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Diabetes mellitus is a worldwide epidemic whose incidence and prevalence have significantly increased in recent decades. Diabetic patients have an increased mortality and morbidity related to ischemic heart disease and are more likely to develop multivessel coronary artery disease than non-diabetic patients. An acute coronary event is the leading cause of death among diabetics. These patients have an increased risk of complications after an acute coronary syndrome both during the acute phase and in the post-infarction period. Experimental evidences showed an increased prevalence of atherosclerosis as well as platelet and coagulation abnormalities in patients with diabetes, even after data adjustment for other risk factors. Both hyperglycemia and insulin resistance play a role in the pathogenic link between diabetes and atherosclerosis. Diabetic patients, therefore, could derive a greater benefit from therapies shown to be effective in treating and preventing ischemic heart disease. An aggressive correction of cardiovascular risk factors and accurate risk stratification of patients with diabetes are needed.

Urocortins and the corticotropin releasing hormone have a long evolutionary history. In the nervous system the corticotropin releasing hormone is responsible of anxiogenic effects associated with stress, while urocortins are concerned with adaptive behavior. Urocortins are also expressed in the heart, where they may play an autocrine/paracrine role binding to corticotropin releasing hormone-R2 receptors. The expression of endogenous cardiac urocortin is increased by in vitro ischemia-reperfusion damage, and the addiction of exogenous urocortins is associated with reduction of myocardial cell death during ischemia-reperfusion damage in vitro, ex vivo and in vivo. In isolated perfused heart urocortin enhances cardiac contractility and decreases high energy phosphates reduction after ischemia-reperfusion damage. Urocortin is also associated with peripheral and coronary vasodilation and with positive inotropic effect. There are experimental data which suggest a beneficial effect of urocortins in subjects with heart failure and a possible beneficial role of urocortin in preventing the iatrogenic ischemia-reperfusion damage caused by cardioplegic arrest during cardiac surgery. These early observations suggest that assessment of the clinical use of urocortin in heart failure and for the prevention of ischemia-reperfusion damage in cardiac surgery should be actively pursued.