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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
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Polymorphisms of factor V, factor VII, and fibrinogen genes. Relevance to severity of coronary artery disease

X L Wang1, J Wang, R M McCredie

  • 1Department of Cardiovascular Medicine, University of New South Wales, Prince Henry/Prince of Wales Hospitals, Sydney, Australia. X.L.Wang@unsw.EDU.AU

Arteriosclerosis, Thrombosis, and Vascular Biology
|February 1, 1997
PubMed

Insights

Elevated fibrinogen levels correlate with more severe coronary artery disease (CAD). Genetic variants in factor V, factor VII, and fibrinogen genes did not predict CAD severity, but smoking dose significantly increased fibrinogen levels.

Area of Science:

  • Cardiovascular Genetics
  • Thrombosis and Hemostasis

Background:

  • Coronary artery disease (CAD) is a significant health concern.
  • Genetic factors and clotting proteins like fibrinogen play roles in atherogenesis.
  • The predictive value of specific gene variants for CAD severity requires further investigation.

Purpose of the Study:

  • To investigate the association between factor V, factor VII, and fibrinogen gene polymorphisms and the severity of coronary artery disease (CAD).
  • To assess the relationship between these genetic variants, circulating fibrinogen levels, and other atherogenic risk factors, including smoking.
  • To determine if genetic variants predict angiographically assessed CAD severity.

Main Methods:

  • A cohort of 545 white Australian patients (aged <= 65 years) underwent angiographic assessment for CAD severity.
  • Genotyping was performed for factor V (G-->A), factor VII (G-->A), and fibrinogen (Hae III polymorphism).
  • Associations between genotypes, circulating fibrinogen levels, smoking history (pack-years), and CAD severity (number of diseased vessels) were analyzed.

Main Results:

  • Elevated circulating fibrinogen levels were significantly associated with more severe CAD (P < .05).
  • No significant association was found between factor V, factor VII, or fibrinogen DNA variants and CAD severity.
  • A strong positive correlation existed between lifetime smoking dose (pack-years) and fibrinogen levels (r = .184, P = .001), indicating a dosage effect.
  • Fibrinogen genotype did not significantly contribute to circulating fibrinogen levels in this population.

Conclusions:

  • Elevated fibrinogen levels are linked to both the occurrence and severity of CAD.
  • The specific genetic variants of factor V, factor VII, and fibrinogen assessed do not appear to predict CAD severity beyond circulating fibrinogen levels.
  • Smoking history, particularly lifetime dose, has a significant dosage-dependent effect on circulating fibrinogen levels, independent of genotype.

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