title: Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia.
abstract: Studies in animals and humans indicate a pivotal role for adhesion molecules (AMs) in the pathogenesis of atherosclerosis. Whereas an association between hypercholesterolaemia and AM expression has been suggested, it is unclear whether lowering cholesterol decreases AM expression and release. We compared the effects of a 3-month treatment with standard doses of three different statins (atorvastatin, simvastatin and pravastatin) on plasma levels of circulating AM (cAM) in 75 hypercholesterolaemic patients in a randomized clinical trial. Plasma levels of circulating (c)E-selectin, circulating intercellular adhesion molecule-1 (cICAM-1) and circulating vascular cell adhesion molecule-1 (cVCAM-1) were measured before and after 3 months of therapy. None of the statins lowered plasma cAM levels and pooled analyses of all patients showed a 1.7% [95% confidence interval (CI), -1.4-4.9%] increase in cE-selectin, a 2.1% (95% CI, -0.2-4.4%) increase in cICAM-1, and a 2.7% (95% CI, -0.6-6.1%) increase in cVCAM-1 levels. cAM levels did not decrease, even in patients with a >50% decrease ( n =19) in low-density lipoprotein cholesterol levels. This study provides strong evidence that 3 months of therapy with three different statins does not decrease cAM levels, despite normalization of cholesterol levels, and a minor decrease in C-reactive protein levels in patients with moderate hypercholesterolaemia.
authors.affiliation: Department of Clinical Pharmacology-TARGET, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. bernd.jilma@univie.ac.at
authors.forename: Bernd
authors.initials: B
authors.lastname: Jilma
authors.forename: Christian
authors.initials: C
authors.lastname: Joukhadar
authors.forename: Ulla
authors.initials: U
authors.lastname: Derhaschnig
authors.forename: Fausi
authors.initials: F
authors.lastname: Rassoul
authors.forename: Volker
authors.initials: V
authors.lastname: Richter
authors.forename: Michael
authors.initials: M
authors.lastname: Wolzt
authors.forename: Guido T
authors.initials: GT
authors.lastname: Dorner
authors.forename: Vanessa
authors.initials: V
authors.lastname: Petternel
authors.forename: Oswald F
authors.initials: OF
authors.lastname: Wagner
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D003430:Cross-Sectional Studies; D004311:Double-Blind Method; D019040:E-Selectin / Q000097:blood; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use; D019821:Simvastatin / Q000627:therapeutic use; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D006538:Heptanoic Acids; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin; D019821:Simvastatin; D017035:Pravastatin