Association study of the thrombomodulin −33G>A polymorphism with coronary artery disease and myocardial infarction in Chinese Han population

Background Thrombomodulin (TM) is the anticoagulant endothelial cell membrane-bound protein cofactor in the thrombin-mediated activation of protein C. Recently, conflicting data have been reported regarding the possible contribution of the TM −33G>A polymorphism to coronary artery disease (CAD) or myocardial infarction (MI) in some Asian populations. We investigated this polymorphism in northern Han Chinese. Methods We performed a case-control study, including 808 patients with angiographically verified CAD or a history of an acute MI and 813 age- and sex-matched controls. The TM −33G>A polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism (PCR–RFLP) analysis. Results We did not find a significant difference in the frequency of the A allele between CAD patients (11%) and controls (9.8%; P=0.249), between MI patients (11.5%) and controls (P=0.163), or between premature MI patients (11.7%) and controls (P=0.265). Similarly, the difference of the genotypic distributions could be neglected across the groups: GG: (GA/AA) was 81.4%:18.6% in controls, 79.7%:20.3% in patients with CAD, 78.8%:21.2% in patients with MI, and 77.7%:22.3% in patients with premature MI, respectively (vs. controls, all P>0.05). The lack of association also persisted after adjusting for other conventional risk factors. Conclusions Our results seemed not to support a significant association of the TM −33G>A polymorphism with CAD, MI or premature MI in our population.