The antiplatelet effects of aspirin are not well understood, say researchers who found large variations in rates of aspirin resistance diagnosed using different assays.
Antiplatelet treatment is an important primary and secondary preventive measure in patients at low or moderate risk for stroke and cardiovascular events. It is also vital in high-risk patients who have contraindications to anticoagulation therapy.
But research suggests that a substantial minority of patients are resistant to antiplatelet treatment, with the rate of aspirin nonresponse reported to be as high as 35%.
Dr Paul Gurbel, of Sinai Center for Thrombosis Research, Baltimore, USA, and co-workers used several popular assays to assess platelet function in 125 patients with stable coronary heart disease. The patients took 81, 162, and 325mg/day doses of aspirin, taking each dose for four weeks.
Just two patients were resistant to 81 and 162mg/day aspirin as assessed using arachidonic acid-induced light transmittance aggregation, and no patient was resistant to the highest aspirin dose.
In contrast, 32 and 21 patients were resistant to the lowest and highest aspirin doses, respectively, according to the results of the PFA-100 assay, in which aggregation is induced by epinephrine and collagen.
All assays involving arachidonic acid detected substantially lower rates of aspirin resistance than did those using other agonists, the team reports in the journal Circulation.
Assays that did not involve arachidonic acid revealed dose-dependent rates of aspirin resistance, suggesting dose increases could overcome the phenomenon.
Although aspirin is thought to prevent platelet aggregation via inhibition of COX-1, “the observation of dose-related effects despite near-complete inhibition of arachidonic acid-induced aggregation suggests that aspirin may also exert antiplatelet effects through non