title: Reduction of soluble P-selectin by statins is inversely correlated with the progression of coronary artery disease.
abstract: BACKGROUND
  Cell adhesion molecules (CAM) play an important role in the pathogenesis of atherosclerosis by mediating the binding of leukocytes to the endothelium. Soluble CAM isoforms are known to be elevated in the sera of patients suffering from coronary artery disease (CAD).
  
  
  METHODS
  We measured the concentrations of soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, P-selectin, platelet endothelial cell adhesion molecule-1, and highly sensitive C-reactive protein (hs-CRP) in the blood of 47 CAD patients before and 6 months after starting statin therapy and in 16 untreated CAD patients. The progression of CAD was monitored by calculating the coronary calcium score using electron beam computed tomography.
  
  
  RESULTS
  Soluble P-selectin (92+/-11 ng/ml vs. 59 +/- 4 ng/ml, p < 0.0001) and hs-CRP (0.92 +/- 0.14 mg/dl vs. 0.42 +/- 0.11 mg/dl, p < 0.001) decreased significantly in the statin-treated group compared to baseline levels. None of the other proteins studied showed significant changes. In contrast to hs-CRP, the reduction of soluble P-selectin concentrations correlated directly with the lowering of total cholesterol (r(2) = 0.236, p < 0.005) and inversely with the progression of CAD (r(2) = 0.393, p < 0.0001).
  
  
  CONCLUSIONS
  Our results suggest P-selectin as an additional marker for the beneficial action of statins in patients with CAD.
authors.affiliation: Clinical Division of General Internal Medicine, Clinical Department of Internal Medicine, Innsbruck Medical University, Austria.
authors.forename: Peter
authors.initials: P
authors.lastname: Marschang
authors.forename: Guy J
authors.initials: GJ
authors.lastname: Friedrich
authors.forename: Heidi
authors.initials: H
authors.lastname: Ditlbacher
authors.forename: Alfons
authors.initials: A
authors.lastname: Stoeger
authors.forename: Dieter Zur
authors.initials: DZ
authors.lastname: Nedden
authors.forename: Rudolf
authors.initials: R
authors.lastname: Kirchmair
authors.forename: Anton
authors.initials: A
authors.lastname: Dienstl
authors.forename: Otmar
authors.initials: O
authors.lastname: Pachinger
authors.forename: Josef R
authors.initials: JR
authors.lastname: Patsch
mesh_terms: D000704:Analysis of Variance; D002097:C-Reactive Protein / Q000378:metabolism; D002114:Calcinosis / Q000000981:diagnostic imaging; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy*; D018450:Disease Progression; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000097:blood; D019007:P-Selectin / Q000097:blood*; D011509:Proteoglycans / Q000097:blood; D018709:Statistics, Nonparametric; D014057:Tomography, X-Ray Computed; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D019040:E-Selectin; C101134:ESM1 protein, human; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D009363:Neoplasm Proteins; D019007:P-Selectin; D011509:Proteoglycans; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein