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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/19256
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dc.contributor.authorLekakis, J.en
dc.contributor.authorBisti, S.en
dc.contributor.authorTsougos, E.en
dc.contributor.authorPapathanassiou, A.en
dc.contributor.authorDagres, N.en
dc.contributor.authorIkonomidis, I.en
dc.contributor.authorSoteriadou, E.en
dc.contributor.authorTselepis, A. D.en
dc.contributor.authorGoudevenos, J.en
dc.contributor.authorKremastinos, D. T.en
dc.date.accessioned2015-11-24T18:58:12Z-
dc.date.available2015-11-24T18:58:12Z-
dc.identifier.issn1874-1754-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/19256-
dc.rightsDefault Licence-
dc.subjectAcute Coronary Syndrome/*genetics/mortalityen
dc.subjectAgeden
dc.subjectAllelesen
dc.subjectAnalysis of Varianceen
dc.subjectCase-Control Studiesen
dc.subjectChi-Square Distributionen
dc.subjectFemaleen
dc.subjectGenotypeen
dc.subjectHumansen
dc.subjectLogistic Modelsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectPlatelet Glycoprotein GPIIb-IIIa Complex/*geneticsen
dc.subjectPolymerase Chain Reactionen
dc.subject*Polymorphism, Geneticen
dc.subjectRisk Factorsen
dc.subjectSex Factorsen
dc.titlePlatelet glycoprotein IIb HPA-3 polymorphism and acute coronary syndromesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.ijcard.2007.04.039-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17561290-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0167527307009278/1-s2.0-S0167527307009278-main.pdf?_tid=295412d9636163be447b5974fc00b6ff&acdnat=1333520863_d1bded1fa6d806e4dbf78ee5c5e3689f-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2008-
heal.abstractBACKGROUND: There is considerable research interest about the platelet GPIIb/IIIa receptor polymorphisms in CAD. METHODS: We investigated differences in the frequency of the polymorphism in the GPIIb subunit of the receptor HPA-3 (a and b allele) between patients with more extensive coronary thrombosis such as patients with ST segment elevation (STEMI) and those with less extensive coronary thrombosis such as those with non-ST elevation myocardial infarction (NSTEMI), unstable angina (UA) or chronic CAD. We studied 118 CAD patients, of which 38 suffered from STEMI, 62 from NSTEMI or UA and 18 from chronic CAD and 15 healthy individuals. Patients were followed-up for 21+/-6 months for occurrence of death, myocardial infarction and revascularization. RESULTS: Seventeen out of 38 (45%) patients with STEMI were homozygous for the HPA-3 b allele compared to 6 out 62 (10%) with NSTEMI-UA , 4 out of 18 (22%) with chronic CAD and 2 out of 15 (13%) healthy controls (chi(2)=16,4, p=0.03.) Homozygous patients for the HPA-3b exhibited a 5-fold higher risk for STEMI compared to heterozygous patients for HPA-3b or homozygous for HPA-3a allele (OR: 5.90, 95% CI: 2.15-16.54, p=0.01) after adjustment for age, sex and risk factors. The HPA-3 genotypes were not related with cardiovascular events during follow-up. CONCLUSIONS: Among patients with an acute coronary syndrome those being HPA-3b homozygous have a tendency to develop ST segment elevation myocardial infarction instead of non-ST segment elevation infarction or unstable angina. There is no association between the HPA-3 genotypes and future cardiovascular events.en
heal.journalNameInt J Cardiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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