Influence of the angiotensin converting enzyme insertion or deletion genetic variant and coronary restenosis risk: evidence based on 11,193 subjects

PLoS One. 2013 Dec 13;8(12):e83415. doi: 10.1371/journal.pone.0083415. eCollection 2013.

Abstract

The insertion/deletion (I/D) polymorphism of the gene encoding angiotensin converting enzyme is a controversial risk factor for restenosis after percutaneous transluminal coronary angioplasties (PTCA) in patients. Genetic association studies can be problematic to reproduce due to insufficient power, phenotypic heterogeneity, population stratification, small effect of the variant and even publication biases. To derive a more precise estimation of the relationship as well as to quantify the between-study heterogeneity and potential bias, a meta-analysis including 11,193 patients from 33 published cohort studies was performed. In a combined analysis, the summary per-allele odds ratio for restenosis was 1.31 (95% CI: 1.08-1.58, P = 0.006), and 1.22 (95% CI: 0.95-1.56, P = 0.12), for PTCA-stent and PTCA-balloon, respectively. In the subgroup analysis by ethnicity, significantly increased restenosis risks after PTCA-stent were found in Asians for the polymorphism; whereas no significant associations were found among Caucasians. As for restenosis risks after PTCA-balloon, no evidence of any gene-disease association was obtained in the stratified analyses according to ethnicity and study size. In conclusion, this meta-analysis demonstrated that the DD homozygous of ACE I/D polymorphism was significantly associated with elevated restenosis susceptibility after PTCA-stent among Asian populations.

Publication types

  • Meta-Analysis
  • Review

MeSH terms

  • Alleles*
  • Angioplasty, Balloon, Coronary*
  • Asian People*
  • Coronary Restenosis / ethnology
  • Coronary Restenosis / genetics*
  • Female
  • Genetic Predisposition to Disease*
  • Humans
  • INDEL Mutation
  • Male
  • Peptidyl-Dipeptidase A / genetics*
  • Risk Factors

Substances

  • ACE protein, human
  • Peptidyl-Dipeptidase A

Grants and funding

The authors have no support or funding to report.