The observation that diabetic patients have a hyper-coagulable state is based both on the increased risk of thrombotic events and on laboratory abnormalities. An angioscopic study performed in patients with acute coronary syndromes (ACS) revealed that plaque ulceration and intracoronary thrombus were more frequent among diabetic patients than among their nondiabetic counterparts. Similarly, the incidence of thrombus was found to be higher in atherectomy specimens from patients with diabetes than in those from nondiabetic patients.15 Diabetic individuals have increased platelet activation and aggregation in response to shear stress and platelet agonists.16 In addition, an increased platelet-surface expression of the glycoprotein (GP) Ib receptor, which mediates binding to von Willebrand factor, and of the GP IIb/IIIa receptor, which mediates platelet-fibrin interaction, have been described. Moreover, decreased endothelial production of the antiaggregants NO and prostacyclin; increased levels of procoagulant agents such as fibrinogen, tissue factor, von Willebrand factor, platelet factor 4, and factor VII; and decreased concentrations of endogenous anticoagulants such as protein C and antithrombin III have been documented (see Fig. 2-2).17 Finally, elevated levels of plasminogen activator inhibitor-1 (PAI-1) may impair endogenous tissue plasminogen activator-mediated fibrinolysis.18 Overall, diabetes is characterized by increased intrinsic platelet activation, decreased endogenous inhibition of platelet activity, and increased blood coagulation in the presence of impaired endogenous fibrinolysis. Ex vivo studies have documented in diabetic patients the association between plasma glucose and level of platelet-dependent thrombosis, as well a reduction of thrombogenicity after improvement in glucose control.
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