Peripheral artery disease in type 2 diabetes: the role of fibrinolysis.

The aim of the present study is to verify the relationship between peripheral artery disease (PAD) and some coagulation/fibrinolysis parameters in type 2 diabetic patients. Sixty-three type 2 diabetic patients, without PAD, were studied at baseline and after 4 years. Assessments included tissue-Plasminogen Activator (t-PA), Plasminogen Activator Inhibitor-1 antigen (PAI-1 Ag), Plasminogen Activator Inhibitor-1 activity (PAI-1 Act), Plasminogen (Pl), Fibrin peptide A (FPA), Fibrinogen (Fr), and the ankle/brachial pressure index (ABI). We observed a significant difference between diabetic patients and controls as regards tPA (11.8 +/- 5.4 vs. 6.6 +/- 3.0 ng/ml; p <0.05) and PAI-1 Act (17.8 +/- 9.2 vs. 11.7 +/- 6.6 ng/dl; p <0.005). After 4 years 13 diabetic patients became vasculopathic and, at baseline, had significantly lower tPA (8.9 +/- 4.8 vs. 12.5 +/- 5.3; p <0.011), and higher PAI-1 Ag (50.8 +/- 22.2 vs. 32 +/- 22.2; p <0.006), and PAI-1 Act values (24.1 +/- 9.5 vs. 16.1 +/- 8.4; p <0.014), compared with 50 diabetic patients who did not develop PAD after 4 years. These data show that the physiological equilibrium which exists between t-PA and PAI-1 moves towards higher levels in our diabetic patients compared with controls, at baseline, whereas diabetic patients who developed PAD showed a shift towards an antifibrinolytic pathway with diminished t-PA, increased PAI-1 Ag and PAI-1 Act and consequently procoagulant activity. Our study suggests that hypofibrinolysis may be involved in the future onset of PAD in type 2 diabetic patients.