• Bartosz Ditkowski, Martyna Bezulska-Ditkowska, Ramadan Jashari, Pieter Baatsen, Philippe Moreillon, Filip Rega, Tiago R Veloso, Marc F Hoylaerts, Ruth Heying, and Congenital Cardiology and Cardiac Surgery Group.
• Cardiovascular Developmental Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.
• J. Thorac. Cardiovasc. Surg. 2021 Jun 1; 161 (6): e457-e472.

ObjectiveAlthough recent advances in pulmonary valve replacement have enabled excellent hemodynamics, infective endocarditis remains a serious complication, particularly for implanted bovine jugular vein (BJV) conduits.MethodsWe 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.ResultsOf all tissues, bovine pericardium (BP) showed the greatest fibrinogen binding. Perfusion of all plasma-precoated tissues identified BP and BJVwall with the greatest affinity for S aureus. Perfusions of anticoagulated human blood over all tissues also triggered more platelet adhesion to BP and BJVwall 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 αIIbβ3 and coated or soluble fibrinogen, respectively, interactions abrogated by the αIIbβ3-antagonist eptifibatide. Also, standard antiplatelet therapy (aspirin/ticagrelor) reduced the adherence of S aureus in blood to BJV 3-fold.ConclusionsBinding of plasma fibrinogen to especially BJV grafts enables adhesion of single platelets via αIIbβ3. S aureus then attaches from blood to (activated) bound platelet αIIbβ3 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.

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