Abstract

The present study investigated the relationship between the genetic polymorphisms in MMP-9 and MMP-3 genes and acute myocardial infarction (AMI). We examined 40 patients with acute myocardial infarction and 40 age and sex matched controls for MMP-9 functional promoter polymorphism (−1562 C>T) and MMP-3 (5A/6A) deletion/insertion polymorphism using restriction fragment length polymorphism (RFLP) for amplified genomic DNA. The frequencies of the combined mutant genotypes CT and TT in the (−1562 C>T) MMP9 were significantly higher in AMI patients (20%) when compared to the controls (0%) (p value=0.005) showing an association between these genotypes and AMI. Also there was a significant difference between 5A/5A genotype and 5A allele frequencies when both are compared in the patients (25% and 35%) and the controls (2.5% and 18.75%) (p=0.009; OR=13; CI=1.576–107.233); and (p=0.02; OR=2.333, CI=1.130–4.820) respectively. In conclusion, the −1562C>T polymorphism of the MMP9 gene is strongly associated with acute myocardial infarction in the Egyptian population. Furthermore, our study supported the presence of the 5A/5A genotype of MMP3 gene promoter polymorphism as a risk factor of AMI in Egyptian patients. Meanwhile, the race selection should be paid more attention since the pathogenesis of a disease might have different bases in different racial population groups.

Highlights

  • Myocardial infarction is caused by several inherited and acquired risk factors that predispose to the development of atherosclerotic lesions and plaque rupture

  • This rupture of an atherosclerotic plaque is a major event in the pathogenesis of an acute myocardial infarction (AMI) [1]

  • The aim of the present study was to investigate whether polymorphisms in MMP-9 and MMP-3 genes are a significant risk factor for acute myocardial infarction in an Egyptian Cohort

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Summary

Introduction

Myocardial infarction is caused by several inherited and acquired risk factors that predispose to the development of atherosclerotic lesions and plaque rupture. This rupture of an atherosclerotic plaque is a major event in the pathogenesis of an acute myocardial infarction (AMI) [1]. Of the many matrix metalloproteinases, MMP-9 (gelatinase B) might play an important role in matrix degradation and the subsequent rupture of the atherosclerotic plaques, owing to its broad substrate specificity distal position in the matrix proteolytic cascade. An association of a SNP in the MMP9 promoter with coronary artery disease and risk of myocardial infarction lesions has been reported [7]

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