Evidence map›Paper›PMID 28056798›Full record

ArticleBMC cardiovascular disorders2017

High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele.

Zsolt Bagyura, Loretta Kiss, Balázs Berta, Ágnes Szilágyi, Kristóf Hirschberg, Gábor Széplaki, Árpád Lux, Zsolt Szelid, Pál Soós, Béla Merkely

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cardiovascular disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

5 citing papers in PubMed, 8 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

10 authors at 1 institution in 2 countries.

Zsolt BagyuraHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary. bagyura@gmail.com.ORCID 0000-0001-8120-2322
Loretta KissHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Balázs BertaHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Ágnes Szilágyi3rd Department of Internal Medicine, Research Laboratory, Semmelweis University, Budapest, Hungary.
Kristóf HirschbergHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Gábor SzéplakiHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Árpád LuxHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Zsolt SzelidHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Pál SoósHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Béla MerkelyHeart and Vascular Center, Semmelweis University, Varosmajor utca 68, Budapest, H-1122, Hungary.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn-stent restenosis occurs in 10-30% of patients following bare metal stent (BMS) implantation and has various risk factors. Mannose-binding lectin (MBL) is known to have effect on the progression of atherosclerosis. Single nucleotide polymorphisms (SNP) of the MBL2 gene intron 1 (codon 52, 54, 57) are known to modulate the bioavailability of the MBL protein. Our aim was to identify the association of these polymorphisms of the MBL gene in the occurrence of in-stent restenosis after coronary artery bare metal stent implantation.

methodsIn a non-randomized prospective study venous blood samples were collected after recoronarography from 225 patients with prior BMS implantation. Patients were assigned to diffuse restenosis group and control group based on the result of the coronarography. MBL genotypes were determined using quantitative real-time PCR. Proportion of different genotypes was compared and adjusted with traditional risk factors using multivariate logistic regression.

resultsAverage follow-up time was 1.0 (+ - 1.4) year in the diffuse restenosis group (N = 117) and 2.7 (+ - 2.5) years in the control group (N = 108). The age, gender distribution and risk status was not different between study groups. Proportion of the MBL variant genotype was 26.8% (29 vs. 79 normal homozygous) in the control group and 39.3% (46 vs. 71 normal homozygous) in the restenosis group (p = 0.04). In multivariate analysis the mutant allele was an independent risk factor (OR = 1.96, p = 0.03) of in-stent restenosis.

conclusionsMBL polymorphisms are associated with higher incidence of development of coronary in-stent restenosis. The attenuated protein function in the mutant allelic genotype may represent the underlying mechanism.

Indexed as

Polymorphism, Single NucleotideStentsAgedCase-Control StudiesChi-Square DistributionCoronary AngiographyCoronary Artery DiseaseCoronary RestenosisFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHeterozygoteHomozygoteHumansLogistic ModelsMannose-Binding LectinMBL2 protein, humanMetalsBare metal stentCardiologyGene associationIn-stent restenosisMBL genetic variant

Identifiers

PMID28056798
PMCPMC5217188
OpenAlexW2569003561

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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.