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Published on: November 8, 2024
Low platelet reactivity in patients with myocardial infarction treated with aspirin plus ticagrelor
Thiago Guarato Rodrigues Costa1, Marcelo Katz1, Pedro Alves Lemos Neto1
1Hospital Israelita Albert Einstein, São Paulo, SP, Brazil.
Insights
Low platelet reactivity is common in acute myocardial infarction patients on dual antiplatelet therapy with ticagrelor and aspirin. This suggests exploring less intensive strategies to reduce bleeding risk.
Area of Science:
- Cardiology
- Pharmacology
- Hematology
Background:
- Dual antiplatelet therapy (DAPT) with aspirin and ticagrelor is standard for acute myocardial infarction (AMI).
- Low platelet reactivity is linked to increased bleeding risk in patients on DAPT.
- Optimal platelet inhibition is crucial, but excessive inhibition may increase bleeding.
Purpose of the Study:
- To determine the prevalence of low platelet reactivity in AMI patients treated with ticagrelor and aspirin.
- To assess platelet reactivity at peak and trough ticagrelor levels.
- To inform potential adjustments in antiplatelet therapy strategies.
Main Methods:
- Prospective enrollment of 50 AMI patients on aspirin and ticagrelor.
- Platelet reactivity assessment using Multiplate®, PFA-100®/Innovance® PFA-P2Y, and PFA-100®/Collagen/ADP assays.
- Measurements taken at peak and trough ticagrelor levels.
Main Results:
- Low platelet reactivity was highly prevalent across all tested methods.
- Prevalence varied by assay: PFA-100®/Innovance® PFA-P2Y (86%), Multiplate® (74%), PFA-100®/Collagen/ADP (48%).
- Peak and trough platelet reactivity levels were markedly low and did not significantly differ between methods.
Conclusions:
- Low platelet reactivity is very common in AMI patients receiving ticagrelor and aspirin.
- These findings support investigating de-escalation strategies, such as lower ticagrelor doses or P2Y12 inhibitor monotherapy.
- Reducing antiplatelet intensity may mitigate bleeding risk in this patient population.
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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