Evidence map›Paper›PMID 25959001›Full record

ArticleBMC cardiovascular disorders2015

Genetic association study of coronary collateral circulation in patients with coronary artery disease using 22 single nucleotide polymorphisms corresponding to 10 genes involved in postischemic neovascularization.

Joan Duran, Pilar Sánchez Olavarría, Marina Mola, Víctor Götzens, Julio Carballo, Eva Martín Pelegrina, Màrius Petit, Omar Abdul-Jawad, Imanol Otaegui, Bruno García del Blanco and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
0.3field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. 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 7 institutions in 4 countries.

Joan DuranUnitat d'Anatomia i Embriologia Humanes, Departament de Patologia i Terapèutica Experimental, Facultat de Medicina, Campus de Ciències de la Salut de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. joanduranf@ub.edu.
Pilar Sánchez OlavarríaUnitat d'Anatomia i Embriologia Humanes, Departament de Patologia i Terapèutica Experimental, Facultat de Medicina, Campus de Ciències de la Salut de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. mariapilar.sanchez@uv.cl.
Marina MolaUnitat d'Anatomia i Embriologia Humanes, Departament de Patologia i Terapèutica Experimental, Facultat de Medicina, Campus de Ciències de la Salut de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. mmola@imim.es.
Víctor GötzensUnitat d'Anatomia i Embriologia Humanes, Departament de Patologia i Terapèutica Experimental, Facultat de Medicina, Campus de Ciències de la Salut de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. vgotzens@ub.edu.
Julio CarballoDepartment of Cardiology and Hemodynamics, Centre Cardiovascular Sant Jordi, Barcelona, Spain. jcgllo@wanadoo.es.
Eva Martín PelegrinaDepartment of Cardiology and Hemodynamics, Centre Cardiovascular Sant Jordi, Barcelona, Spain. emartinp76@hotmail.com.
Màrius PetitDepartment of Cardiology and Hemodynamics, Centre Cardiovascular Sant Jordi, Barcelona, Spain. 4021mpg@comb.cat.
Omar Abdul-JawadDepartment of Cardiology, Hospital Mútua de Terrassa, Terrassa, Barcelona, Spain. uzarasl@yahoo.es.
Imanol OtaeguiDepartment of Cardiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. iotaegui@vhebron.net.
Bruno García del BlancoDepartment of Cardiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. brugarci@vhebron.net.
David García-DoradoDepartment of Cardiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. dgdorado@vhebron.net.
Josep ReigDepartament of Morphological Sciences, Universitat Autònoma de Barcelona, Bellaterra, Cerdanyola del Vallès, Barcelona, Spain. josep.reig@uab.cat.
Alex CorderoUnitat d'Anatomia i Embriologia Humanes, Departament de Patologia i Terapèutica Experimental, Facultat de Medicina, Campus de Ciències de la Salut de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. acordero@idibell.cat.
Josep Maria de AntaUnitat d'Anatomia i Embriologia Humanes, Departament de Patologia i Terapèutica Experimental, Facultat de Medicina, Campus de Ciències de la Salut de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Barcelona, 08907, Spain. janta@ub.edu.
Bellvitge University Hospital · ESVall d'Hebron Hospital Universitari · ESBarcelona Centre for International Affairs · ESCardiovascular Research Center · BRMontavid Thermodynamic Research Group · HUUniversitat Autònoma de Barcelona · ESUniversity Hospital Mútua de Terrassa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCollateral growth in patients with coronary artery disease (CAD) is highly heterogeneous. Although multiple factors are thought to play a role in collateral development, the contribution of genetic factors to coronary collateral circulation (CCC) is largely unknown. The goal of this study was to assess whether functional single nucleotide polymorphisms (SNPs) in genes involved in vascular growth are associated with CCC.

methods677 consecutive CAD patients were enrolled in the study and their CCC was assessed by the Rentrop method. 22 SNPs corresponding to 10 genes involved in postischemic neovascularization were genotyped and multivariate logistic regression models were adjusted using clinically relevant variables to estimate odds ratios and used to examine associations of allelic variants, genotypes and haplotypes with CCC.

resultsStatistical analysis showed that the HIF1A rs11549465 and rs2057482; VEGFA rs2010963, rs1570360, rs699947, rs3025039 and rs833061; KDR rs1870377, rs2305948 and rs2071559; CCL2 rs1024611, rs1024610, rs2857657 and rs2857654; NOS3 rs1799983; ICAM1 rs5498 and rs3093030; TGFB1 rs1800469; CD53 rs6679497; POSTN rs3829365 and rs1028728; and LGALS2 rs7291467 polymorphisms, as well as their haplotype combinations, were not associated with CCC (p < 0.05).

conclusionsWe could not validate in our cohort the association of the NOS3 rs1799983, HIF1A rs11549465, VEGFA rs2010963 and rs699947, and LGALS2 rs7291467 variants with CCC reported by other authors. A validated SNP-based genome-wide association study is required to identify polymorphisms influencing CCC.

Indexed as

Collateral CirculationCoronary CirculationNeovascularization, PhysiologicPolymorphism, Single NucleotideAgedCoronary Artery DiseaseFemaleGenotypeHumansMaleMiddle Aged

Identifiers

PMID25959001
PMCPMC4493944
OpenAlexW1705320075

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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.