Skip to main content
. 2022 Dec 1;14(4):358–372. doi: 10.3390/hematolrep14040050

Table 1.

Brief comparison between COVID-19 thrombosis and VITT.

COVID-19 Thrombosis VITT
Pathophysiology
  • -

    Angiotensin II elevation

  • -

    Endotheliopathy

  • -

    Complement activation

  • -

    NETosis and platelet activation
  • -

    Working mechanism: Adenoviral capsid-PF4 or hexon-PF4 interactions

  • -

    Vaccine trace constituents (EDTA, trace cell proteins) possibly promoting inflammation but requires more evidence

  • -

    Non-viral binding partners still unclear

  • -

    Formation of anti-PF4 antibodies
Hemostatic abnormalities
  • -

    Seen in severe COVID-19 usually 6 to 21 days after ICU admission

  • -

    Elevated prothrombin time, D-dimer, and fibrinogen

  • -

    Mild thrombocytopenia
  • -

    Seen 4–28 days after adenoviral COVID-19 vaccination

  • -

    Normal to mildly elevated prothrombin time

  • -

    Elevated D-dimer

  • -

    Decreased fibrinogen

  • -

    Moderate to severe thrombocytopenia
Complications
  • -

    Pulmonary embolism, VTE, DVT, stroke, mesenteric or myocardial infarction

  • -

    Uncommon CVST
  • -

    CVST, thrombosis of adrenal or splanchnic veins

  • -

    Uncommon DVT, stroke, or MI
Treatment
  • -

    Parenteral LMWH (preferred) or unfractionated heparin (UFH)

  • -

    No benefit in oral anticoagulants for thromboprophylaxis (NIH)
  • -

    Non-heparin anticoagulants (argatroban, fondaparinux, or danaparoid),

  • -

    IVIG, plasma exchange therapy

  • -

    Case-to-case glucocorticoid use