Epicardial Fat and Clinical Outcomes After Coronary Artery Bypass Grafting in Diabetics vs. Non Diabetics
Status:
Unknown status
Trial end date:
2019-08-20
Target enrollment:
Participant gender:
Summary
Cardiovascular disease (CVD) is a group of diseases including both the heart and blood
vessels, thereby including coronary heart disease (CHD). To date, diabetics have a higher
incidence and prevalence of multivessels CHD. Treatments in multivessels CHD in diabetics
include full medical anti ischemic therapy, and revascularization therapy (Percutaneous
coronary intervention (PCI) and/or Coronary artery bypass grafting (CABG)). Randomized trials
comparing multivessel PCI to 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. 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,
an increased epicardial fat tissue thickness may be independently associated with the
prevalence of diabetes, and diabetics have an higher epicardial fat tissue thickness,
volumetry, and enhanced metabolism. Therefore, after CABG, lifestyle and medical improvements
may lead to the reduction of epicardial fat thickness, extension, and metabolism in both
non-diabetics, and diabetics, ameliorating the prognosis. At moment, epicardial tissue
function in diabetics is not well investigated in literature, and no data has been reported
about new hypoglycemic drugs, and its pleiotropic effects on diabetics after CABG. Indeed,
our 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. Therefore, incretin therapy may be associated to the reduction in
epicardial fat tissue thickness, and extension, with 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 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.