title: Simvastatin does not inhibit intimal hyperplasia and restenosis but promotes plaque regression in normocholesterolemic patients undergoing coronary stenting: a randomized study with intravascular ultrasound.
abstract: BACKGROUND
  Restenosis after coronary stenting is mainly caused by intimal hyperplasia. Both experimental and clinical studies suggest that statins may be able to inhibit intimal hyperplasia and, therefore, in-stent restenosis (ISR), by mechanisms beyond lipid lowering.
  
  
  METHODS
  In a 12-month study, we randomized 71 normocholesterolemic patients to 20 mg simvastatin or no treatment, 2 weeks before elective coronary stenting. Patients were evaluated by quantitative coronary angiography and intravascular ultrasound, immediately after the index procedure and at the 12-month catheterization.
  
  
  RESULTS
  Binary ISR was present in 15% and in 18% of simvastatin-treated patients and controls, respectively (P = NS). Intimal hyperplasia did not differ significantly between the 2 groups (3.6 +/- 1.8 vs 3.8 +/- 2.3 mm3/mm, 34% +/- 15% vs 35% +/- 23% for simvastatin vs controls, P = NS). However, persistent plaque decreased with simvastatin but increased in controls (-4.0 +/- 4.0 vs +1.6 +/- 3.8 mm3/mm, -14% +/- 10% vs +6% +/- 12%, P < .05). The same behavior was shown by intermediate plaques at nonstented sites (-2.5 +/- 3.0 vs +1.0 +/- 3.0 mm3/mm, -10% +/- 8% vs +9% +/- 9%, P < .05). Major adverse events at 12 months were present in 11% and 24% of simvastatin-treated patients and controls, respectively (P = .20).
  
  
  CONCLUSIONS
  In normocholesterolemic patients undergoing coronary stenting, simvastatin does not prevent intimal hyperplasia or ISR, but it promotes atherosclerotic regression both at stented and at nonstented sites.
authors.affiliation: Cardiothoracic Department, Pisa, Italy.
authors.forename: Anna Sonia
authors.initials: AS
authors.lastname: Petronio
authors.forename: Giovanni
authors.initials: G
authors.lastname: Amoroso
authors.forename: Ugo
authors.initials: U
authors.lastname: Limbruno
authors.forename: Barbara
authors.initials: B
authors.lastname: Papini
authors.forename: Marco
authors.initials: M
authors.lastname: De Carlo
authors.forename: Andrea
authors.initials: A
authors.lastname: Micheli
authors.forename: Nicola
authors.initials: N
authors.lastname: Ciabatti
authors.forename: Mario
authors.initials: M
authors.lastname: Mariani
mesh_terms: D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000628:therapy*; D023903:Coronary Restenosis / Q000175:diagnosis / Q000517:prevention & control*; D003331:Coronary Vessels / Q000000981:diagnostic imaging*; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D006965:Hyperplasia / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D011292:Premedication; D019821:Simvastatin / Q000494:pharmacology* / Q000627:therapeutic use; D015607:Stents; D018084:Ultrasonography, Interventional
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019821:Simvastatin