Evidence map›Paper›PMID 23676293›Full record

ArticleJournal of the American Heart Association2013

P2Y12 receptor blockade augments glycoprotein IIb-IIIa antagonist inhibition of platelet activation, aggregation, and procoagulant activity.

Michelle A Berny-Lang, Joseph A Jakubowski, Atsuhiro Sugidachi, Marc R Barnard, Alan D Michelson, Andrew L Frelinger

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Improving the Quality of EDTA-treated Blood Specimens from Mice.Journal of the American Association for Laboratory Animal Science : JAALAS · 2022
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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

6 authors at 5 institutions in 2 countries.

Michelle A Berny-LangCenter for Platelet Research Studies, Division of Hematology/Oncology, Boston Children's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, Japan.
Joseph A Jakubowski
Atsuhiro Sugidachi
Marc R Barnard
Alan D Michelson
Andrew L Frelinger
Harvard University · USBoston Children's Hospital · USDaiichi-Sankyo (Japan) · JPDana-Farber Cancer Institute · USEli Lilly (United States) · US

Funding

Harvard Clinical and Translational Science Center (UL1)UL1TR000170 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2012 to 2013
$31.4M
PATHOPHYSIOLOGY OF HUMAN BLOOD CELLST32HL007574 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Daniel Evan Bauer · 1985 to 2026
$18.4M
NCATS NIH HHS 8UL1TR000170-05NCATS NIH HHS UL1 TR000170NHLBI NIH HHS 5T32HL007574-31NHLBI NIH HHS T32 HL007574
6 · The paper itself

Abstract

backgroundNew antiplatelet agents that provide greater, more consistent inhibition of the platelet ADP receptor P2Y12 may be used in combination with glycoprotein (GP) IIb-IIIa antagonists, but their combined effect on platelet function and procoagulant activity is not well studied. Therefore, the objective of this study was to evaluate the independent and complementary effects of P2Y12 and GPIIb-IIIa inhibition on platelet function and procoagulant activity. METHODS AND

resultsHealthy donor blood was treated with the active metabolite of prasugrel (R-138727 5 μmol/L), GPIIb-IIIa antagonists (abciximab 3 μg/mL or eptifibatide 0.9 μg/mL), and combinations thereof, exposed to physiologically relevant agonists (collagen and ADP) and then evaluated for markers of platelet activation and procoagulant activity. Significant interactions between R-138727 and GPIIb-IIIa antagonists were observed. R-138727 and the GPIIb-IIIa antagonists had additive inhibitory effects on collagen-stimulated platelet aggregation and on the collagen plus ADP-stimulated level of activated platelet surface GPIIb-IIIa. R-138727 and abciximab each inhibited collagen plus ADP-stimulated platelet phosphatidylserine expression and prothrombin cleavage, and the combination produced greater inhibition than achieved with abciximab alone. In contrast, eptifibatide did not inhibit, but instead enhanced, collagen plus ADP-stimulated prothrombin cleavage. Addition of R-138727 reduced prothrombin cleavage in eptifibatide-treated samples, suggesting a novel mechanism for potential benefit from combined prasugrel and eptifibatide treatment.

conclusionsThe complementary effects of abciximab and R-138727 on platelet activation, aggregation, and procoagulant activity suggest their combined use may, to a greater degree than with either agent alone, reduce thrombus formation in vivo.

Indexed as

AbciximabAntibodies, MonoclonalBlood PlateletsEptifibatideHumansImmunoglobulin Fab FragmentsPeptidesPiperazinesPlatelet ActivationPlatelet AggregationPlatelet Aggregation InhibitorsPlatelet Glycoprotein GPIIb-IIIa ComplexReceptors, Purinergic P2Y12AbciximabAntibodies, MonoclonalEptifibatideImmunoglobulin Fab FragmentsP2RY12 protein, humanPeptidesPiperazinesPlatelet Aggregation InhibitorsPlatelet Glycoprotein GPIIb-IIIa ComplexR-138727Receptors, Purinergic P2Y12glycoprotein IIb‐IIIa receptor antagonistsplateletsprasugrel

Identifiers

PMID23676293
PMCPMC3698756
OpenAlexW2055382468

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.