Key result
An ADP-induced platelet inhibition rate of <76% measured by thromboelastography independently predicted a higher risk of 1-year primary ischemic events in ticagrelor-treated patients with acute coronary syndrome (HR 8.21).
Why the study?
Despite ticagrelor therapy, serious ischemic events still occur in ACS, and the predictability of platelet reactivity for residual ischemic risk during treatment remains uncertain.
Does the ADP-induced platelet inhibition rate measured by TEG predict ischemic events in ticagrelor-treated patients with ACS?
Cohort (n=751)
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No
Does the ADP-induced platelet inhibition rate measured by TEG predict ischemic events in ticagrelor-treated patients with ACS?
Hazard Ratio: 8.21 (95% CI 4.82–13.99)
Absolute Event Rate: 54.12% vs 7.97%
p-value: p=<0.001
TEG-measured ADP% may stratify ischemic risk on ticagrelor; leaves open whether monitoring improves outcomes or warrants practice change.
BACKGROUND: Despite strong antiplatelet therapy with ticagrelor, serious ischemic events still occur in patients with acute coronary syndrome (ACS). The predictability of platelet reactivity to the residual risk of ischemic events during ticagrelor treatment remains uncertain. OBJECTIVES: We aimed to investigate the predictability of the thromboelastography (TEG)-measured adenosine disphosphate (ADP)-induced platelet inhibition rate (ADP%) to the ischemic events in ticagrelor-treated patients with ACS. METHODS: A cohort of ticagrelor-treated patients with ACS were consecutively recruited. ADP% was measured by TEG after 3 days of ticagrelor maintenance treatment. The primary ischemic event was defined as rehospitalization for unstable angina (UA) within 1 year, and the secondary ischemic event was a composite of the primary ischemic event plus all-cause death, nonfatal myocardial infarction (MI), stent thrombosis, stroke, and unplanned revascularization within 1 year. RESULTS: A total of 751 eligible patients with ACS were included in the analysis, with 336 patients randomly assigned to the derivation group and 415 to the validation group. The overall rates of primary and secondary ischemic events were 14.51% (n = 109) and 16.91% (n = 127), respectively. Compared to the patients without ischemic events, those with ischemic events had a significantly lower ADP% both in the derivation group (for primary ischemic events: 66.05% vs. 92.80%, p < 0.001; for secondary ischemic events: 66.05% vs. 93.20%, p < 0.001) and in the validation group (for primary ischemic events: 66.40% vs. 89.20%, p < 0.001; for secondary ischemic events: 66.90% vs. 89.20%, p < 0.001). Receiver operating characteristic curve (ROC) analysis showed that an ADP% < 76% was the optimal cut-off value for predicting 1-year primary ischemic events, with an area under the curve (AUC) of 0.80 (95% CI: 0.72-0.86, p < 0.001) in the derivation group and 0.77 (95% CI: 0.69-0.85, p < 0.001) in the validation group. The multivariate Cox regression hazard analysis consistently identified an ADP% < 76% as an independent predictor of primary ischemic events in the derivation group (HR: 8.21, 95% CI: 4.82-13.99, p < 0.001) and in the validation group (HR: 6.34 95% CI: 3.32-12.11, p < 0.001). There was also a strong association between an ADP% < 76 and the occurrence of secondary ischemic events in the derivation group (HR: 7.33, 95% CI: 4.47-12.00, p < 0.001) and in the validation group (HR: 4.76, 95% CI: 2.73-8.32, p < 0.001). CONCLUSION: The ADP-induced platelet inhibition rate measured by TEG could predict ischemic events in ticagrelor-treated patients with ACS.
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Zou et al. (2022) conducted a cohort in Acute coronary syndrome (n=751). ADP-induced platelet inhibition rate (ADP%) < 76% vs. ADP% ≥ 76% was evaluated on Rehospitalization for unstable angina within 1 year (primary ischemic event) (HR 8.21, 95% CI 4.82-13.99, p=<0.001). An ADP-induced platelet inhibition rate of <76% measured by thromboelastography independently predicted a higher risk of 1-year primary ischemic events in ticagrelor-treated patients with acute coronary syndrome (HR 8.21).
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