科研之友
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摘要
Background: Recent studies have shown that the thromboxane A(2)-dependent pathway is dependent on the ADP-P2Y(12) pathway, and that strong P2Y(12) receptor blockade alone causes inhibition of platelet aggregation that is minimally enhanced by aspirin. Data from the PLATO trial suggested that, among ticagrelor-treated patients, high-dose versus low-dose (< 100 mg day(-1)) aspirin is associated with an increased risk fof ischemic events. Objectives: To evaluate the impact of aspirin withdrawal on platelet reactivity in acute coronary syndrome (ACS) patients treated with a potent P2Y(12) blocker. Patients/Methods: This was a current prospective, randomized, placebo-controlled, double-blind, cross-over study. The study population comprised 22 consecutive ACS patients who underwent percutaneous coronary intervention and were treated with aspirin (100 mg day(-1)) and ticagrelor. Thirty days post-ACS, open-label aspirin was stopped, and patients were randomized to either blinded aspirin or placebo for 2 weeks, with each patient crossing over to the other arm for an additional 2 weeks. Platelet reactivity to arachidonic acid and ADP determined with light-transmission aggregometry (LTA) and VerifyNow was evaluated at baseline, and 2 weeks and 4 weeks later. Results: Aspirin withdrawal resulted in an increase in arachidonic-acid induced platelet reactivity as determined with both LTA (77.0% +/- 11.3% versus 20.8% +/- 4.4%) and VerifyNow (607.7 +/- 10.6 aspirin reaction units [ARU] versus 408.5 +/- 14.4 ARU). Platelet response to ADP, as determined with both LTA and VerifyNow, did not differ with either aspirin or placebo (32.9% +/- 2.6% versus 35.8% +/- 3.6%, and 33.5 +/- 6.4 P2Y(12) reaction units (PRU) versus 29.6 +/- 5.7 PRU, respectively). Conclusions: Aspirin withdrawal early post-ACS results in increased platelet reactivity in response to arachidonic acid, despite concomitant treatment with the potent P2Y(12) blocker ticagrelor.
- 出版日期2018-4
