Abstract
The cardinal pathology of coronavirus disease 2019 (COVID-19) is a primary infection
of pulmonary tract cells by severe acute respiratory syndrome coronavirus 2, provoking
a local inflammatory response, often accompanied by cytokine storm and acute respiratory
distress syndrome, especially in patients with severe disease. Systemic propagation
of the disease may associate with thrombotic events, including deep vein thrombosis,
pulmonary embolism, and thrombotic microangiopathy, which are important causes of
morbidity and mortality in patients with COVID-19. This narrative review describes
current knowledge of the pathophysiological mechanisms of COVID-19-associated coagulopathy,
with focus on prothrombotic changes in hemostatic mediators, including plasma levels
of clotting factors, natural anticoagulants, components of fibrinolytic system, and
platelets. It will also highlight the central role of endothelial cells in COVID-19-associated
coagulopathy. This narrative review discusses also potential therapeutic strategies
for managing thrombotic complications. Awareness by medical experts of contributors
to the pathogenesis of thrombotic events in COVID-19 is imperative to develop therapeutics
not limited to regular anticoagulants. Instituting cooperation among medical personnel
and researchers may lessen this novel virus' impact now, and in the event of recurrence.
Keywords
SARS-CoV-2 - COVID-19 - coagulopathy - thrombosis