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The authors evaluated 38 patients with confirmed SARS-CoV-2 infection and 24 controls to evaluate the mechanisms of respiratory failure and complicating renal and myocardial involvement in COVID-19 patients. Organ involvement and prothrombotic features appear to be linked by immunothrombosis. Inflammatory microvascular thrombi are evident in the lung, kidney, and heart of COVID-19 patients. The blood of COVID-19 patients has neutrophil–platelet aggregates and a distinct neutrophil and platelet activation pattern, which is associated with disease severity. Patients with intermediate-severity disease have an exhausted platelet and hyporeactive neutrophil phenotype, while patients with severe disease have excessive platelet and neutrophil activation. Dysregulated immunothrombosis in patients with COVID-19 pneumonia is associated with ARDS and systemic hypercoagulability.
Immunothrombotic dysregulation is a marker of the severity of disease in patients with COVID-19 pneumonia, and further research is warranted to evaluate the role of immunothrombosis.
This abstract is available on the publisher's site.
SARS-CoV-2 infection causes severe pneumonia (COVID-19), but the mechanisms of subsequent respiratory failure and complicating renal and myocardial involvement are poorly understood. In addition, a systemic prothrombotic phenotype has been reported in COVID-19 patients.
A total of 62 subjects were included in our study (n=38 patients with RT-PCR confirmed COVID-19 and n=24 non-COVID-19 controls). We performed histopathological assessment of autopsy cases, surface-marker based phenotyping of neutrophils and platelets, and functional assays for platelet, neutrophil functions as well as coagulation tests.
We provide evidence that organ involvement and prothrombotic features in COVID-19 are linked by immunothrombosis. We show that in COVID-19 inflammatory microvascular thrombi are present in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets and fibrin. COVID-19 patients also present with neutrophil-platelet aggregates and a distinct neutrophil and platelet activation pattern in blood, which changes with disease severity. Whereas cases of intermediate severity show an exhausted platelet and hyporeactive neutrophil phenotype, severely affected COVID-19 patients are characterized by excessive platelet and neutrophil activation compared to healthy controls and non-COVID-19 pneumonia. Dysregulated immunothrombosis in SARS-CoV-2 pneumonia is linked to both ARDS and systemic hypercoagulability.
Taken together, our data point to immunothrombotic dysregulation as a key marker of disease severity in COVID-19. Further work is necessary to determine the role of immunothrombosis in COVID-19.
Immunothrombotic Dysregulation in COVID-19 Pneumonia Is Associated With Respiratory Failure and Coagulopathy
Circulation 2020 Jul 28;[EPub Ahead of Print], L Nicolai, A Leunig, S Brambs, R Kaiser, T Weinberger, M Weigand, M Muenchhoff, JC Hellmuth, S Ledderose, H Schulz, C Scherer, M Rudelius, M Zoller, D Höchter, O Keppler, D Teupser, B Zwißler, M Bergwelt-Baildon, S Kääb, S Massberg, K Pekayvaz, K Stark