Thromb Haemost 2002; 87(04): 614-621
DOI: 10.1055/s-0037-1613057
Review Article
Schattauer GmbH

No Association of Plasma Prothrombin Concentration or the G20210A Mutation with Incident Cardiovascular Disease

Results from the Cardiovascular Health Study

Authors

  • Adam M. Smiles

    1   Department of Pathology, College of Medicine, University of Vermont, Burlington, VT
  • Nancy S. Jenny

    1   Department of Pathology, College of Medicine, University of Vermont, Burlington, VT
  • Zhonghua Tang

    1   Department of Pathology, College of Medicine, University of Vermont, Burlington, VT
  • Alice Arnold

    2   Department of Biostatistics, University of Washington, Seattle, WA
  • Mary Cushman

    1   Department of Pathology, College of Medicine, University of Vermont, Burlington, VT
    3   Department of Medicine, College of Medicine, University of Vermont, Burlington, VT
  • Russell P. Tracy

    1   Department of Pathology, College of Medicine, University of Vermont, Burlington, VT
    4   Department of Biochemistry, College of Medicine, University of Vermont, Burlington, VT, USA
Further Information

Publication History

Received 18 May 2001

Accepted after resubmission 29 November 2001

Publication Date:
08 December 2017 (online)

Preview

Summary

Prothrombin is a key factor in blood clotting, a process intimately involved in thrombotic disease. We assessed prothrombin levels and G20210A genotype in a case-control study within the Cardiovascular Health Study. Cases included angina, myocardial infarction, stroke, and the presence of MRI-detectable infarcts (n ≈ 250 each). Populationbased controls free of clinical cardiovascular disease (CVD) (n ≈ 500) and a subset free of clinical and subclinical CVD (n ≈ 250) were used for comparison. The 20210 A allele, frequency 2.9%, was associated with higher mean prothrombin levels: 166.3 vs. 139.5 µg/ml (P <0.001). Significant correlates of prothrombin included gender, plasma lipids, other vitamin K-dependent proteins, and inflammatory markers, but not race, smoking, hypertension, diabetes, measures of subclinical CVD, or markers of procoagulant activity. Compared to controls, neither genotype nor prothrombin level was associated with any CVD case group. We conclude that, in the elderly, neither prothrombin level nor 20210 genotype were associated with either CVD risk factors or events. This is consistent with the lack of association of prothrombin levels with measures of underlying CVD or procoagulant markers.