title: Difference in statin effects on neointimal coverage after implantation of drug-eluting stents.
abstract: OBJECTIVE
  This study was carried out to examine the difference in effects between rosuvastatin and pravastatin on neointimal formation after the placement of a drug-eluting stent (DES).
  
  
  METHODS
  Forty patients who underwent placement of a DES in our hospital were prospectively randomized to receive rosuvastatin (n=20) or pravastatin (n=20), and analyzed by optical coherence tomography at the chronic stage. The main outcome measure was comparison of neointimal coverage analyzed at a strut level.
  
  
  RESULTS
  A significant reduction in total cholesterol, low-density lipoprotein, and white blood cell count was observed during the study in the rosuvastatin group (total cholesterol, from 4.82±0.90 to 4.43±0.77 mmol/l, P=0.038; low-density lipoprotein, from 2.85±0.76 to 2.34±0.57 mmol/l, P=0.006; white blood cell count, from 5810±1399 to 5355±1257/µl, P=0.048), but not in the pravastatin group. Although not statistically significant, C-reactive protein was lower in the rosuvastatin than in the pravastatin group at the chronic stage (1.14±1.21 vs. 7.67±13.67 mg/l, P=0.051). Malapposed and uncovered struts were significantly less frequent in the rosuvastatin group than in the pravastatin group (malapposed, 0.06 vs. 0.60%, P<0.001; uncovered, 6.49 vs. 11.29%, P<0.001). The difference in uncovered struts was maintained even when stent types were analyzed separately (everolimus-eluting stent, 4.81 vs. 6.21%, P=0.007; sirolimus-eluting stent, 14.40 vs. 20.86%, P<0.001). Comparison of neointimal thickness between the rosuvastatin and the pravastatin groups showed inconsistent results depending on the stent types analyzed.
  
  
  CONCLUSIONS
  Compared with pravastatin, the use of rosuvastatin resulted in lower frequency of uncovered and malapposed struts after the placement of a DES, which might be mediated through improved inflammatory and lipid profiles.
authors.affiliation: Department of Medicine, Division of Cardiology, Faculty of Medicine, Kinki University, Osaka, Japan.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Shinichiro
authors.initials: S
authors.lastname: Ikuta
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Kobuke
authors.forename: Masakazu
authors.initials: M
authors.lastname: Yasuda
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Ikeda
authors.forename: Kenji
authors.initials: K
authors.lastname: Yamaji
authors.forename: Masafumi
authors.initials: M
authors.lastname: Ueno
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Iwanaga
authors.forename: Shunichi
authors.initials: S
authors.lastname: Miyazaki
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D054855:Drug-Eluting Stents; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007564:Japan; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D058426:Neointima; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000295:instrumentation*; D017035:Pravastatin / Q000627:therapeutic use*; D011446:Prospective Studies; D011743:Pyrimidines / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use*; D013997:Time Factors; D041623:Tomography, Optical Coherence; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D002097:C-Reactive Protein; D017035:Pravastatin