Key result
In post-MI patients on potent P2Y12 inhibitors, adding vorapaxar to DAPT reduced CAT-induced platelet aggregation at 30 days (MD -27; 95% CI -35 to -19; P<0.001), an effect persisting without aspirin.
Why the study?
The pharmacodynamic effects of vorapaxar combined with potent P2Y12 inhibitors and the impact of dropping aspirin in post-myocardial infarction patients were unexplored.
Does vorapaxar added to potent P2Y12 inhibitors with or without aspirin reduce platelet-mediated global thrombogenicity in post-myocardial infarction patients?
RCT (n=130)
Does vorapaxar added to potent P2Y12 inhibitors with or without aspirin reduce platelet-mediated global thrombogenicity in post-myocardial infarction patients?
Mean Difference: -27 (95% CI -35–-19)
p-value: p=<0.001
In post-MI patients on potent P2Y12 inhibitors, adding vorapaxar reduces platelet-driven global thrombogenicity, an effect that persists even when aspirin is withdrawn.
Authors
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Vorapaxar may augment platelet inhibition beyond potent P2Y12 therapy post-MI; leaves open whether aspirin omission improves net outcomes.
Franchi et al. (2020) conducted an RCT in Prior myocardial infarction (n=130). Vorapaxar (with or without aspirin) vs. Standard DAPT (aspirin + prasugrel or ticagrelor) was evaluated on CAT (collagen-ADP-TRAP)-induced platelet aggregation at 30 days (MD -27, 95% CI -35 to -19, p=<0.001). In post-MI patients on potent P2Y12 inhibitors, adding vorapaxar to DAPT reduced CAT-induced platelet aggregation at 30 days (MD -27; 95% CI -35 to -19; P<0.001), an effect persisting without aspirin.
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