Evaluating the frequency of ER2 polymorphisms in coronary heart disease patients and healthy controls

Background: The leading cause of mortality and rising healthcare costs globally is coronary heart disease (CHD). Interactions between environmental and genetic variables may be the cause of CHD. Research on the role of several genes in the etiology of coronary heart disease is still underway. The estrogen receptor 2 (ER2) gene, which is present in the layers of the vessel wall in the vasculature, is one of the genes thought to be related to CHD. Aim: The objective is to evaluate the rs1271572 A/T SNP of the ER2 gene's connection with CHD in a sample of Iraqis and investigate how gender affects the onset of the illness. Method: A sample of CHD patients and a group of healthy people were the subjects of a case-control study. Participants' serum lipid levels were assessed, and T-ARMS was used to genotype the ER2 gene, rs1271572 A/T SNP. Results: The carriers of the variant allele in the sick group were significantly higher (P: 0.0022-0.015) than in the control group, according to the assessment of genotype frequencies under various inheritance models. It was discovered that the odd ratio was around 2. It was clear that the co-dominant model had the lowest Akaike information criterion (AIC) score. The recruited participants' genotype-gender cross-classification interaction was assessed. With an odd ratio of 2.28, a significant correlation was demonstrated in females with the heterozygous variant genotype. When the biochemical parameter and BMI values were compared to the genotype frequencies, bearers of the variant alleles showed noticeably higher levels. However, in a comparable comparison, HDL-C significantly decreased. It was discovered that the variant alleles were substantially associated with an increase in atherogenic parameters.Conclusion: In the Iraqi population, the ER2 gene polymorphism, rs1271572 SNPs, is a risk factor for the development of CHD. Elevated atherogenic lipids are associated with this relationship. Females are more susceptible to the illness than males due to the mutant allele.