Platelet and endothelial activation as potential mechanisms behind the thrombotic complications of COVID-19 patients
P Canzano, M Brambilla, B Porro, N Cosentino… - Basic to Translational …, 2021 - jacc.org
P Canzano, M Brambilla, B Porro, N Cosentino, E Tortorici, S Vicini, P Poggio, A Cascella…
Basic to Translational Science, 2021•jacc.orgThe 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 …
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 …
Summary
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 P2Y12 inhibitor.
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