The molecular markers of hemostatic activation on coronary artery disease.

Endothelial cells, circulating platelets, and proteins of the coagulation and fibrinolytic systems are known to contribute to the hemostatic processes. Various molecular markers of hemostatic alteration are found in increased amounts in the circulation during the activation of this process. In this study, we investigated serum lipoprotein (a) and plasma platelet factor 4, beta-thromboglobulin, thrombin-anthithrombin complex, fibrinopeptid A, D-dimer, tissue plasminogen activator, tissue plasminogen activator inhibitor, and fibronectin levels in patients with coronary artery disease.

The importance of Lp(a)-fibronectin interaction in atherogenesis.

An elevated concentration of lipoprotein (a) (Lp(a)) in serum has been considered a risk factor for coronary heart disease by various investigators. The apo(a) portion of Lp(a) binds to the carboxyterminal heparin binding domain of fibronectin. Lp(a) bound to fibronectin is internalized through the fibronectin receptor pathway and thereby causes increased accumulation of lipid and foam cell formation.

Plasma Lp(a) and t-PA-PAI-1 complex levels in coronary heart disease.

In this study we investigated serum Lp(a) and plasma t-PA-PAI-1 complex levels in patients with coronary heart disease (CHD). Serum total cholesterol, triglyceride, LDL and VDL cholesterol levels (p < 0.001) and HDL cholesterol levels (p < 0.

The relationship between the electrophoretic mobility of lipoproteins and coronary heart disease.

Low density lipoproteins (LDL) in patients with coronary atherosclerosis have a substantially lower content of sialic acid when compared with the LDL from healthy subjects. Desialylated LDL have smaller sizes and greater electrophoretic mobilities than sialylated ones. Desialylated LDL may be responsible for the accelerated development of foam cells in atherosclerosis.