title: Association of fibrinogen with cardiovascular risk factors and cardiovascular disease in the Framingham Offspring Population.
abstract: BACKGROUND
  Fibrinogen has been identified as an independent risk factor for cardiovascular disease and associated with traditional cardiovascular risk factors. Also, the role of elevated fibrinogen in thrombosis suggests that it may be on the causal pathway for certain risk factors to exert their effect. These associations remain incompletely characterized. Moreover, the optimal fibrinogen assay for risk stratification is uncertain.
  
  
  RESULTS
  In 2632 subjects from cycle 5 of the Framingham Offspring Population, fibrinogen levels were determined with a newly developed immunoprecipitation test (American Biogenetic Sciences) and the functional Clauss method. With the immunoprecipitation method, there were significant linear trends across fibrinogen tertiles (P:<0.001) for age, body mass index, smoking, diabetes mellitus, total cholesterol, HDL cholesterol, and triglycerides in men and women. The Clauss method had significant results (P:<0.030), except for triglycerides in men. Fibrinogen levels were higher for those with compared with those without cardiovascular disease. After covariate adjustment, fibrinogen remained significantly higher in those with cardiovascular disease with the use of the immunoprecipitation test (P:=0.035 and P:=0.018 for men and women, respectively) but not with the Clauss method.
  
  
  CONCLUSIONS
  Fibrinogen was associated with traditional cardiovascular risk factors. Elevation of fibrinogen may provide a mechanism for risk factors to exert their effect. Also, fibrinogen levels were higher among subjects with cardiovascular disease compared with those without disease. The immunoprecipitation test showed a stronger association with cardiovascular disease than the Clauss method, suggesting that it may be a useful screening tool to identify individuals at increased thrombotic risk.
authors.affiliation: Institute for Prevention of Cardiovascular Disease, Cardiovascular Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
authors.forename: J J
authors.initials: JJ
authors.lastname: Stec
authors.forename: H
authors.initials: H
authors.lastname: Silbershatz
authors.forename: G H
authors.initials: GH
authors.lastname: Tofler
authors.forename: T H
authors.initials: TH
authors.lastname: Matheney
authors.forename: P
authors.initials: P
authors.lastname: Sutherland
authors.forename: I
authors.initials: I
authors.lastname: Lipinska
authors.forename: J M
authors.initials: JM
authors.lastname: Massaro
authors.forename: P F
authors.initials: PF
authors.lastname: Wilson
authors.forename: J E
authors.initials: JE
authors.lastname: Muller
authors.forename: R B
authors.initials: RB
authors.lastname: D'Agostino
mesh_terms: D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism*; D015331:Cohort Studies; D005260:Female; D005340:Fibrinogen / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D005340:Fibrinogen