Association study of dimethylarginine dimethylaminohydrolase 2 gene polymorphisms and coronary heart disease

While a number of genetic and environmental risk factors for coronary heart disease (CHD) have been identified, the list of potential risk factors remains long. One candidate is dimethylarginine dimethylaminohydrolase (DDAH2), which is known to be polymorphic in humans. The gene product indirectly increases the endogenous production of nitric oxide, an anti-atherogenic molecule. Therefore, alterations in DDAH2 activity may indirectly result in an increased risk of CHD. We studied allele and genotype distributions for two polymorphic loci of DDAH2, rs805305 and rs2272592, in 180 patients with CHD and 180 healthy controls. Disease history and other clinical data were recorded. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to determine the genotype at rs805305, and ligase detection reaction (LDR) was used to determine the genotype at rs2272592. Systolic blood pressure and blood triglyceride and glucose levels were higher, and history of hypertension, diabetes, smoking and alcohol use was more common in the patients with CHD (P<0.05). However, the genotype and allele frequencies at the two polymorphic loci of DDAH2 were not statistically different between the two groups. Therefore, no association was observed between the DDAH2 polymorphisms at rs805305 and rs2272592 and CHD.