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Fibrinogen/fibrin in atherogenesis.

E B Smith¹, W D Thompson, L Crosbie

¹Department of Clinical Biochemistry, University of Aberdeen, Aberdeen Royal Infirmary.

European Journal of Epidemiology

|May 1, 1992

Summary

Fibrin in atherosclerotic plaques can release lipoprotein(a) [Lp(a)] via plasmin. Lp(a)

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Area of Science:

Cardiovascular research
Atherosclerosis and thrombosis
Lipoprotein metabolism

Background:

Fibrin is a key component of atherosclerotic plaques.
Continuous fibrin formation and breakdown occur within the arterial intima.
Lipoprotein(a) [Lp(a)] is implicated in cardiovascular disease.

Purpose of the Study:

To investigate the relationship between fibrin and Lp(a) in aortic lesions.
To explore the atherogenic mechanisms of Lp(a).

Main Methods:

Analysis of aortic lesions.
Incubation with plasmin to release bound lipoproteins.
Characterization of released lipoproteins, primarily Lp(a).

Main Results:

A fibrin-bound lipoprotein, largely Lp(a), can be released from aortic lesions by plasmin.
Lp(a)'s atherogenicity may stem more from lipid deposition than fibrinolysis inhibition.
Fibrin degradation products may attract monocyte-macrophages and promote smooth muscle cell proliferation.

Conclusions:

Fibrin plays a role in retaining Lp(a) within atherosclerotic plaques.
Lp(a) contributes to atherosclerosis through lipid accumulation.
Fibrin breakdown products may influence inflammatory and proliferative processes in the arterial wall.

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