Evidence map›Paper›PMID 28076455›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2017

Decreased platelet responsiveness to clopidogrel correlates with CYP2C19 and PON1 polymorphisms in atherosclerotic patients.

J F M Marchini, M R Pinto, G C Novaes, A V Badran, R B Pavão, G L Figueiredo, I M Lago, M O Lima-Filho, D C Lemos, M Tonani and 4 more

Open access · goldAbstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2017. 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
2.0field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Observational
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  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

14 authors at 4 institutions in 1 country.

J F M MarchiniUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
M R PintoDepartamento de Odontologia, Universidade de Uberaba, Uberaba, MG, Brasil.
G C NovaesUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
A V BadranUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
R B PavãoUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
G L FigueiredoUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
I M LagoUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
M O Lima-FilhoUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
D C LemosUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
M TonaniUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
C M AntlogaUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
L OliveiraDivisão de Hematologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
J C LorenziDepartamento de Genética, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
J A Marin-NetoUnidade de Hemodinâmica e Cardiologia Intervencionista, Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil.
Universidade de São Paulo · BRUniversidade Brasil · BRUniversidade de Ribeirão Preto · BRUniversidade de Uberaba · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clopidogrel and aspirin are the most commonly used medications worldwide for dual antiplatelet therapy after percutaneous coronary intervention. However, clopidogrel hyporesponsiveness related to gene polymorphisms is a concern. Populations with higher degrees of genetic admixture may have increased prevalence of clopidogrel hyporesponsiveness. To assess this, we genotyped CYP2C19, ABCB1, and PON1 in 187 patients who underwent percutaneous coronary intervention. Race was self-defined by patients. We also performed light transmission aggregometry with adenosine diphosphate (ADP) and arachidonic acid during dual antiplatelet therapy. We found a significant difference for presence of the CYP2C19*2 polymorphism between white and non-white patients. Although 7% of patients had platelet resistance to clopidogrel, this did not correlate with any of the tested genetic polymorphisms. We did not find platelet resistance to aspirin in this cohort. Multivariate analysis showed that patients with PON1 and CYP2C19 polymorphisms had higher light transmission after ADP aggregometry than patients with native alleles. There was no preponderance of any race in patients with higher light transmission aggregometry. In brief, PON1 and CYP2C19 polymorphisms were associated with lower clopidogrel responsiveness in this sample. Despite differences in CYP2C19 polymorphisms across white and non-white patients, genetic admixture by itself was not able to identify clopidogrel hyporesponsiveness.

Indexed as

AllelesAryldialkylphosphataseAspirinATP Binding Cassette Transporter, Subfamily BBlood PlateletsClopidogrelCoronary Artery DiseaseCytochrome P-450 CYP2C19Drug Therapy, CombinationFemaleGenotypeHumansMaleMiddle AgedPercutaneous Coronary InterventionPlatelet Aggregation InhibitorsABCB1 protein, humanAryldialkylphosphataseAspirinATP Binding Cassette Transporter, Subfamily BClopidogrelCYP2C19 protein, humanCytochrome P-450 CYP2C19Platelet Aggregation InhibitorsPON1 protein, humanTiclopidineAspirinClopidogrelPercutaneous coronary interventionPlatelet function testsSingle nucleotide polymorphism

Identifiers

PMID28076455
PMCPMC5264542
OpenAlexW2571139424

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.