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Published on: February 26, 2013
[Clinical significance of the cardiovascular risk factor fibrinogen in secondary prevention]
D Baller1, U Gleichmann, E Miche
1Herz- und Diabeteszentrum NRW, Kardiologische Klinik, Bad Oeynhausen.
Insights
High plasma fibrinogen levels are a significant cardiovascular risk factor, increasing the likelihood of heart attack and stroke. Lowering fibrinogen through smoking cessation and lifestyle changes can reduce this risk.
Area of Science:
- Cardiovascular Medicine
- Hematology
Context:
- Epidemiological studies identify plasma fibrinogen as a key cardiovascular risk factor.
- Clinical research links fibrinogen levels to the severity of coronary heart disease.
Purpose:
- To elucidate the role of plasma fibrinogen in cardiovascular disease pathogenesis.
- To explore mechanisms linking fibrinogen to thrombosis and atherogenesis.
- To review methods for reducing elevated fibrinogen levels.
Summary:
- Elevated plasma fibrinogen (over 300-350 mg/dl) is an independent risk factor for myocardial infarction and stroke.
- Fibrinogen impacts blood viscosity, platelet aggregation, and coagulation, promoting a hypercoagulable state.
- It also contributes to atherogenesis by influencing smooth muscle cell proliferation and migration.
Impact:
- Identifies smoking as a major determinant of fibrinogen levels, emphasizing smoking cessation for risk reduction.
- Highlights lifestyle modifications like weight reduction and physical activity.
- Discusses pharmacological interventions including fibrates, low-dose Urokinase, and LDL-apheresis for managing fibrinogen levels.
Abstract:
Seven prospective, epidemiological studies indicate plasma fibrinogen levels (over 300-350 mg/dl) as an important, independent cardiovascular risk factor for subsequent myocardial infarction and stroke. Furthermore, several clinical studies revealed an association between fibrinogen and both the angiographic and clinical degree of coronary heart disease. In addition, a significant relation of fibrinogen with the number of occluded coronary vessels was found. The following pathophysiologic mechanism are of particular importance: Fibrinogen is a main determinant of plasma viscosity and red cell aggregation. Both phenomena deteriorate blood fluidity especially in the microcirculation. Fibrinogen plays a central role in platelet aggregation and performs an essential substrate in the coagulation cascade. Thus, high fibrinogen levels may favor a hypercoagulable state resulting in final thrombotic events of cardiovascular disease. Fibrinogen is also involved in atherogenesis by stimulating proliferation and migration of smooth muscle cells. Several determinants of fibrinogen levels are known. Smoking is the strongest one in healthy persons. This clinically important effect is dose related. Consequently, cessation of smoking is a major step to lower fibrinogen and subsequently the individual cardiovascular risk. Reduction of overweight and maintenance of regular physical activity are further nonpharmacologic means. Fibrates decrease fibrinogen about 10-30% on an average. Finally, intermittent low-dose Urokinase for end-stages of coronary artery disease and LDL-apheresis (HELP) represent additional approaches to reduce fibrinogen.
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