Coronary Artery Disease and Epicardial Adipose Tissue

Abstract

Epicardial adipose tissue (EAT) can locally affect the coronary arteries and play a significant role in the development and progression of coronary artery disease (CAD), as emerged only recently. The mechanisms through which epicardial fat can cause atherosclerosis are complex and multifactorial. Its anatomical proximity to the heart, the unique transcriptome, and intense proteasome are the major atherogenic factors of the epicardial adipose tissue. EAT can cause atherosclerosis via several mechanisms that could be summarized in inflammation, innate immunity, oxidative stress, lipotoxicity, and glucotoxicity. EAT, regardless of whether it is measured as volume or thickness, is higher in patients with CAD as compared to individuals without CAD. The more proximal EAT is to the coronary arteries, the higher is its inflammatory activity. EAT provides prognostic information and improves the prediction of first coronary events. EAT volume is greater in subjects with incident coronary heart disease. The incidence of fatal or nonfatal coronary event significantly increased with higher EAT and remains significant even after adjustment for coronary calcium calcification score and obesity. EAT is linked to early coronary plaque components and, therefore, plays a role in the early phases of asymptomatic atherosclerosis. Routine assessment of EAT could be implemented for a better prediction and stratification of CAD.