Evidence map›Paper›PMID 25993271›Full record

ArticlePloS one2015

Determinants of reduced antiplatelet effect of aspirin in patients with stable coronary artery disease.

Sanne Bøjet Larsen, Erik Lerkevang Grove, Søs Neergaard-Petersen, Morten Würtz, Anne-Mette Hvas, Steen Dalby Kristensen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
3.6field-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.

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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Whole Blood Platelet Aggregation Test and Prediction of Hemostatic Difficulty After Tooth Extraction in Patients Receiving Antiplatelet Therapy.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018
    Trial
  7. Review
  8. Review
  9. Research and practice in thrombosis and haemostasis · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Fibrin Clot Formation and Lysis in Plasma.Methods and protocols · 2020
    Article
  17. Article
  18. Article
  19. Obesity and Altered Aspirin Pharmacology.Clinical pharmacokinetics · 2018
    Review
  20. Observational
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 2 institutions in 1 country.

Sanne Bøjet LarsenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Erik Lerkevang GroveDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Søs Neergaard-PetersenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Morten WürtzDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Anne-Mette HvasDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark; Faculty of Health Sciences, Aarhus University, Aarhus, Denmark.
Steen Dalby KristensenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Faculty of Health Sciences, Aarhus University, Aarhus, Denmark.
Aarhus University Hospital · DKAarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAspirin is a cornerstone in management of coronary artery disease (CAD). However, considerable variability in the antiplatelet effect of aspirin has been reported.

aimTo investigate independent determinants of reduced antiplatelet effect of aspirin in stable CAD patients.

methodsWe performed a cross-sectional study including 900 stable, high-risk CAD patients. Among these, 795 (88%) had prior myocardial infarction, 250 (28%) had type 2 diabetes, and 170 (19%) had both. All patients received 75 mg aspirin daily as mono antiplatelet therapy. The antiplatelet effect of aspirin was assessed by measurement of platelet aggregation employing 1) multiple electrode aggregometry (MEA, Multiplate Analyzer) in whole blood anticoagulated with citrate or hirudin using arachidonic acid (AA) or collagen as agonists, and 2) VerifyNow Aspirin Assay. Compliance was assessed by measurement of serum thromboxane B2.

resultsPlatelet count, prior myocardial infarction, type 2 diabetes and body mass index were independent determinants of increased AA-induced MEA platelet aggregation in citrate and hirudin anticoagulated blood (p-values ≤ 0.045). Similar results were found with VerifyNow. Prior coronary artery bypass grafting, age, smoking (MEA, AA/citrate) and female gender (MEA, AA/hirudin) were also independent determinants of increased platelet aggregation (p-values ≤ 0.038). Compliance was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 0.97 [0.52;1.97], range 0.02-26.44 ng/ml).

conclusionPlatelet count, prior myocardial infarction, type 2 diabetes and body mass index were independent determinants of increased platelet aggregation, indicating that these characteristics may be key factors in reduced antiplatelet effect of aspirin in stable CAD patients.

Indexed as

AgedAspirinBody Mass IndexCoronary Artery DiseaseCross-Sectional StudiesDiabetes Mellitus, Type 2FemaleHumansMaleMiddle AgedMyocardial InfarctionPlatelet AggregationPlatelet Aggregation InhibitorsPlatelet CountThromboxane B2AspirinPlatelet Aggregation InhibitorsThromboxane B2

Identifiers

PMID25993271
PMCPMC4436265
OpenAlexW1583518427

What OpenQuestion holds

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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.