Print Email Facebook Twitter Elevated plasma fibrinogen: Cause or consequence of cardiovascular disease? 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 Healthβ- fibrinogen gene-455G/A polymorphismCardiovascular disease riskHaeIII polymorphismThrombotic tendencyAgedBlood PressureCardiovascular DiseasesCase-Control StudiesCholesterolCholesterol, HDLCross-Sectional StudiesFemaleFibrinogenGenotypeHumansMaleMiddle AgedMyocardial InfarctionPolymerase Chain ReactionPolymorphism, GeneticRisk FactorsSmoking To reference this document use: http://resolver.tudelft.nl/uuid:ccb787fd-3710-4858-9df7-748d46e2c453 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 Files To receive the publication files, please send an e-mail request to TNO Library.