Key result
Ticagrelor-based DAPT in AMI shows ~74% prevalence of low platelet reactivity.
Why the study?
Low platelet reactivity is linked to increased bleeding risk during DAPT, prompting evaluation of its prevalence in acute myocardial infarction patients treated with ticagrelor and aspirin.
Does dual antiplatelet therapy with ticagrelor and aspirin cause low platelet reactivity in patients with acute myocardial infarction?
Observational (n=50)
No
Does dual antiplatelet therapy with ticagrelor and aspirin cause low platelet reactivity in patients with acute myocardial infarction?
High low-reactivity rates on ticagrelor-aspirin in AMI warrant assay-specific monitoring; extends RCT data on DAPT response variability.
OBJECTIVE: Low platelet reactivity levels are associated with higher risk of bleeding in patients receiving dual antiplatelet therapy relative to patients with optimal platelet blockade. This study set out to evaluate the prevalence of low platelet reactivity in patients with acute myocardial infarction treated with ticagrelor and aspirin. METHODS: Patients admitted with acute myocardial infarction who were already undergoing dual antiplatelet therapy with aspirin and ticagrelor were enrolled. Blood samples were collected 1 hour before and 2 hours after the maintenance dose of ticagrelor to investigate trough and the peak effects of the drug respectively. Platelet reactivity was measured by three methods: Multiplate®, PFA-100® with Innovance® PFA-P2Y cartridge and PFA-100® with Collagen/ADP cartridge. Platelet reactivity was assessed in the presence of peak levels of ticagrelor and defined according to previously validated cut-offs for each method (<19 AUC, >299 seconds and >116 seconds respectively). The level of significance was set at p<0.05. RESULTS: Fifty patients were enrolled (44% with ST-elevation). Median duration of DAPT was 3 days (interquartile range, 2-5 days). On average, peak and trough platelet reactivity were markedly low and did not differ between different methods. Low platelet reactivity was common, but varied according to analytic method (PFA-100®/Innovance®PFA-P2Y: 86%; Multiplate®: 74%; PFA-100®/Collagen/ADP: 48%; p<0.001). CONCLUSION: Low platelet reactivity was very common in patients with acute myocardial infarction submitted to dual antiplatelet therapy with ticagrelor and aspirin. Findings of this study justify the investigation of less intensive platelet inhibition strategies aimed at reducing the risk of bleeding in this population, such as lower dose regimens or monotherapy with P2Y12 inhibitors.
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Costa et al. (2022) conducted an observational in Acute myocardial infarction (n=50). Ticagrelor plus aspirin was evaluated on Prevalence of low platelet reactivity (LPR) at peak drug activity (Multiplate assay). In patients with acute myocardial infarction, dual antiplatelet therapy with ticagrelor and aspirin resulted in a high prevalence of low platelet reactivity, ranging from 48% to 86% depending on the assay.
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