Authors: Barrett TJ, Lee AH, Xia Y, Lin LH, Black M, Cotzia P
PMID: 32757722 PMCID: PMC7478197 DOI: 10.1161/CIRCRESAHA.120.317803
Abstract
The SARS-CoV-2 (SARS-CoV-2 severe acute respiratory syndrome coronavirus 2) coronavirus disease (COVID-19) is a global pandemic. Laboratory testing suggests a coagulopathy with up to 30% of hospitalized patients with COVID-19 developing thrombotic events.1 Platelets are central protagonists in both arterial and venous thrombosis, and virus-platelet interactions contribute to thrombotic risk, promoting an overall procoagulant and inflammatory states during viral infection.2 Furthermore, recent studies report platelets to be hyperactivated in subjects with COVID-19.3
We speculated that in COVID-19, biomarkers of platelet activation are associated with incident thrombosis or death. Thus, we investigated in vivo surrogate biomarkers of platelet activation and vascular inflammation collected in the early phase of COVID-19 hospitalization. Plasma levels of soluble CD40 ligand (sCD40L), P-selectin, the metabolite of thromboxane A2, thromboxane B2 (TxB2), and mean platelet volume (MPV) were assessd. Venous blood samples were collected within 24 hours of hospital admission to NYU Langone Health between March 15 and April 20, 2020, in accordance with the policies of the NYU Langone Health Institutional Review Board. Plasma was collected by centrifugation of PST tubes; MPV was measured during routine care from EDTA tubes on a SYSMEX analyzer.
Keywords: COVID-19; pandemics; platelet activation; thrombosis; thromboxane.
