No association found between the insertion/deletion of a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene in Mexican patients and binary restenosis after coronary stenting

Clin Chim Acta. 2008 Nov;397(1-2):65-7. doi: 10.1016/j.cca.2008.07.019. Epub 2008 Jul 25.

Abstract

Background: It has been suggested that the incidence of coronary restenosis after a percutaneous coronary intervention is much higher in patients with a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene (deletion allele) than in others, but published studies are conflicting.

Methods: The presence (insertion) or absence (deletion) of a 287-bp alu repeat sequence within intron 16 of the ACE gene (I/D polymorphism) was analyzed by polymerase chain reaction in a group of 168 patients with coronary artery disease who underwent coronary artery stenting. Basal and procedure coronary angiographies were analyzed searching for angiographic predictors of restenosis and follow-up angiography was analyzed looking for binary restenosis.

Results: Distribution of angiotensin converting enzyme I/D polymorphisms was similar in patients with and without restenosis. Similar results were observed when the analysis was made considering the type of stent implanted. On the other hand, the whole group of coronary artery disease patients showed increased frequencies of the D allele (p=0.00001, OR=2.17, 95% CI=1.49-3.16) and ID genotype (p=0.0002, OR=2.58, 95%CI=1.49-4.47) when compared to healthy controls.

Conclusions: Genetic variations of the ACE gene could be a genetic factor related to coronary artery disease in the Mexican mixed racial ancestry individuals, but do not support its role as a risk factor for developing restenosis after coronary stenting.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alleles
  • Alu Elements / genetics*
  • Coronary Angiography
  • Coronary Restenosis / genetics*
  • Female
  • Gene Frequency
  • Genotype
  • Heart
  • Humans
  • INDEL Mutation*
  • Introns / genetics
  • Male
  • Mexico
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic

Substances

  • Peptidyl-Dipeptidase A