OBJECTIVE: Matrix metalloproteinases, such as gelatinase B, are important in connective tissue remodelling processes associated with atherogenesis and plaque rupture. The T allele of the gelatinase B C((-1562)) T polymorphism has been reported to be associated with an almost 2-fold increase in promoter activity and with the extent of coronary artery disease (CAD). The aim of this study was to analyse the relation of this gene variation to the risk and severity of CAD and the risk of myocardial infarction (MI). MATERIAL AND METHODS: This case-control study comprised 535 healthy controls and 2731 participants who had undergone coronary angiography. RESULTS: In the total sample, the gelatinase B promoter polymorphism was not associated with the risk of CAD and MI or with the extent of CAD defined either by the number of diseased coronary arteries or--in patients with coronary angiography--by a score for coronary heart disease (CHD) according to the Gensini score. However, patients with TT genotype had higher CHD scores than the other genotypes in subgroups of individuals with high apolipoprotein B levels, high lipoprotein (a) plasma concentrations and high fibrinogen levels, or with combinations of increased levels of these coronary risk factors. These observations were made in the entire sample of individuals with coronary angiography and in the population of patients with documented CHD. CONCLUSIONS: Obviously, the gelatinase B C((-1562))T gene polymorphism is not a risk indicator for CAD and MI. With respect to the extent of CHD, the impact of this gene variation may be restricted to individuals with high apolipoprotein B, lipoprotein (a) and/or fibrinogen levels.
OBJECTIVE: Matrix metalloproteinases, such as gelatinase B, are important in connective tissue remodelling processes associated with atherogenesis and plaque rupture. The T allele of the gelatinase B C((-1562)) T polymorphism has been reported to be associated with an almost 2-fold increase in promoter activity and with the extent of coronary artery disease (CAD). The aim of this study was to analyse the relation of this gene variation to the risk and severity of CAD and the risk of myocardial infarction (MI). MATERIAL AND METHODS: This case-control study comprised 535 healthy controls and 2731 participants who had undergone coronary angiography. RESULTS: In the total sample, the gelatinase B promoter polymorphism was not associated with the risk of CAD and MI or with the extent of CAD defined either by the number of diseased coronary arteries or--in patients with coronary angiography--by a score for coronary heart disease (CHD) according to the Gensini score. However, patients with TT genotype had higher CHD scores than the other genotypes in subgroups of individuals with high apolipoprotein B levels, high lipoprotein (a) plasma concentrations and high fibrinogen levels, or with combinations of increased levels of these coronary risk factors. These observations were made in the entire sample of individuals with coronary angiography and in the population of patients with documented CHD. CONCLUSIONS: Obviously, the gelatinase B C((-1562))T gene polymorphism is not a risk indicator for CAD and MI. With respect to the extent of CHD, the impact of this gene variation may be restricted to individuals with high apolipoprotein B, lipoprotein (a) and/or fibrinogen levels.