Diabetes is associated with significant morbidity and mortality in the setting of acute coronary syndromes. Exists a progressive relationship between glucose levels and cardiovascular risk. Hyperglycemy in fact produces endothelial dysfunction recognised to be a key accessory to diabetic microangiopathy and macroangiopathy. Furthermore diabetics present high levels of cholesterol which elevate the risk of CHD. The statins, for their effects, may represent the fit therapy. The beneficial effects of statins may extend beyond improving the lipid profile. There are several proposed mechanisms for event reduction by lipid-lowering therapy, which include improved endothelium-dependent vasodilation, stabilization of atherosclerotic lesions, reduction in inflammatory stimuli, and prevention, slowed progression, or regression of atherosclerotic lesions (pleiotropic effects). Cellular experiments suggest that statins have an impact on endothelial function by preventing oxidized LDL-induced reduction of nitric oxide production and increased nitric oxide synthesis. Statins also impact chronic inflammation by reducing mitogen (PDGF) responsiveness, inhibiting smooth muscle cell proliferation, inhibiting monocyte chemotaxis and migration, and by reducing macrophage protease production. The absolute clinical benefit achieved may be greater in diabetic than in nondiabetic patients with CHD because diabetic patients have a higher absolute risk of recurrent CHD events and other atherosclerotic events.