title: Effect of intensive lipid-lowering treatment compared to moderate lipid-lowering treatment with rosuvastatin on endothelial function in high risk patients.
abstract: BACKGROUND
  The healthy endothelium plays a key roll in vascular regulation. This function can be examined non-invasively by use of B-mode ultrasound on the brachial artery. The aim of this study was to measure the effect of low-dose and high-dose lipid-lowering treatment with rosuvastatin on the endothelial function evaluated with endothelium-dependent and endothelium-independent flow-mediated dilatation (FMD).
  
  
  METHODS
  87 Statin-naive patients with ST-segment elevation myocardial infarction (STEMI) were randomized to 5mg or 40 mg rosuvastatin. The FMD was assessed at baseline, 6 months and after 12 months of follow-up by use of B-mode ultrasound of the brachial artery.
  
  
  RESULTS
  Baseline low-density lipoprotein (LDL) cholesterol level was reduced by 31.8% in the low-dose group (from 3.1 ± 0.7 mmol/l to 2.0 ± 0.4 mmol/l, p<0.001) vs. 49.0% in the high-dose group (from 3.1 ± 1.0 mmol/l to 1.6 ± 0.7 mmol/l, p<0.001) (between groups p=0.001). Treatment with low-dose rosuvastatin did not change the endothelium-dependent FMD (-1.4 ± 8.2%, p=0.32) whereas the endothelium-dependent FMD increased significantly in the high-dose group (3.7 ± 11.0%, p=0.045) (between group p=0.029). No significant changes in endothelium-independent FMD were seen.
  
  
  CONCLUSIONS
  In the present study treatment of statin-naive STEMI patients with high-dose rosuvastatin for 12 months resulted in a significant increase in endothelium-dependent FMD of the brachial artery whereas no significant change was seen in the low-dose rosuvastatin group (Clinicaltrials.gov Identifier: NCT01223625).
authors.affiliation: Department of Cardiology, Odense University Hospital, Odense, Denmark. rasmusegede@hotmail.com
authors.forename: Rasmus
authors.initials: R
authors.lastname: Egede
authors.forename: Lisette Okkels
authors.initials: LO
authors.lastname: Jensen
authors.forename: Henrik Steen
authors.initials: HS
authors.lastname: Hansen
authors.forename: Lisbeth
authors.initials: L
authors.lastname: Antonsen
authors.forename: Knud Nørregaard
authors.initials: KN
authors.lastname: Hansen
authors.forename: Anders
authors.initials: A
authors.lastname: Junker
authors.forename: Per
authors.initials: P
authors.lastname: Thayssen
mesh_terms: D000368:Aged; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage*; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology; D011446:Prospective Studies; D011743:Pyrimidines / Q000008:administration & dosage*; D012307:Risk Factors; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage*; D014280:Triglycerides / Q000097:blood; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D014280:Triglycerides; D000068718:Rosuvastatin Calcium