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ASAIO journal (American Society for Artificial Internal Organs : 1992) · 2025

Understanding Platelet Activation in the Aeson Bioprosthetic Total Artificial Heart: Insights From Aspirin Treatment and Outcomes.

СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Smadja David M, Roux de Bezieux Joseph, Peronino Christophe, Jilet Léa, Ivak Peter, Pya Yuri, Philippe Aurélien, Latremouille Christian, Gustafsson Finn, Ramjankhan Faiz Z, Roussel Jean Christian, Courbebaisse Marie, Parfait Béatrice, Lebeaux David, Friedlander Gérard, Vincentelli André, Flecher Erwan, Gaussem Pascale, Jansen Piet, Netuka Ivan

Аннотация

This study aimed to assess platelet activation following implantation of the Aeson bioprosthetic total artificial heart (A-TAH). We monitored plasma levels of platelet activation markers in patients receiving A-TAH support (n = 16) throughout the follow-up period. Before implantation, soluble CD40 ligand (sCD40L) levels averaged 3,909.06 pg/ml (standard deviation [SD] = 3,772.37), remaining stable postimplantation at 3,964.56 pg/ml (SD = 2,198.85) during months 1-3 and at 3,519.27 pg/ml (SD = 1,647.04) during months 3-6. Similarly, P-selectin (sP-sel) levels were 35,235.36 pg/ml (SD = 14,940.47) before implantation, stabilizing to 33,158.96 pg/ml (SD = 9,023.11) (1-3 months) and 31,022.58 pg/ml (SD = 9,249.95) (3-6 months). Preimplantation platelet factor 4 (PF4) measured 2,593.47 ng/ml (SD = 2,167.85), remaining consistent at 2,136.10 ng/ml (SD = 1,264.47) (1-3 months) and 1,991.26 ng/ml (SD = 1,234.16) (3-6 months). Levels of neutrophil-activating peptide 2 (NAP2) were also steady, measuring 785.63 ng/ml (SD = 605.26) preimplantation, 935.10 ng/ml (SD = 517.73) at 1-3 months, and 907.21 ng/ml (SD = 501.96) at 3-6 months postimplantation. Importantly, neither aspirin nor heparin treatment affected these platelet biomarker levels. No correlation was observed between platelet activation marker levels and clinical outcomes such as pericardial effusion, nor with the timing of aspirin initiation and drain removal. Our findings confirm that A-TAH does not trigger platelet activation. The lack of association between aspirin, platelet activation, and clinical outcomes suggests the possibility of discontinuing antiplatelet therapy following A-TAH implantation in the future.

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