Antiplatelet Therapy Guided by Platelet Function Testing after Successful Percutaneous Coronary Intervention

Alfonsina Candiello, Fernando Cura, Marcelo Trivi, Lucio Padilla, Mariano Albertal, Gerardo Nau, Maria Esther Aris Cancela, Sebastian Peralta, Fabricio Torrent, Jorge Belardi



Dual antiplatelet therapy with aspirin and clopidogrel is an essential treatment to prevent ischemic events in patients undergoing percutaneous coronary intervention (PCI). However, a significant interindividual variability exists in response to clopidogrel treatment, which is responsible for failure in the therapeutic effect and in the development of high residual platelet reactivity (HRPR). Prasugrel could reduce this prothrombotic state.


To evaluate: 1) the antiaggregant response in clopidogrel or prasugrel pretreated patients undergoing successful PCI, and 2) the response to prasugrel loading in patients with low residual platelet reactivity on clopidogrel therapy.

Material and Methods

Eighty three patients were prospectively included in the study. They underwent successful PCI under dual antiplatelet therapy: aspirin plus clopidogrel (600 mg loading dose or a maintenance dose of 75 mg for more than 7 days; n=42) or prasugrel (60 mg loading dose or a maintenance dose of 10 mg for more than 7 days; n=41). The selection of thienopyridine was left at the discretion of the treating physician. Patients with high hemorrhagic risk were excluded. Platelet function was tested 12-24 hours after PCI with the VerifyNowTMP2Y12 Assay. High residual platelet reactivity (HRPR) was defined as P2Y12-reaction units (PRU) ³ 230. In case of HRPR, patients received a loading dose of prasugrel 60 mg and platelet function was reassessed 2 hours later.


Baseline characteristics did not differ in patients who initially received clopidogrel or prasugrel. At 12-24 hours post PCI, patients treated with prasugrel presented significantly less PRU compared with the clopidogrel cohort (median 49 (9-78) vs. 160 (82-224); p < 0.001). HRPR was observed in 24% of patients in the clopidogrel group and in no patients in the prasugrel cohort (p < 0.001). All patients with HRPR on clopidogrel treatment corrected this value after the loading dose of prasugrel.


After successful PCI, prasugrel administration achieved greater platelet inhibition compared to clopidogrel. Moreover, in patients with high-on treatment platelet reactivity with clopidogrel, optimal platelet inhibition was accomplished by additional prasugrel administration.


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