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

This record contains raw data related to the article "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-<br> based tissue factor (TF)-mediated activation of coagulation, procoagulant microvesicles (MVs) release, and<br> massive platelet activation. COVID-19 patients have higher levels of TFþ platelets, TFþ granulocytes, and TFþ<br> MVs than healthy subjects and coronary artery disease patients. Plasma MV-associated thrombin generation is<br> present in prophylactic anticoagulated patients. A sustained platelet activation in terms of P-selectin expression<br> and platelet–leukocyte aggregate formation, and altered nitric oxide/prostacyclin synthesis are also observed.<br> COVID-19 plasma, added to the blood of healthy subjects, induces platelet activation similar to that observed<br> in vivo. This effect was blunted by pre-incubation with tocilizumab, aspirin, or a P2Y12 inhibitor.