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European Heart Journal 2002 23(16):1276-1281; doi:10.1053/euhj.2001.3117
Copyright © 2002 by the European Society of Cardiology.
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Elevated fibrinogen in the healthy male relatives of patients with severe, premature coronary artery disease

J.D. Millsf1, M.W. Mansfield and P.J. Grant

Academic Unit of Molecular Vascular Medicine, University of Leeds, U.K.

Received October 30, 2001; accepted November 21, 2001

Abstract

Aims To assess the possible role of certain coagulation factors and associated genetic polymorphisms in families in which coronary disease has occurred prematurely.

Methods and Results One hundred and eighty-five healthy male relatives aged 65 or less were recruited following the identification of 125 patients with confirmed, premature coronary artery disease and compared to a control group of 185 healthy, age-matched volunteers. None of the control subjects had a personal or family history of coronary artery disease. The relatives and controls were similar in terms of conventional coronary artery disease risk factors. Fibrinogen levels were elevated in relatives compared with controls and remained higher after adjustment for significant correlates, 3·0g.l–1 (2·9–3·1) vs 2·8g.l–1 (2·8–2·9),P =0·004. Factor VII coagulant activity and von Willebrand factor antigen did not differ between the groups nor were there any differences in genotype frequency for the fibrinogen Bß-455 G/A polymorphism or the factor VII promoter deletion/insertion and Arg-Gln coding polymorphisms.

Conclusions A significant increase in fibrinogen levels was demonstrated in the healthy, male, first-degree relatives of patients with severe coronary artery disease. Fibrinogen may be of particular importance in subjects who, other than their family history, appear to be at low risk in terms of conventional coronary artery disease risk factors. Copyright 2002 The European Society of Cardiology Published by Elsevier Science Ltd. All rights reserved.

Key Words: Family history, coronary artery disease, fibrinogen, factor VII, von Willebrand factor

f1 Correspondence: Dr Joseph D. Mills, Academic Unit of Molecular Vascular Medicine, G Floor, Martin Wing, Leeds General Infirmary, Leeds LS1 3EX, U.K.


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