Why the study?
Does low-dose aspirin reduce platelet aggregability and serum thromboxane B2 concentrations in poststroke patients?
Does low-dose aspirin reduce platelet aggregability and serum thromboxane B2 concentrations in poststroke patients?
Despite significant reductions in serum thromboxane B2 with low-dose aspirin, individual variation in platelet aggregability suggests alternative pathways of platelet activation.
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Variable platelet inhibition despite thromboxane suppression with low-dose aspirin in post-stroke patients; hypothesis-generating for alternative pathways and should not yet change practice.
The effects of low daily oral doses of aspirin (40 mg/day) on platelet aggregability and serum thromboxane B2 concentrations were studied in 19 poststroke patients. Although platelet aggregation was reduced significantly after 1 week, there was wide individual variation in the inhibition of platelet function in spite of marked decreases of serum thromboxane B2 concentrations by greater than 90% (from 224 +/- 58 to 8 +/- 8 ng/ml). There was no correlation between collagen-induced platelet aggregability and serum thromboxane B2 concentration before aspirin administration in the range 100-350 ng/ml, but after 1 week of repeated administration of aspirin, there was a correlation between platelet aggregability and serum thromboxane B2 concentrations of less than 25 ng/ml (r = 0.68, p less than 0.01). However, platelet inhibition was insufficient even in some patients with markedly decreased thromboxane B2 concentrations (less than 5 ng/ml). Our results suggest that individual variation of platelet aggregability in response to low-dose aspirin may be due to variation not only in the degree of inhibition of thromboxane A2 production but also in the relative dependence of platelet aggregation on extra-arachidonic pathways.
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Tohgi et al. (1988) studied this question.
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