title: Plasma activity and insertion/deletion polymorphism of angiotensin I-converting enzyme: a major risk factor and a marker of risk for coronary stent restenosis.
abstract: BACKGROUND
  Tissue proliferation is almost invariably observed in recurrent lesions within stents, and ACE, a factor of smooth muscle cell proliferation, may play an important role. Plasma ACE level is largely controlled by the insertion/deletion (I/D) polymorphism of the enzyme gene. The association among restenosis within coronary stents, plasma ACE level, and the I/D polymorphism is analyzed in the present prospective study.
  
  
  RESULTS
  One hundred seventy-six consecutive patients with successful, high-pressure, elective stenting of de novo lesions in the native coronary vessels were considered. At follow-up angiography, recurrence was observed in 35 patients (19.9%). Baseline clinical and demographic variables, plasma glucose and serum fibrinogen levels, lipid profile, descriptive and quantitative angiographic data, and procedural variables were not significantly different in patients with and without restenosis; mean plasma ACE levels (+/-SEM) were 40.8+/-3.5 and 20.7+/-1.0 U/L, respectively (P<.0001). Diameter stenosis percentage and minimum luminal diameter at 6 months showed statistically significant correlation with plasma ACE level (r=.352 and -.387, respectively P<.001). Twenty-one of 62 patients (33.9%) with D/D genotype, 13 of 80 (16.3%) with I/D genotype, and 1 of 34 (2.9%) with I/I genotype showed recurrence; the restenosis rate for each genotype is consistent with a codominant expression of the allele D.
  
  
  CONCLUSIONS
  In a selected cohort of patients, both the D/D genotype of the ACE gene, and high plasma activity of the enzyme are significantly associated with in-stent restenosis. Continued study with clinically different subsets of patients and various stent designs is warranted.
authors.affiliation: Cardiac Catheterization Unit, Ospedale Santa Croce, Cuneo, Italy. emodinam@www.lrcser.it
authors.forename: F
authors.initials: F
authors.lastname: Ribichini
authors.forename: G
authors.initials: G
authors.lastname: Steffenino
authors.forename: A
authors.initials: A
authors.lastname: Dellavalle
authors.forename: G
authors.initials: G
authors.lastname: Matullo
authors.forename: E
authors.initials: E
authors.lastname: Colajanni
authors.forename: T
authors.initials: T
authors.lastname: Camilla
authors.forename: A
authors.initials: A
authors.lastname: Vado
authors.forename: G
authors.initials: G
authors.lastname: Benetton
authors.forename: E
authors.initials: E
authors.lastname: Uslenghi
authors.forename: A
authors.initials: A
authors.lastname: Piazza
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D003327:Coronary Disease / Q000201:enzymology* / Q000235:genetics / Q000601:surgery; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D012008:Recurrence; D012307:Risk Factors; D015607:Stents
chemical_list: D007703:Peptidyl-Dipeptidase A