Comparing efficacy of antiplatelet agents in PCI patients heterozygous to CYP2C19*2/*3 mutations

摘要

Introduction: Clopidrogel is the most common, cost effective medicationavailable for patients undergoing PCI. But variations inCYP2C19 has been associated in decreased metabolismof this drugleading to MACE. The other anti-platelet drugs considered in suchsituations include Prasugrel and Ticagrelor, which are highly efficientwhen compared to Clopidrogel but are sometimes associatedwith bleeding and Ticagrelor is expensive. CYP2C19*2/*3 is the mostcommon, loss of function mutation in this gene, which reduces itsactivity and hence low metabolismof Clopidrogel. Patients heterozygousto anyone of these SNPs have to be put on alternativetreatment regime, which included Prasugrel and Ticagrelor orhigher doses of Clopidrogel.Objective: To evaluate the efficiency of Clopidrogel (75 mg), Prasugrel(10 mg) and Ticagrelor (90 mg) in PCI patients heterozygous forCYP2C19*2/*3.Methodology: A total of 20 patients who have undergone PCI andheterozygous for CYP2C19*2 and CYP2C19*3 variations wererecruited from Sri Balaji Hospital, Chrompet after obtaining writteninformed consent. The patients were randomly categorized into 3regimens: double dose Clopidrogel (75 mg), Prasugrel (10 mg), andTicagrelor (90 mg). Each group has 8, 8, and 4 patients, respectively.The efficacy of these drugs was evaluated by platelet responsearray using FACS. Based on platelet reactivity index (PRI), they wereclassified as normal (50) response.Results: Of the 8 patients who had Clopidrogel (75 mg), two hadborderline response and the rest 6 had poor response, and ofthe 8 patients, who were on Prasugrel (10 mg), two had borderlineand 6 had good response. The 4 patients on Ticagrelor had goodresponse.Conclusion: Evaluation of the efficacy of these three anti-plateletdrugs in the heterozygous group of CYP2C19*2/*3 showed Ticagreloris highly efficient in preventing platelet aggregation followed byPrasugrel in our cohort. Patients on double dose Clopidogrel havehigh residual platelet reactivity.