Association between UCP2 A55V polymorphism and risk of cardiovascular events in patients with multi-vessel coronary arterial disease

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorGIOLI-PEREIRA, Luciana
dc.contributor.authorSANTOS, Paulo C. J. L.
dc.contributor.authorSUGAYA, Luisa S.
dc.contributor.authorFERREIRA, Noely E.
dc.contributor.authorKRIEGER, Jose Eduardo
dc.contributor.authorPEREIRA, Alexandre C.
dc.contributor.authorHUEB, Whady A.
dc.date.accessioned2013-09-23T16:36:36Z
dc.date.available2013-09-23T16:36:36Z
dc.date.issued2013
dc.description.abstractBackground: UCP2 (uncoupling protein 2) plays an important role in cardiovascular diseases and recent studies have suggested that the A55V polymorphism can cause UCP2 dysfunction. The main aim was to investigate the association of A55V polymorphism with cardiovascular events in a group of 611 patients enrolled in the Medical, Angioplasty or Surgery Study II (MASS II), a randomized trial comparing treatments for patients with coronary artery disease and preserved left ventricular function. Methods: The participants of the MASS II were genotyped for the A55V polymorphism using allele-specific PCR assay. Survival curves were calculated with the Kaplan-Meier method and evaluated with the log-rank statistic. The relationship between baseline variables and the composite end-point of cardiac death, acute myocardial infarction (AMI), refractory angina requiring revascularization and cerebrovascular accident were assessed using a Cox proportional hazards survival model. Results: There were no significant differences for baseline variables according genotypes. After 2 years of follow-up, dysglycemic patients harboring the W genotype had higher occurrence of AMI (p=0.026), Death+AMI (p=0.033), new revascularization intervention (p=0.009) and combined events (p=0.037) as compared with patients carrying other genotypes. This association was not evident in normoglycemic patients. Conclusions: These findings support the hypothesis that A55V polymorphism is associated with UCP2 functional alterations that increase the risk of cardiovascular events in patients with previous coronary artery disease and dysglycemia.
dc.description.indexMEDLINE
dc.description.sponsorshipZerbini Foundation, Sao Paulo, Brazil
dc.description.sponsorshipFAPESP, Sao Paulo, Brazil [Proc. 2010-17465-8]
dc.identifier.citationBMC MEDICAL GENETICS, v.14, article ID 40, 7p, 2013
dc.identifier.doi10.1186/1471-2350-14-40
dc.identifier.issn1471-2350
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/1822
dc.language.isoeng
dc.publisherBIOMED CENTRAL LTD
dc.relation.ispartofBMC Medical Genetics
dc.rightsopenAccess
dc.rights.holderCopyright BIOMED CENTRAL LTD
dc.subjectUCP2
dc.subjectA55V polymorphism
dc.subjectCoronary artery disease
dc.subjectDiabetes
dc.subject.otheruncoupling protein-2 gene
dc.subject.othercontrolled clinical-trial
dc.subject.other3 therapeutic strategies
dc.subject.otherenergy-expenditure
dc.subject.otherdiabetes-mellitus
dc.subject.othermass-ii
dc.subject.otherpromoter
dc.subject.otheratherosclerosis
dc.subject.otherangioplasty
dc.subject.othermedicine
dc.subject.wosGenetics & Heredity
dc.titleAssociation between UCP2 A55V polymorphism and risk of cardiovascular events in patients with multi-vessel coronary arterial disease
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.citation.scopus13
hcfmusp.contributor.author-fmusphcLUCIANA GIOLI PEREIRA
hcfmusp.contributor.author-fmusphcPAULO CALEB JUNIOR DE LIMA SANTOS
hcfmusp.contributor.author-fmusphcLUISA SHIGUEMI SUGAYA
hcfmusp.contributor.author-fmusphcNOELY EVANGELISTA FERREIRA
hcfmusp.contributor.author-fmusphcJOSE EDUARDO KRIEGER
hcfmusp.contributor.author-fmusphcALEXANDRE DA COSTA PEREIRA
hcfmusp.contributor.author-fmusphcWHADY ARMINDO HUEB
hcfmusp.description.articlenumber40
hcfmusp.description.volume14
hcfmusp.origemWOS
hcfmusp.origem.pubmed23537071
hcfmusp.origem.scopus2-s2.0-84875349441
hcfmusp.origem.wosWOS:000317466700001
hcfmusp.publisher.cityLONDON
hcfmusp.publisher.countryENGLAND
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hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipFund Zerbini
hcfmusp.scopus.lastupdate2024-06-16
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