title: Effect of atorvastatin on peripheral endothelial function and systemic inflammatory markers in patients with stable coronary artery disease.
abstract: BACKGROUND
  Endothelial dysfunction, detectable by an impaired flow-mediated vasodilation (FMD) of the brachial artery, has been shown to be associated with increased levels of circulating proinflammatory markers. Therapeutic interventions such as lipid-lowering with statins increase FMD and decrease inflammatory markers, like soluble (s) E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) or high-sensitivity Creactive protein (hsCRP). The effect of atorvastatin therapy on both FMD and inflammatory markers in patients with stable coronary artery disease (CAD) has not been investigated.
  
  
  METHODS
  Thirty hypercholesterolemic patients with angiographically documented stable coronary artery disease (CAD) were randomized to placebo or atorvastatin (20 mg/d) for 3 months. FMD was assessed using highresolution ultrasound (13 MHz, Acuson Sequoia, C256). High-sensitivity CRP was measured with Latex agglutination assay, sE-selectin and sICAM-1 were determined with ELISA.
  
  
  RESULTS
  Baseline characteristics were not different between groups. FMD improved in patients on atorvastatin (6.7+/-3.8% to 8.5+/-4.4%; p<0.01), but remained unchanged in placebo-treated patients (8.2+/-3.3% to 8.9+/-5.1%; p=NS). Atorvastatin treatment was associated with decreases of sICAM-1 (from 274.2+/-92.2 to 197.9+/-70.0 ng/ml; p<0.01) and hsCRP (from 0.57+/-0.45 to 0.18+/-0.15 mg/dl; p<0.01), whereas placebo treatment had no effect on these markers. sE-selectin levels were not influenced by either treatment. No correlations were found between changes in FMD, lipids and inflammatory markers.
  
  
  CONCLUSIONS
  Treatment with atorvastatin leads to an improvement in endothelial function and a reduction in inflammatory markers in patients with stable CAD. The lack of correlation between changes in FMD and inflammatory markers may support the concept of pleiotropic effects of statins in humans.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Medical University of Innsbruck, Innsbruck, Austria.
authors.forename: Hannes Franz
authors.initials: HF
authors.lastname: Alber
authors.forename: Matthias
authors.initials: M
authors.lastname: Frick
authors.forename: Alois
authors.initials: A
authors.lastname: Süssenbacher
authors.forename: Jakob
authors.initials: J
authors.lastname: Dörler
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Dichtl
authors.forename: Eva-Maria
authors.initials: EM
authors.lastname: Stocker
authors.forename: Otmar
authors.initials: O
authors.lastname: Pachinger
authors.forename: Franz
authors.initials: F
authors.lastname: Weidinger
mesh_terms: D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D001916:Brachial Artery / Q000187:drug effects / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology; D004311:Double-Blind Method; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D000924:Anticholesteremic Agents; D019040:E-Selectin; D006538:Heptanoic Acids; D018836:Inflammation Mediators; D011758:Pyrroles; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D000069059:Atorvastatin