title: Insertion/deletion polymorphism of the angiotensin I-converting enzyme gene is not associated with restenosis after coronary stent placement.
abstract: BACKGROUND
  The renin-angiotensin system is thought to play a role in coronary thrombosis and restenosis. Plasma angiotensin I-converting enzyme (ACE) activity is associated with an insertion/deletion polymorphism in the gene coding for ACE. The objective of this study was to test the hypothesis that the D allele of the ACE gene is associated with a higher risk for restenosis after coronary stent placement.
  
  
  RESULTS
  This prospective study included 1850 consecutive patients with coronary artery disease who underwent intracoronary stent implantation. The adverse clinical events recorded were death, myocardial infarction, and target vessel revascularization. The primary end point of the study was restenosis (>/=50% diameter stenosis at follow-up angiography performed in 84% of the patients). The secondary end point was clinical outcome 1 year after the procedure. The restenosis rate at the 6-month angiographic follow-up was 32.8% in patients with the II genotype, 34.0% for patients with the ID genotype, and 31.2% for patients with the DD genotype (P=0.62). One-year event-free survival was 77.7% in patients with genotype II, 75.2% in patients with genotype ID, and 75.5% in patients with genotype DD (P=0.54). The lack of association was also present in the subgroup of patients with a low risk for restenosis: the restenosis rate was 21.7% in II carriers, 23.4% in ID carriers, and 19.7% in DD carriers (P=0.83).
  
  
  CONCLUSIONS
  The ACE DD genotype or D allele does not influence the 1-year clinical and angiographic outcome of patients undergoing coronary stent placement. These data suggest that routine determination of the ACE genotype may not help identify patients who are at a higher risk of thrombotic and restenotic events after coronary stent placement.
authors.affiliation: Deutsches Herzzentrum München and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany.
authors.forename: W
authors.initials: W
authors.lastname: Koch
authors.forename: A
authors.initials: A
authors.lastname: Kastrati
authors.forename: J
authors.initials: J
authors.lastname: Mehilli
authors.forename: C
authors.initials: C
authors.lastname: Böttiger
authors.forename: N
authors.initials: N
authors.lastname: von Beckerath
authors.forename: A
authors.initials: A
authors.lastname: Schömig
mesh_terms: D000368:Aged; D003251:Constriction, Pathologic; D017023:Coronary Angiography; D003327:Coronary Disease / Q000453:epidemiology / Q000235:genetics / Q000601:surgery; D003328:Coronary Thrombosis / Q000453:epidemiology / Q000235:genetics* / Q000601:surgery; D005260:Female; D005500:Follow-Up Studies; D017353:Gene Deletion; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009204:Myocardial Revascularization; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012008:Recurrence; D012307:Risk Factors; D015607:Stents; D016896:Treatment Outcome
chemical_list: D007703:Peptidyl-Dipeptidase A