Evidence map›Paper›PMID 21320154›Full record

ReviewBritish journal of clinical pharmacology2011

Anti-platelet therapy: cyclo-oxygenase inhibition and the use of aspirin with particular regard to dual anti-platelet therapy.

Timothy D Warner, Sven Nylander, Carl Whatling

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of clinical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02741817 (WilL LOWer Dose Aspirin be More Effective Following ACS?), which is not on this map. Cited by 118 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 11 pooled it
3.7field-weighted citation impact, top 7% 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.

NCT02741817 phase4completednot on this mapstarted 2016, after this paper: background citation

WilL LOWer Dose Aspirin be More Effective Following ACS? (WILLOW-ACS)

TypeinterventionalSponsorSheffield Teaching Hospitals NHS Foundation TrustRan2016 to 2017Enrolled20ConditionsAcute Coronary SyndromeArmsAspirin
3 · Its place in the literature

Who cites it

118 citing papers in PubMed, 11 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Pooled it
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  4. Ticagrelor Paradox: Systematic Review and Network Meta-Analysis.Journal of the American Heart Association · 2025
    Pooled it
  5. Antiplatelet agents for the treatment of adults with COVID-19.The Cochrane database of systematic reviews · 2023
    Pooled it
  6. Pooled it
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  12. Trial
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  15. Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Trial
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58 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Timothy D WarnerThe William Harvey Research Institute, Barts and London School of Medicine and Dentistry, Queen Mary University of London, London, UK. t.d.warner@qmul.ac.uk
Sven Nylander
Carl Whatling
AstraZeneca (Sweden) · SEWilliam Harvey Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aspirin and P2Y(12) antagonists are commonly used anti-platelet agents. Aspirin produces its effects through inhibition of thromboxane A(2) (TXA(2)) production, while P2Y(12) antagonists attenuate the secondary responses to ADP released by activated platelets. The anti-platelet effects of aspirin and a P2Y(12) antagonist are often considered to be separately additive. However, there is evidence of an overlap in effects, in that a high level of P2Y(12) receptor inhibition can blunt TXA(2) receptor signalling in platelets and reduce platelet production of TXA(2). Against this background, the addition of aspirin, particularly at higher doses, could cause significant reductions in the production of prostanoids in other tissues, e.g. prostaglandin I(2) from the blood vessel wall. This review summarizes the data from clinical studies in which dose-dependent effects of aspirin on prostanoid production have been evaluated by both plasma and urinary measures. It also addresses the biology underlying the cardiovascular effects of aspirin and its influences upon prostanoid production throughout the body. The review then considers whether, in the presence of newer, more refined P2Y(12) receptor antagonists, aspirin may offer less benefit than might have been predicted from earlier clinical trials using more variable P2Y(12) antagonists. The possibility is reflected upon, that when combined with a high level of P2Y(12) blockade the net effect of higher doses of aspirin could be removal of anti-thrombotic and vasodilating prostanoids and so a lessening of the anti-thrombotic effectiveness of the treatment.

Indexed as

AspirinBlood PlateletsClinical Trials as TopicCyclooxygenase InhibitorsDose-Response Relationship, DrugDrug InteractionsDrug Therapy, CombinationHumansPlatelet AggregationPlatelet Aggregation InhibitorsProstaglandinsPurinergic P2Y Receptor AntagonistsThrombosisThromboxane A2AspirinCyclooxygenase InhibitorsPlatelet Aggregation InhibitorsProstaglandinsPurinergic P2Y Receptor AntagonistsThromboxane A2

Identifiers

PMID21320154
PMCPMC3195738
OpenAlexW1608454038

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.