Association of serum levels of AngII, KLK1, and ACE/KLK1 polymorphisms with acute myocardial infarction induced by coronary artery stenosis

J Renin Angiotensin Aldosterone Syst. 2016 Jun 21;17(2):1470320316655037. doi: 10.1177/1470320316655037. Print 2016 Apr-Jun.

Abstract

Introduction: The study aims to confirm the association of acute myocardial infarction (AMI) with serum angiotensin II (AngII), kallikrein1 (KLK1), and ACE/KLK1 polymorphisms.

Materials and methods: Serum AngII/KLK1 levels and ACE and KLK1 genotypes were determined in 208 patients with AMI and 216 normal controls. Binary logistic regression was used for data analysis.

Results: The differences in serum AngII levels were statistically significant between the groups. After adjusting for potential confounding factors, high serum levels of AngII and KLK1 significantly increased the risk of AMI. The individuals with ACE DD and KLK1 GG genotypes significantly increased the risk of AMI compared with those harboring the ACE II and KLK1 AA genotypes (OR = 8.77, 95% CI = 1.74-44.16).

Conclusions: (1) Increasing the serum levels of AngII increased the risk of AMI. (2) The risk of AMI increased significantly when the serum levels of AngII and KLK1 simultaneously increased. (3) Individuals with the combined genotypes of ACE DD and KLK1 GG showed significantly increased risk of AMI compared with those with the combined genotypes of ACE II and KLK1 AA.

Keywords: Coronary artery stenosis; acute myocardial infarction; angiotensin converting enzyme gene; kallikrein1 gene; polymorphism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / blood*
  • Case-Control Studies
  • Chi-Square Distribution
  • Coronary Stenosis / blood
  • Coronary Stenosis / complications*
  • Female
  • Gene Frequency
  • Humans
  • INDEL Mutation / genetics
  • Logistic Models
  • Male
  • Middle Aged
  • Myocardial Infarction / blood
  • Myocardial Infarction / etiology*
  • Myocardial Infarction / genetics*
  • Peptidyl-Dipeptidase A / genetics*
  • Polymerase Chain Reaction
  • Polymorphism, Single Nucleotide / genetics*
  • Tissue Kallikreins / blood*
  • Tissue Kallikreins / genetics*

Substances

  • Angiotensin II
  • ACE protein, human
  • Peptidyl-Dipeptidase A
  • Tissue Kallikreins