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Genotype- and Phenotype-Directed Personalization of Antiplatelet Treatment in Patients with Non-ST Elevation Acute Coronary Syndromes Undergoing Coronary Stenting

DC Field Value Language
dc.contributor.authorAhn, SG-
dc.contributor.authorYoon, J-
dc.contributor.authorKim, J-
dc.contributor.authorUh, Y-
dc.contributor.authorKim, KM-
dc.contributor.authorLee, JH-
dc.contributor.authorLee, JW-
dc.contributor.authorYoun, YJ-
dc.contributor.authorAhn, MS-
dc.contributor.authorKim, JY-
dc.contributor.authorYoo, BS-
dc.contributor.authorLee, SH-
dc.contributor.authorTahk, SJ-
dc.contributor.authorChoe, KH-
dc.date.accessioned2014-07-16-
dc.date.available2014-07-16-
dc.date.issued2013-
dc.identifier.issn1738-5520-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/10589-
dc.description.abstractBackground and Objectives: We evaluated the effectiveness of genotype- and phenotype-directed individualization of P2Y12 inhibitors to decrease high on-treatment platelet reactivity (HOPR).



Subjects and Methods: Sixty-five patients undergoing percutaneous coronary intervention for non-ST elevation acute coronary syndromes were randomly assigned to genotype- or phenotype-directed treatment. All patients were screened for CYP2C19*2, *3, or *17 alleles by using the Verigene CLO assay (Nanosphere, Northbrook, IL, USA). The P2Y12 reaction unit (PRU) was measured using the VerifyNow P2Y12 assay (Accumetrics, San Diego, CA, USA). 21 CYP2C19 *2 or *3 carriers (65.6%) and 11 patients with HOPR (33.3%), defined as a PRU value ≥230, were given 90 mg ticagrelor twice daily; non-carriers and patients without HOPR were given 75 mg clopidogrel daily. The primary endpoint was the percentage of patients with HOPR after 30 days of treatment.



Results: PRU decreased following both genotype- and phenotype-directed therapies (242±83 vs. 109±90, p<0.001 in the genotype-directed group; 216±74 vs. 109±90, p=0.001 in the phenotype-directed group). Five subjects (16.2%) in the genotype-directed group and one (3.3%) in the phenotype-directed group had HOPR at day 30 (p=0.086). All patients with HOPR at the baseline who received ticagrelor had a PRU value of <230 after 30 days of treatment. Conversely, clopidogrel did not lower the number of patients with HOPR at the baseline.



Conclusion: Tailored antiplatelet therapy according to point-of-care genetic and phenotypic testing may be effective in decreasing HOPR after 30 days.
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dc.language.isoen-
dc.titleGenotype- and Phenotype-Directed Personalization of Antiplatelet Treatment in Patients with Non-ST Elevation Acute Coronary Syndromes Undergoing Coronary Stenting-
dc.typeArticle-
dc.identifier.urlhttp://www.koreancircj.kr/search.php?where=aview&id=10.4070/kcj.2013.43.8.541&code=0054KCJ&vmode=FULL-
dc.subject.keywordAntiplatelet agents-
dc.subject.keywordGenetic testing-
dc.subject.keywordPlatelet function tests-
dc.subject.keywordPoint-of-care systems-
dc.contributor.affiliatedAuthor탁, 승제-
dc.type.localJournal Papers-
dc.identifier.doi10.4070/kcj.2013.43.8.541-
dc.citation.titleKorean circulation journal-
dc.citation.volume43-
dc.citation.number8-
dc.citation.date2013-
dc.citation.startPage541-
dc.citation.endPage549-
dc.identifier.bibliographicCitationKorean circulation journal, 43(8):541-549, 2013-
dc.identifier.eissn1738-5555-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Cardiology
Files in This Item:
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