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

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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 TFþ platelets, TFþ granulocytes, and TFþ
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.