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Updated: Oct 5, 2025
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Longitudinal multiparametric characterization of platelet dysfunction in COVID-19: Effects of disease severity,
Alexey A Martyanov1, Anna E Boldova2, Maria G Stepanyan3
1Center for Theoretical Problems of Physico-Сhemical Pharmacology, Russian Academy of Sciences, 30 Srednyaya Kalitnikovskaya str., Moscow 109029, Russia; National Medical Research Centеr of Pediatric Hematology, Oncology and Immunology named after Dmitry Rogachev, 1 Samory Mashela St, Moscow 117198, Russia; Institute for Biochemical Physics (IBCP), Russian Academy of Sciences (RAS), Moscow, Kosyigina 4, 119334, Russia.
Insights
COVID-19 patients exhibit platelet dysfunction, characterized by impaired responses to activation. This thrombocytopathy appears to stem from intravascular coagulation, not direct viral effects or inflammation, and may improve with heparin treatment.
Area of Science:
- Hematology
- Virology
- Immunology
Background:
- Platelet functional defects in COVID-19 have been observed but their origins and significance remain unclear.
- Understanding these platelet abnormalities is crucial for managing COVID-19 complications.
Purpose of the Study:
- To characterize the nature and underlying mechanisms of thrombocytopathy in patients with COVID-19.
Main Methods:
- Flow cytometry and aggregometry were used to analyze platelet function in 46 COVID-19 patients.
- Coagulation, inflammatory markers, and NETosis were assessed.
- Platelet responses were evaluated across different COVID-19 severity groups (non-ICU, ICU, ECMO).
Main Results:
- COVID-19 patients showed increased procoagulant platelets and decreased agonist-induced platelet activation (GPIb shedding, P-Selectin exposure, aggregation).
- Severe cases (ECMO) exhibited more pronounced thrombocytopenia and platelet dysfunction.
- Increased NETosis correlated with platelet dysfunction, while SARS-CoV-2 RNA presence did not.
- Low molecular weight heparin (LMWH) treatment improved platelet parameters.
Conclusions:
- Platelet dysfunction in COVID-19 is primarily due to intravascular coagulation-induced refractoriness.
- Mechanisms are distinct from inflammation or direct viral activation.
- Findings suggest potential therapeutic strategies targeting coagulation pathways.
Introduction:
Defects of platelet functional responses in COVID-19 were reported, but their origin and pathophysiological significance are unclear. The objective of this study was to characterize the thrombocytopathy in COVID-19.
Materials And Methods:
Analysis of platelet functional responses to activation by flow cytometry and aggregometry in 46 patients with confirmed COVID-19 of different severity (non-ICU, ICU, and ECMO) over the course of hospitalization alongside with plasma coagulation, inflammatory markers (CRP, fibrinogen, NETosis assays in smears) was performed.
Results And Conclusions:
All patients had increased baseline percentage of procoagulant platelets (healthy: 0.9 ± 0.5%; COVID-19: 1.7 ± 0.6%). Patients had decreased agonist-induced platelet GPIb shedding (1.8 ± 0.7 vs 1.25 ± 0.4), P-Selectin exposure (1.51 ± 0.21 vs 1.1 ± 0.3) and aggregation. The values of these parameters among the non-ICU and ICU cohorts differed modestly, while the ECMO cohort differed significantly. Only ECMO patients had pronounced thrombocytopenia. While inflammatory markers improved over time, the observed platelet functional responses changed only moderately. SARS-CoV-2 RNA was found in 8% of blood samples and it did not correlate with platelet counts or responses. All patients had increased NETosis that moderately correlated with platelet dysfunction. High cumulative dosages of LMWH (average > 12,000 IU/day over 5 days) resulted in an improvement in platelet parameters. The observed pattern of platelet refractoriness was reproduced by in vitro pre-treatment of washed platelets with subnanomolar thrombin or perfusion of blood through a collagen-covered flow chamber. We conclude that platelet dysfunction in COVID-19 is consistent with the intravascular-coagulation-induced refractoriness rather than with an inflammation-induced mechanism or a direct activation by the virus.
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