Key result
Appropriate clopidogrel response matches prasugrel or ticagrelor for MACE risk in ACS after PCI.
Why the study?
Whether new P2Y12 inhibitors reduce thrombotic events similarly to appropriate P2Y12 inhibition by clopidogrel in PCI-treated ACS patients was uncertain.
Does prasugrel or ticagrelor reduce the composite of cardiovascular death, myocardial infarction, stent thrombosis, and stroke compared to clopidogrel in clopidogrel-responsive ACS patients undergoing urgent PCI?
Cohort (n=730)
Single-blind (outcome assessors)
No
Does prasugrel or ticagrelor reduce the composite of cardiovascular death, myocardial infarction, stent thrombosis, and stroke compared to clopidogrel in clopidogrel-responsive ACS patients undergoing urgent PCI?
Absolute Event Rate: 7.1% vs 4.1%
p-value: p=0.43
In PCI-treated ACS patients who are clopidogrel responders, clopidogrel therapy provides similar protection against thrombotic events as prasugrel or ticagrelor, with fewer minor bleeding events.
High on-treatment ADP reactivity on clopidogrel associated with increased events post-PCI; leaves open whether prasugrel or ticagrelor reduces risk in this population.
AIM: In percutaneous coronary intervention (PCI)-treated acute coronary syndrome (ACS) patients on clopidogrel therapy, high on-treatment platelet adenosine diphosphate (ADP) reactivity was observed in numerous studies, with significant increases in non-fatal myocardial infarction, definite/probable stent thrombosis, or cardiovascular mortality. Compared to clopidogrel, prasugrel and ticagrelor provide more potent platelet inhibition. Whether new P2Y12 inhibitors reduce thrombotic events in a similar manner compared to the rate observed with appropriate P2Y12 inhibition by clopidogrel must still be determined. This study sought to compare long-term outcomes between clopidogrel responders (platelet reactivity index [PRI] vasodilator-stimulated phosphoprotein [VASP] ＜61%) and patients under prasugrel or ticagrelor therapy following PCI-treated ACS. METHODS: 730 ACS patients undergoing urgent PCI were prospectively enrolled into two groups: clopidogrel responders (n=448) and those under ticagrelor or prasugrel therapy (n=282). The primary endpoint was a composite of cardiovascular death, myocardial infarction, stent thrombosis, and stroke; the secondary endpoint comprised major hemorrhagic events. RESULTS: The median follow-up was 260±186 days. Clopidogrel patients were older and more likely to present non-ST segment elevation myocardial infarction, cardiovascular risk factors, atrial fibrillation, or prior vascular disease. After propensity score matching, the primary endpoint was met in 7.1% of the clopidogrel group and 4.1% of the prasugrel/ticagrelor group (p=0.43). Minor bleeding events were significantly reduced in the clopidogrel group (1.1% vs. 3%; p=0.03). In a multivariate analysis, the antiplatelet treatment strategy was not an independent primary endpoint predictor. CONCLUSION: In PCI-treated ACS patients, clopidogrel therapy and PRI VASP ＜61% were not associated with increased risks of thrombotic events compared to prasugrel or ticagrelor therapy.
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Ristorto et al. (2018) conducted a cohort in Acute Coronary Syndrome (ACS) treated with PCI (n=730). Clopidogrel (responders with PRI VASP <61%) vs. Prasugrel or Ticagrelor was evaluated on Composite of cardiovascular death, myocardial infarction, stent thrombosis, and stroke (p=0.43). Appropriate platelet inhibition by clopidogrel (PRI VASP <61%) did not significantly increase the risk of major adverse cardiac events compared to prasugrel or ticagrelor therapy in PCI-treated ACS patients.
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