Key result
Cessation of aspirin at 1 month post-PCI significantly increased arachidonic acid-induced platelet aggregation (11.1 to 64.9 U), while ticagrelor cessation increased ADP-induced aggregation.
Why the study?
Discontinuing one component of DAPT after PCI increases ischemic event risk, but whether stopping aspirin is preferable to stopping an oral P2Y12 inhibitor remains uncertain.
Does cessation of aspirin versus ticagrelor differentially affect recovery of platelet reactivity in patients treated with DAPT following PCI?
Cohort (n=34)
Open-label
Randomized
No
Does cessation of aspirin versus ticagrelor differentially affect recovery of platelet reactivity in patients treated with DAPT following PCI?
Cessation of either aspirin or ticagrelor leads to a substantial increase in platelet reactivity with differential effects on specific pathways of platelet activation.
Answers are grounded in this paper and cite their sources.
Supports differential platelet reactivity recovery after aspirin vs ticagrelor cessation post-PCI; informs de-escalation timing and guides targeted DAPT trials.
Cessation of one component of dual antiplatelet therapy (DAPT) following percutaneous coronary intervention (PCI) has been associated with increased risk of ischemic events but it is uncertain whether discontinuation of aspirin is preferable to discontinuation of the oral P2Y12 inhibitor. The GLOBAL LEADERS study compared two antiplatelet strategies following PCI, cessation of aspirin at 1 month with continued ticagrelor monotherapy for 23 months versus standard DAPT for 12 months followed by aspirin monotherapy for a further 12 months. We assessed recovery of platelet reactivity after withdrawal of either aspirin or ticagrelor at 1 month and 12 months, respectively, in this study. Platelet aggregation (PA) was assessed before cessation of DAPT (‘baseline’) and after 2, 7, and 14 days post-cessation using Multiplate whole-blood aggregometry with collagen, thrombin-receptor-activating peptide (TRAP), adenosine diphosphate (ADP) and arachidonic acid (AA) as agonists. Following cessation of aspirin at 1 month, there was marked recovery of PA induced by AA (baseline [mean ± SD]: 11.1 ± 7.4 U vs. 14 days: 64.9 ± 19.6 U, p < .0001) and collagen (37.4 ± 22.9 U vs. 79.8 ± 13.8 U, p < .0001), whereas PA induced by ADP (18.6 ± 6.6 vs. 69.1 ± 20.5, p < .0001) and collagen (34.4 ± 18.7 U vs. 43.0 ± 21.0, p = .0018) recovered following cessation of ticagrelor at 12 months. There were no significant changes in TRAP-induced PA in either group. In conclusion, cessation of either component of DAPT leads to substantial increase in platelet reactivity with differential effects on different pathways of platelet activation when aspirin or the P2Y12 inhibitor is stopped. Further work is required to determine which patients receive net benefit from long-term continuation of DAPT.
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Hennigan et al. (2020) conducted a cohort in Percutaneous coronary intervention (n=34). Cessation of aspirin vs. Baseline (on dual antiplatelet therapy) was evaluated on Arachidonic acid-induced platelet aggregation at 14 days post-cessation of aspirin (p=<0.0001). Cessation of aspirin at 1 month post-PCI significantly increased arachidonic acid-induced platelet aggregation (11.1 to 64.9 U), while ticagrelor cessation increased ADP-induced aggregation.
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