Why the study?
Does increasing aspirin dose to 162 mg or greater improve platelet responsiveness in patients nonresponsive to aspirin 81 mg?
Does increasing aspirin dose to 162 mg or greater improve platelet responsiveness in patients nonresponsive to aspirin 81 mg?
Increasing the aspirin dose to 162 mg or higher successfully overcomes platelet nonresponsiveness in the majority of patients who are resistant to 81 mg.
May support dose escalation in aspirin nonresponders; hypothesis-generating and should not yet change practice.
This study demonstrates that patients who are taking 81 mg of aspirin and are nonresponsive benefit from a dose of 162 mg or greater vs a different antiplatelet therapy. We identified 100 patients who were nonresponsive to aspirin 81 mg via whole blood aggregometry and observed how many patients became responsive at a dose of 162 mg or greater. Platelet nonresponsiveness was defined as >10 Ω of resistance to collagen 1 µg/mL and/or an ohms ratio of collagen 1 µg/mL to collagen 5 µg/mL >0.5 and/or >6 Ω to arachidonate. Borderline response was defined as an improvement in 1 but not both of the above criteria. Of the initial 100 patients who were nonresponsive to an aspirin dose of 81 mg, 79% became responsive at a dose of 162 mg or >162 mg. Only 6% did not respond to any increase in dose. We believe that patients treated with low-dose aspirin who have significant risk for secondary vascular events should be individually assessed to determine their antiplatelet response. Those found to have persistent platelet aggregation despite treatment with 81 mg of aspirin have a higher likelihood of obtaining an adequate antiplatelet response at a higher aspirin dose.
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Gengo et al. (2015) studied this question.
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