Lipid-thrombosis interface.

Abstract

Remnants produced on the lipolysis of triglyceride-rich lipoproteins provide a contact surface that activates the contact system of coagulation and therefrom factor VII. New evidence is reviewed suggesting that increased levels of circulating activated factor VII (VIIa) initiates coagulation and produces thrombin at higher rate at the site of an atheromatous lesion or at an injury site. This may have profound significance for the propagation of thrombus and for the thrombin-induced inflammatory and proliferative responses. Vascular homeostasis is achieved by the regulated interaction of the coagulation and fibrinolytic systems. An imbalance in this equilibrium may lead to an increased risk of thrombosis or a bleeding diathesis. The role of PAI-1, a potent inhibitor of enzymes that generate plasmin, in the regulation of fibrinolytic activity, is discussed and the evidence linking the expression of its activity to hypertriglyceridaemia is reviewed. Moreover, the association between lipoprotein (a) and coronary heart disease is attributed to its interference in the normal activation of plasminogen to plasmin.