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Thromb Haemost 1998; 79(02): 400-404
DOI: 10.1055/s-0037-1614999
Letters to the Editor
Schattauer GmbH

Fibrinogen, Plasminogen Activator Inhibitor-1, and Carotid Intima-Media Wall Thickness in the NHLBI Family Heart Study

Aaron R. Folsom
1   Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN
,
James S. Pankow
2   Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, NC
,
Roger R. Williams
3   Cardiovascular Genetics, University of Utah, Salt Lake City, UT
,
Gregory W. Evans
4   Department of Public Health Sciences, Bowman Gray School of Medicine, Winston-Salem, NC
,
Michael A. Province
5   Division of Biostatistics, Washington University, St. Louis, MO
,
John H. Eckfeldt
6   Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN, USA
› InstitutsangabenSupport was provided by National Heart, Lung, and Blood Institute contracts N01-HC-25104, N01-HC-25105, N01-HC-25106, N01-HC-25107, N01-HC-25108, and N01-HC-25109, and institutional training grant T32 HL07036.
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Publikationsverlauf

Received 16. Juni 1997

Accepted after revision 17. September 1997

Publikationsdatum:
08. Dezember 2017 (online)

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Summary

Several studies have linked higher plasma fibrinogen and plasminogen activator inhibitor (PAI-1) concentrations with increased risk of cardiovascular disease. We studied whether members of families with increased occurrence of coronary heart disease (CHD) have increased levels of fibrinogen and PAI-1 and whether subclinical carotid atherosclerosis is associated with these two hemostatic factors. Contrary to our hypothesis, fibrinogen and PAI-1 antigen levels were not different between high CHD risk families versus random families. Adjusted for age and family type, fibrinogen and PAI-1 were both associated positively with carotid intima-media thickness assessed by B-mode ultrasound. However, adjustment for lifestyle and medical covariates essentially eliminated these associations. These data suggest 1) elevated fibrinogen and PAI-1 do not explain clustering of CHD in families and 2) fibrinogen and PAI-1 may partly mediate the effects of other risk factors on carotid atherosclerosis, though the data are also consistent with them playing no causal role.

 

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