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A randomised study for optimising crossover from ticagrelor to clopidogrel in patients with acute coronary syndrome.
Ali Pourdjabbar, Benjamin Hibbert, Aun-Yeong Chong
1Derek Y. F. So MD, University of Ottawa Heart Institute, 40 Ruskin Street, Room H3408, Ottawa, Ontario K1Y 4W7, Canada, Tel.: +1 613 761 5387, Fax: +1 613 761 4338,
Insights
Switching from ticagrelor to clopidogrel: A clopidogrel bolus strategy did not improve P2Y12 reactivity units (PRU) at 72 hours but showed superior platelet inhibition at 48 hours and reduced high on-treatment platelet reactivity (HPR).
Area of Science:
- Cardiology
- Pharmacology
- Clinical Trials
Background:
- Ticagrelor is the preferred P2Y12 inhibitor for acute coronary syndrome (ACS).
- Optimal strategies for switching from ticagrelor to clopidogrel and its pharmacodynamic effects are not well-defined.
- Patients with ACS on ticagrelor may require a switch to clopidogrel due to various clinical reasons.
Purpose of the Study:
- To compare the pharmacodynamic effects of a clopidogrel bolus versus no bolus strategy in patients switching from ticagrelor.
- To assess P2Y12 reactivity units (PRU) and high on-treatment platelet reactivity (HPR) after switching antiplatelet therapy.
- To evaluate the incidence of major adverse cardiac events (MACE) and bleeding complications.
Main Methods:
- Randomized controlled trial involving 60 patients switching from ticagrelor to clopidogrel.
- Patients were assigned to either a 600 mg clopidogrel bolus followed by daily 75 mg or a no-bolus group receiving daily 75 mg.
- Platelet reactivity was measured using PRU at multiple time points up to 72 hours.
Main Results:
- No significant difference in PRU was observed at 72 hours between the bolus and no-bolus groups (p=0.19).
- The clopidogrel bolus group showed significantly lower PRU at 48 hours (p=0.0076).
- A significant reduction in high on-treatment platelet reactivity (HPR) was observed at 72 hours in the bolus arm (26.7% vs 56.7%, p=0.02).
Conclusions:
- A clopidogrel bolus strategy did not improve platelet inhibition at 72 hours but demonstrated superior inhibition at 48 hours.
- The bolus strategy led to a reduced incidence of HPR at 72 hours.
- Further research is needed to determine the clinical significance of these findings, with decisions on clopidogrel bolus potentially influenced by bleeding risk and indication for switching.
Abstract:
Ticagrelor has been endorsed by guidelines as the P2Y12 inhibitor of choice in patients with acute coronary syndrome. Clinically, some patients on ticagrelor will require a switch to clopidogrel; however, the optimal strategy and pharmacodynamics effects of switching remain unknown. Patients with an indication to switch were randomly assigned to either a bolus arm (Clopidogrel 600 mg bolus followed by 75 mg daily, n=30) or a no-bolus arm (Clopidogrel 75 mg daily, n=30). Blood samples were collected at baseline, 12, 24, 48, 54, 60 and 72 hours (h) for assessment of platelet reactivity. The primary outcome was P2Y12 reactivity units (PRU) at 72 h. Secondary outcomes included: PRUs at each time point, incidence of high on-treatment platelet reactivity (HPR), major adverse cardiac events (MACE) and TIMI bleeding at 30 days. Serial PRUs increased after switching to clopidogrel in both groups. At 72 h, no difference in PRU was observed (165.8 ± 71.0 vs 184.1 ± 67.7, bolus vs no bolus, respectively, p=0.19). At 48 h the PRUs were significantly lower in the bolus arm (114 ± 73.1 vs 165.1 ± 70.5, respectively; p=0.0076) and at 72 h, there was a significant reduction in incidence of HPR (26.7 % vs 56.7 %, p=0.02). No differences in MACE or TIMI bleeding were observed. Although a bolus strategy was not associated with improved platelet inhibition at 72 h; at 48 h, platelet inhibition was superior with reduced incidence of HPR. Larger studies will be required to determine its clinical significance. Until then, decision for giving a bolus of clopidogrel at the time of a switch may in part be dependent on the indication for switching, especially if there are concerns for bleeding risk.
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