Abstract
Epicardial adipose tissue is a distinct fat depot with local and systemic effects. Distinguished from other visceral fat depots by a number of anatomical and metabolic features, this tissue exhibits increased fatty acid metabolism and a unique transcriptome enriched for genes associated with inflammation and endothelial function. As epicardial fat and the heart share an unobstructed microcirculation, it is suggested that these tissues may interact. Under normal physiological conditions, epicardial fat exhibits metabolic and thermogenic properties similar to those of brown fat, as well as mechanical properties that provide cardioprotection. However, the development of pathological conditions could cause the phenotype of epicardial fat to become detrimental to the myocardium and coronary arteries. The balance between the protective and detrimental effects of this tissue is fragile. The expression of the epicardial fat-specific transcriptome is downregulated in severe and advanced coronary artery disease. Improved local vascularisation, weight loss and targeted drugs can restore the protective physiological functions of epicardial fat. Accurate measurement of epicardial fat thickness or volume has several important clinical applications, as it correlates with visceral adiposity, coronary artery disease, metabolic syndrome, fatty liver disease, cardiac changes, arrhythmias and ventricular dysfunction. Due to the simplicity of this clinical assessment, epicardial fat is a reliable marker of cardiovascular risk and an attractive surrogate for evaluating the efficacy of drugs that modulate adipose tissue. In this article, we review the rapidly emerging evidence suggesting a specific role for epicardial adipose tissue as a marker of cardiac risk and an active player in the development of cardiac pathology, as well as a potentially modifiable therapeutic target for new drugs, even in high-risk populations.