Key result
Ticagrelor monotherapy significantly reduced ADP-induced platelet aggregation compared to clopidogrel monotherapy (27.30% vs. 35.55%; P=0.0254) in patients with chronic coronary syndrome.
Why the study?
Data were lacking on platelet reactivity comparing ticagrelor monotherapy versus clopidogrel monotherapy after discontinuing aspirin.
Does ticagrelor monotherapy reduce platelet reactivity compared to clopidogrel monotherapy in Chinese patients with chronic coronary syndrome?
RCT (n=50)
Single-blind
randomized
Does ticagrelor monotherapy reduce platelet reactivity compared to clopidogrel monotherapy in Chinese patients with chronic coronary syndrome?
Absolute Event Rate: 27.3% vs 35.55%
p-value: p=0.0254
Ticagrelor monotherapy provides stronger inhibition of ADP- and AA-induced platelet aggregation than clopidogrel monotherapy in Chinese patients with chronic coronary syndrome.
Ticagrelor monotherapy lacks platelet reactivity data versus clopidogrel in Chinese CCS patients; leaves open optimal P2Y12 monotherapy choice.
Increasing clinical trials demonstrated that the discontinuation of aspirin while maintaining a P2Y12 inhibitor monotherapy could decrease the risk of bleeding without losing the antithrombotic effect. However, no data are available on the platelet reactivity of patients undergoing ticagrelor monotherapy vs. clopidogrel. Therefore, we performed this study to observe the efficacy of ticagrelor monotherapy vs. clopidogrel in Chinese patients with chronic coronary syndrome. This randomized, single-blinded, crossover trial enrolled 50 patients who were administered with ticagrelor (90 mg twice daily for 2 weeks) or clopidogrel (75 mg once daily for 2 weeks). Followed by a 2-week washout period, the two groups of patients underwent a crossover trial. Light transmission aggregometry (LTA) and thromboelastography (TEG) assays were used to test platelet reactivity. The platelet aggregation rate (PAgR) of ADP and AA was significantly lower with ticagrelor than clopidogrel (PAgR of ADP, 27.30% (7.30%-42.635%) vs. 35.55% (12.03%-69.25%), P = .0254; PAgR of AA, 77.80% (21.60%-86.43%) vs. 83.10% (67.13%-87.20%), P = .0400). There was no significant difference in PAgR of collagen and epinephrine between the two groups. The TEG assay showed that ADP and AA, which induced the inhibition of platelet aggregation, were significantly higher in the ticagrelor group than those in the clopidogrel group [ADP%, 69.00% (59.68%–88.95%) vs. 60.55% (35.98%–78.35%), P = .0020; AA%, 53.65% (22.75%–79.28%) vs. 15.15% (5.75%–70.25%), P = .0127]. High on-treatment platelet reactivity (HTPR) on ADP was 2.17% with ticagrelor and 19.57% with clopidogrel. HTPR on AA was 50.00% with ticagrelor and 69.57% with clopidogrel. Ticagrelor and clopidogrel caused the inhibition of ADP and AA-induced platelet aggregation. Moreover, ticagrelor monotherapy had a stronger inhibitory effect than clopidogrel monotherapy (except on collagen and epinephrine).
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He et al. (2022) conducted an RCT in chronic coronary syndrome (n=50). Ticagrelor vs. Clopidogrel (75 mg once daily) was evaluated on Platelet aggregation rate (PAgR) of ADP (p=0.0254). Ticagrelor monotherapy significantly reduced ADP-induced platelet aggregation compared to clopidogrel monotherapy (27.30% vs. 35.55%; P=0.0254) in patients with chronic coronary syndrome.
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