Collective review
Fibrinolysis Shutdown in COVID-19: Clinical Manifestations, Molecular Mechanisms, and Therapeutic Implications

https://doi.org/10.1016/j.jamcollsurg.2021.02.019Get rights and content

The COVID-19 pandemic has introduced a global public health threat unparalleled in our history. The most severe cases are marked by ARDS attributed to microvascular thrombosis. Hypercoagulability, resulting in a profoundly prothrombotic state, is a distinct feature of COVID-19 and is accentuated by a high incidence of fibrinolysis shutdown. The aims of this review were to describe the manifestations of fibrinolysis shutdown in COVID-19 and its associated outcomes, review the molecular mechanisms of dysregulated fibrinolysis associated with COVID-19, and discuss potential implications and therapeutic targets for patients with severe COVID-19.

Abbreviations and Acronyms

DIC
disseminated intravascular coagulation
INR
international normalized ratio
LY30
lysis at 30 minutes
MCF
maximum clot firmness
ML
maximum lysis
PAI-1
plasminogen activator inhibitor 1
ROTEM
rotational thromboelastometry
SARS-CoV-2
severe acute respiratory syndrome coronavirus 2
TAFI
thrombin activatable fibrinolysis inhibitor
TEG
thrombelastography
tPA
tissue plasminogen activator
VTE
venous thromboembolism

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Disclosure Information: Nothing to disclose.

Disclosures outside the scope of this work: Drs HB Moore and EE Moore have received grant support from Haemonetics and Instrumentation Laboratories; have patents pending related to coagulation and fibrinolysis diagnostics and therapeutic fibrinolytics; and are co-founders with stock options in Thrombo Therapeutics, Inc. Dr EE Moore has received grant support from Stago, Hemosonics, and Diapharma. Dr Meizoso has nothing to declare.

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© 2021 by the American College of Surgeons. Published by Elsevier Inc. All rights reserved.