Reperfusion failure is attributed to different factors, including diabetes. Several mechanisms have been proposed for the harmful effects of hyperglycemia after acute myocardial infarction. Association of hyperglycemia with the activation of blood coagulation has been well studied; it could induce a shortening of the fibrinogen half-life, increase in fibrinopeptide A, fragments of pro-thrombin in factor VII, and platelet aggregation, all of which could lead to increased activation of thrombosis. Hyperglycemia at admission is associated with increased levels of inflammatory markers, enhanced expression of cytotoxic T-cells, and reduced expression of cytotoxic T-lymphocyte-associated protein 4, indicating its association with increased inflammatory immune process after acute myocardial infarction. It also could be associated with endothelial dysfunction, oxidative stress, and possibly, abolition of protective ischemic preconditioning. Other possible mechanism of harmful effects of acute hyperglycemia is microvascular dysfunction after coronary revascularization.