title: Influence of short-term rosuvastatin therapy on endothelial progenitor cells and endothelial function.
abstract: Endothelial progenitor cells maintain endothelium integrity by replacing injured endothelial cells. Cholesterol-lowering promotes either endothelial progenitor cells mobilization or improves endothelial function. It is unknown whether improving endothelial function with statin is associated with a parallel increased endothelial progenitor cells availability. Thirty-two hypercholesterolemic patients were assigned to 4-week rosuvastatin (10 mg daily) and 16 hypercholesterolemic served as controls. Circulating endothelial progenitor cells, brachial artery flow-mediated vasodilatation, an index of endothelial function, and the lipid profile were measured before and after the 4-week statin therapy. At baseline, we found a correlation between circulating endothelial progenitor cells and flow-mediated vasodilatation (r = .31, P = .029). At the end of the 4-week intervention with rosuvastatin there was a 37% reduction in low-density lipoprotein cholesterol (P < .001) and a significant 72% increase in the number of endothelial progenitor cells and flow-mediated vasodilatation (4.7 + 0.7% to 8.8 + 0.4%, P < .001). Endothelial progenitor cells and flow-mediated vasodilatation were unchanged at the end of the study in patients not taking statin. A correlation emerged between endothelial progenitor cells and flow-mediated vasodilatation variations (r = .52, P < .001), this correlation being still significant after controlling for blood cholesterol reduction. In conclusion, short-term rosuvastatin therapy contributes in hyperchoelsterolemic patients to improving endothelial function by lowering cholesterol and increasing the number of circulating endothelial progenitor cells; the latter effect appears to be partly independent from reduction in plasma cholesterol.
authors.affiliation: Unit of Internal Medicine, Angiology and Arteriosclerosis Diseases, Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy. mpirro@unipg.it
authors.forename: Matteo
authors.initials: M
authors.lastname: Pirro
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Schillaci
authors.forename: Paolo F
authors.initials: PF
authors.lastname: Romagno
authors.forename: Massimo R
authors.initials: MR
authors.lastname: Mannarino
authors.forename: Francesco
authors.initials: F
authors.lastname: Bagaglia
authors.forename: Rolando
authors.initials: R
authors.lastname: Razzi
authors.forename: Leonella
authors.initials: L
authors.lastname: Pasqualini
authors.forename: Gaetano
authors.initials: G
authors.lastname: Vaudo
authors.forename: Elmo
authors.initials: E
authors.lastname: Mannarino
mesh_terms: D002784:Cholesterol / Q000097:blood; D004334:Drug Administration Schedule; D042783:Endothelial Cells / Q000187:drug effects* / Q000473:pathology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011743:Pyrimidines / Q000008:administration & dosage*; D000068718:Rosuvastatin Calcium; D013234:Stem Cells / Q000187:drug effects* / Q000473:pathology; D013449:Sulfonamides / Q000008:administration & dosage*; D016896:Treatment Outcome; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D002784:Cholesterol