ArticleJournal of thrombosis and thrombolysis2025
Exploring the relationship of platelet aggregation function with efficacy and safety outcomes following the administration of prasugrel and clopidogrel in patients with thrombotic stroke: a post hoc analysis of PRASTRO pooled studies.
Article in Journal of thrombosis and thrombolysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Prasugrel: Reassessing Its Role in Contemporary Antiplatelet Therapy.Cardiovascular therapeutics · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The P2Y12 receptor inhibitor prasugrel was approved for thrombotic stroke in Japan following the phase 3 clinical trials PRASTRO-I, -II, and -III. However, correlations between elevated platelet reaction unit (PRU) and ischemic event risk remain unclear. This post hoc integrated analysis of PRASTRO-I, -II, and -III assessed the relationships of PRU with efficacy and safety outcomes, and risk factors for high PRU (HPR). Patients from PRASTRO-I, -II, and -III receiving prasugrel or clopidogrel and with PRU values at 4 and 24 weeks after treatment initiation were included. The primary endpoint was PRU at 4 weeks; secondary endpoints included cumulative incidence of ischemic and bleeding events from study drug initiation to 48 weeks. Exploratory univariate and multivariate analyses were conducted to identify HPR risk factors. Of 2688 patients analyzed, 2595 and 2434 had PRU values available at 4 and 24 weeks, respectively. Mean PRU was numerically lower with prasugrel than clopidogrel at 4 weeks (151.3 vs. 195.4) and 24 weeks (143.8 vs. 188.0). CYP2C19 polymorphisms affected PRU at 4 and 24 weeks with clopidogrel but not with prasugrel. PRU at 4 weeks did not predict ischemic and bleeding event incidence up to 48 weeks. The CYP2C19 poor metabolizer phenotype was the strongest HPR risk factor. PRU values at 4 and 24 weeks were numerically lower with prasugrel and unaffected by CYP2C19 genetic polymorphisms. Further research is needed to clarify the relationship of PRU with ischemic and bleeding events.
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Registered trials
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