Literature DB >> 21816455

High levels of platelet-monocyte aggregates after valve replacement for aortic stenosis: relation to soluble P-selectin and P-selectin glycoprotein ligand-1 genes.

Roza Badr Eslam1, Thomas Gremmel, Alexandra Schneller, Michael Stegfellner, Alexandra Kaider, Christine Mannhalter, Irene Lang, Simon Panzer.   

Abstract

BACKGROUND: Calcific aortic valve stenosis is linked to atherosclerosis. The latter is associated with increased levels of platelets adhering to monocytes (PMA).
OBJECTIVE: The hemodynamic impairment in symptomatic aortic valve stenosis can be abated by valve replacement. We investigated the effect of valve replacement on PMA and receptor-ligand axis P-selectin - P-selectin glycoprotein ligand-1 (PSGL-1) in severe aortic valve stenosis. PATIENTS AND METHODS: PMA, plasma P-selectin (sP-selectin) and polymorphisms within the coding region for PSGL-1 (SELPLG) were determined in 42 patients with severe aortic valve stenosis before and 4 to 8 months after valve replacement. Ten patients suffered from significant coronary artery disease and received also a coronary artery bypass graft. Thirty-four patients received a bioprosthetic valve and 8 patients who were <65 years old received a mechanical valve.
RESULTS: Before the intervention, PMA levels were significantly higher in patients with aortic valve stenosis than in two control cohorts, namely healthy indviduals and 88 age- and sex-matched patients with severe atherosclerosis, but without aortic valve stenosis (p<0.001). PMA decreased after surgery, but normalized in only 3 patients, while further increases were noted in 11 patients. sP-selectin was elevated in 3 and 4 patients before and after valve replacement, respectively. sP-selectin increased significantly after surgery, but remained within the normal range. There was no correlation between changes of PMA and sP-selectin or any of the polymorphisms within SELPLG.
CONCLUSIONS: Exceedingly high PMA in aortic stenosis are independent of SELPLG polymorphisms, and largely of the hemodynamic compromise caused by the stenotic valve.
Copyright © 2011 Elsevier Ltd. All rights reserved.

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Year:  2011        PMID: 21816455     DOI: 10.1016/j.thromres.2011.07.021

Source DB:  PubMed          Journal:  Thromb Res        ISSN: 0049-3848            Impact factor:   3.944


  2 in total

1.  Increased Smad2/3 phosphorylation in circulating leukocytes and platelet-leukocyte aggregates in a mouse model of aortic valve stenosis: Evidence of systemic activation of platelet-derived TGF-β1 and correlation with cardiac dysfunction.

Authors:  Wei Wang; Nathalie Burg; Spandana Vootukuri; Barry S Coller
Journal:  Blood Cells Mol Dis       Date:  2016-01-23       Impact factor: 3.039

2.  Peri-procedural hemostasis disorders in surgical and transcatheter aortic valve implantation.

Authors:  Katarzyna Czerwińska-Jelonkiewicz; Krzysztof Milewski; Piotr Buszman; Przemysław Kwasiborski; Krzysztof Sanetra; Wojciech Domaradzki; Paweł Buszman
Journal:  Postepy Kardiol Interwencyjnej       Date:  2019-03-15       Impact factor: 1.426

  2 in total

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