Evidence map›Paper›PMID 26786608›Full record

ArticleSao Paulo medical journal = Revista paulista de medicina2016

Gene mutations of platelet glycoproteins and response to tirofiban in acute coronary syndrome.

Antonio de Padua Mansur, Alessandra Roggerio, Júlio Yoshio Takada, Pérola Michelle Vasconcelos Caribé, Solange Desirée Avakian, Célia Maria Cassaro Strunz

Open access · diamondAbstract read
In one paragraph

Article in Sao Paulo medical journal = Revista paulista de medicina, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Antonio de Padua MansurMD, PhD. Associate Professor, Department of Cardiopulmonology, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Alessandra RoggerioBSc, PhD. Biochemist, Department of Cardiopulmonology, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Júlio Yoshio TakadaMD, PhD. Attending Physician, Department of Cardiopulmonology, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Pérola Michelle Vasconcelos CaribéMD, MSc. Doctoral Student, Department of Cardiopulmonology, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Solange Desirée AvakianMD, PhD. Attending Physician, Department of Cardiopulmonology, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Célia Maria Cassaro StrunzBSc. Central Laboratory Director, Department of Cardiopulmonology, Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CONTEXT AND

objectivesGlycoprotein inhibitors (abciximab, eptifibatide and tirofiban) are used in patients with unstable angina and non-ST-segment elevation myocardial infarction before percutaneous coronary intervention. Of these, tirofiban is the least effective. We hypothesized that the response to tirofiban might be associated with glycoprotein gene mutations. DESIGN AND

settingProspective study at Emergency Unit, Heart Institute (InCor), University of São Paulo.

methodIntrahospital evolution and platelet aggregation in response to tirofiban were analyzed in relation to four glycoprotein mutations in 50 patients indicated for percutaneous coronary intervention: 17 (34%) with unstable angina and 33 (66%) with non-ST-segment elevation myocardial infarction. Platelet aggregation was analyzed using the Born method. Blood samples were obtained before and one hour after tirofiban infusion. Glycoproteins Ia (807C/T ), Ib (Thr/Met) , IIb (Ile/Ser ) and IIIa (PIA ) were the mutations selected.

resultsHypertension, dyslipidemia, diabetes, smoking, previous coronary artery disease and stroke were similar between the groups. Mutant glycoprotein IIIa genotypes had lower platelet aggregation before tirofiban administration than that of the wild genotype (41.0% ± 22.1% versus 55.9% ± 20.8%; P = 0.035). Mutant glycoprotein IIIa genotypes correlated moderately with lower platelet inhibition (r = -0.31; P = 0.030). After tirofiban administration, platelet glycoprotein Ia, Ib, IIb and IIIa mutations did not influence the degree of inhibition of platelet aggregation or intrahospital mortality.

conclusionsMutations of glycoproteins Ia, Ib, IIb and IIIa did not influence platelet aggregation in response to tirofiban in patients with unstable angina and non-ST-segment elevation myocardial infarction.

Indexed as

MutationAbciximabAcute Coronary SyndromeAgedAngina, UnstableAntibodies, MonoclonalEptifibatideFemaleGenotypeHumansImmunoglobulin Fab FragmentsMaleMiddle AgedPeptidesPlatelet AggregationPlatelet Aggregation InhibitorsAbciximabAntibodies, MonoclonalEptifibatideImmunoglobulin Fab FragmentsPeptidesPlatelet Aggregation InhibitorsPlatelet Glycoprotein GPIIb-IIIa ComplexPlatelet Membrane GlycoproteinsTirofibanTyrosine

Identifiers

PMID26786608
PMCPMC10496600
OpenAlexW2274384593

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Registered trials

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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.