title: Acetylsalicylate reduces endothelial and platelet-derived microparticles in patients with coronary artery disease.
abstract: Previous studies suggest that endothelial progenitor cells (EPCs) contribute to vascular repair processes. In contrast, circulating microparticles (MPs) are reported to be part of a process that is damaging to vascular cells. Numerous studies suggest that the "balance" between EPCs and MPs is important for the integrity of vascular cells and preservation of endothelial function. In the present study, we assess the impact of acetylsalicylate (ASA) - which is, beside statins and physical exercise, a third basic column in the preventive therapy of coronary artery disease (CAD) - on EPCs and MPs in patients with CAD. We investigated the effect of treatment (8 weeks) with ASA (100 mg/d) on endothelial function (flow-mediated vasodilation, FMD), number of circulating EPCs, and endothelial- and platelet-derived microparticles (eMP, pMP) in 15 male patients (age 59.5 ± 12.3 years) with CAD but nonsignificant stenosis. The number of pMPs and eMPs decreased by 62.7% (p < 0.05) and 28.4% (p < 0.05), respectively. The number of circulating EPCs (VEGFR2(+)CD34(+)), expressed as ‰ of circulating polymorphonuclear leukocytes, remained unchanged. Despite the reduced number of pMPs and eMPs in response to the ASA therapy, the FMD responses and the maximal dilator effects of nitroglycerin were unaffected. In a control experiment, patients (n = 6) treated with the selective COX-2 inhibitor etoricoxib (90 mg/day) for 8 weeks showed no changes in the number of pMPs, eMPs, and EPCs and in FMD. We report on a novel effect of ASA treatment on the number of circulating endothelial- and platelet-derived microparticles in patients with cardiovascular disease. The mechanism remains elusive, and appears not to be associated with the COX-2 pathway.
authors.affiliation: Herz- und Kreislaufzentrum der Ruhr-Universität, Standort St. Josef-Hospital, Gudrunstraße, Bochum, Germany. daniel.bulut@rub.de
authors.forename: Daniel
authors.initials: D
authors.lastname: Bulut
authors.forename: Vanessa
authors.initials: V
authors.lastname: Becker
authors.forename: Andreas
authors.initials: A
authors.lastname: Mügge
mesh_terms: D001241:Aspirin / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D055252:Cell-Derived Microparticles / Q000187:drug effects*; D003324:Coronary Artery Disease / Q000097:blood* / Q000473:pathology / Q000517:prevention & control*; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000077613:Etoricoxib; D006801:Humans; D008297:Male; D008875:Middle Aged; D011725:Pyridines / Q000494:pharmacology; D013234:Stem Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D013450:Sulfones / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D011725:Pyridines; D013450:Sulfones; D001241:Aspirin; D000077613:Etoricoxib