We determined the prevalence and clinical predictors of aspirin resistance by prospectively
studying 325 patients with stable cardiovascular disease who were receiving aspirin
(325 mg/day for > or =7 days) but no other antiplatelet agents. We also compared the
detection of aspirin resistance with optical platelet aggregation, a widely accepted
method, with a newer, more rapid method, the platelet function analyzer (PFA)-100,
a whole blood test that measures platelet adhesion and aggregation ex vivo. Blood
samples were analyzed in a blinded fashion for aspirin resistance by optical aggregation
using adenosine diphosphate (ADP) and arachidonic acid, and by PFA-100 using collagen
and/or epinephrine and collagen and/or ADP cartridges to measure aperture closure
time. Aspirin resistance was defined as a mean aggregation of > or =70% with 10 microM
ADP and a mean aggregation of > or =20% with 0.5 mg/ml arachidonic acid. Aspirin semiresponders
were defined as meeting one, but not both of the above criteria. Aspirin resistance
by PFA-100 was defined as having a normal collagen and/or epinephrine closure time
(< or =193 seconds). By optical aggregation, 5.5% of the patients were aspirin resistant
and 23.8% were aspirin semiresponders. By PFA-100, 9.5% of patients were aspirin resistant.
Of the 18 patients who were aspirin resistant by aggregation, 4 were also aspirin
resistant by PFA-100. Patients who were either aspirin resistant or aspirin semiresponders
were more likely to be women (34.4% vs 17.3%, p = 0.001) and less likely to be smokers
(0% vs 8.3%, p = 0.004) compared with aspirin-sensitive patients. There was a trend
toward increased age in patients with aspirin resistance or aspirin semiresponders
(65.7 vs 61.3 years, p = 0.06). There were no differences in aspirin sensitivity by
race, diabetes, platelet count, renal disease, or liver disease.