Evidence map›Paper›PMID 23981082›Full record

ReviewBritish journal of clinical pharmacology2014

Genetics of platelet inhibitor treatment.

Dietmar Trenk, Willibald Hochholzer

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
3.0field-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.

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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Dietmar TrenkKlinik für Kardiologie und Angiologie II, Universitäts-Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany.
Willibald Hochholzer
Universitäts-Herzzentrum Freiburg-Bad Krozingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dual antiplatelet therapy with aspirin and a P2Y12 receptor antagonist is the standard of care in patients undergoing percutaneous coronary intervention (PCI) and in patients with acute coronary syndromes (ACS) because this regimen has markedly decreased the rate of cardiovascular events. The substantial variability in pharmacodynamic response as well as the moderate antiplatelet efficacy of clopidogrel has raised major concerns, since high on-clopidogrel platelet reactivity has consistently been associated with increased risk for ischaemic events in PCI patients. Baseline demographic and clinical variables contributing to the observed variability have been identified. Besides this, research within the past decade has focused on the impact of genetic polymorphisms encoding transport systems or enzymes involved in the absorption and metabolism of these drugs. Loss-of-function polymorphisms in CYP2C19 are the strongest individual variables affecting pharmacokinetics and antiplatelet response to clopidogrel, but explain no more than 5 to 12% of the variability in adenosine diphosphate-induced platelet aggregation on clopidogrel. No genetic variables contributing to clinical outcomes of patients treated with the newer P2Y12 receptor antagonists, prasugrel or ticagrelor, have been identified so far. This review aims to provide an update on the current status of genotype-based personalized therapy with clopidogrel.

Indexed as

Precision MedicineAryldialkylphosphataseATP Binding Cassette Transporter, Subfamily BCarboxylic Ester HydrolasesClopidogrelCytochrome P-450 CYP2C19Genotyping TechniquesHumansMolecular Sequence DataPharmacogeneticsPlatelet Aggregation InhibitorsPolymorphism, GeneticPurinergic P2Y Receptor AntagonistsTiclopidineABCB1 protein, humanAryldialkylphosphataseATP Binding Cassette Transporter, Subfamily BCarboxylic Ester HydrolasesCES1 protein, humanClopidogrelCYP2C19 protein, humanCytochrome P-450 CYP2C19Platelet Aggregation InhibitorsPON1 protein, humanPurinergic P2Y Receptor AntagonistsTiclopidineclopidogrelP2Y12 antagonistplatelet inhibitorprasugrelsingle nucleotide polymorphismticagrelor

Identifiers

PMID23981082
PMCPMC3971981
OpenAlexW1508125153

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.