Prasugrel reduced platelet reactivity units by 24.4 to 42.0 units more than clopidogrel at Day 5 and lowered odds of high platelet reactivity in high-risk subgroups including CKD (OR 8.06, p=0.012) and age ≥75 years (OR 5.02, p=0.025) in patients with acute atherothrombotic stroke or high-risk TIA.
RCT (n=176)
Randomized
Open-label
Yes
Does prasugrel improve early platelet inhibition compared to clopidogrel across different patient background subgroups with acute atherothrombotic stroke or high-risk TIA?
176 patients with acute atherothrombotic stroke (large artery atherosclerosis) or high-risk TIA (ABCD2 score ≥ 4 or paralysis) treated within 48 hours of symptom onset. Mean age ~71 years. Key inclusion: NIHSS score ≤ 10, ≥ 1 risk factor (CKD, DM, hypertension, dyslipidemia, or prior stroke).
Prasugrel 3.75 mg or 2.5 mg oral once daily (without initial loading dose) plus aspirin for the first 21 days, continued for 90 days.
Clopidogrel (initial dose 300 mg or 75 mg, maintenance dose 75 mg or 50 mg once daily at physician discretion) plus aspirin for the first 21 days, continued for 90 days.
High platelet reactivity (HPR; defined as PRU >208) and absolute platelet reaction units (PRU) on Day 5 after starting treatment.surrogate
Prasugrel provides more potent early platelet inhibition than clopidogrel in acute stroke patients, particularly in high-risk subgroups such as those with advanced age, chronic kidney disease, or metabolic comorbidities.
Effect estimate: OR 2.73 for non-HPR in ABCD-GENE score ≥10 subgroup favoring prasugrel (p=0.076); OR 8.06 for non-HPR in CKD patients favoring prasugrel (p=0.012); OR 5.02 for age ≥75 years favoring prasugrel (p=0.025); OR 4.61 for BMI <25 kg/m2 favoring prasugrel (p=0.012); OR 4.73 for dyslipidemia favoring prasugrel (p=0.009); OR 3.86 for diabetes favoring prasugrel (p=0.038); OR 3.31 for treatment initiation ≤24 hours favoring prasugrel (p=0.010); OR 2.77 (NIHSS ≤3) and 9.00 (NIHSS ≥4) favoring prasugrel
Aim: To explore whether the antiplatelet effects of prasugrel and clopidogrel vary according to patient background factors in the ACUTE-PRAS study.
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Shigeru Fujimoto
Yasuyuki Iguchi
Jikei University School of Medicine
Hiroshi Yamagami
Journal of Atherosclerosis and Thrombosis
University of Tsukuba
Jichi Medical University
National Cerebral and Cardiovascular Center
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Fujimoto et al. (Thu,) conducted a rct in Patients with acute atherothrombotic stroke or high-risk transient ischemic attack initiating antiplatelet therapy within 48 hours of symptom onset (n=176). Prasugrel vs. Clopidogrel 75 mg or 300 mg initial dose followed by 50 mg or 75 mg once daily as maintenance was evaluated on Platelet reaction units (PRU) on Day 5 post-treatment initiation as a measure of platelet inhibition; defined high platelet reactivity (HPR) as PRU ≥ 208 (OR 2.73 for non-HPR in ABCD-GENE score ≥10 subgroup favoring prasugrel (p=0.076); OR 8.06 for non-HPR in CKD patients favoring prasugrel (p=0.012); OR 5.02 for age ≥75 years favoring prasugrel (p=0.025); OR 4.61 for BMI <25 kg/m2 favoring prasugrel (p=0.012); OR 4.73 for dyslipidemia favoring prasugrel (p=0.009); OR 3.86 for diabetes favoring prasugrel (p=0.038); OR 3.31 for treatment initiation ≤24 hours favoring prasugrel (p=0.010); OR 2.77 (NIHSS ≤3) and 9.00 (NIHSS ≥4) favoring prasugrel). Prasugrel reduced platelet reactivity units by 24.4 to 42.0 units more than clopidogrel at Day 5 and lowered odds of high platelet reactivity in high-risk subgroups including CKD (OR 8.06, p=0.012) and age ≥75 years (OR 5.02, p=0.025) in patients with acute atherothrombotic stroke or high-risk TIA.
synapsesocial.com/papers/69a91cbed6127c7a504bfaa9 — DOI: https://doi.org/10.5551/jat.66056