Evidence map›Paper›PMID 25360888›Full record

Observational studyPloS one2014

Genetic determinants of on-aspirin platelet reactivity: focus on the influence of PEAR1.

Morten Würtz, Peter H Nissen, Erik Lerkevang Grove, Steen Dalby Kristensen, Anne-Mette Hvas

Registry-linked trialOpen access · goldAbstract readObservational Study
In one paragraph

Observational study in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01383304 (Is a Reduced Biochemical Response to Aspirin Associated With Increased Cardiovascular Morbidity and Mortality in High Risk Patients With Coronary Artery Disease?), which is not on this map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 8% 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.

NCT01383304 unknown statusnot on this map

Is a Reduced Biochemical Response to Aspirin Associated With Increased Cardiovascular Morbidity and Mortality in High Risk Patients With Coronary Artery Disease?

TypeobservationalSponsorUniversity of AarhusRan2007 to 2017Enrolled906ConditionsCoronary Artery Disease, Myocardial Infarction, Diabetes Mellitus, Renal Insufficiency, Chronic
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  3. Review
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  7. Using theBrain sciences · 2023
    Article
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  10. Effect ofFrontiers in pharmacology · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Observational
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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

5 authors at 1 institution in 1 country.

Morten WürtzDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Department of Internal Medicine, Regional Hospital West Jutland, Herning, Denmark.
Peter H NissenDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Erik Lerkevang GroveDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Steen Dalby KristensenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Anne-Mette HvasDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Aarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlatelet aggregation during aspirin treatment displays considerable inter-individual variability. A genetic etiology likely exists, but it remains unclear to what extent genetic polymorphisms determine platelet aggregation in aspirin-treated individuals.

aimTo identify platelet-related single nucleotide polymorphisms (SNPs) influencing platelet aggregation during aspirin treatment. Furthermore, we explored to what extent changes in cyclooxygenase-1 activity and platelet activation may explain such influence.

methodsWe included 985 Danish patients with stable coronary artery disease treated with aspirin 75 mg/day mono antiplatelet therapy. Patients were genotyped for 16 common SNPs in platelet-related genes using standard PCR-based methods (TaqMan). Platelet aggregation was evaluated by whole blood platelet aggregometry employing Multiplate Analyzer (agonists: arachidonic acid and collagen) and VerifyNow Aspirin. Serum thromboxane B2 was measured to confirm aspirin adherence and was used as a marker of cyclooxygenase-1 activity. Soluble P-selectin was used as marker of platelet activation. Platelet aggregation, cyclooxygenase-1 activity, and platelet activation were compared across genotypes in adjusted analyses.

resultsThe A-allele of the rs12041331 SNP in the platelet endothelial aggregation receptor-1 (PEAR1) gene was associated with reduced platelet aggregation and increased platelet activation, but not with cyclooxygenase-1 activity. Platelet aggregation was unaffected by the other SNPs analyzed.

conclusionA common genetic variant in PEAR1 (rs12041331) reproducibly influenced platelet aggregation in aspirin-treated patients with coronary artery disease. The exact biological mechanism remains elusive, but the effect of this polymorphism may be related to changes in platelet activation. Furthermore, 14 SNPs previously suggested to influence aspirin efficacy were not associated with on-aspirin platelet aggregation. CLINICAL

trial registrationClinicalTrials.gov NCT01383304.

Indexed as

AgedAspirinCoronary Artery DiseaseCyclooxygenase 1FemaleGenotypeHumansMalePlatelet AggregationPolymorphism, Single NucleotideReceptors, Cell SurfaceAspirinCyclooxygenase 1PEAR1 protein, humanPTGS1 protein, humanReceptors, Cell Surface

Identifiers

PMID25360888
PMCPMC4216141
OpenAlexW2077898124

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.