An open lable,two arms,randomized controlled pilot study comparing the platelet aggregation rate in patients with stable coronary artery disease treated with Ticagrelor monotherapy or Ticagrelor combined with Asprin
An open lable,two arms,randomized controlled pilot study comparing the platelet aggregation rate in patients with stable coronary artery disease treated with Ticagrelor monotherapy or Ticagrelor combined with Asprin
Objective To evaluate platelet aggregation after 14 days of treatment with ticagrelor alone or aspirin plus ticagrelor in patients with stable coronary artery disease.Methods Patients with stable coronary artery disease receiving dual antiplatelet therapy with aspirin 100 mg/d plus clopidogrel 75 mg/d were randomly assigned to ticagrelor monotherapy group or ticagrelor plus aspirin group after washout of ticagrelor monotherapy.Platelet aggregation rate was measured after 7 days and 14 days.Results 57 patients(32 in Ticagrelor monotherapy group and 25 in Ticagrelor+Aspirin group)completed the follow-up.The mean age was(61.16±7.87)years.The platelet aggregation rates induced by arachidonic acid(AA),adenosine diphosphate(ADP),and collagen-induced were similar at baseline and randomization in both groups.After 14 days of treatment,the ADP-induced platelet aggregation rates in both groups were significantly lower than the baseline,but there was no statistical difference between the two groups[(21.50±7.86)％vs.(21.92±10.21)％,P=0.864].The ADP-induced platelet aggregation rates in both groups decreased compared to randomization,but the Ticagrelor monotherapy group was significantly higher than the Ticagrelor+Aspirin group[(48.22±24.01)％vs.(8.67±5.96)％,P＜0.001].In the monotherapy group,5 patients had a significant increase in the AA-induced platelet aggregation after the discontinuation of aspirin.After 14 days of continued Ticagrelor monotherapy,the AA-induced platelet aggregation rate decreased significantly again(＜30％).Conclusions Ticagrelor monotherapy exerts a strong inhibitory effect on ADP-induced platelet aggregation and a mild inhibitory effect on the AA-induced platelet aggregation.In addition to its strong inhibitory effect on ADP-induced platelet aggregation,the mild inhibitory effect of Ticagrelor on the AA-induced pathway may have some clinical significance for the early de-escalation of dual antiplatelet therapy to monotherapy in patients.
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