We determined the prevalence and clinical predictors of aspirin resistance
by prospectively studying 325 patients with stable cardiovascular disease w
ho were receiving aspirin (325 mg/day for greater than or equal to7 days) b
ut no other antiplatelet agents. We also compared the detection of aspirin
resistance with optical platelet aggregation, a widely accepted method, wit
h a newer, more rapid method, the platelet function analyzer (PFA)-100, a w
hole blood test that measures platelet adhesion and aggregation ex vivo. Bl
ood samples were analyzed in a blinded fashion for aspirin resistance by op
tical aggregation using adenosine diphosphate (ADP) and arachidonic acid, a
nd by PFA-100 using collagen and/or epinephrine and collagen and/or ADP car
tridges to measure aperture closure time. Aspirin resistance was defined as
a mean aggregation of greater than or equal to 70% with 10 muM ADP and a m
ean aggregation of greater than or equal to 20% with 0.5 mg/ml arachidonic
acid. Aspirin semiresponders were defined as meeting one, but not both of t
he above criteria. Aspirin resistance by PFA-100 was defined as having a no
rmal collagen and/or epinephrine closure time (less than or equal to 193 se
conds). 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 a
spirin resistant. Of the 18 patients who were aspirin resistant by aggregat
ion, 4 were also aspirin resistant by PFA-100. Patients who were either asp
irin 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 increa
sed 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. (C) 20
01 by Excerpta Medica, Inc.