Background Inflammation plays an important role in coronary artery disease (CAD). Complement Factor H (CFH) gene has been analyzed in relation to CAD in several studies with conflicting results. The aim of the present study was to investigate the association between the CFH Y402H polymorphism and CAD in Chinese. Methods and results About 336 patients were enrolled, included 166 patients with CAD and 170 controls. The SNP at CFH Y402H was genotyped by ligase detection reaction and plasma levels of CFH were assayed by enzyme-linked immunosorbent assay. Analysis of genotype frequencies did not reveal any significant difference between CAD patients and controls. There were significant differences in the frequencies of C allele and C allele carriers between early-onset CAD and controls. After adjustment of clinical parameters, significant association was identified for CFH Y402H polymorphism, with C allele carriers having a higher risk of early-onset CAD than carriers of TT genotype (odds ratio [OR] 4.66, 95% CI: 1.23-17.62, P=0.02). There was no difference of plasma CFH levels between CAD group and controls. Conclusions CFH Y402H polymorphism is associated with early-onset CAD in Chinese.

Toll-like receptors (TLRs) play roles in innate and adaptive immune responses. Some TLRs are involved in the pathogenesis of cardiovascular diseases. Coronary artery disease (CAD) has an inflammatory and immunological basis. We investigated whether TLR8 Met1Val and TLR8-129G＞C single nucleotide polymorphisms (SNPs rs3764879 and rs3764880) are associated with CAD in the Chinese population. We enrolled 412 consecutive patients (185 with coronary stenosis ≥50% or previous myocardial infarction and 227 controls). Ligase detection reaction was performed to detect SNPs rs3764879 and rs3764880 of TLR8. The SNP at rs3764879 is in complete linkage disequilibrium with rs3764880. No significant difference was found in genotypic or allelic frequencies of these two common SNPs between CAD cases and controls (P＞0.05, respectively). No associations existed between these two SNPs and the severity of coronary artery stenosis (All P＞0.05). These results do not support an involvement of SNPs rs3764879 and rs3764880 of TLR8 in predisposition to CAD.

Objective: Tetramethylpyrazine, a drug originally isolated from the rhizome of Ligusticum walliichi, is an inhibitor of phosphodiesterase and inhibits platelet aggregation and smooth muscle cell proliferation. The effect of the tetramethylpyrazine-eluting stent (TES) on preventing in-stent restenosis was investigated in comparison with control bare metal stents in a porcine coronary stent restenosis model. Methods: The TES was prepared by spray-coating the 2.5 to 3.0mm×15 to 20mm bare metal stents with Tetramethylpyrazine monomer, methyl methacrylate copolymer, and polyglycolic acid. Stent overdilation injury (stent:artery=1.1 to 1.2:1.0) was made with control bare stents (n=5) and TES (n=5) in porcine coronary arteries. Follow-up quantitative coronary angiography (QCA) and histopathological assessments of stented coronary arteries were performed 4 weeks after stenting. Results: Quantitative coronary angiography showed the late lumen loss (0.28±0.08mm versus 1.70±0.52mm; P=0.004) and percentage diameter stenosis (10.0±2.1% versus 60.2±23.5%; P=0.01) were significantly lower in the TES group than that in the control group. Histopathological assessments of stented coronary arteries showed that the injury score and the in-stent area were similar between the groups (P＞0.05), whereas the lumen area was significantly larger (4.34±0.93 mm2 versus 1.29±1.02mm2; P=0.011) in the TES group than that in the control group. The number of proliferating cell nuclear antigen-positive cells was also significantly decreased in the TES group compared with the control group (14.7±2.5% versus 23.6±3.2%; P=0.008). Moreover, apoptosis was enhanced in TES group while regrowth of endothelium was similar between the groups. Conclusions: TES inhibited the neointimal hyperplasia and reduced in-stent restenosis in a porcine coronary artery restenosis model.

Background We examined the -2518G/A polymorphism of the MCP-1 gene, its plasma levels, and premature stableCADin a Chinese population. Methods The study comprised 132 patients with premature stable CAD (cases) and 153 controls. Genotypes were determined by ligase detection reaction-polymerase chain reaction sequencing and grouping. Plasma MCP-1 level was detected with enzyme-linked immunosorbent assay. Results No differences were found between genotype distribution and allele frequencies of MCP-1 gene -2518 G/A polymorphism (AA:18.1%; AG:51.5%; GG:30.3% in cases; AA:16.3%; AG:52.9%; GG:30.7% in controls; P=0.918). The G allele prevalence was 0.561 in cases and 0.572 in controls (P=0.786). No significant difference was found in plasma MCP-1 level between cases and controls [(47.50±26.65) vs. (41.05±15.71)pg/ml, P=0.272)] or among the 3 genotypes [AA, (43.49±10.50) pg/ml; AG, (46.09±25.08)pg/ml; GG, (40.03±18.13)pg/ml; P=0.381]. Logistic regression analysis confirmed the lack of association between MCP-1-2518 G/A single nucleotide polymorphism and premature stable CAD after adjustment for confounding parameters. Conclusions The MCP-1-2518 G/A single nucleotide polymorphism does not affect plasma levels of MCP-1 or susceptibility to premature stableCADin a Chinese population.