Intercellular Adhesion Molecule-1 K469E and Angiotensinogen T207M Polymorphisms in Coronary Slow Flow

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dc.contributor.authorGazi, Emine
dc.contributor.authorBarutcu, Ahmet
dc.contributor.authorAltun, Burak
dc.contributor.authorTemiz, Ahmet
dc.contributor.authorBekler, Adem
dc.contributor.authorUrfali, Mine
dc.contributor.authorSılan, Fatma
dc.date.accessioned2025-01-27T20:58:08Z
dc.date.available2025-01-27T20:58:08Z
dc.date.issued2014
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractObjective: To investigate intercellular adhesion molecule-1 (ICAM1) and angiotensinogen (AGT) gene polymorphisms, as related to atherosclerosis and endothelial dysfunction, in coronary slow flow (CSF). Subjects and Methods: The participants in this study were 48 patients with CSF and 67 patients with normal coronary flow as controls. The K469E polymorphism of ICAM1 (rs5498) and the T207M polymorphism of AGT (rs4762) were determined using the polymerase chain reaction amplification method. Results: Baseline demographic parameters were similar in both groups. The mean thrombolysis in myocardial infarction frame count was significantly higher in patients with CSF (23.8 +/- 5.1) compared to the controls (13.3 +/- 2.6, p < 0.001). A significant association was found between the ICAM1 K allele and CSF (OR: 1.96, 95% CI: 1.15-3.35, p = 0.013). There was no difference in the frequency of AGT T207M genotypes in the patients with CSF and the control subjects. Conclusion: This study showed that K469E polymorphisms of ICAM1 that play a role in atherosclerotic pathogenesis are related to CSF. (C) 2014 S. Karger AG, Basel
dc.description.sponsorshipCanakkale Onsekiz Mart University [TSA-2013-99]
dc.description.sponsorshipOur study on genetic polymorphisms in CSF was supported by the Research Fund of the Canakkale Onsekiz Mart University (project No. TSA-2013-99).
dc.identifier.doi10.1159/000363451
dc.identifier.endpage350
dc.identifier.issn1011-7571
dc.identifier.issn1423-0151
dc.identifier.issue4
dc.identifier.pmid24942509
dc.identifier.scopus2-s2.0-84905050194
dc.identifier.scopusqualityQ1
dc.identifier.startpage346
dc.identifier.urihttps://doi.org/10.1159/000363451
dc.identifier.urihttps://hdl.handle.net/20.500.12428/26619
dc.identifier.volume23
dc.identifier.wosWOS:000339731600010
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherKarger
dc.relation.ispartofMedical Principles and Practice
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20250125
dc.subjectICAM1 polymorphism
dc.subjectAngiotensinogen polymorphism
dc.subjectCoronary slow flow
dc.subjectAtherosclerosis
dc.titleIntercellular Adhesion Molecule-1 K469E and Angiotensinogen T207M Polymorphisms in Coronary Slow Flow
dc.typeArticle

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