptor agonists, sodium-glucose cotransporter 2 inhibitors, dipeptidyl peptidase-4 inhibitors, and statins, have been shown to influence EAT thickness. Additionally, EAT thickness can also be managed more invasively through bariatric surgery, or noninvasively through lifestyle changes to diet and exercise routines.