Personalized antiplatelet therapy did not significantly reduce new stroke compared to standard care (P=0.842), but reduced poor functional prognosis (14.88% vs 18.20%; HR 0.77; 95% CI 0.63-0.95).
RCT (n=2,663)
randomized
Yes
Does personalized antiplatelet therapy based on CYP2C19 genotype and 11-dhTxB2 testing reduce new stroke in patients with acute ischaemic stroke or transient ischaemic attack?
Genotype- and metabolite-guided personalized antiplatelet therapy did not reduce new strokes but improved functional prognosis and reduced bleeding risk in patients with acute ischemic stroke or TIA.
p-value: p=.842
AIMS: The aim of this study was to determine whether the testing strategy for clopidogrel and/or aspirin resistance using CYP2C19 genotyping or urinary 11-dhTxB2 testing has an impact on clinical outcomes. METHODS: A multicentre, randomized, controlled trial was conducted at 14 centres in China from 2019 to 2021. For the intervention group, a specific antiplatelet strategy was assigned based on the CYP2C19 genotype and 11-dhTxB2, a urinary metabolite of aspirin, and the control group received nonguided (ie, standard of care) treatment. 11-dhTXB2 is a thromboxane A2 metabolite that can help quantify the effects of resistance to aspirin in individuals after ingestion. The primary efficacy outcome was new stroke, the secondary efficacy outcome was a poor functional prognosis (a modified Rankin scale score ≥3), and the primary safety outcome was bleeding, all within the 90-day follow-up period. RESULTS: A total of 2815 patients were screened and 2663 patients were enrolled in the trial, with 1344 subjects assigned to the intervention group and 1319 subjects assigned to the control group. A total of 60.1% were carriers of the CYP2C19 loss-of-function allele (*2, *3) and 8.71% tested positive for urinary 11-dhTxB2- indicating aspirin resistance in the intervention group. The primary outcome was not different between the intervention and control groups (P = .842). A total of 200 patients (14.88%) in the intervention group and 240 patients (18.20%) in the control group had a poor functional prognosis (hazard ratio 0.77, 95% confidence interval CI 0.63 to 0.95, P = .012). Bleeding events occurred in 49 patients (3.65%) in the intervention group and 72 patients (5.46%) in the control group (hazard ratio 0.66, 95% CI 0.45 to 0.95, P = .025). CONCLUSIONS: Personalized antiplatelet therapy based on the CYP2C19 genotype and 11-dhTxB2 levels was associated with favourable neurological function and reduced bleeding risk in acute ischaemic stroke and transient ischaemic attack patients. The results may help support the role of CYP2C19 genotyping and urinary 11-dhTxB2 testing in the provision of precise clinical treatment.
Han et al. (Wed,) conducted a rct in acute ischaemic stroke or transient ischaemic attack (n=2,663). Personalized antiplatelet therapy based on CYP2C19 genotype and 11-dhTxB2 vs. Nonguided (standard of care) treatment was evaluated on new stroke (p=.842). Personalized antiplatelet therapy did not significantly reduce new stroke compared to standard care (P=0.842), but reduced poor functional prognosis (14.88% vs 18.20%; HR 0.77; 95% CI 0.63-0.95).
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