Association between angiotensin-converting enzyme insertion/deletion gene polymorphism and atrial fibrillation: a meta-analysis

Europace. 2011 Mar;13(3):346-54. doi: 10.1093/europace/euq407. Epub 2010 Nov 13.

Abstract

Aims: Recent observations have raised concerns regarding the activation of the renin-angiotensin system and the development of atrial fibrillation (AF). Some initial studies indicated an association between an angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism and AF, however, the results have been inconsistent. Our aim was to perform a meta-analysis of relevant studies to assess the validity of this association.

Methods and results: PubMed, Cochrane clinical trials database, and EMBASE were searched through July 2009, and a manual search was also performed. Of the 68 initially identified studies, 18 case-control studies with 7577 patients were finally analysed. No statistically significant associations were found between the ACE I/D polymorphism and AF risk in the genetic additive model and dominant model, whereas a significant association was observed in the recessive model. A significant heterogeneity between individual studies was evident in all three models. Subgroup analyses showed a strong association between the ACE I/D polymorphism and hypertensive AF without significant heterogeneity.

Conclusion: Our meta-analysis suggests that there is insufficient evidence to demonstrate an association between ACE I/D polymorphism and AF risk. However, there seems to be a significant association between ACE I/D gene polymorphic variation and AF in patients with hypertension. Additional studies are warranted to further explore this association in ethnically diverse populations and varied cardiovascular substrates.

Publication types

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

MeSH terms

  • Adult
  • Aged
  • Atrial Fibrillation / epidemiology
  • Atrial Fibrillation / genetics*
  • Atrial Fibrillation / physiopathology
  • Case-Control Studies
  • Female
  • Humans
  • INDEL Mutation / genetics*
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic / genetics
  • Renin-Angiotensin System / physiology
  • Risk Factors

Substances

  • Peptidyl-Dipeptidase A