title: Predictors of coronary in-stent restenosis: importance of angiotensin-converting enzyme gene polymorphism and treatment with angiotensin-converting enzyme inhibitors.
abstract: OBJECTIVE
  This study aimed to clarify the role of the angiotensin-converting enzyme (ACE) gene polymorphism in the development of in-stent restenosis.
  
  
  BACKGROUND
  In-stent restenosis occurs after treatment of coronary artery stenosis in 12% to 32% of coronary interventions with stents. Experimental and clinical studies have suggested that the deletion/insertion (D/I) polymorphism of the ACE gene plays a role in this.
  
  
  METHODS
  Quantitative coronary angiography before, immediately after and six months after stent implantation were compared in 369 patients, in whom D/I typing of the ACE gene was performed.
  
  
  RESULTS
  At follow-up we found no differences between the three genotypes in minimal lumen diameter (homozygotes with two deletion alleles in the ACE gene [DD], 2.20 mm; heterozygotes with one deletion and one insertion allele in the ACE gene [DI], 2.19 mm; and homozygotes with two insertion alleles in the ACE gene [II], 2.25 mm). The corresponding diameter stenoses were: DD: 25%, DI: 27%, II: 27% (p = NS), and the frequency of restenosis (>50% diameter stenosis) was: DD: 15.7%, DI: 11.0% and II: 16.4% (p = NS). Logistic regression analysis identified diabetes (odds ratio [OR]: 3.0, 95% confidence interval [CI]: 1.0 to 8.7), lesion length (OR: 1.1, 95% CI: 1.01 to 1.30) and minimal lumen diameter immediately after the intervention (OR: 0.3, 95% CI: 0.14 to 0.85) as predictors of in-stent restenosis. In a post hoc analysis of patients treated versus those not treated with an ACE-inhibitor antagonist or an angiotensin receptor antagonist, we found an increased frequency of in-stent restenosis in the DD genotypes (40% vs. 12%, p = 0.006).
  
  
  CONCLUSIONS
  The D/I polymorphism is not an independent predictor of coronary in-stent restenosis in general, but it may be of clinical importance in patients treated with ACE inhibitors or angiotensin receptor antagonists.
authors.affiliation: Department of Cardiology, The Heart Centre, Rigshospitalet, Copenhagen, Denmark. erikj@rh.dk
authors.forename: E
authors.initials: E
authors.lastname: Jørgensen
authors.forename: H
authors.initials: H
authors.lastname: Kelbaek
authors.forename: S
authors.initials: S
authors.lastname: Helqvist
authors.forename: G V
authors.initials: GV
authors.lastname: Jensen
authors.forename: K
authors.initials: K
authors.lastname: Saunamäki
authors.forename: J
authors.initials: J
authors.lastname: Kastrup
authors.forename: O
authors.initials: O
authors.lastname: Havndrup
authors.forename: H
authors.initials: H
authors.lastname: Bundgaard
authors.forename: J
authors.initials: J
authors.lastname: Kyst Madsen
authors.forename: M
authors.initials: M
authors.lastname: Christiansen
authors.forename: P S
authors.initials: PS
authors.lastname: Andersen
authors.forename: J H
authors.initials: JH
authors.lastname: Reiber
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000295:instrumentation / Q000379:methods; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D003131:Combined Modality Therapy; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000235:genetics* / Q000628:therapy*; D016172:DNA Fingerprinting; D005260:Female; D005500:Follow-Up Studies; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D011237:Predictive Value of Tests; D012008:Recurrence; D012307:Risk Factors; D015607:Stents / Q000009:adverse effects; D017211:Treatment Failure
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007703:Peptidyl-Dipeptidase A