Antiplatelet therapy abrogates platelet-assisted Staphylococcus aureus infectivity of biological heart valve conduits.

Autor: Ditkowski B; Cardiovascular Developmental Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium., Bezulska-Ditkowska M; Cardiovascular Developmental Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium; Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium., Jashari R; European Homograft Bank, Saint Jean Clinique, Brussels, Belgium., Baatsen P; Department of Neurosciences, VIB-KU Leuven Center for Brain & Disease Research, KU Leuven and EM-platform of VIB Bio Imaging Core @KULeuven, Leuven, Belgium., Moreillon P; Department of Fundamental Microbiology, University Lausanne, Lausanne, Switzerland., Rega F; Division of Clinical Cardiac Surgery, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium., Veloso TR; Cardiovascular Developmental Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium., Hoylaerts MF; Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium., Heying R; Cardiovascular Developmental Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium. Electronic address: ruth.heying@uzleuven.be.
Jazyk: angličtina
Zdroj: The Journal of thoracic and cardiovascular surgery [J Thorac Cardiovasc Surg] 2021 Jun; Vol. 161 (6), pp. e457-e472. Date of Electronic Publication: 2019 Nov 23.
DOI: 10.1016/j.jtcvs.2019.10.188
Abstrakt: Objective: Although recent advances in pulmonary valve replacement have enabled excellent hemodynamics, infective endocarditis remains a serious complication, particularly for implanted bovine jugular vein (BJV) conduits.
Methods: We investigated contributions by platelets and plasma fibrinogen to endocarditis initiation on various grafts used for valve replacement. Thus, adherence of Staphylococcus aureus and platelets to 5 graft tissues was studied quantitatively in perfusion chambers, assisted by microscopic analysis. We also evaluated standard antiplatelet therapy to prevent onset of S aureus endocarditis.
Results: Of all tissues, bovine pericardium (BP) showed the greatest fibrinogen binding. Perfusion of all plasma-precoated tissues identified BP and BJV wall with the greatest affinity for S aureus. Perfusions of anticoagulated human blood over all tissues also triggered more platelet adhesion to BP and BJV wall as single platelets. Several controls confirmed that both S aureus and platelets were recruited on immobilized fibrinogen. In addition, perfusions (and controls) over plasma-coated tissues with whole blood, spiked with S aureus, revealed that bacteria exclusively bound to adhered platelets. Both the platelet adhesion and platelet-mediated S aureus recruitment required platelet α IIb β 3 and coated or soluble fibrinogen, respectively, interactions abrogated by the α IIb β 3 -antagonist eptifibatide. Also, standard antiplatelet therapy (aspirin/ticagrelor) reduced the adherence of S aureus in blood to BJV 3-fold.
Conclusions: Binding of plasma fibrinogen to especially BJV grafts enables adhesion of single platelets via α IIb β 3 . S aureus then attaches from blood to (activated) bound platelet α IIb β 3 via plasma fibrinogen. Dual antiplatelet therapy appears a realistic approach to prevent endocarditis and its associated mortality.
(Copyright © 2019 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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