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COVID-19 and Hypercoagulability: A Review
Asim Kichloo1,2, Kirk Dettloff2, Michael Aljadah3
1St. Mary's of Saginaw Hospital, Saginaw, MI, USA.
Insights
Thrombotic complications in COVID-19 are linked to a hypercoagulable state. Understanding the pathophysiology and targeting specific pathways may improve outcomes for patients with coronavirus disease 2019.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pathophysiology
Background:
- Thrombotic complications are a significant concern in coronavirus disease (COVID-19), particularly in critically ill patients.
- COVID-19 is associated with a hypercoagulable state, but the underlying pathophysiology remains incompletely understood.
Purpose of the Study:
- To review the proposed pathophysiologic mechanisms contributing to thrombotic complications in COVID-19.
- To discuss current and potential treatment strategies for these thrombotic complications.
Main Methods:
- Literature review of existing studies on COVID-19 and thrombosis.
- Analysis of proposed mechanisms including immune response, endothelial injury, coagulation activation, and fibrinolysis shutdown.
Main Results:
- COVID-19 pathogenesis involves immune response, endothelial cell injury, and activation of coagulation via tissue factor.
- Impaired fibrinolysis also contributes to the hypercoagulable state observed in COVID-19 patients.
Conclusions:
- Effective treatments targeting the identified pathophysiologic pathways are crucial for improving clinical outcomes.
- Addressing thrombotic complications may decrease overall mortality in patients with COVID-19.
Abstract:
Thrombotic complications of the novel coronavirus (COVID-19) are a concerning aspect of the disease, due to the high incidence in critically ill patients and poor clinical outcomes. COVID-19 predisposes patients to a hypercoagulable state, however, the pathophysiology behind the thrombotic complications seen in this disease is not well understood. Several mechanisms have been proposed and the pathogenesis likely involves a host immune response contributing to vascular endothelial cell injury, inflammation, activation of the coagulation cascade via tissue factor expression, and shutdown of fibrinolysis. Treatments targeting these pathways may need to be considered to improve clinical outcomes and decrease overall mortality due to thrombotic complications. In this review, we will discuss the proposed pathophysiologic mechanisms for thrombotic complications in COVID-19, as well as treatment strategies for these complications based on the current literature available.
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