title: D allele of the angiotensin I-converting enzyme is a major risk factor for restenosis after coronary stenting.
abstract: BACKGROUND
  Although intracoronary stent implantation significantly reduces restenosis compared with balloon angioplasty, a minority of patients still develop restenosis predominantly due to neointimal hyperplasia. Experimental studies suggest that the renin-angiotensin system is involved in neointimal hyperplasia after arterial injury. In humans, the plasma and cellular levels of ACE are associated with an I/D genetic polymorphism in the ACE gene, DD patients having higher levels.
  
  
  RESULTS
  We investigated a possible relation between the ACE I/D polymorphism and restenosis in 146 patients who underwent successful implantation of a Palmaz-Schatz stent and had 6-month follow-up angiography. The minimal lumen diameter (MLD) before and after the procedure did not differ significantly among the three groups of genotypes (DD, ID, and II). At follow-up, MLD had a significant inverse relationship to the number of D alleles present (DD, 1.65 +/- 0.71 mm; ID, 1.84 +/- 0.60 mm; II, 2.05 +/- 0.61 mm; P < .007). Late luminal loss during the follow-up period was significantly related to the number of D alleles (DD, 0.89 +/- 0.61 mm; ID, 0.60 +/- 0.52 mm; II, 0.40 +/- 0.53 mm; P < .0001). The relative risk of restenosis (defined as a > 50% diameter stenosis at follow-up) approximated by the adjusted odds ratio was 2.00 per number of D alleles (95% confidence interval, 1.03 to 3.88, P < .04).
  
  
  CONCLUSIONS
  The ACE I/D polymorphism influences the level of late luminal loss after coronary stent implantation. These results suggest that the renin-angiotensin system may be implicated in the pathogenesis of restenosis after coronary stenting.
authors.affiliation: INSERM CJF 95-05, Institut Pasteur de Lille, France.
authors.forename: C
authors.initials: C
authors.lastname: Amant
authors.forename: C
authors.initials: C
authors.lastname: Bauters
authors.forename: J C
authors.initials: JC
authors.lastname: Bodart
authors.forename: J M
authors.initials: JM
authors.lastname: Lablanche
authors.forename: G
authors.initials: G
authors.lastname: Grollier
authors.forename: N
authors.initials: N
authors.lastname: Danchin
authors.forename: M
authors.initials: M
authors.lastname: Hamon
authors.forename: F
authors.initials: F
authors.lastname: Richard
authors.forename: N
authors.initials: N
authors.lastname: Helbecque
authors.forename: E P
authors.initials: EP
authors.lastname: McFadden
authors.forename: P
authors.initials: P
authors.lastname: Amouyel
authors.forename: M E
authors.initials: ME
authors.lastname: Bertrand
mesh_terms: D000368:Aged; D000483:Alleles; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000601:surgery*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009204:Myocardial Revascularization; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011446:Prospective Studies; D012008:Recurrence; D012086:Reoperation; D012307:Risk Factors; D015607:Stents
chemical_list: D007703:Peptidyl-Dipeptidase A