Matrix metalloproteinase-2 and angiotensin-1 gene polymorphisms in patient who have coronary artery disease

Abstract

Introduction: The rupture of atherosclerotic plaques is caused by the impact of matrix metalloproteinases (MMPs) upon the local fibrous valve and so might convert a chronic disease to a myocardial infarction, ultimately leading to instant death. Angiotensin converting enzyme (ACE) is actively engaged in the pathogenesis of ischemic heart disease. This study tries to unravel whether/how ACE and MMP-2 gene polymorphism contributes to the occurrence of Coronary Artery Disease (CAD). Materials and methods: A total of 300 individuals (100 healthy/200 patients) were included in the study. A PCR-RFLP method was utilized for ACE gene I/D and DNA sequencing MMP-2 (-1306 C/T) polymorphisms. Results: The ACE-1 gene D/D, I/D and I/I genotype frequency of the CAD cohort was 50%, 29%, and 21%, respectively whereas that of the healthy control cohort was 37%, 45% and 18%, respectively. Our findings indicate that the groups differed significantly in relation to the ACE-1 genotypes (p=0.021). The frequencies of ACE-1 gene allele I and D in both cohorts did not reveal a significant difference (p=0.314). In addition, the two groups did not manifest MMP-2 (rs243865) gene polymorphism. Conclusion: The association between MMP-2 gene polymorphism and CAD is too weak to suggest a conclusive evidence. The I/D genotype frequency remained higher in the healthy individuals than in the CAD cohort, while in the CAD group D/D genotype was more frequently than control group. Finally, the patients with D/D genotype tend to bear greater risk for cardiovascular diseases.