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Thrombotic Mechanism Involving Platelet Activation, Hypercoagulability and Hypofibrinolysis in Coronavirus Disease
Hideo Wada1, Katsuya Shiraki1, Hideto Shimpo2
1Department of General and Laboratory Medicine, Mie Prefectural General Medical Center, Yokkaichi 5450-132, Japan.
Insights
COVID-19 is linked to increased thrombosis, differing from bacterial infections. Key differences involve platelet activation and fibrinolysis, suggesting unique mechanisms driving blood clots in COVID-19 patients.
Area of Science:
- Medical Science
- Infectious Diseases
- Hematology
Background:
- Coronavirus disease 2019 (COVID-19) has emerged globally, frequently associated with thrombotic complications.
- Thrombosis in COVID-19 patients presents distinct characteristics compared to bacterial infections.
- Reported incidences of thrombosis in COVID-19 range from 6-26%, with venous thromboembolism (VTE) and arterial thrombosis being significant concerns.
Purpose of the Study:
- To investigate and differentiate the thrombotic complications in COVID-19 from those observed in bacterial infections.
- To elucidate the specific hemostatic and fibrinolytic profiles associated with COVID-19-related thrombosis.
- To identify potential mechanisms underlying hypercoagulability in COVID-19.
Main Methods:
- Comparative analysis of thrombosis incidence and characteristics between COVID-19 and bacterial sepsis.
- Measurement and comparison of fibrin-related markers, including D-dimer and soluble C-type lectin-like receptor 2 (sCLEC-2) levels.
- Assessment of coagulation and fibrinolysis states, focusing on platelet activation and fibrinolytic activity.
Main Results:
- COVID-19 exhibits a distinct thrombotic profile compared to bacterial infections, with varying incidences of venous (4.8-21.0%) and arterial (0.7-3.7%) thrombosis.
- Disseminated intravascular coagulation (DIC) is less common in COVID-19 than in bacterial infections.
- Elevated sCLEC-2 levels are observed in COVID-19, contrasting with extremely high D-dimer levels in bacterial infections, indicating hypercoagulable and hypofibrinolytic states with platelet activation in COVID-19.
Conclusions:
- COVID-19 is associated with a unique hemostatic profile characterized by hypercoagulability, hypofibrinolysis, and marked platelet activation.
- These distinct pathophysiological states contribute to the thrombotic complications observed in COVID-19 patients.
- Understanding these differences is crucial for managing thrombosis in COVID-19 and differentiating it from sepsis-induced coagulopathy.
Abstract:
Coronavirus disease 2019 (COVID-19) has spread, with thrombotic complications being increasingly frequently reported. Although thrombosis is frequently complicated in septic patients, there are some differences in the thrombosis noted with COVID-19 and that noted with bacterial infections. The incidence (6-26%) of thrombosis varied among reports in patients with COVID-19; the incidences of venous thromboembolism and acute arterial thrombosis were 4.8-21.0% and 0.7-3.7%, respectively. Although disseminated intravascular coagulation (DIC) is frequently associated with bacterial infections, a few cases of DIC have been reported in association with COVID-19. Fibrin-related markers, such as D-dimer levels, are extremely high in bacterial infections, whereas soluble C-type lectin-like receptor 2 (sCLEC-2) levels are high in COVID-19, suggesting that hypercoagulable and hyperfibrinolytic states are predominant in bacterial infections, whereas hypercoagulable and hypofibrinolytic states with platelet activation are predominant in COVID-19. Marked platelet activation, hypercoagulability and hypofibrinolytic states may cause thrombosis in patients with COVID-19.
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