Genotype frequency of gelatinase B C-1562 T polymorphism in coronary heart disease and myocardial infarction

Background One of the characteristics of atherosclerosis is a change in the content of extracellular matrix in the arterial wall. Gelatinase B, a member of the family of matrix metalloproteinase, can regulate extracellular matrix metabolism and play a role in the pathogenesis of atherosclerosis, coronaiy heart disease (CHD) and myocardial infarction (MI). Gelatinase B is polymorphic due to a C to T change at the position -1562 bp in the promoter region. Its relationship with gene product concentration in serum and its role in mediating the risk of CHD and MI in Germans is still unknown. Methods We enrolled 102 controls and 322 patients with angiographically documented CHD, including a sub-group of 173 patients with acute or chronic MI and 80 patients with acute coronary syndrome (ACS). All patients and controls were Germans and genotyped by polymerase chain reaction and digestion with SphI. Results We found that several classical risk factors for CHD and MI, including hypercholesterolemia and cigarette smoking, were significantly increased in CHD and MI patients compared with controls. Serum levels of gelatinase B and tissue inhibitor of metalloproteinase-1 were increased in the peripheral blood of patients with acute coronary syndrome. No significant differences in genotype or allelic frequencies between CHD, MI and control subjects of either men or women were found. Our search for a possible association of the polymorphisms with CHD and MI by logistic regression analysis was also negative. The serum concentrations of gelatinase B showed no differences between genotypes. Conclusions Our data showed that gelatinase B might provide an index of plaque activity in ACS, but gelatinase B protein was not affected by genotypes. Also, the T variant of gelatinase B was not associated with CHD or MI in Germans.