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J Thromb Haemost . Fibrinolysis and COVID-19: A Plasmin Paradox

tetano

Editor, Senior Moderator
J Thromb Haemost


. 2020 Jun 16.
doi: 10.1111/jth.14960. Online ahead of print.
Fibrinolysis and COVID-19: A Plasmin Paradox


Robert L Medcalf[SUP] 1 [/SUP], Charithani B Keragala[SUP] 1 [/SUP], Paul S Myles[SUP] 2 3 [/SUP]



Affiliations

Abstract

The COVID-19 pandemic has provided many challenges in the field of thrombosis and haemostasis. Among these is a novel form of coagulopathy that includes exceptionally high levels of D-dimer. D-dimer is a marker of poor prognosis, but does this also imply a causal relationship? These spectacularly raised D-dimer levels may actually signify the failing attempt of the fibrinolytic system to remove fibrin and necrotic tissue from the lung parenchyma, being consumed or overwhelmed in the process. Indeed, recent studies suggest that increasing fibrinolytic activity might offer hope for patients with critical disease and severe respiratory failure. However, the fibrinolytic system can also be harnessed by coronavirus to promote infectivity and where anti-fibrinolytic measures would also seem appropriate. Hence, there is a clinical paradox where plasmin formation can be either deleterious or beneficial in COVID-19, but not at the same time. Hence, it all comes down to timing.

Keywords: COVID-19; D-dimer; coronavirus; fibrinolysis; tranexamic acid.
 
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