Coronary artery disease (CAD) represents one of the most important causes of morbility, hospitalization and death, and its incidence greatly increases in the elderly population. In the last decades, several pieces of evidence have suggested a pathogenetic role of systemic and visceral fat inflammation in the development and progression of CAD. The epicardial adipose tissue (EAT), the visceral fat depot of heart, produces and secretes numerous pro-inflammatory mediators that could be involved in the pathogenesis of coronary atherosclerosis. Furthermore, age-related low-grade inflammation leads to the accumulation and inflammation of EAT. Therefore, this review aims to explore the potential implication of EAT in the pathogenesis of CAD, the link between systemic inflammation and an EAT pro-inflammatory phenotype, and, finally the perspectives for novel therapeutic strategies targeting the cardiac visceral fat.