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dc.creatorBacković, D.
dc.creatorIgnjatović, Svetlana
dc.creatorRakicević, Ljiljana
dc.creatorNovković, Mirjana
dc.creatorKusić-Tisma, Jelena
dc.creatorRadojković, Dragica
dc.creatorStrugarević, Evgenija
dc.creatorČalija, Branko
dc.creatorRadak, Đorđe
dc.creatorKovac, M.
dc.date.accessioned2019-09-02T11:55:57Z
dc.date.available2019-09-02T11:55:57Z
dc.date.issued2016
dc.identifier.issn1538-7933
dc.identifier.urihttps://farfar.pharmacy.bg.ac.rs/handle/123456789/2744
dc.description.abstractBackground: Carotid endarterectomy (CEA) is the standard treatment for carotid stenosis. Dual antiplatelet therapy, including aspirin and clopidogrel, has a potential role in reducing the risk of stroke after car- otid surgery. However, clopidogrel high on-treatment platelet reactiv- ity (HTPR) is quite a common phenomenon. Aims: Our study aimed to evaluate genetic and non-genetic factors as possible risks for clopidogrel-HTPR in patients with carotid artery stenosis undergoing CEA. Methods: Using multiple-electrode impedance aggregometry (MEA) the antiplatelet effectiveness of clopidogrel was prospectively evaluated in 112 patients (66.2 8.1 years). Measurements were made after 24 h, 7 and 30 days of clopidogrel treatment, which was introduced after elective CEA at a dose of 75 mg daily, for at least 30 days. Clopido- grel-HTPR was defined as an adenosine diphosphate (ADP) - throm- bin receptor activating peptide (TRAP) platelet aggregation ratio ≥ 52%. CYP2C19*2 genotyping was performed by TaqMan assay. Logistic regression models were used to estimate predictors for low responsiveness. The Ethics Committee of the “Dedinje” Institute for Cardiovascular Diseases approved the research protocol. All patients gave written informed consent prior to study inclusion. Results: According to this specific cut-off value for our population, the number of patients with HTPR declined from 79.5% 24 h after intro- ducing clopidogrel to 25% after 30 days of treatment. Analysis showed that 16/30 patients carrying the CYP2C19*2 gene variant had HTPR, in contrast to 12/82 non-carriers of this allele (P< 0.001). Multivariate logistic regression analysis identified the CYP2C19*2 gene variant (OR 4.384, 95% CI 1.296-14.833, P=0.017) and high total cholesterol (OR 2.090, 95% CI 1.263-3.459, P=0.004) as the only independent risk factors for clopidogrel-HTPR. Conclusions: The CYP2C19*2 gene variant and high total cholesterol level were risk factors for clopidogrel-HTPR in patients with carotid artery stenosis undergoing CEA.
dc.publisherElsevier
dc.rightsopenAccess
dc.sourceJournal of Thrombosis and Haemostasis
dc.titleRisk factors for clopidogrel high on-treatment platelet reactivity in patients with carotid artery stenosis undergoing endarterectomyen
dc.typeconferenceObject
dc.rights.licenseARR
dcterms.abstractРадак, Ђорђе; Игњатовић, Светлана; Чалија, Бранко; Стругаревић, Евгенија; Радојковић, Драгица; Бацковић, Д.; Кусић-Тисма, Јелена; Новковић, Мирјана; Ракицевић, Љиљана; Ковац, М.;
dc.citation.volume14
dc.citation.issueS1
dc.citation.spage110
dc.citation.epage110
dc.citation.other14: 110-110
dc.citation.rankM21
dc.description.other62nd Annual Meeting of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis May 25–28, 2016
dc.identifier.wos000379164000276
dc.identifier.doi10.1111/jth.13325
dc.type.versionpublishedVersion


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