Genotype- and Phenotype-Directed Personalization of Antiplatelet Treatment in Patients with Non-ST Elevation Acute Coronary Syndromes Undergoing Coronary Stenting.
10.4070/kcj.2013.43.8.541
- Author:
Sung Gyun AHN
1
;
Junghan YOON
;
Juwon KIM
;
Young UH
;
Kyung Min KIM
;
Ji Hyun LEE
;
Jun Won LEE
;
Young Jin YOUN
;
Min Soo AHN
;
Jang Young KIM
;
Byung Su YOO
;
Seung Hwan LEE
;
Seung Jea TAHK
;
Kyung Hoon CHOE
Author Information
1. Division of Cardiology, Yonsei University Wonju College of Medicine, Wonju, Korea. jyoon@yonsei.ac.kr
- Publication Type:Original Article ; Randomized Controlled Trial
- Keywords:
Antiplatelet agents;
Genetic testing;
Platelet function tests;
Point-of-care systems
- MeSH:
Acute Coronary Syndrome;
Adenosine;
Alleles;
Blood Platelets;
Genetic Testing;
Humans;
Percutaneous Coronary Intervention;
Platelet Aggregation Inhibitors;
Platelet Function Tests;
Point-of-Care Systems;
Stents;
Ticlopidine
- From:Korean Circulation Journal
2013;43(8):541-549
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND 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 > or =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.
