The angiotensin-converting-enzyme insertion/deletion polymorphism is not a risk factor for peripheral arterial disease

Atherosclerosis. 2002 Nov;165(1):175-8. doi: 10.1016/s0021-9150(02)00207-1.


Background: An insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting-enzyme (ACE) is associated with ACE plasma levels and activity. Conflicting results have been reported about the relevance of this polymorphism for atherosclerotic vascular disease. The aim of the present study was to analyze the role of this polymorphism for peripheral arterial disease (PAD).

Methods: The study was designed as a case-control study including 522 patients with documented PAD and 522 sex- and age-matched controls. ACE genotype was determined by size-analysis of polymerase chain reaction products.

Results: ACE genotype frequencies were similar between patients (II: 23.4%; ID: 44.8%; DD: 31.8%) and controls (II: 23.8%; ID: 48.3%; DD: 27.9%, P=0.37). The adjusted odds ratio of carriers of the DD genotype for PAD was 1.29 (95% confidence interval 0.95-1.75). The polymorphism was furthermore not associated with age at onset of PAD (P=0.56), Fontaine stage of the disease (P=0.68) or ankle/brachial index of patients (P=0.86).

Conclusion: The ACE I/D polymorphism is not a significant risk factor for PAD.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Age Distribution
  • Aged
  • Austria / epidemiology
  • Case-Control Studies
  • Cohort Studies
  • Female
  • Gene Deletion*
  • Genetic Markers / genetics
  • Humans
  • Incidence
  • Logistic Models
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Peripheral Vascular Diseases / diagnosis
  • Peripheral Vascular Diseases / epidemiology
  • Peripheral Vascular Diseases / genetics*
  • Polymorphism, Genetic*
  • Probability
  • Reference Values
  • Risk Assessment
  • Risk Factors
  • Sensitivity and Specificity
  • Severity of Illness Index
  • Sex Distribution
  • Statistics, Nonparametric


  • Genetic Markers
  • Peptidyl-Dipeptidase A