Authors: Zaid Y, Guessous F, Puhm F, Elhamdani W, Chentoufi L, Morris AC
PMID: 33560374 PMCID: PMC7846461 DOI: 10.1182/bloodadvances.2020003513
Abstract
In addition to preserving homeostasis and contributing to immunity, platelets may exhibit a dysregulated state, in acute respiratory distress syndrome (ARDS) and potentially exacerbate lung injury.Although thrombocytopenia has been associated with increased mortality in ARDS,and particularly in patients infected with H1N1 influenza, analysis of quantitative changes in platelet activation levels in ARDS and of how these may differ between the various etiologies of ARDS is limited.
Coronavirus disease 2019 (COVID-19) is clinically associated with a high incidence of thrombosis and with a high burden of pulmonary and systemic platelet-rich microthrombi.Interestingly, in contrast to a cohort of patients with H1N1-influenza infection with ARDS of equal severity, patients with COVID-19 ARDS displayed a 9 times higher burden of alveolar capillary platelet-rich microthrombi. Patients with COVID-19 who were autopsied demonstrated an abundance of platelet-rich thrombi in the pulmonary and systemic microvasculature despite having received anticoagulation therapy. Clinically, thromboelastography (TEG) studies have also demonstrated a hypercoagulable profile in patients with severe COVID-19, despite prophylactic anticoagulation. TEG profiles remained hypercoagulable, with parameters suggesting a significant hypercoagulable effect from platelet activity and fibrin.
Keywords: platelet reactivity, thrombin, COVID-19, ARDS, acute respiratory distress syndrome
