The factor II G20210A and factor V G1691A gene transitions and coronary heart disease

Background: G to A transitions at nucleotide position 20210 of the factor I I (Fn) gene and at 1691 of the factor V (FV) gene have been shown to be ass ociated with an increased risk of venous thrombosis. Since it is still uncl ear whether both gene variations are also related to an increased risk of c oronary heart disease (CHD), we studied the relation of both gene variation s to coronary artery disease (CAD) and myocardial infarction (MI) in a samp le of 2210 male individuals whose coronary anatomy were defined by coronary angiography. Results: In the total sample, the FII G20210A gene variation was not associ ated with the presence or the extent of CAD, the latter defined either by t he degree of vessel disease or by a CHD score according to Gensini. However , individuals with unfavourable lipid profiles showed pronounced difference s in CHD scores between GA heterozygotes and GG homozygotes; this observati on applied in particular to younger patients (<62 years; mean age of total sample) who simultaneously had low apoAI/apoB ratios (< 1.19, mean value) a nd high Lp(a) plasma levels (>28 mg/dl; mean value). In addition, in subjec ts without acetylsalicylic acid treatment GA heterozygotes had clearly high er CHD scores than AA genotypes. Further restriction to smokers, to subject s 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 increa se the difference in CHD score between FII G20210A genotypes. An associatio n of the FII G20210A gene variation with non-fatal 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 ex tent 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 facto r 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 r isk of CHD.