Haemostatic factors in human aortic intima.

Area of Science:

• Cardiovascular Biology
• Thrombosis and Hemostasis
• Atherosclerosis Research

Background:

• Lipid accumulation in atherosclerotic plaques correlates with high fibrin concentrations.
• Fibrin may play a crucial role in the development of atherosclerotic lesions.
• The origin of fibrin within lesions (mural thrombus vs. in situ clotting) remains unclear.

Purpose of the Study:

• To investigate the role of fibrin and clotting factors in atherosclerotic plaque development.
• To determine the source of fibrin within human aortic intima and lesions.
• To elucidate the mechanisms of fibrin-mediated lipid and clotting factor accumulation.

Main Methods:

• Immunoelectrophoresis was employed to quantify fibrinogen and clotting system components.
• Analysis was performed on human aortic intima, atherosclerotic lesions, and mural thrombi.
• Concentrations of prothrombin, antithrombin III, alpha 2-macroglobulin, and factor-VIII-related antigen were measured.

Main Results:

• Prothrombin concentration was elevated in plaque centers compared to normal intima, while thrombin inhibitors decreased.
• Mural thrombi showed preferential sequestration of fibrinogen and prothrombin.
• Factor-VIII-related antigen distribution was variable, with highest concentrations in endothelium-denuded deep lesion layers.

Conclusions:

• Findings support the conversion of fibrinogen to fibrin within atherosclerotic lesions.
• Accumulated fibrin appears to bind low-density lipoprotein and sequester clotting factors.
• This process may create a self-amplifying system contributing to atherosclerosis progression.