Key result
Ticagrelor loading dose did not achieve noninferiority to tirofiban for inhibition of platelet aggregation at 2 hours (mean difference -9.9%; 95% CI -25.7% to 5.9%).
Why the study?
Does a ticagrelor loading dose provide non-inferior inhibition of platelet aggregation compared to tirofiban in NSTE-ACS patients planned for PCI?
RCT (n=95)
Does a ticagrelor loading dose provide non-inferior inhibition of platelet aggregation compared to tirofiban in NSTE-ACS patients planned for PCI?
Mean Difference: -9.9 (95% CI -25.7–5.9)
In NSTE-ACS patients undergoing PCI, the early antiplatelet effect of a ticagrelor loading dose is strong but does not reach the level of platelet inhibition achieved by tirofiban at 2 hours.
Ticagrelor loading not noninferior to tirofiban at 2 hours in NSTE-ACS PCI; challenges early equivalence assumptions and warrants outcome trials.
Addition of a potent P2Y12 inhibitor to aspirin is the standard therapy for non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients undergoing percutaneous coronary intervention (PCI). Glycoprotein IIb/IIIa inhibitor, together with antiplatelet therapy, may be considered as part of initial therapy in NSTE-ACS patients with high-risk features. This study investigated the antiplatelet effect of ticagrelor loading dose (LD) versus tirofiban bolus injection with a post-bolus infusion on top of aspirin among NSTE-ACS patients planned to PCI. NSTE-ACS patients were randomised to receive either ticagrelor (n = 47) or tirofiban (n = 48). Platelet reactivity was assessed by light transmittance aggregometry at 0, 2, 8, and 24 hours (h) after treatment initiation. Primary endpoint was inhibition of platelet aggregation (IPA, 20 µM ADP, final extent) at 2 h after LD therapy, with a non-inferiority margin of 10%. The prevalence of high on-treatment platelet reactivity (HPR) was also compared at 0, 2, 8, and 24 h. The mean difference in IPA between ticagrelor and tirofiban was -9.9% (95% confidence interval: -25.7% to 5.9%) at 2 h, -1.6% (-8.0% to 4.8%) at 8 h, and -3.3% (-18.4% to 12.0%) at 24 h. The prevalence of HPR did not differ between the two groups at any time point (all p values ≥ 0.059), which was almost abolished by 8 h post-LD (< 5%). In conclusion, the antiplatelet effect during the early phase (~2 h) after ticagrelor LD appeared to be relatively strong, but it did not reach that of tirofiban in NSTE-ACS patients.
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Jeong et al. (2015) conducted an RCT in Non-ST-segment elevation acute coronary syndrome (NSTE-ACS) (n=95). Ticagrelor vs. Tirofiban bolus injection with a post-bolus infusion was evaluated on Inhibition of platelet aggregation (IPA, 20 µM ADP, final extent) at 2 h after LD therapy (MD -9.9%, 95% CI -25.7% to 5.9%). Ticagrelor loading dose did not achieve noninferiority to tirofiban for inhibition of platelet aggregation at 2 hours (mean difference -9.9%; 95% CI -25.7% to 5.9%).
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