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Abstract Venous thromboembolism (VTE) is a major cause of morbidity and mortality in western countries. The main clinical manifestations are represented by deep venous thrombosis (DVT) and pulmonary embolism (PE) (Ascari E, et al., 1995).Venous thrombosis is a multifactorial disease and usually occurs as a result of an imbalance between prothrombotic and antithrombotic potentials, a defective function of the fibrinolytic system or both (Girolami A, et al., 1997).Virchow first elucidated the causes of deep venous thrombosis with a description of a classical triad: stasis, hypercoagulabih’ty, and endothelial injury (Cogo A, et al., 1994).Among the leading causes of impaired fibrinolysis, lipoprotein (a) [ Lp(a)] plays a pivotal role. Lp(a) is a genetic variant of a low density lipoprotein (LDL) composed by the association of a unique and highly glycosylated apolipoprotein (a) [apo(a)J with apolipoprotein B100 through a single disulphide bond (Giuseppe, et al., 1999).Due to the structural mimicry with plasminogen, apo(a) inhibits plasminogen binding and activation at the surface of stabilized fibrin, endothelial cells and platelets in a dose - dependant fashion (Marcucci R, et al., 2003). |