We compared the ability of
aspirin to suppress platelet aggregation and
thromboxane synthesis in ten normal subjects and ten patients with
diabetic angiopathy and high rate of entry of new platelets into the circulation. When single doses of 100 to 1,000 mg
aspirin were ingested daily for 1 month, there were time gaps between doses in which platelets from diabetics and normals aggregated and formed
thromboxane ex vivo in response to the combination of
arachidonic acid plus
collagen. Similar gaps were also found for diabetics, but not for normals, following four daily doses (every six hours) of 25 or 100 mg. Our data show that dose schedules of
aspirin which may suffice in normals are not effective in patients with
diabetic angiopathy, presumably because these patients have a high rate of entry of new platelets into the circulation. We suggest that continual suppression of platelet
thromboxane synthesis and aggregation by low-dose, "slow-release" preparations of
aspirin would be an ideal long-term approach for the prevention of
thrombosis in patients with a high rate of entry of new platelets into the circulation.