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

Detalhes bibliográficos
Autor(a) principal: Mansur, Antonio P.
Data de Publicação: 2013
Outros Autores: Takada, Julio Y., Strunz, Celia M. C., Avakian, Solange D., Cesar, Luiz Antonio M., Ramires, Jose A.F.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/77051
Resumo: OBJECTIVE: To examine the association of atherogenic and thrombogenic markers and lymphotoxin-alfa gene mutations with the risk of premature coronary disease. METHODS: This cross-sectional, case-control, age-adjusted study was conducted in 336 patients with premature coronary 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. RESULTS: Coronary 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
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spelling The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery diseaseOBJECTIVE: To examine the association of atherogenic and thrombogenic markers and lymphotoxin-alfa gene mutations with the risk of premature coronary disease. METHODS: This cross-sectional, case-control, age-adjusted study was conducted in 336 patients with premature coronary 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. RESULTS: Coronary 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 (pHospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2013-12-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/7705110.1590/clin.v68i12.77051Clinics; Vol. 68 No. 12 (2013); 1502-1508Clinics; v. 68 n. 12 (2013); 1502-1508Clinics; Vol. 68 Núm. 12 (2013); 1502-15081980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/77051/80916Mansur, Antonio P.Takada, Julio Y.Strunz, Celia M. C.Avakian, Solange D.Cesar, Luiz Antonio M.Ramires, Jose A.F.info:eu-repo/semantics/openAccess2014-03-24T18:38:58Zoai:revistas.usp.br:article/77051Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2014-03-24T18:38:58Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
title The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
spellingShingle The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
Mansur, Antonio P.
title_short The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
title_full The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
title_fullStr The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
title_full_unstemmed The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
title_sort The involvement of multiple thrombogenic and atherogenic markers in premature coronary artery disease
author Mansur, Antonio P.
author_facet Mansur, Antonio P.
Takada, Julio Y.
Strunz, Celia M. C.
Avakian, Solange D.
Cesar, Luiz Antonio M.
Ramires, Jose A.F.
author_role author
author2 Takada, Julio Y.
Strunz, Celia M. C.
Avakian, Solange D.
Cesar, Luiz Antonio M.
Ramires, Jose A.F.
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Mansur, Antonio P.
Takada, Julio Y.
Strunz, Celia M. C.
Avakian, Solange D.
Cesar, Luiz Antonio M.
Ramires, Jose A.F.
description OBJECTIVE: To examine the association of atherogenic and thrombogenic markers and lymphotoxin-alfa gene mutations with the risk of premature coronary disease. METHODS: This cross-sectional, case-control, age-adjusted study was conducted in 336 patients with premature coronary 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. RESULTS: Coronary 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
publishDate 2013
dc.date.none.fl_str_mv 2013-12-31
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/77051
10.1590/clin.v68i12.77051
url https://www.revistas.usp.br/clinics/article/view/77051
identifier_str_mv 10.1590/clin.v68i12.77051
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/77051/80916
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 68 No. 12 (2013); 1502-1508
Clinics; v. 68 n. 12 (2013); 1502-1508
Clinics; Vol. 68 Núm. 12 (2013); 1502-1508
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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