Evidence map›Paper›PMID 34957266›Full record

ArticleFrontiers in cardiovascular medicine2021

Adverse Outcome in COVID-19 Is Associated With an Aggravating Hypo-Responsive Platelet Phenotype.

Waltraud C Schrottmaier, Anita Pirabe, David Pereyra, Stefan Heber, Hubert Hackl, Anna Schmuckenschlager, Laura Brunnthaler, Jonas Santol, Kerstin Kammerer, Justin Oosterlee and 12 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 29 citations in OpenAlex.

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  9. Alterations in platelet proteome signature and impaired platelet integrin αJournal of thrombosis and haemostasis : JTH · 2023
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  12. Early SARS-CoV-2 infection: Platelet-neutrophil complexes and platelet function.Research and practice in thrombosis and haemostasis · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 4 institutions in 2 countries.

Waltraud C SchrottmaierDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Anita PirabeDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
David PereyraDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Stefan HeberInstitute of Physiology, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Hubert HacklInstitute of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
Anna SchmuckenschlagerDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Laura BrunnthalerDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Jonas SantolDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Kerstin KammererDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Justin OosterleeDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Erich PawelkaDepartment of Medicine IV, Clinic Favoriten, Vienna, Austria.
Sonja M TreiberDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Abdullah O KhanInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Matthew PughInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Marianna T TraugottDepartment of Medicine IV, Clinic Favoriten, Vienna, Austria.
Christian SchörgenhoferDepartment of Clinical Pharmacology, Medical University of Vienna, General Hospital Vienna, Vienna, Austria.
Tamara SeitzDepartment of Medicine IV, Clinic Favoriten, Vienna, Austria.
Mario KarolyiDepartment of Medicine IV, Clinic Favoriten, Vienna, Austria.
Bernd JilmaDepartment of Clinical Pharmacology, Medical University of Vienna, General Hospital Vienna, Vienna, Austria.
Julie RayesInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Alexander ZoufalyDepartment of Medicine IV, Clinic Favoriten, Vienna, Austria.
Alice AssingerDepartment of Vascular Biology and Thrombosis Research, Centre of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATUniversity of Birmingham · GBInnsbruck Medical University · ATVienna General Hospital · AT

Funding

Austrian Science Fund FWF P 32064Austrian Science Fund FWF P 34783British Heart Foundation FS/IBSRF/20/25039Wellcome Trust
6 · The paper itself

Abstract

Thromboembolic complications are frequently observed in Coronavirus disease 2019 (COVID-19). While COVID-19 is linked to platelet dysregulation, the association between disease outcome and platelet function is less clear. We prospectively monitored platelet activation and reactivity in 97 patients during the first week of hospitalization and determined plasma markers of platelet degranulation and inflammation. Adverse outcome in COVID-19 was associated with increased basal platelet activation and diminished platelet responses, which aggravated over time. Especially GPIIb/IIIa responses were abrogated, pointing toward impeded platelet aggregation. Moreover, platelet-leukocyte aggregate formation was diminished, pointing toward abrogated platelet-mediated immune responses in COVID-19. No general increase in plasma levels of platelet-derived granule components could be detected, arguing against platelet exhaustion. However, studies on platelets from healthy donors showed that plasma components in COVID-19 patients with unfavorable outcome were at least partly responsible for diminished platelet responses. Taken together this study shows that unfavorable outcome in COVID-19 is associated with a hypo-responsive platelet phenotype that aggravates with disease progression and may impact platelet-mediated immunoregulation.

Indexed as

COVID-19infectionoutcomeplateletplatelet activation and reactivityplatelet dysfunctionplatelet-leukocyte interaction

Identifiers

PMID34957266
PMCPMC8702807
OpenAlexW4200201338

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.