ON LIPOPROTEIN(A) AND THE COAGULATION FIBRINOLYSIS BALANCE IN THE ACUTE PHASE OF DEEP VENOUS THROMBOSIS

In vitro studies have suggested that lipoprotein(a) (Lp(a)), an important risk factor for the development of atherosclerotic cardiovascular and cerebrovascular disease, might interfere with fibrinolysis. We studied the correlations in vivo between Lp(a) and various coagulation and fibrinolysis factors in acute deep venous thrombosis, a state associated with an activated coagulation system and increased reactive fibrinolysis. In 31 patients with established acute deep venous thrombosis of the lower limb, coagulation parameters (fibrin monomers, thrombin-antithrombin III) and fibrinolysis parameters (D-dimers, tissue plasminogen activator antigen, plasminogen) were studied in relation to Lp(a) concentrations. Elevated thrombin-antithrombin III and fibrin monomer levels were found together with enhanced D-dimers and tissue plasminogen activator concentrations, signs of an activated coagulation system and of increased reactive fibrinolysis. Significant correlations were obtained for fibrin monomers with thrombin-antithrombin III and D-dimers (r=0.56; p=0.002 and r=0.68; p=0.0002 respectively), between fibrin monomers and plasminogen (r=0.38; p=0.03) and for thrombin-antithrombin III with tissue plasminogen activator antigen (r=0.64, p=0.006). These data are indicative of a normally functioning coagulation/fibrinolysis axis in acute deep venous thrombosis. No correlation between Lp(a) concentrations and coagulation or fibrinolysis parameters was found in these patients with acute deep venous thrombosis, which suggests that variations in Lp(a) concentrations are not accompanied by parallel changes in coagulation and fibrinolysis parameters.