title: Angiotensin-converting enzyme insertion/deletion gene polymorphism in a Tunisian healthy and acute myocardial infarction population.
abstract: BACKGROUND
  The role of the insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme gene (ACE) on acute myocardial infarction (AMI) is controversial.
  
  
  OBJECTIVE
  To assess the effect of the ACE I/D polymorphism on AMI compared with the healthy controls and its relationship with serum ACE activity in a Tunisian population.
  
  
  METHODS
  A total of 119 patients with AMI were compared with 238 healthy controls from the same geographical area. ACE genotyping was determined by polymerase chain reaction, and serum ACE activity was measured with N-[3-(2-furylacryloyl]-L-phenylalanyl-L-glycyl-L-glycine as substrate.
  
  
  RESULTS
  The ACE I/D polymorphism was significantly different between patients and controls (p < 0.0001). The frequencies of the DD genotype and the D allele were statistically higher in patients with AMI as compared with the controls and were associated with increased risk of AMI (DD vs. ID and II: odds ratio = 4.27, p < 0.0001, 95% confidence interval = 2.65-6.86; D vs. I: odds ratio = 3.15, p < 0.0001, 95% confidence interval = 2.26-4.40). This association was independent of other cardiovascular risk factors but dyslipidemia (p = 0.002) that was not represented in AMI patients with II genotype and in a lower extent with hypertension (p < 0.05). Serum ACE activity was significantly higher in AMI patients with ACE DD genotype compared with the subjects with ID or II genotype (p = 0.034) and was not correlated with other cardiovascular risk factors.
  
  
  CONCLUSIONS
  ACE DD genotype associated with higher serum ACE activity is increased in the studied population and might be clinically useful as markers to assess risk for AMI.
authors.affiliation: Unity of Genetic and Molecular Epidemiology, Faculty of Medicine, Tunis, Tunisia.
authors.forename: Sounira
authors.initials: S
authors.lastname: Mehri
authors.forename: Bruno
authors.initials: B
authors.lastname: Baudin
authors.forename: Sinda
authors.initials: S
authors.lastname: Mahjoub
authors.forename: Amira
authors.initials: A
authors.lastname: Zaroui
authors.forename: Bénédicte
authors.initials: B
authors.lastname: Bénéteau-Burnat
authors.forename: Rachid
authors.initials: R
authors.lastname: Mechmeche
authors.forename: Mohamed
authors.initials: M
authors.lastname: Hammami
authors.forename: Saïda
authors.initials: S
authors.lastname: Ben Arab
mesh_terms: D000368:Aged; D000483:Alleles; D001483:Base Sequence; D016022:Case-Control Studies; D017931:DNA Primers / Q000235:genetics; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D054643:INDEL Mutation; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology* / Q000209:etiology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000235:genetics*; D012307:Risk Factors; D014416:Tunisia
chemical_list: D017931:DNA Primers; D007703:Peptidyl-Dipeptidase A