Why the study?
Considerable inter-individual variation in clopidogrel response results in suboptimal therapy, with CYP2C19 polymorphisms reported as strong predictors of impaired response.
Does the CYP2C19*2 polymorphism increase clopidogrel resistance in patients with high cardiovascular risk?
Does the CYP2C19*2 polymorphism increase clopidogrel resistance in patients with high cardiovascular risk?
The presence of the CYP2C19*2 polymorphism is significantly associated with reduced clopidogrel effectiveness and higher platelet reactivity in Mexican patients with high cardiovascular risk.
Answers are grounded in this paper and cite their sources.
Clopidogrel response variability warrants caution in high-risk patients; leaves open whether CYP2C19 genotyping improves outcomes.
Objective: Oral antiplatelet drugs are a key to modern pharmacotherapy in cardiovascular atherothrombotic diseases. Clopidogrel (CLO) constitutes the main preventive treatment of atherothrombosis. However, a considerable inter-individual variation in CLO response has been documented, resulting in suboptimal therapy and an increased risk of recurrent adverse effects in some patients. The enzyme CYP2C19 has been reported to be the CYP isoform that activates CLO to its active metabolite. Several single nucleotide polymorphisms in the CYP2C19 gene have been identified as strong predictors of CLO-impaired pharmacological response. At least 16 variants have been associated with changes in CYP2C19 activity.
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Cedillo-Salazar et al. (2020) studied this question.
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