title: Insertion/deletion polymorphism of the angiotensin I-converting enzyme gene is associated with coronary artery plaque calcification as assessed by intravascular ultrasound.
abstract: OBJECTIVE
  We evaluated the influence of the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene on coronary plaque morphology and calcification in patients with angiographically documented coronary artery disease (CAD).
  
  
  BACKGROUND
  The ACE I/D polymorphism has been associated with an increased risk of myocardial infarction in patients with the DD genotype but not with the presence of native CAD.
  
  
  METHODS
  We studied 146 patients undergoing percutaneous transluminal coronary angioplasty for stable angina pectoris by means of preinterventional intravascular ultrasound (IVUS). Qualitative and quantitative criteria were used to classify the target lesions as poorly or highly echoreflective or as calcified. Genomic deoxyribonucleic acid was analyzed by polymerase chain reaction (PCR) to identify the I/D polymorphism, with a second insertion-specific PCR in DD genotypes to prevent mistyping.
  
  
  RESULTS
  The ACE genotype groups (DD 46, ID 68, II 32) were well matched for the basic characteristics. Patients with the DD genotype had significantly more calcified lesions (DD 80%, ID 57%, II 66%; unadjusted odds ratio [OR] 2.88, 95% confidence interval [CI] 1.30 to 6.92, p = 0.008) and more calcifications >180 degrees of the vessel circumference (DD 22%, ID 10%, II 6%; OR 2.80, 95% CI 1.05 to 7.63, p = 0.03). The prevalence of myocardial infarction was not significantly associated with coronary calcification (OR 1.44, 95% CI 0.72 to 2.88, p = 0.31).
  
  
  CONCLUSIONS
  Patients with CAD and the ACE DD genotype have a significantly higher incidence and greater extent of coronary lesion calcification, as determined by IVUS. This finding indicates that the ACE I/D gene polymorphism is related to the development or progression of atherosclerotic plaque calcification.
authors.affiliation: Department of Medicine, University of Tübingen, Germany. martin.pfohl@t-online.de
authors.forename: M
authors.initials: M
authors.lastname: Pfohl
authors.forename: A
authors.initials: A
authors.lastname: Athanasiadis
authors.forename: M
authors.initials: M
authors.lastname: Koch
authors.forename: P
authors.initials: P
authors.lastname: Clemens
authors.forename: N
authors.initials: N
authors.lastname: Benda
authors.forename: H U
authors.initials: HU
authors.lastname: Häring
authors.forename: K R
authors.initials: KR
authors.lastname: Karsch
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000235:genetics* / Q000473:pathology; D005260:Female; D017353:Gene Deletion; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D018084:Ultrasonography, Interventional
chemical_list: D007703:Peptidyl-Dipeptidase A