title: Effects of statin treatments on coronary plaques assessed by volumetric virtual histology intravascular ultrasound analysis.
abstract: OBJECTIVE
  We evaluated the effects of statin treatments for each component of coronary plaques.
  
  
  BACKGROUND
  Effects of statin treatments on coronary plaques have not been sufficiently evaluated.
  
  
  METHODS
  One hundred patients without significant lesion stenosis underwent baseline and 12-month follow-up virtual histology (VH) intravascular ultrasound (IVUS) studies and were treated with statin for 1 year. They were randomized to simvastatin (20 mg/day, n = 50) or rosuvastatin (10 mg/day, n = 50). With VH-IVUS, plaque was characterized as fibrotic, fibrofatty, dense calcium, and necrotic core.
  
  
  RESULTS
  In overall patients, necrotic core volume significantly reduced (15.7 to 13.7 mm(3), p = 0.010) and fibrofatty plaque volume increased (4.3 to 5.5 mm(3), p = 0.006) after statin treatments for 1 year. There were no significant differences of changes in either plaque component volume between simvastatin- and rosuvastatin-treated subgroups. In serial comparisons during 1-year follow-up, simvastatin treatment did not achieve statistically significant changes in fibrofatty plaque (4.1 to 5.1 mm(3), p = 0.131) and necrotic core volume (15.8 to 14.4 mm(3), p = 0.216). However, there was a significant decrease in necrotic core volume (15.5 to 13.0 mm(3), p = 0.015) and an increase in fibrofatty plaque volume (4.5 to 5.9 mm(3), p = 0.017) in the rosuvastatin-treated subgroup.
  
  
  CONCLUSIONS
  Serial volumetric VH-IVUS analysis showed that statin treatments might be associated with significant changes in necrotic core and fibrofatty plaque volume in overall patients. The changes in both plaques' component volume were not statistically different between simvastatin- and rosuvastatin-treated subgroup.
authors.affiliation: Division of Cardiology, Yonsei Cardiovascular Center, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Myeong-Ki
authors.initials: MK
authors.lastname: Hong
authors.forename: Duk-Woo
authors.initials: DW
authors.lastname: Park
authors.forename: Cheol-Whan
authors.initials: CW
authors.lastname: Lee
authors.forename: Seung-Whan
authors.initials: SW
authors.lastname: Lee
authors.forename: Young-Hak
authors.initials: YH
authors.lastname: Kim
authors.forename: Duk-Hyun
authors.initials: DH
authors.lastname: Kang
authors.forename: Jae-Kwan
authors.initials: JK
authors.lastname: Song
authors.forename: Jae-Joong
authors.initials: JJ
authors.lastname: Kim
authors.forename: Seong-Wook
authors.initials: SW
authors.lastname: Park
authors.forename: Seung-Jung
authors.initials: SJ
authors.lastname: Park
mesh_terms: D000368:Aged; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000188:drug therapy; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000188:drug therapy*; D005260:Female; D005355:Fibrosis; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D011237:Predictive Value of Tests; D011743:Pyrimidines / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D012720:Severity of Illness Index; D019821:Simvastatin / Q000627:therapeutic use*; D013449:Sulfonamides / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D014584:User-Computer Interface
chemical_list: D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D019821:Simvastatin