Platelet and Endothelial Activation as Potential Mechanisms Behind the Thrombotic Complications of COVID-19 Patients

The authors hypothesized that the cytokine storm described in COVID-19 patients may lead to consistent cell-based tissue factor (TF)-mediated activation of coagulation, procoagulant microvesicles (MVs) release, and massive platelet activation. COVID-19 patients have higher levels of TF(+) platelets,...

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Detalles Bibliográficos
Autores principales: Canzano, Paola, Brambilla, Marta, Porro, Benedetta, Cosentino, Nicola, Tortorici, Elena, Vicini, Stefano, Poggio, Paolo, Cascella, Andrea, Pengo, Martino F., Veglia, Fabrizio, Fiorelli, Susanna, Bonomi, Alice, Cavalca, Viviana, Trabattoni, Daniela, Andreini, Daniele, Omodeo Salè, Emanuela, Parati, Gianfranco, Tremoli, Elena, Camera, Marina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Clinical Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7904280/
https://www.ncbi.nlm.nih.gov/pubmed/33649738
http://dx.doi.org/10.1016/j.jacbts.2020.12.009
Descripción
Sumario:The authors hypothesized that the cytokine storm described in COVID-19 patients may lead to consistent cell-based tissue factor (TF)-mediated activation of coagulation, procoagulant microvesicles (MVs) release, and massive platelet activation. COVID-19 patients have higher levels of TF(+) platelets, TF(+) granulocytes, and TF(+) MVs than healthy subjects and coronary artery disease patients. Plasma MV-associated thrombin generation is present in prophylactic anticoagulated patients. A sustained platelet activation in terms of P-selectin expression and platelet–leukocyte aggregate formation, and altered nitric oxide/prostacyclin synthesis are also observed. COVID-19 plasma, added to the blood of healthy subjects, induces platelet activation similar to that observed in vivo. This effect was blunted by pre-incubation with tocilizumab, aspirin, or a P2Y(12) inhibitor.

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