Evidence map›Paper›PMID 20628791›Full record

ReviewPharmaceutical research2010

Old and new molecular mechanisms associated with platelet resistance to antithrombotics.

Antonio J López Farré, Juan Tamargo, Petra J Mateos-Cáceres, Luís Azcona, Carlos Macaya

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pharmaceutical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. The Impact ofHospital pharmacy · 2024
    Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Platelet aggregation pathway.Pharmacogenetics and genomics · 2011
    Article
  9. Article
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.

Antonio J López FarréCardiovascular Research Unit, Cardiology Department, Hospital Clínico San Carlos, C/ Profesor Martín Lagos s/n, Madrid, 28040, Spain. lcarinv.hcsc@salud.madrid.org
Juan Tamargo
Petra J Mateos-Cáceres
Luís Azcona
Carlos Macaya

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current available data show that about 5 to 40% of coronary patients treated with conventional doses of antithrombotic drugs do not display adequate antiplatelet response. Nowadays, aspirin remains the main antiplatelet therapy. However, a significant number of patients show platelet resistance to aspirin therapy, and recurrent thrombotic events occur. Combined antithrombotic therapies with thienopyridines, such as clopidogrel have been used to resolve this problem. However, clopidogrel treatment has been also associated with wide response variability, and non-responsiveness to clopidogrel also occurs in some patients. Therefore, the main question arising about the antithrombotic therapy is why particular patients do not benefit from the therapy and how they might be identified to improve their treatment. Different hypotheses have been suggested, including genetic factors, platelet heterogeneity, non-compliance and others. However, it is probably that many molecular mechanisms involved in platelet resistance to antithrombotic therapies still remains unknown. New technologies, such as proteomics and genetic, are beginning to show new unknown biological biomarkers and molecular mechanisms which may be associated with platelet antithrombotic drug resistance.

Indexed as

AntithrombinsAspirinBlood PlateletsClopidogrelHumansPatient ComplianceTiclopidineAntithrombinsAspirinClopidogrelTiclopidine

Identifiers

What OpenQuestion holds

Textmetadata
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.