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Fibrinogen and coronary risk
1Department of Internal Medicine II, Cardiology, University of Ulm Medical Center, Robert-Koch-Str 8, D-89081, Ulm, Germany.
Insights
Fibrinogen is a key marker for coronary risk, linked to atherosclerosis and heart disease. While its exact role is still debated, elevated fibrinogen levels indicate increased cardiovascular risk.
Area of Science:
- Cardiovascular Science
- Hematology
- Epidemiology
Background:
- Fibrinogen is widely accepted as a significant independent risk factor for coronary heart disease.
- Numerous prospective studies and clinical observations support the link between fibrinogen and cardiovascular risk.
- The precise pathophysiological mechanisms underlying elevated fibrinogen in atherosclerosis remain incompletely understood.
Purpose of the Study:
- To explore the multifaceted roles of fibrinogen in atherothrombogenesis.
- To elucidate the mechanisms by which elevated fibrinogen contributes to coronary risk.
- To assess the current understanding of fibrinogen's causal involvement in cardiovascular disease.
Main Methods:
- Review of prospective epidemiological studies.
- Analysis of clinical observations.
- Examination of cellular and molecular mechanisms involved in fibrinogen's role in atherosclerosis.
Main Results:
- Fibrinogen acts as a substrate for thrombin, crucial in coagulation.
- It plays a role in platelet aggregation and endothelial function.
- Elevated fibrinogen is associated with smooth muscle cell proliferation and modulates plasminogen binding.
Conclusions:
- Fibrinogen is a major acute phase protein and an important marker of coronary risk.
- Its causal role in atherothrombogenesis requires further investigation.
- Understanding fibrinogen's mechanisms is key to managing cardiovascular risk.
Abstract:
The notion that fibrinogen is strongly, consistently, and independently related to coronary risk has been widely accepted. The evidence is based on numerous prospective epidemiological studies and clinical observations. However, the reasons why fibrinogen is elevated in coronary disease and in atherosclerosis are only incompletely understood. All cells involved in the atherogenetic process are able to produce cytokines which induce an acute phase reaction. The potential pathophysiologic mechanisms by which elevated fibrinogen levels mediate coronary risk are manifold: It forms the substrate for thrombin and represents the final step in the coagulation cascade; it is essential for platelet aggregation; it modulates endothelial function; it promotes smooth muscle cell proliferation and migration; it interacts with the binding of plasminogen with its receptor; and finally it represents a major acute phase protein. Whether or not fibrinogen is causally involved in atherothrombogenesis still remains to be determined, and even though other unsolved issues await conclusive answers, fibrinogen has emerged as an important additional marker of coronary risk.