Thromb Haemost 1998; 80(01): 134-139
DOI: 10.1055/s-0037-1615152
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Correlates of Antithrombin, Protein C, Protein S, and TFPI in a Healthy Elderly Cohort

Pamela A. Sakkinen
1   Depts of Pathology and Biochemistry
,
Mary Cushman
2   Depts of Medicine and Pathology, University of Vermont
,
Bruce M. Psaty
3   Depts of Medicine, Epidemilogy and Health Services, University of Washington, Seattle, Washington
,
Lewis H. Kuller
4   Dept of Epidemiology, University of Pittsburgh
,
S. Paul Bajaj
5   Depts of Medicine and Biochemistry
,
Arun K. Sabharwal
6   Dept of Biochemistry, St. Louis University
,
Robin Boineau
7   Division of Epidemiology and Clinical Applications, NHLBI, NIH, Bethesda, MD
,
Elizabeth Macy
8   Dept of Pathology, University of Vermont, USA
,
Russell P. Tracy
1   Depts of Pathology and Biochemistry
› Institutsangaben
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Publikationsverlauf

Received 24. November 1997

Accepted after revision 19. Februar 1998

Publikationsdatum:
08. Dezember 2017 (online)

Summary

The majority of fatal acute myocardial infarctions occur in the elderly. Since these events are predominantly thrombotic, we studied the cross-sectional associations of the anticoagulant proteins Anti-thrombin, Protein C, Protein S, and Tissue Factor Pathway Inhibitor (TFPI) in a subgroup (n = 400) of the Cardiovascular Health Study (a study of healthy men and women ≥65 years) free of clinical cardiovascular disease (CVD).

We did not observe any strong age-associated trends, although Protein C was lower in older women (p ≤0.001), and TFPI was higher in older men (p ≤0.01). The inhibitors were highly intercorrelated, and were associated with increased levels of inflammation-sensitive proteins (e.g., fibrinogen, plasminogen), lipids (especially total and LDL-cholesterol), and coagulation factors, such as Factors VIIc, IXc, and Xc. None was associated with the procoagulant markers Prothrombin Fragment F1-2 or Fibrinopeptide A. Only TFPI was associated with subclinical atherosclerosis: ankle-arm index and internal carotid artery stenosis, p trend ≤0.01; and carotid wall thickness, p trend ≤0.05. In multivariate analysis the independent predictors of TFPI were levels of fibrinogen; the fibrinolytic marker plasminantiplasmin complex; LDL-cholesterol; and carotid wall thickness (R2 for the model = 0.35).

In summary, the inhibitors did not appear to increase with age, and were predominantly associated with inflammation markers and lipids. Since markers of thrombin production do increase with age, we hypothesize that an age-related hemostatic imbalance may ensue, with associated increased thrombotic risk. Only TFPI was associated with subclinical CVD, suggesting that it may more closely reflect endothelial damage. (250)

 
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