Genetic effects versus bias for candidate polymorphisms in myocardial infarction: case study and overview of large-scale evidence

dc.contributor.authorNtzani, E. E.en
dc.contributor.authorRizos, E. C.en
dc.contributor.authorIoannidis, J. P.en
dc.date.accessioned2015-11-24T19:14:57Z
dc.date.available2015-11-24T19:14:57Z
dc.identifier.issn0002-9262-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21422
dc.rightsDefault Licence-
dc.subjectAllelesen
dc.subject*Bias (Epidemiology)en
dc.subjectCoronary Artery Disease/epidemiology/*geneticsen
dc.subjectEthnic Groups/geneticsen
dc.subjectGreece/epidemiologyen
dc.subjectHumansen
dc.subjectMyocardial Infarction/epidemiology/*geneticsen
dc.subject*Polymorphism, Geneticen
dc.subjectReceptor, Angiotensin, Type 1/*geneticsen
dc.subjectRisk Factorsen
dc.titleGenetic effects versus bias for candidate polymorphisms in myocardial infarction: case study and overview of large-scale evidenceen
heal.abstractSeveral genetic polymorphisms have been proposed to be associated with myocardial infarction (MI). The authors examined the evidence and biases underlying such associations using a case-study meta-analysis and an overview of large-scale data. In a meta-analysis of 27 studies addressing the association of the angiotensin type 1 receptor (AT1R)+1166A/C polymorphism with MI (10,180 cases, 17,129 controls), the *C allele conferred an increase in MI risk (odds ratio = 1.13 per allele, p = 0.005). However, there was large between-study heterogeneity; the largest study showed no effect, contradicting smaller studies; and studies with blinded genotyping showed no effect. The authors conducted an overview of meta-analyses of genetic associations for MI or coronary artery disease, including at least three studies and 3,000 subjects. In their latest meta-analysis, another 14 polymorphisms were found to have formally significant associations. If true, these associations would already explain 42% of the MI risk for Caucasian populations. Significant between-study heterogeneity was common. Across the 32 largest studies, only two found formally significant results (nine would be expected if each meta-analysis showed a true association). Even with large-scale evidence from meta-analyses, significant associations for MI may be subject to bias. Large-scale single studies and prospective consortia should be used for detecting and validating the genetic determinants of MI.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1093/aje/kwk085-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17293603-
heal.identifier.secondaryhttp://aje.oxfordjournals.org/content/165/9/973.full.pdf-
heal.journalNameAm J Epidemiolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2007-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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