Prognostic value of an automated thrombin generation assay in COVID-19 patients entering hospital: A multicentric, prospective observational study

Gris, Jean‐Christophe; Guillotin, Florence; Santos, Taissa Pereira dos; Chéa, Mathias; Loubet, Paul; Laureillard, Didier; Sotto, Albert; Muller, Laurent; Barbar, Saber Davide; Roger, Claire; Lefrant, Jean‐Yves; Jung, Boris; Klouche, Kada; Mura, Thibault; Quéré, Isabelle; Pérez‐Martin, A.

doi:10.1016/j.thromres.2022.12.019

Cited by 1 publication

(2 citation statements)

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“…In quite a few cases with SARS-CoV-2 pneumonia, testing results by this approach were not consistent with the anticipated increase of thrombin generation. For instance, most studies demonstrated that the patients had delayed 'Lag Time' (time until thrombin is generated) and/or unchanged 'Time to Peak Thrombin' (time needed to reach the peak level of generated thrombin) (42,(61)(62)(63)(64)(65)(66)(67)(68)(69). Furthermore, only a subset of studies reported increases in 'Peak Thrombin' , 'Endogenous Thrombin Potential' (ETP), and thrombin generation 'Velocity' .…”

Section: Thrombin Generationmentioning

confidence: 99%

“…Furthermore, only a subset of studies reported increases in 'Peak Thrombin' , 'Endogenous Thrombin Potential' (ETP), and thrombin generation 'Velocity' . These unexpected observations in the CAT assay may be attributed to elevated plasma levels of anticoagulant factors, such as thrombomodulin (TM) -a tissue factor pathway inhibitor (TFPI), existing in certain COVID-19 patients, as shown by published data (41,42,68,70). Moreover, it is crucial to conduct further evaluations to determine the reliability of using Coagulation Assays (CAT) for testing COVID-19 samples that potentially contain antiphospholipid antibodies (aPLs).…”

Section: Thrombin Generationmentioning

confidence: 99%

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COVID-19: Not a thrombotic disease but a thromboinflammatory disease

He,

Blombäck,

Wallén

2024

ujms

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While Coronavirus Disease in 2019 (COVID-19) may no longer be classified as a global public health emergency, it still poses a significant risk at least due to its association with thrombotic events. This study aims to reaffirm our previous hypothesis that COVID-19 is fundamentally a thrombotic disease. To accomplish this, we have undertaken an extensive literature review focused on assessing the comprehensive impact of COVID-19 on the entire hemostatic system. Our analysis revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection significantly enhances the initiation of thrombin generation. However, it is noteworthy that the thrombin generation may be modulated by specific anticoagulants present in patients’ plasma. Consequently, higher levels of fibrinogen appear to play a more pivotal role in promoting coagulation in COVID-19, as opposed to thrombin generation. Furthermore, the viral infection can stimulate platelet activation either through widespread dissemination from the lungs to other organs or localized effects on platelets themselves. An imbalance between Von Willebrand Factor (VWF) and ADAMTS-13 also contributes to an exaggerated platelet response in this disease, in addition to elevated D-dimer levels, coupled with a significant increase in fibrin viscoelasticity. This paradoxical phenotype has been identified as ‘fibrinolysis shutdown’. To clarify the pathogenesis underlying these hemostatic disorders in COVID-19, we also examined published data, tracing the reaction process of relevant proteins and cells, from ACE2-dependent viral invasion, through induced tissue inflammation, endothelial injury, and innate immune responses, to occurrence of thrombotic events. We therefrom understand that COVID-19 should no longer be viewed as a thrombotic disease solely based on abnormalities in fibrin clot formation and proteolysis. Instead, it should be regarded as a thromboinflammatory disorder, incorporating both classical elements of cellular inflammation and their intricate interactions with the specific coagulopathy.

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