Fibrinogen As a Cardiovascular Risk Marker

Authors

• André Luis Valera Gasparoto Intensive Care Unit, BP - A Beneficência Portuguesa de São Paulo, São Paulo – Brazil
• Tania Leme da Rocha Martinez, Anita L. R. Saldanha, Ana Paula Pantoja Margeotto Nephrology Department, BP - A Beneficência Portuguesa de São Paulo, São Paulo, Brazil

Abstract

International comparations show that the level of fibrinogen increases with the national risk of ischemic heart disease except in rural Africa and Eskimos who have high levels of fibrinogen despite the low risk of ischemic heart disease. Fibrinogen is a probable cofactor of multi factorial disease, atherosclerosis in cardiovascular disease. Epidemiological studies have shown that fibrinogen levels are a strong and consistent primary and secondary risk factor for coronary artery disease, cerebral and peripheral arterial disease, as well as is associated with prevalence of arterial disease in these three sites. Epidemiological studies also suggest that fibrinogen may be an important link between genetics (difference in nationality, family history, fibrinogen genotype) and environmental influences (fetal development, smoking, alcoholism, obesity, diabetes, infections, menopause, estrogen use) and the development of arterial disease. Fibrinogen level is the major determinant of cardiovascular risk in people with hypercholesterolemia, hypertension or diabetes; should then be included in the cardiovascular risk profile and clinical management. Persistent fibrinogen greater than 3.0 g/L is associated with significant increase in cardiovascular risk and indicates the target population for intervention. Epidemiological and path physiological studies show that there are at least four possible mechanisms by which fibrinogen can promote arterial disease: atherogenesis, platelet aggregation and thrombus formation, fibrin thrombus formation, increased plasma and blood viscosity. Clinical studies have shown that reducing plasma fibrinogen increases blood flow, reduces platelet aggregability, reduces plasma and blood viscosity, and the risk of ischemic symptoms and events. The reduction of fibrinogen needs to be considered in people with ischemic symptoms and those at high risk of arterial disease, also by lifestyle (smoking) or drug therapy (fibrates). Further studies of fibrinogen reduction are desirable for prevention and symptomatic treatment of arterial disease.