Thrombotic storm in coronavirus disease 2019: from underlying mechanisms to its management

Arghavan Zebardast1,2, Tayebeh Latifi1, Mehdi Shabani1

  • 1Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Insights

COVID-19 coagulopathy involves overactive renin-angiotensin system (RAS) and inflammation. Further research is needed for optimal anticoagulant therapy in COVID-19 patients.

Area of Science:

  • Internal Medicine
  • Pathophysiology
  • Infectious Diseases

Background:

  • Coronavirus disease 2019 (COVID-19) presents with high mortality and significant thrombotic complications.
  • Coagulopathy and thrombosis occur frequently in COVID-19 patients, even with anticoagulation, particularly in intensive care settings.
  • The precise mechanisms driving COVID-19 coagulopathy remain incompletely understood.

Approach:

  • This review synthesizes current knowledge on the pathophysiology of COVID-19-induced coagulopathy.
  • It explores potential mechanisms including renin-angiotensin system (RAS) overactivation, cytokine storm, endothelial damage, neutrophil extracellular traps (NETs), and extracellular vesicles (EVs).
  • Diagnostic markers and therapeutic strategies for managing coagulopathy in COVID-19 patients are discussed.

Key Points:

  • COVID-19 coagulopathy is linked to systemic inflammation and endothelial dysfunction.
  • Multiple pathways, including RAS, cytokine storm, NETs, and EVs, contribute to hypercoagulability.
  • Early identification and management of coagulopathy are crucial for COVID-19 patient outcomes.

Conclusions:

  • While several mechanisms contributing to COVID-19 coagulopathy have been identified, a complete understanding is still lacking.
  • Further research is essential to establish optimal anticoagulant regimens and explore novel therapeutic interventions.
  • Continued investigation is needed to refine treatment strategies for COVID-19-associated thrombosis.

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