Background and Aim Asymmetric dimethylarginine(ADMA),an endogenous inhibitor of nitric oxide synthase(NOS),has been shown to be an independent predictor of coronary heart disease(CHD).Dimethylarginine dimethylaminohydrolase-2(DDAH2) promotes the metabolism of ADMA and plays a key role in formation of the atherosclerosis.We hypothesized that genetic variation inDDAH2 gene might alter the susceptibility to CHD.Methods We tested our hypothesis in a case-control studies.We used ahaplotype-tagging single nucleotide polymorphisms(SNP) approach to identify tag SNP in DDAH2.The SNP were genotyped by poly-merase chain reaction-restriction fragment length polymorphism(PCR-RFLP) and ligase detection reaction(LDR)-sequencing in 1650patients with CHD and 1920 control subjects.Results Apromoter variant-449C/G(rs805305) and -1415G/A(rs2272592)in DDAH2 was identified in the region containing DDAH2.The frequency of those polymorphism were consistent with the lawof Har-dy-Weinberg.The frequency of rs805305 CG +GG or G allele was not significantly different between CHD and wild-type genotype(OR: 0.667,95%CI: 0.374 to 1.187,p>0.05).The frequency of rs2272592 GA +AA or A allele also showed no significant difference between CHD and wild-type genotype(OR: 1.420,95%CI: 0.899 to 2.242,p>0.05).No association was observed be-tween the DDAH2 variant and CHD.These results was independent of age,gender,hypertension,diabetes and hyperlipidemia.Conclusions Our results suggest that although DDAH2/ADMA pathway acts as a critical regulator of coronary atherosclerotic heartdisease,the DDAH2 common variant may not predict the susceptibility to CHD in Chinese population.