Evidence map›Paper›PMID 39295604›Full record

ArticleTurkish journal of medical sciences2024

Can prothrombotic gene variants and Apoa1 rs5069 polymorphism be the predictors of early myocardial infarctions?

Hüseyin Balcioğlu, Elif Fatma Özkan Pehlivanoğlu, Uğur Bilge, Kadir Uğur Mert, Muhammet Dural, Ebru Erzurumluoğlu Gökalp, Oğuz Çilingir, Sevilhan Artan

Abstract read
In one paragraph

Article in Turkish journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Hüseyin BalcioğluDepartment of Family Medicine, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0003-1648-3206
Elif Fatma Özkan PehlivanoğluEskişehir Local Health Authority, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0002-7529-2576
Uğur BilgeDepartment of Family Medicine, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0002-9310-3070
Kadir Uğur MertDepartment of Cardiology, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0002-1331-5365
Muhammet DuralDepartment of Cardiology, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0001-7227-8114
Ebru Erzurumluoğlu GökalpDepartment of Medical Genetics, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0002-1275-5174
Oğuz ÇilingirDepartment of Medical Genetics, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0002-5593-4164
Sevilhan ArtanDepartment of Medical Genetics, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.ORCID https://orcid.org/0000-0001-7658-6309

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/aim: We aimed to determine the genetic risk factors in patients aged 45 years and below with a history of early myocardial infarction (MI), compared to individuals over 60 years of age with no history of MI. Materials and methods: In this study, we selected different age groups to more clearly distinguish genetic differences. Accordingly, we compared individuals who had experienced MI at an early age with those who were older and had not experienced any cardiovascular events. The patient group consisted of 99 volunteers under the age of 45 with a history of MI, while the control group included 99 volunteers aged 60 and over without a history of MI. MTHFR (C677T, A1298C), Factor V Leiden (G1691A), Prothrombin (G20210A), PAI (4G/5G), Factor XIII (V34L), APOA1 (rs670, rs1799837, rs5069), and APOB were studied using blood samples taken from the patients. Results: In the logistic regression analysis of thrombophilia markers and gene polymorphisms in the patient and control groups, no statistically significant increase was observed in markers other than APOA1 rs5069 gene polymorphism. APOA1 rs5069 gene polymorphism was found to be higher in the patient group than those without this polymorphism. The frequencies of homozygous MTHFR (C677T, A1298C) and heterozygous Factor XIII V34L were higher in the patient cohort compared to the controls. Conclusion: In our study, we found that prothrombotic gene variants and APOA1 rs5069 polymorphism were statistically significantly associated with coronary artery disease. Thus, prothrombotic gene variants and APOA1 rs5069 polymorphism may serve as predictors of early myocardial infarctions. Individuals with early family histories of coronary artery disease could be screened for these mutations.

Indexed as

Apolipoprotein A-IMyocardial InfarctionAdultAgedCase-Control StudiesFactor VFemaleGenetic Predisposition to DiseaseHumansMaleMethylenetetrahydrofolate Reductase (NADPH2)Middle AgedPolymorphism, GeneticPolymorphism, Single NucleotideProthrombinRisk FactorsAPOA1 protein, humanApolipoprotein A-IFactor Vfactor V LeidenMethylenetetrahydrofolate Reductase (NADPH2)MTHFR protein, humanProthrombinGene mutationmyocardial infarction at a young agepolymorphism

Identifiers

PMID39295604
PMCPMC11407368

What Socratic holds

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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 Socratic graph.