The Factor II G20210A and Factor V G1691A Gene Transitions and Coronary Heart Disease

Andreas Gardemann; Tanja Arsic; Norbert Katz; Harald Tillmanns; Friedrich Wilhelm Hehrlein; Werner Haberbosch

doi:10.1055/s-0037-1614444

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1999; 81(02): 208-213
DOI: 10.1055/s-0037-1614444

Review Articles

Schattauer GmbH

The Factor II G20210A and Factor V G1691A Gene Transitions and Coronary Heart Disease

Autor*innen

Andreas Gardemann

¹From the Institut für klinische Chemie und Pathobiochemie, Gießen, Germany
Tanja Arsic

¹From the Institut für klinische Chemie und Pathobiochemie, Gießen, Germany
Norbert Katz

¹From the Institut für klinische Chemie und Pathobiochemie, Gießen, Germany
Harald Tillmanns

²Abteilung Kardiologie und Angiologie, Gießen, Germany
Friedrich Wilhelm Hehrlein

³Klinik für Herz- und Gefäßchirurgie der Justus-Liebig-Universität Gießen, Gießen, Germany
Werner Haberbosch

⁴Max-Planck-Institut für experimentelle und klinische Forschung, Kerckhoff-Klinik, Bad Nauheim, Germany

Abstract

Summary

Background: G to A transitions at nucleotide position 20210 of the factor II (FII) gene and at 1691 of the factor V (FV) gene have been shown to be associated with an increased risk of venous thrombosis. Since it is still unclear whether both gene variations are also related to an increased risk of coronary heart disease (CHD), we studied the relation of both gene variations to coronary artery disease (CAD) and myocardial infarction (MI) in a sample of 2210 male individuals whose coronary anatomy were defined by coronary angiography.

Results: In the total sample, the FII G20210A gene variation was not associated with the presence or the extent of CAD, the latter defined either by the degree of vessel disease or by a CHD score according to Gensini. However, individuals with unfavourable lipid profiles showed pronounced differences in CHD scores between GA heterozygotes and GG homozygotes; this observation applied in particular to younger patients (<62 years; mean age of total sample) who simultaneously had low apoAI/apoB ratios (< 1.19, mean value) and high Lp(a) plasma levels (>28 mg/dl; mean value). In addition, in subjects without acetylsalicylic acid treatment GA heterozygotes had clearly higher CHD scores than AA genotypes. Further restriction to smokers, to subjects with high fibrinogen plasma levels (>3.47 g/l; mean value) or to patients with high glucose concentrations (>112 mg/dl; mean value) tended to increase the difference in CHD score between FII G20210A genotypes. An association of the FII G20210A gene variation with nonfatal MI was not observed. In the total sample and in high and low risk subpopulations, an association of the FV G1691A gene variation was not detected neither with presence and extent of CAD or with nonfatal MI.

Conclusion: The importance of the factor II G20210A gene variation for CHD may be restricted to individuals with major cardiovascular risk factors. In addition, the present study did not strengthen the hypothesis of the factor V G1691A transition as a risk factor of coronary heart disease neither in the total sample nor in subgroups of individuals who were at high or low risk of CHD.

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Referenzen

References
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