title: Time course of statin-induced changes in coronary atherosclerosis using intravascular ultrasound with virtual histology.
abstract: OBJECTIVE
  Recent trials using intravascular ultrasound (IVUS) have shown that statins induce regression and stabilization of coronary artery plaques. However, there are no reports on whether regression and stabilization in coronary artery plaques associated with statin therapy continue or not. The purpose of the present study was to examine the time course of statin-induced changes in coronary atherosclerosis.
  
  
  METHODS
  Coronary atherosclerosis was evaluated using virtual histology-IVUS in 39 patients at the time of a percutaneous coronary intervention, 8 months after statin therapy (mid-term), and at 48-month (long-term) follow-up. IVUS images qualified for evaluation obtained from 30 of these patients at three time points.
  
  
  RESULTS
  Significant decreases in low-density lipoprotein cholesterol and high-sensitivity C-reactive protein were observed at 8 months and these decreases continued for 48 months. A decrease in external elastic membrane volume was observed at 8 months (-1.1%) and reached significance at 48 months (-5.9%, P=0.0001). Plaque volume tended to decrease over time, but this was not statistically significant (-1.6% at 8 months and -3.8% at 48 months). An increase in the calcified plaque component was observed at 8 months (0.09±0.34 mm/mm) and reached significance at 48 months (0.21±0.33 mm/mm, P=0.002). Change in the calcified component and change in the external elastic membrane volume showed a significant negative correlation at the long-term follow-up (r=-0.598, P=0.0005).
  
  
  CONCLUSIONS
  Continued negative vessel remodeling associated with an increase in the calcified plaque component was observed following prolonged statin therapy by serial virtual histology-IVUS analysis.
authors.affiliation: Department of Internal Medicine, Division of Cardiology, Yokohama Sakae Kyosai Hospital, Yokohama, Japan. nozue2493@yahoo.co.jp
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Nozue
authors.forename: Kazuki
authors.initials: K
authors.lastname: Fukui
authors.forename: Shingo
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Kunishima
authors.forename: Shigeo
authors.initials: S
authors.lastname: Umezawa
authors.forename: Yuko
authors.initials: Y
authors.lastname: Onishi
authors.forename: Shinichi
authors.initials: S
authors.lastname: Tohyama
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Hibi
authors.forename: Takashi
authors.initials: T
authors.lastname: Sozu
authors.forename: Mitsuyasu
authors.initials: M
authors.lastname: Terashima
authors.forename: Ichiro
authors.initials: I
authors.lastname: Michishita
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging* / Q000188:drug therapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000187:drug effects*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007564:Japan; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic; D011237:Predictive Value of Tests; D011446:Prospective Studies; D011804:Quinolines / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D061205:Vascular Calcification / Q000000981:diagnostic imaging / Q000188:drug therapy
chemical_list: D015415:Biomarkers; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011804:Quinolines; D002097:C-Reactive Protein; C108475:pitavastatin