Please use this identifier to cite or link to this item:
http://hdl.handle.net/10553/43693
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Martínez Quintana, Efrén | en_US |
dc.contributor.author | Chirino Godoy, Ricardo | en_US |
dc.contributor.author | Nieto-Lago, Vicente | en_US |
dc.contributor.author | Pérez-Jiménez, Patricia | en_US |
dc.contributor.author | López-Ríos, Laura | en_US |
dc.contributor.author | Rodríguez-González, Fayna | en_US |
dc.date.accessioned | 2018-11-21T17:07:27Z | - |
dc.date.available | 2018-11-21T17:07:27Z | - |
dc.date.issued | 2014 | en_US |
dc.identifier.issn | 1897-5593 | en_US |
dc.identifier.uri | http://hdl.handle.net/10553/43693 | - |
dc.description.abstract | BACKGROUND: Coronary artery disease (CAD) has turned into a prevalent cause of morbi-mortality contributing some polymorphisms in the recurrence of major adverse cardiac events (MACE). METHODS: Three hundred and fifty six patients with first myocardial infarction (MI) were followed up during a 60-month period to find out if ACE I/D, AT1R A1166C, PAI-I 4G/5G and GPIIIa a1/a2 polymorphisms, in combination with other classical cardiovascular risk factors, can contribute to the relapse of MACE. RESULTS: Two hundred and eighty five (80.1%) men and 71 (19.9%) women were followed up after first MI. The primary clinical endpoint, a composite of MACE, was reached in 106 (29.8%) patients. In the Cox univariate survival analysis those risk factors influencing a poorer prognosis were age (p = 0.004), a positive family history of CAD (p = 0.007), diabetes (p = 0.004), smoking (p = 0.024), fibrinolytic therapy (p = 0.012) and having 2 or 3 vessels CAD (p = 0.046). Cox proportional hazards regression model showed that patients with the DD genotype had a 1.5 increased risk of having an unfavorable outcome when compared with No-DD genotype patients (RR 1.561, 95% CI 1.048-2.326, p = 0.028) and that patients with the ACE DD genotype plus the AT1R No-AA genotype, the GPIIIa No-a1a1 genotype or a combination of both, had a twice higher risk than any other genotype of MACE in the follow-up (RR 1.978, 95% CI 1.286-3.043, p = 0.002). CONCLUSIONS: Patients with the ACE DD genotype plus 1 or 2 unfavorable genotypes, the AT1R No-AA, the GPIIIa No-a1a1 or a combination of both, have twice higher the risk of MACE during their clinical follow-up | en_US |
dc.language | eng | en_US |
dc.publisher | 1897-5593 | - |
dc.relation.ispartof | Cardiology Journal | en_US |
dc.source | Cardiology Journal [ISSN 1897-5593], v. 21, p. 229-237 | en_US |
dc.subject | 320501 Cardiología | en_US |
dc.subject.other | ACE I/D | en_US |
dc.subject.other | AT1R A1166C | en_US |
dc.subject.other | PAI-I 4G/5G | en_US |
dc.subject.other | GPIIIa a1/a2 | en_US |
dc.subject.other | Polymorphisms | en_US |
dc.subject.other | Myocardial infarction | en_US |
dc.title | Prognostic value of ACE I/D, AT1R A1166C, PAI-I 4G/5G and GPIIIa a1/a2 polymorphisms in myocardial infarction | en_US |
dc.type | info:eu-repo/semantics/Article | es |
dc.type | Article | es |
dc.identifier.doi | 10.5603/CJ.a2013.0107 | |
dc.identifier.scopus | 84902182890 | - |
dc.identifier.isi | 000343853600003 | |
dc.contributor.authorscopusid | 23485891800 | - |
dc.contributor.authorscopusid | 6701324062 | - |
dc.contributor.authorscopusid | 8642874100 | - |
dc.contributor.authorscopusid | 37665747500 | - |
dc.contributor.authorscopusid | 33068166900 | - |
dc.contributor.authorscopusid | 24825586600 | - |
dc.description.lastpage | 237 | - |
dc.description.firstpage | 229 | - |
dc.relation.volume | 21 | - |
dc.investigacion | Ciencias de la Salud | en_US |
dc.type2 | Artículo | en_US |
dc.contributor.daisngid | 614797 | |
dc.contributor.daisngid | 880609 | |
dc.contributor.daisngid | 4448649 | |
dc.contributor.daisngid | 10057424 | |
dc.contributor.daisngid | 1964185 | |
dc.contributor.daisngid | 648988 | |
dc.contributor.wosstandard | WOS:Martinez-Quintana, E | |
dc.contributor.wosstandard | WOS:Chirino, R | |
dc.contributor.wosstandard | WOS:Nieto-Lago, V | |
dc.contributor.wosstandard | WOS:Perez-Jimenez, P | |
dc.contributor.wosstandard | WOS:Lopez-Rios, L | |
dc.contributor.wosstandard | WOS:Rodriguez-Gonzalez, F | |
dc.date.coverdate | Enero 2014 | |
dc.identifier.ulpgc | Sí | es |
dc.description.sjr | 0,496 | |
dc.description.jcr | 1,062 | |
dc.description.sjrq | Q3 | |
dc.description.jcrq | Q4 | |
dc.description.scie | SCIE | |
item.grantfulltext | none | - |
item.fulltext | Sin texto completo | - |
crisitem.author.dept | Departamento de Ciencias Médicas y Quirúrgicas | - |
crisitem.author.dept | GIR IUIBS: Diabetes y endocrinología aplicada | - |
crisitem.author.dept | IU de Investigaciones Biomédicas y Sanitarias | - |
crisitem.author.dept | Departamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología | - |
crisitem.author.orcid | 0000-0002-5681-8931 | - |
crisitem.author.parentorg | IU de Investigaciones Biomédicas y Sanitarias | - |
crisitem.author.fullName | Martínez Quintana, Efrén | - |
crisitem.author.fullName | Chirino Godoy, Ricardo | - |
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