Genetic polymorphism of angiotensin converting enzyme and risk of coronary restenosis after percutaneous transluminal coronary angioplasties: evidence from 33 cohort studies

PLoS One. 2013 Sep 30;8(9):e75285. doi: 10.1371/journal.pone.0075285. eCollection 2013.

Abstract

Background: In the past decade, a number of cohort studies studies have been carried out to investigate the relationship between the insertion/deletion polymorphism of the gene encoding angiotensin-converting enzyme and risk of restenosis after percutaneous transluminal coronary angioplasties in patients. However, these studies have yielded contradictory results. Genetic association studies addressing this issue are frequently hampered by insufficient power. We therefore performed a meta-analysis of the published studies to clarify this inconsistency and to establish a comprehensive picture of the relationship between ACE I/D polymorphism and post-PTCA restenosis risk.

Methods: Databases including Pubmed, EMBASE, ISI Web of Science, EBSCO, Cochrane Library databases and CNKI were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association. The random-effects model was applied, addressing heterogeneity and publication bias.

Results: A total of 33 cohort studies involving 11,099 subjects were included. In a combined analysis, the OR for post-PTCA restenosis of the ACE DD genotype was 1.61 (95% CI: 1.27-2.04; P<10(-5)). In the subgroup analysis by intervention, significantly increased risks were also found in PTCA-stent and PTCA-balloon for the DD genotype of the polymorphism.

Conclusions: Our meta-analysis showed that the DD genotype of ACE I/D polymorphism was significantly associated with increased risk of restenosis, particularly for PTCA-stent.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angioplasty, Balloon, Coronary / adverse effects*
  • Coronary Restenosis / epidemiology*
  • Coronary Restenosis / genetics*
  • Databases, Bibliographic
  • Humans
  • Odds Ratio
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Risk Assessment
  • Sensitivity and Specificity

Substances

  • ACE protein, human
  • Peptidyl-Dipeptidase A

Grants and funding

This study was supported by Nature Scientific Foundation of Wenling (2010WLCA0047). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.