Key result
Routine CYP2C19 genotyping triples clopidogrel prescribing post-PCI, increasing use from 25% to ~77%.
Why the study?
The relationship between routine CYP2C19 genotyping, real-world P2Y12 inhibitor prescribing, and clinical outcomes after PCI remains uncertain.
Does routine CYP2C19 genotyping influence P2Y12 inhibitor prescription patterns in CHD patients after PCI?
Cohort (n=364)
No
Does routine CYP2C19 genotyping influence P2Y12 inhibitor prescription patterns in CHD patients after PCI?
Absolute Event Rate: 76.6% vs 25%
p-value: p=<0.001
Routine CYP2C19 genotyping significantly altered the real-world prescribing patterns of P2Y12 inhibitors following PCI, demonstrating high clinical uptake of pharmacogenomic data.
Routine CYP2C19 genotyping was associated with increased clopidogrel use post-PCI; leaves open effects on ischemic and bleeding outcomes.
Background CYP2C19 genotype can influence clopidogrel response, but the relationship between routine genotyping, real‐world P2Y12 inhibitor prescribing, and clinical outcomes remains uncertain. Aims To characterize P2Y12 inhibitor prescription patterns before and after routine CYP2C19 genotyping and to describe ischemic and bleeding outcomes in a retrospective real‐world cohort. Methods This single‐center retrospective study included 364 adults with coronary heart disease who underwent percutaneous coronary intervention (PCI) from January to December 2023. During the study period, CYP2C19 genotyping was routinely performed as part of the hospital’s antiplatelet management policy, and all 364 participants were genotyped. Prescription patterns before and after genotype results were compared; clinical outcome analyses were restricted to the 271 patients with complete linked postdischarge medication and outcome data. Results Before genotyping, 273/364 patients (75.0%) received ticagrelor, and 91/364 (25.0%) received clopidogrel; after genotype results, 279/364 (76.6%) received clopidogrel, and 85/364 (23.4%) received ticagrelor. From the reported adjustment counts, 258 patients switched from ticagrelor to clopidogrel, 70 switched from clopidogrel to ticagrelor, and 36 remained on the same agent (exact McNemar p < 0.001). CYP2C19 genotypes were ∗1/∗1 in 132 (36.3%; normal metabolizer), ∗1/∗2 or ∗1/∗3 in 179 (49.2%; intermediate metabolizer), and two loss‐of‐function alleles in 53 (14.5%; poor metabolizer). In the 271‐patient outcome subset, event counts were low, and treatment strata were highly imbalanced. Fisher exact comparisons were therefore considered exploratory, and no causal effect of genotyping or drug selection was inferred. Conclusions Routine CYP2C19 genotyping was associated with a substantial change in P2Y12 inhibitor prescribing in this single‐center cohort. Because treatment was physician‐directed and outcome data were sparse and incomplete for the full cohort, the clinical event comparisons should be interpreted as exploratory rather than evidence that genotype‐guided therapy reduced bleeding or ischemic events.
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Niu et al. (2026) conducted a cohort in Coronary heart disease post-PCI (n=364). Routine CYP2C19 genotype availability vs. Before genotype availability was evaluated on Change in P2Y12 inhibitor prescription (clopidogrel use) before vs after genotype results (p=<0.001). Routine CYP2C19 genotyping availability significantly changed P2Y12 inhibitor prescribing, with clopidogrel use increasing from 25.0% to 76.6% (p<0.001).
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