Evidence map›Paper›PMID 37647652›Full record

ArticleBlood2023

A signature of platelet reactivity in CBC scattergrams reveals genetic predictors of thrombotic disease risk.

Hippolyte Verdier, Patrick Thomas, Joana Batista, Carly Kempster, Harriet McKinney, Nicholas Gleadall, John Danesh, Andrew Mumford, Johan W M Heemskerk, Willem H Ouwehand and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 5 countries.

Hippolyte VerdierInstitut Pasteur, CNRS UMR 3751, Decision and Bayesian Computation, Université Paris Cité, Paris, France.
Patrick ThomasDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Joana BatistaDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0001-5406-6353
Carly KempsterDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0001-5721-1050
Harriet McKinneyDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Nicholas GleadallDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0002-1132-1059
John DaneshBritish Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.
Andrew MumfordSchool of Cellular and Molecular Medicine, University of Bristol, Bristol, United Kingdom.ORCID 0000-0002-5523-511X
Johan W M HeemskerkSynapse Research Institute, Maastricht, The Netherlands.ORCID 0000-0002-2848-5121
Willem H OuwehandDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0002-7744-1790
Kate DownesCambridge Genomics Laboratory, Cambridge University Hospitals NHS Foundation Trust, Cambridge Biomedical Campus, Cambridge, United Kingdom.
William J AstleNational Health Service Blood and Transplant, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0001-8866-6672
Ernest TurroDepartment of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0002-1820-6563
University of Cambridge · GBNational Health Service · GBCambridge University Hospitals NHS Foundation Trust · GBCentre National de la Recherche Scientifique · FRSynapse (Netherlands) · NL

Funding

Medical Research Council MR/L003120/1
6 · The paper itself

Abstract

Genetic studies of platelet reactivity (PR) phenotypes may identify novel antiplatelet drug targets. However, such studies have been limited by small sample sizes (n < 5000) because of the complexity of measuring PR. We trained a model to predict PR from complete blood count (CBC) scattergrams. A genome-wide association study of this phenotype in 29 806 blood donors identified 21 distinct associations implicating 20 genes, of which 6 have been identified previously. The effect size estimates were significantly correlated with estimates from a study of flow cytometry-measured PR and a study of a phenotype of in vitro thrombus formation. A genetic score of PR built from the 21 variants was associated with the incidence rates of myocardial infarction and pulmonary embolism. Mendelian randomization analyses showed that PR was causally associated with the risks of coronary artery disease, stroke, and venous thromboembolism. Our approach provides a blueprint for using phenotype imputation to study the determinants of hard-to-measure but biologically important hematological traits.

Indexed as

Platelet Aggregation InhibitorsThrombosisBlood Cell CountBlood PlateletsGenome-Wide Association StudyHumansPlatelet Aggregation Inhibitors

Identifiers

PMID37647652
PMCPMC10733829
OpenAlexW4386279217

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.