Thromboembolic complications in critically ill COVID-19 patients are associated with impaired fibrinolysis
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RESEARCH
Thromboembolic complications in critically ill COVID‑19 patients are associated with impaired fibrinolysis Jan Matthias Kruse1†, Abakar Magomedov2†, Annika Kurreck3, Frédéric H. Münch1, Roland Koerner1, Julian Kamhieh‑Milz4,5, Andreas Kahl1, Inka Gotthardt1, Sophie K. Piper6,7, Kai‑Uwe Eckardt1, Thomas Dörner8,9 and Daniel Zickler1*
Abstract Background: There is emerging evidence for enhanced blood coagulation in coronavirus 2019 (COVID-19) patients, with thromboembolic complications contributing to morbidity and mortality. The mechanisms underlying this pro‑ thrombotic state remain enigmatic. Further data to guide anticoagulation strategies are urgently required. Methods: We used viscoelastic rotational thromboelastometry (ROTEM) in a single-center cohort of 40 critically ill COVID-19 patients. Results: Clear signs of a hypercoagulable state due to severe hypofibrinolysis were found. Maximum lysis, especially following stimulation of the extrinsic coagulation system, was inversely associated with an enhanced risk of thrombo‑ embolic complications. Combining values for maximum lysis with D-dimer concentrations revealed high sensitivity and specificity of thromboembolic risk prediction. Conclusions: The study identifies a reduction in fibrinolysis as an important mechanism in COVID-19-associated coagulopathy. The combination of ROTEM and D-dimer concentrations may prove valuable in identifying patients requiring higher intensity anticoagulation. Keywords: COVID-19, Coagulopathy, Hypofibrinolysis, ROTEM, D-dimers Background The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing coronavirus disease 2019 (COVID-19) has led to a global pandemic posing a major threat to humans [1]. More than 500 000 deaths related to COVID-19 have been so far reported [2].
*Correspondence: [email protected] † Jan Matthias Kruse and Abakar Magomedov have contributed equally to this work 1 Department of Nephrology and Medical Intensive Care, Charité – Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany Full list of author information is available at the end of the article
SARS-CoV-2 primarily affects the respiratory system with a widely heterogeneous clinical presentation, ranging from none or minimal symptoms to significant hypoxia with viral pneumonia, potentially leading to severe acute respiratory distress syndrome (ARDS) and cytokine storm [3]. ARDS with related lung injury is considered one of the main causes of death in COVID-19 patients [4]. However, there is emerging evidence that involvement of other pathomechanisms contributes to morbidity and mortality. Both clinical and autopsy studies have revealed a high incidence of venous and arterial thromboembolic events, including pulmonary embolism, even in patients receiving therapeutic anticoagulation [5–7]. These
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