Left ventricular assist device implantation causes platelet dysfunction and proinflammatory platelet-neutrophil interaction
Autor: | Tiago Granja, Harry Magunia, Patricia Schüssel, Claudius Fischer, Thomas Prüfer, David Schibilsky, Lina Serna-Higuita, Hans Peter Wendel, Christian Schlensak, Helene Häberle, Peter Rosenberger, Andreas Straub |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: | |
Zdroj: | Platelets, Vol 33, Iss 1, Pp 132-140 (2022) |
Druh dokumentu: | article |
ISSN: | 0953-7104 1369-1635 09537104 |
DOI: | 10.1080/09537104.2020.1859101 |
Popis: | Blood flow through left ventricular assist devices (LVAD) may induce activation and dysfunction of platelets. Dysfunctional platelets cause coagulation disturbances and form platelet-neutrophil conjugates (PNC), which contribute to inflammatory tissue damage. This prospective observational cohort study investigated patients, who underwent implantation of a LVAD (either HeartMate II (HM II) (n = 7) or HeartMate 3 (HM 3) (n = 6)) and as control patients undergoing coronary artery bypass grafting (CABG) and/or aortic valve replacement (AVR) (n = 10). We performed platelet and leukocyte flow cytometry, analysis of platelet activation markers, and platelet aggregometry. Platelet CD42b expression was reduced at baseline and perioperatively in HM II/3 compared to CABG/AVR patients. After surgery the platelet activation marker β-thromboglobulin and platelet microparticles increased in all groups while platelet aggregation decreased. Platelet aggregation was more significantly impaired in LVAD compared to CABG/AVR patients. PNC were higher in HM II compared to HM 3 patients. We conclude that LVAD implantation is associated with platelet dysfunction and proinflammatory platelet-leukocyte binding. These changes are less pronounced in patients treated with the newer generation LVAD HM 3. Future research should identify device-specific LVAD features, which are associated with the least amount of platelet activation to further improve LVAD therapy. |
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