title: The angiotensin converting enzyme D allele is an independent risk factor for early onset coronary artery disease.
abstract: OBJECTIVE
  The role of angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in early onset coronary artery disease age < 55years (ECAD) is controversial. The aim of this study was to further evaluate the role of this ACE(I/D) gene polymorphism on the risk of premature CAD in patients from western Iran.
  
  
  METHODS
  The ACE(I/D) genotypes were detected by PCR-RFLP in 323 individuals undergoing their first coronary angiography. Patients were placed into two groups: ECAD and late onset CAD age ≥ 55years (LCAD).
  
  
  RESULTS
  We found a statistically significant association of the ACE D allele, as homozygous or ACE ID plus DD genotypes (ID+DD), only in the ECAD subjects OR=1.35, p=0.015, OR=3.27, p=0.014, and OR=2.8, p=0.013, respectively. In addition, there was a significant association after adjustment for the absence of history of diabetes, presence of normolipidemia and absence of history of blood pressure [OR 1.38, p=0.017 and 2.35, p=0.02]. Our results indicated that the ACE D allele is a risk factor for early onset of CAD even after correcting for conventional risk factors. The incidence of triple vessel disease was significantly higher in individuals carrying ACE(D/D) genotype in ECAD patients compared to those who carried ACE(I/I) genotype (OR 3.38; p=0.019; 57.5% vs. 42.5%; p=0.013).
  
  
  CONCLUSIONS
  The presence of D allele of ACE can be important independent risk factor in the onset of CAD patients less than 55 years old in a west population of Iran. Larger collaborative studies are needed to confirm these results.
authors.affiliation: Fertility and Infertility Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran. asadvaisiraygani@kums.ac.ir
authors.forename: Asad
authors.initials: A
authors.lastname: Vaisi-Raygani
authors.forename: Hori
authors.initials: H
authors.lastname: Ghaneialvar
authors.forename: Zohreh
authors.initials: Z
authors.lastname: Rahimi
authors.forename: Hamid
authors.initials: H
authors.lastname: Nomani
authors.forename: Mohmadreza
authors.initials: M
authors.lastname: Saidi
authors.forename: Fariborz
authors.initials: F
authors.lastname: Bahrehmand
authors.forename: Aliakbar
authors.initials: A
authors.lastname: Vaisi-Raygani
authors.forename: Haidar
authors.initials: H
authors.lastname: Tavilani
authors.forename: Tayebeh
authors.initials: T
authors.lastname: Pourmotabbed
mesh_terms: D017668:Age of Onset; D000483:Alleles; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000201:enzymology / Q000453:epidemiology* / Q000235:genetics*; D023921:Coronary Stenosis / Q000097:blood / Q000150:complications / Q000201:enzymology / Q000235:genetics; D003710:Demography; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D054643:INDEL Mutation / Q000235:genetics*; D007492:Iran / Q000453:epidemiology; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A