Thrombotic Events in COVID-19 Are Associated With a Lower Use of Prophylactic Anticoagulation Before Hospitalization and Followed by Decreases in Platelet Reactivity

Clark, Chantal C.; Jukema, Bernard N.; Barendrecht, Arjan D.; Spanjaard, Judith S.; Jorritsma, Nikita K.N.; Smits, Simone M.; Maat, Steven de; Seinen, Cor; Verhoef, Sandra; Parr, Naomi M. J.; Sebastian, Silvie; Koekman, Cornelis A.; Wesel, Annet C.W. van; Goor, Harriët M. R. van; Spijkerman, Roy; Bongers, Suzanne; Vries, Erhard van der; Nierkens, Stefan; Boes, Marianne; Koenderman, Leo; Kaasjager, Karin A H; Maas, Coen

doi:10.3389/fmed.2021.650129

Cited by 9 publications

(7 citation statements)

References 25 publications

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“…Platelet reactivity to physiological stimulus with TRAP was not altered after vaccination in contrast to the dysregulation observed during SARS-CoV-2 infection. 8,24 Clustering analysis of nonstimulated platelets did not detect a phenotypic modification after vaccination, in contrast to the specific cluster activation observed previously during SARS-CoV-2 infection. 8 Hence, our study shows that the vaccination does not generally lead to platelet activation or dysfunctional reactivity.…”

Section: Discussioncontrasting

confidence: 79%

Platelet Surface Protein Expression and Reactivity upon TRAP Stimulation after BNT162b2 Vaccination

et al. 2021

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces a coagulopathy characterized by platelet activation and a hypercoagulable state with an increased incidence of cardiovascular events. The viral spike protein S has been reported to enhance thrombosis formation, stimulate platelets to release procoagulant factors, and promote the formation of platelet–leukocyte aggregates even in absence of the virus. Although SARS-CoV-2 vaccines induce spike protein overexpression to trigger SARS-CoV-2-specific immune protection, thrombocyte activity has not been investigated in this context. Here, we provide the first phenotypic platelet characterization of healthy human subjects undergoing BNT162b2 vaccination. Using mass cytometry, we analyzed the expression of constitutive transmembrane receptors, adhesion proteins, and platelet activation markers in 12 healthy donors before and at five different time points within 4 weeks after the first BNT162b2 administration. We measured platelet reactivity by stimulating thrombocyte activation with thrombin receptor-activating peptide. Activation marker expression (P-selectin, LAMP-3, LAMP-1, CD40L, and PAC-1) did not change after vaccination. All investigated constitutive transmembrane proteins showed similar expressions over time. Platelet reactivity was not altered after BNT162b2 administration. Activation marker expression was significantly lower compared with an independent cohort of mild symptomatic COVID-19 patients analyzed with the same platform. This study reveals that BNT162b2 administration does not alter platelet protein expression and reactivity.

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Section: Discussioncontrasting

confidence: 79%

Platelet Surface Protein Expression and Reactivity upon TRAP Stimulation after BNT162b2 Vaccination

et al. 2021

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“…In a retrospective cohort analysis of 79 hospitalized COVID-19 patients, Clark et al [ 62 ] looked at platelet reactivity. They were unable to add healthy controls for comparison during the early stages of the pandemic, which hampered this study.…”

Section: Resultsmentioning

confidence: 99%

The Role of P-Selectin in COVID-19 Coagulopathy: An Updated Review

Agrati

Sacchi

Tartaglia

et al. 2021

IJMS

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In severe COVID-19, which is characterized by blood clots and neutrophil-platelet aggregates in the circulating blood and different tissues, an increased incidence of cardiovascular complications and venous thrombotic events has been reported. The inflammatory storm that characterizes severe infections may act as a driver capable of profoundly disrupting the complex interplay between platelets, endothelium, and leukocytes, thus contributing to the definition of COVID-19-associated coagulopathy. In this frame, P-selectin represents a key molecule expressed on endothelial cells and on activated platelets, and contributes to endothelial activation, leucocyte recruitment, rolling, and tissue migration. Briefly, we describe the current state of knowledge about P-selectin involvement in COVID-19 pathogenesis, its possible use as a severity marker and as a target for host-directed therapeutic intervention.

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“…Several reports have tried to find out the relationship between the previous use of antithrombotic drugs and the evolution of the disease in terms of mortality, admission to intensive care units, recourse to mechanical ventilation and thus the occurrence of thromboembolic events, but this is done on patients with or without heart disease, to our knowledge, this is the first cohort that studies this question in a rather special population: patients with previous heart disease. Concerning published reports, Chantal et al, 17 reported the same result as our study, with a protective effect on thromboembolic complications (OR = 0.19, 95% CI (0.04; 0.84) P = .029), but no effect on mortality, as well as in the same series, thromboembolic complications were more frequent in patients with high platelet reactivity to TRAP-6 with (0.96 95%CI (0.930.99), P = .02). Rivera et al, 18 reported in a large cohort, in COVID-19 positive patients, prior treatment with direct oral anticoagulants at the time of diagnosis was not associated with an improvement in thromboembolic events or rehospitalization compared to patients not taking OAC therapy, but this was in a population quite different from mine.…”

Section: Discussionmentioning

confidence: 97%

The Impact of Prior Antithrombotic use on Thromboembolic Events in Patients with Cardiovascular Disease and Severe COVID-19 Infection

Bouchlarhem

Boulouiz

Aidouni

et al. 2022

Clin Appl Thromb Hemost

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Objective Our objective in this study was to determine the predictive factors of thromboembolic complications in patients with previous heart disease and severe covid-19 infection and the impact of previous use of antithrombotics on protection against these complications. Methods We conducted a single-center retrospective study of 158 patients with heart disease admitted to an intensive care unit for severe SARS-COV-2 infection. In order to determine the predictive factors, we used logistic regression analysis. Results Out of 158 patients, 22 were complicated by a thrombo-embolic event (13.9%), mean age of our population 64.03 (SD = 15.27), with a male predominance of 98 (62%). For the predictive factors of thromboembolic complications, and after multivariate analysis, we find the short duration of hospitalization (OR = 0.92; 95%CI (0.863–0.983), P = .014, previous use of antithrombotic drugs ((OR = 0.288, 95%CI (0.091–0.911), P = .034 for antiplatelet agents) and (OR = 0.322, 95% CI (0, 131–0.851), P = .021) for anticoagulants) as protective factors, and admission thrombocytosis as a risk factor (OR = 4.58, 95%CI (1.2–10.627), P = .021). D-dimer was not detected as a risk factor, and this can be explained by the characteristics of our population. Although prior use of antithrombotic drugs protects against thromboembolic complications during severe infection, there was no benefit in mortality. Conclusion Prior use of antithrombotic drugs is a protective factor against thromboembolic complications in patients with a history of heart disease but without effect on mortality.

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Thrombotic Events in COVID-19 Are Associated With a Lower Use of Prophylactic Anticoagulation Before Hospitalization and Followed by Decreases in Platelet Reactivity

Cited by 9 publications

References 25 publications

Platelet Surface Protein Expression and Reactivity upon TRAP Stimulation after BNT162b2 Vaccination

Platelet Surface Protein Expression and Reactivity upon TRAP Stimulation after BNT162b2 Vaccination

The Role of P-Selectin in COVID-19 Coagulopathy: An Updated Review

The Impact of Prior Antithrombotic use on Thromboembolic Events in Patients with Cardiovascular Disease and Severe COVID-19 Infection

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