Title
Elevated plasma fibrinogen: Cause or consequence of cardiovascular disease?
Author
van der Bom, J.G.
de Maat, M.P.M.
Bots, M.L.
Haverkate, F.
de Jong, P.T.V.M.
Hofman, A.
Kluft, C.
Grobbee, D.E.
Gaubius Instituut TNO
Publication year
1998
Abstract
An association between increased plasma fibrinogen and an increased risk for myocardial infarction (MI) is well established, but the nature of this association is subject to debate. Our aim was to shed light on the potentially causal nature of this association. We examined whether increased plasma fibrinogen, due to a condition that is independent of cardiovascular events, also increases the risk for MI. A case-control study was performed in 139 subjects with a history of MI and 287 control subjects selected from the Rotterdam Study, a population-based cohort of 7983 subjects aged 55 years and older. The genotype of the -455G/A polymorphism in the fibrinogen β-gene was determined by polymerase chain reaction. Functional-plasma fibrinogen levels were determined according to yon Clauss. The plasma level of fibrinogen was significantly higher in subjects with one or two A alleles compared with subjects with the GG genotype: 3.8 (95% confidence interval [CI], 3.6 to 3.9) g/L and 3.6 (3.5 to 3.7) g/L, respectively. With increasing plasma fibrinogen level, the risk for MI increased gradually; a rise in fibrinogen of 1 g/L was associated with a 45% increased risk (odds ratio adjusted for age, sex, and smoking, 1.45; 95% CI, 1.12 to 1.88). There was no association between the genotype of the -455G/A polymorphism and the risk for MI. The -455G/A polymorphism is therefore associated with increased plasma fibrinogen levels but not with an increased risk for MI. These findings indicate that an increased plasma fibrinogen level due to this genetic factor does not increase the risk for MI.
Subject
Health
β- fibrinogen gene
-455G/A polymorphism
Cardiovascular disease risk
HaeIII polymorphism
Thrombotic tendency
Aged
Blood Pressure
Cardiovascular Diseases
Case-Control Studies
Cholesterol
Cholesterol, HDL
Cross-Sectional Studies
Female
Fibrinogen
Genotype
Humans
Male
Middle Aged
Myocardial Infarction
Polymerase Chain Reaction
Polymorphism, Genetic
Risk Factors
Smoking
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DOI
https://doi.org/10.1161/01.atv.18.4.621
TNO identifier
234449
ISSN
1079-5642
Source
Arteriosclerosis, Thrombosis, and Vascular Biology, 18 (4), 621-625
Document type
article