Key result
Combining CYP2C19 genotyping and platelet reactivity predicts post-PCI MACCEs on clopidogrel better than either alone.
Why the study?
To investigate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity and its association with long-term clinical outcome in patients with coronary heart disease undergoing PCI.
Does CYP2C19 gene polymorphism and clopidogrel reactivity predict long-term clinical outcomes in patients with CHD after PCI?
Does CYP2C19 gene polymorphism and clopidogrel reactivity predict long-term clinical outcomes in patients with CHD after PCI?
CYP2C19 genotyping combined with platelet reactivity testing is an independent predictor of 12-month MACCEs in CHD patients treated with clopidogrel after PCI, performing better than either test alone.
Combined CYP2C19 genotyping plus reactivity testing was associated with better MACCE prediction post-PCI; hypothesis-generating and should not yet change practice.
Objective To investigate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity and its association with long-term clinical outcome in patients with coronary heart disease (CHD) undergoing percutaneous coronary intervention (PCI). Methods In total, 675 patients were enrolled. Based on the platelet inhibition rate, patients were categorized into two groups: clopidogrel low responsiveness (CLR) and normal clopidogrel responsiveness (NCR). The CLR group was divided into ticagrelor and clopidogrel group based on the antiplatelet drugs used in the follow-up treatment. Patients were classified into three groups (normal metabolizer, intermediate metabolizer, and poor metabolizer) based on the CYP2C19 genotype. We aimed to evaluate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity. The cumulative rates of 12-month all-cause deaths, major adverse cardiovascular events (MACCEs), and bleeding events were calculated. Results CLR was observed in 44.4% of the overall population. Significant differences were observed in the platelet inhibition rate of clopidogrel among the three metabolic genotypes (P < 0.05). At the 12-month follow-up, 13 patients (1.9%) died and 96 patients (14.2%) experienced MACCEs. Patients with CLR (9.6% vs. 11.7% vs. 22.1%, P < 0.05) or poor metabolizer (10.7% vs. 16.4% vs. 22.6%, P = 0.026) experienced a higher rate of MACCEs. A MACCEs risk score between zero and two was calculated. The highest incidence of MACCEs significantly increased with the 2-positive results, and the area under the curve (AUC) was 0.712 (95% CI: 0.650–0.774, P < 0.05). There was no significant difference between the group with a score of one and the occurrence of MACCEs (P > 0.05). Conclusions Low response to clopidogrel in CHD patients is correlated with CYP2C19 gene polymorphism. CYP2C19 genotyping combined with platelet reactivity is an independent predictor of 12-months MACCEs in patients with clopidogrel treatment after PCI, which is better than either test alone.
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Hu et al. (2024) studied this question. CYP2C19 genotyping combined with platelet reactivity independently predicted 12-month MACCEs in post-PCI patients on clopidogrel better than either test alone (AUC 0.712, 95% CI 0.650-0.774).
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