Key result
High on-clopidogrel residual platelet aggregation is linked to ~3-fold greater 1-year death and MI risk.
Why the study?
Cytochrome P450-dependent conversion of clopidogrel to its active metabolite may contribute to response variability, prompting investigation into whether the CYP2C19 681G>A *2 polymorphism relates to high residual platelet aggregation and impacts clinical outcome after elective PCI.
Does the CYP2C19 681G>A *2 polymorphism increase residual platelet aggregation and the risk of death or myocardial infarction in patients undergoing elective PCI treated with clopidogrel?
Population
797 consecutive patients undergoing PCI
Comparison
CYP2C19*2 allele carriers vs wild-type homozygotes (*1/*1)
Design
Cohort study
Follow-up
1 year
Authors
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CYP2C19 polymorphism may flag higher-risk clopidogrel-treated PCI patients; leaves open prospective outcome trials before guiding therapy.
Cohort (n=797)
Does the CYP2C19 681G>A *2 polymorphism increase residual platelet aggregation and the risk of death or myocardial infarction in patients undergoing elective PCI treated with clopidogrel?
Effect estimate: 3.0-fold increase (95% CI 1.4-6.8)
p-value: p=0.004
Carriage of the CYP2C19*2 loss-of-function allele is associated with higher on-clopidogrel platelet reactivity and an increased risk of death and myocardial infarction at 1 year after elective PCI.
Trenk et al. (2008) conducted a cohort in Elective percutaneous coronary intervention (n=797). Residual platelet aggregation >14% at pre-discharge vs. Residual platelet aggregation ≤14% was evaluated on 1-year incidence of death and myocardial infarction (3.0-fold increase, 95% CI 1.4-6.8, p=0.004). High on-clopidogrel residual platelet aggregation (>14%) at pre-discharge was associated with a 3.0-fold increase in the 1-year incidence of death and myocardial infarction (95% CI 1.4-6.8; p=0.004).
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