Evidence map›Paper›PMID 24473507›Full record

ArticleClinics (Sao Paulo, Brazil)2013

The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease.

Antonio P Mansur, Julio Y Takada, Célia M C Strunz, Solange D Avakian, Luiz Antonio M César, José A F Ramires

Open access · goldAbstract read
In one paragraph

Article in Clinics (Sao Paulo, Brazil), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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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

6 authors at 1 institution in 1 country.

Antonio P MansurHeart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo/SP, Brazil.
Julio Y TakadaHeart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo/SP, Brazil.
Célia M C StrunzHeart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo/SP, Brazil.
Solange D AvakianHeart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo/SP, Brazil.
Luiz Antonio M CésarHeart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo/SP, Brazil.
José A F RamiresHeart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo/SP, Brazil.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo examine the association of atherogenic and thrombogenic markers and lymphotoxin-alfa gene mutations with the risk of premature coronary disease.

methodsThis cross-sectional, case-control, age-adjusted study was conducted in 336 patients with premature coronary disease (<50 years old) and 189 healthy controls. The control subjects had normal clinical, resting, and exercise stress electrocardiographic assessments. The coronary disease group patients had either angiographically documented disease (>50% luminal reduction) or a previous myocardial infarction. The laboratory data evaluated included thrombogenic factors (fibrinogen, protein C, protein S, and antithrombin III), atherogenic factors (glucose and lipid profiles, lipoprotein(a), and apolipoproteins AI and B), and lymphotoxin-alfa mutations. Genetic variability of lymphotoxin-alfa was determined by polymerase chain reaction analysis.

resultsCoronary disease patients exhibited lower concentrations of HDL-cholesterol and higher levels of glucose, lipoprotein(a), and protein S. The frequencies of AA, AG, and GG lymphotoxin-alfa mutation genotypes were 55.0%, 37.6%, and 7.4% for controls and 42.7%, 46.0%, and 11.3% for coronary disease patients (p = 0.02), respectively. Smoking, dyslipidemia, family history, and lipoprotein(a) and lymphotoxin-alfa mutations in men were independent variables associated with coronary disease. The area under the curve (C-statistic) increased from 0.779 to 0.802 (p<0.05) with the inclusion of lipoprotein(a) and lymphotoxin-alfa mutations in the set of conventional risk factors.

conclusionsThe inclusion of lipoprotein(a) and lymphotoxin-alfa mutations in the set of conventional risk factors showed an additive but small increase in the risk prediction of premature coronary disease.

Indexed as

AdultAtherosclerosisBiomarkersCase-Control StudiesCoronary Artery DiseaseCross-Sectional StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansLipoproteinsLymphotoxin-alphaMaleMiddle AgedMutationPolymorphism, GeneticBiomarkersLipoproteinsLymphotoxin-alpha

Identifiers

PMID24473507
PMCPMC3840366
OpenAlexW2116156697

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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.