title: Lower level of low-density lipoprotein cholesterol by statin prevents progression of coronary restenosis after successful stenting in acute myocardial infarction.
abstract: OBJECTIVE
  It is unclear whether the reduction of coronary restenosis by statins is due to a decrease in low-density lipoprotein (LDL) cholesterol and/or pleiotropic effects. Therefore, we performed quantitative coronary angiography (QCA) and analyzed the lipid profile and changes in adhesion molecules and chemokines caused by statin in patients with acute myocardial infarction (AMI).
  
  
  METHODS
  The subjects included AMI patients who had initial coronary angiograms and significant coronary stenosis and were implanted with a stent. After stent implantation, patients were treated either with (n = 36) or without (n = 14) statin. The primary end-point for this study was the absolute changes in the lipid profile, C-reactive protein (CRP), adhesion molecules, chemokines and stenosis measured by QCA between the post-stent and follow-up angiogram at 6 months after stenting.
  
  
  RESULTS
  Treatment with statin reduced % coronary diameter stenosis (DS) and was associated with a greater reduction in LDL cholesterol at 6 months after stenting in patients with acute myocardial infarction (AMI), while there were no differences in adhesion molecules, chemokines, CC chemokine receptor or CXC chemokine receptor. Interestingly, changes in % DS between before and after statin treatment at 6 months (Delta%DS) were positively correlated with DeltaLDL cholesterol, and patients who had an LDL cholesterol level of less than 80 mg/dl had a significantly lower Delta%DS. In addition, Delta%DS was significantly related only to the reduction in LDL cholesterol as assessed by a stepwise multivariable regression analysis.
  
  
  CONCLUSIONS
  These results suggest that the lower level of LDL cholesterol is the most critical factor in preventing coronary restenosis.
authors.affiliation: Department of Cardiology, Fukuoka University Hospital, Nanakuma, Fukuoka.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Iwata
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Miura
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shirai
authors.forename: Akira
authors.initials: A
authors.lastname: Kawamura
authors.forename: Sayo
authors.initials: S
authors.lastname: Tomita
authors.forename: Yoshino
authors.initials: Y
authors.lastname: Matsuo
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Nishikawa
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kumagai
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Matsuo
authors.forename: Keijiro
authors.initials: K
authors.lastname: Saku
mesh_terms: D000368:Aged; D018925:Chemokines / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D001026:Coronary Artery Bypass / Q000295:instrumentation*; D023903:Coronary Restenosis / Q000097:blood* / Q000517:prevention & control; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy; D015607:Stents
chemical_list: D018925:Chemokines; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors