Abstract
Platelet primary hemostatic function occurs under high shear conditions. Cyclooxyenase inhibitors such as ibuprofen inhibit this platelet aggregation under high shear rates only to a limited extent. This prompted the present study on 10 healthy volunteers treated with 100 mg aspirin for 4 weeks. The platelet function analyser (PFA-100®) was used to measure the closure time (CT) of a membrane pore coated with collagen and epinephrine by aggregating platelets under shear rates of 5000–6000 s−1. A first dose of 100 mg aspirin prolonged the CT above the normal range in 4 of 10 individuals, but the CT for the whole group (153±42 s) was not different from baseline (112±18 s). After 7 and 28 days of treatment, CTs were >300 s in 8 individuals and the mean values for the group were significantly higher than baseline. However, one subject had an intermediate response and one had an aspirin non-responsiveness, which was not overcome by 300 mg aspirin daily. The CT was normalized in 4 individuals 48 h after the last aspirin dose and in 7 individuals after 72 h, when the mean value for the group became not different from baseline. We conclude that the platelet function measured with the PFA-100 is not inhibited significantly after a single dose of 100 mg aspirin, is thereafter inhibited consistently in the majority, but not all individuals during a 4 week treatment, and returns to normal in 48–72 h. Since large interindividual differences exist, monitoring of platelet inhibition at the beginning of an aspirin treatment should be considered and validated in a prospective study.
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