Key result
Platelet function-guided optimal-antiplatelet therapy significantly reduced the 2-year composite of death, MI, TVR, or stroke compared to standard therapy (4.5% vs. 9.2%, P=0.006).
Why the study?
Does platelet function-guided optimal-antiplatelet therapy reduce the composite of all-cause death, myocardial infarction, clinically driven TVR, or stroke in patients with high on-treatment platelet reactivity undergoing coronary stenting for ACS?
RCT (n=840)
1:2 ratio
Yes
Does platelet function-guided optimal-antiplatelet therapy reduce the composite of all-cause death, myocardial infarction, clinically driven TVR, or stroke in patients with high on-treatment platelet reactivity undergoing coronary stenting for ACS?
Platelet function-guided antiplatelet therapy significantly reduces long-term ischemic events without increasing bleeding in ACS patients with high on-treatment platelet reactivity after stenting.
Answers are grounded in this paper and cite their sources.
Supports platelet function-guided therapy in ACS stenting with high reactivity; extends evidence to long-term ischemic reduction without excess bleeding.
Optimal strategy for the management of high on-treatment platelet reactivity (HPR), an independent predictor of ischaemic events, is not yet clear. The aim of this study was to explore the safety and efficacy of personalized antiplatelet therapy based on platelet function testing in patients with HPR. A total of 840 patients with HPR who underwent coronary stenting for acute coronary syndrome (ACS) were randomly assigned in a 1:2 ratio to receive standard dual-antiplatelet therapy (n = 280) or platelet function-guided optimal-antiplatelet therapy (n = 560). In the optimal group, patients initially received clopidogrel 150 mg/day on top of aspirin and switched to triple antiplatelet therapy with additional cilostazol if repeat platelet function assay after 3 days indicated a sustained HPR. The primary endpoint was the composite of all-cause death, myocardial infarction, clinically driven target vessel revascularization (TVR), or stroke. Optimal therapy resulted in significantly lower 30-day HPR rate (30.1 vs. 44.3%, P < 0.001). At 1-year follow up, optimal therapy was associated with significantly lower incidence of primary endpoint events (2.7 vs. 6.8%, P = 0.006) compared with standard therapy, mainly due to the reduction of TVR. These beneficial effects were sustained at 2 years (4.5 vs. 9.2%, P = 0.006), with similar bleeding event rates between groups (7.3 vs. 6.5%, P = 0.565). Optimal-antiplatelet therapy based on platelet function testing is effective in attenuating HPR and improving long-term outcomes for ACS patients with no increase in bleeding events.
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Li et al. (2015) conducted an RCT in Acute coronary syndrome with high on-treatment platelet reactivity (n=840). Platelet function-guided optimal-antiplatelet therapy vs. Standard dual-antiplatelet therapy was evaluated on Composite of all-cause death, myocardial infarction, clinically driven target vessel revascularization (TVR), or stroke (p=0.006). Platelet function-guided optimal-antiplatelet therapy significantly reduced the 2-year composite of death, MI, TVR, or stroke compared to standard therapy (4.5% vs. 9.2%, P=0.006).
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