Cardiovascular disease (CVD) is a group of diseases that include both the heart and blood vessels, thereby including coronary heart disease (CHD) and coronary artery disease (CAD), and acute coronary syndrome (ACS) among several other conditions. CHD causes about one-third of all deaths in people older than 35 years. Diabetes Mellitus (DM) is independently associated with a 2 to 4-fold increased mortality risk from heart disease, and with an increased mortality after myocardial infarction (MI), and worse overall prognosis with CAD. To date, DM patients have a higher incidence and prevalence of multivessels CAD. Treatments in multivessels CAD diabetics include full medical anti ischemic therapy (antiplatelets drugs, beta blockers, anti-remodelling drugs, anti-diabetic drugs etc), and revascularization therapy (Percutaneous coronary intervention (PCI) and/or Coronary artery bypass grafting (CABG)). Randomized trials comparing multivessel PCI to coronary artery bypass grafting (CABG) have consistently demonstrated the superiority of CABG in reducing mortality, myocardial infarctions and need for repeat revascularizations. After the CABG treatment, diabetics vs. non-diabetics evidenced a worse prognosis, and an increased mortality at follow up. The causes of the worse prognosis after CABG in diabetics are not well known, and under-investigated. Authors may speculate that, numerous molecular, epigenetics (as microRNAs), and other metabolic risk factors may condition the worse prognosis in diabetics vs. non diabetics after CABG. In this context, recently authors investigated the impact of epicardial adipose fat tissue dimension and metabolism on cardiovascular clinical outcomes. Intriguingly, an increased epicardial fat tissue thickness may be independently associated with the prevalence of diabetes. Consequently, diabetics have an higher epicardial fat tissue thickness, volumetry, and enhanced metabolism. Therefore, authors may speculate that, epicardial fat tissue may work as a metabolically active tissue, by a direct action on the heart, and by a cross talking with various metabolic derangements in the body leading to insulin resistance, atherosclerosis, metabolic syndrome, and cardiovascular disease. Moreover, after CABG, lifestyle and medical improvements may lead to the reduction of epicardial fat thickness, extension, and metabolism in both non-diabetics, and diabetics. Therefore, a part of the lifestyle modifications, also the hypoglycemic drugs therapy may lead to modification of epicardial fat tissue. However, authors may speculate that, the epicardial fat tissue thickness, volumetry, and metabolism, probably due to inflammatory and oxidative molecules activity, and epigenetic and anti-apoptotic pathways (as Sirtuins expression), may lead to a balance between epicardial fat tissue growth and/or reduction, and then all these pathways may be consequently involved in the prognosis of diabetics vs. non diabetics patients after CABG. At moment, all these pathways remain not well investigated in literature, and no data has been reported about new hypoglycemic drugs, and its pleiotropic effects on diabetics after CABG. Indeed, authors study hypothesis was that, epicardial fat tissue dimension, and metabolic activity may be related to a different expression of inflammatory, oxidative, and apoptotics molecules, and epigenetic effectors in diabetics vs. non-diabetics. Secondary, these effectors, and epicardial tissue dimension and activity, may be controlled, after CABG, by incretin treatment in diabetics. Moreover, higher epicardial fat tissue thickness, and tissue extension, may be associated with worse prognosis in diabetics after CABG. Secondary, in diabetics with better response to CABG, there may be a more important reduction of epicardial fat tissue tickness at follow up. This effect may be due to the control of different inflammatory, oxidative, and apoptotics molecules, and epigenetic effectors in diabetics undergoing CABG, and related to better clinical outcomes. Authors study hypothesis, is that incretin therapy may be associated to the reduction in epicardial fat tissue thickness, and extension. This effect in diabetics incretin-users vs. never-incretin-users may be due to the down regulation of different inflammatory, oxidative and apoptotics molecules, and epigenetic effectors involved in epicardial fat metabolism. Moreover, in this study authors will evaluate in diabetics vs. non diabetics, and in diabetic incretin-users vs. never.-incretin-users, all cause mortality, cardiac mortality, and Major adverse cardiac events (MACE) after CABG in diabetics vs. non diabetics, and diabetic incretin-users (6 months of incretin therapy) vs. diabetic never-incretin-users. Authors will correlate these clinical endpoints to the study of the epicardial fat anatomy and metabolism before and after CABG, and to the study of circulating inflammatory and pro-apoptotic markers, epigenetic effectors, and stem cells in diabetics vs. non diabetics, and diabetic incretin-users (6 months of incretin therapy) vs. diabetic never-incretin-users. A part of this, authors may speculate to recognize new cellular, molecular, and inflammatory processes, and epigenetic effectors epicardial fat derived related to these effects on clinical outcomes, and then used as specifical targets to improve clinical outcomes after CABG in diabetics.