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

Paola Canzano1, Marta Brambilla1, Benedetta Porro1

  • 1Centro Cardiologico Monzino IRCCS, Milan, Italy.

JACC. Basic to Translational Science
|March 2, 2021
PubMed

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.

Keywords:
ADP, adenosine diphosphateCAD, coronary artery diseaseCOVID-19COVID-19, coronavirus disease-2019CRP, C-reactive proteinGPA, granulocyte–platelet aggregatesHS, healthy subjectIL, interleukinIL-6IL-6R, interleukin-6 receptorLMWH, low-molecular-weight heparinMPA, monocyte–platelet aggregatesMV, microvesicleNO, nitric oxideNOS, nitric oxide synthasePGI2, prostacyclinPLA, platelet–leukocyte aggregatesPS, phosphatidylserineSARS-CoV-2, severe acute respiratory syndrome-coronavirus-2TF, tissue factorantiplatelet drugscirculating microvesiclesplatelet activationtissue factor

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