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.
Canzano P, Brambilla M, Porro B, Cosentino N, Tortorici E, Vicini S, Poggio P, Cascella A, Pengo MF, Veglia F, Fiorelli S, Bonomi A, Cavalca V, Trabattoni D, Andreini D, Omodeo Salè E, Parati G, Tremoli E, Camera M. Platelet and Endothelial Activation as Potential Mechanisms Behind the Thrombotic Complications of COVID-19 Patients. JACC Basic Transl Sci 2021 Feb 24. doi: 10.1016/j.jacbts.2020.12.009