Relationship between angiotensin-converting enzyme gene insertion/deletion polymorphism, angiographically defined coronary artery disease and myocardial infarction in patients with type 2 diabetes mellitus

J Renin Angiotensin Aldosterone Syst. 2012 Dec;13(4):478-86. doi: 10.1177/1470320312448947. Epub 2012 Jun 7.

Abstract

Introduction: The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been implicated in the pathogenesis of cardiovascular diseases. The objective of the present study was to investigate the influence of ACE gene I/D polymorphism on the development and progression of coronary artery disease (CAD) and myocardial infarction (MI) in type 2 diabetic (T2DM) patients.

Materials and methods: We screened 283 T2DM patients, inclusive of 160 patients with angiographically defined CAD, 73 patients with MI, 89 patients without MI and 121 T2DM individuals with no evidence of CAD for ACE gene I /D polymorphism.

Results: There was no significant difference in the distribution of genotypes and alleles of ACE gene I/D polymorphism between T2DM+CAD and T2DM (non-CAD) groups. However, a significant association of this polymorphism with MI in T2DM+CAD patients (p=0.024) was observed. Further analysis revealed that the frequencies of the DD and ID genotypes increased with the number of stenosed coronary vessels (p=0.026). The DD genotype and the D allele were more frequent in the subgroup of T2DM patients with multivessel CAD (p=0.01) than in individuals with single vessel stenosis.

Conclusions: These findings reveal a significant relationship between ACE gene I/D polymorphism, multivessel CAD and also the occurrence of MI in T2DM individuals with significant coronary stenoses in our population.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Coronary Angiography
  • Coronary Artery Disease / complications
  • Coronary Artery Disease / diagnostic imaging*
  • Coronary Artery Disease / enzymology
  • Coronary Artery Disease / genetics*
  • Diabetes Mellitus, Type 2 / complications*
  • Diabetes Mellitus, Type 2 / enzymology
  • Diabetes Mellitus, Type 2 / genetics
  • Female
  • Gene Frequency / genetics
  • Humans
  • INDEL Mutation / genetics*
  • Logistic Models
  • Male
  • Middle Aged
  • Myocardial Infarction / complications*
  • Myocardial Infarction / enzymology
  • Myocardial Infarction / genetics
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Risk Factors

Substances

  • ACE protein, human
  • Peptidyl-Dipeptidase A