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Aspirin has been widely used as a potent antithrombotic drug in clinical practice. However, the optimal dosage for the prevention of thrombo-embolic events is still controversial because high-dose aspirin inhibits PGI2 production in vessel walls as well as TXB2 production in platelets. This study was designed to investigate the optimal clinical aspirin dosage from the view point of its effects on ADP-induced platelet aggregation.The materials were composed of 13 normal subjects (control group) and 71 patients with cardiovascular diseases. Various daily doses of aspirin (80, 160, 330, 660 and 990mg) were given to patients (aspirin group) for more than 4 weeks, and percent ADP aggregation was studied.There was no significant difference in percent aggregation between any two of the aspirin-treated groups, all of which showed a tendency to have lowered percent aggregation as compared with the control group. A single dose of 160mg of aspirin inhibited ADP platelet aggregation within one hour after oral ingestion. The inhibitory effect of aspirin on collagen- and epinephrine-induced aggregation persisted for 4 days when 330mg of aspirin was given and for 5.5 days when 660mg was adminstered. No significant correlation was observed between plasma concentration of aspirin and its effects on platelet aggregation.The present study showed that a daily dose of as small as 80mg of aspirin was sufficient to inhibit platelet aggregation. However, further clinical trials should be made to ascertain that this low daily dosage of aspirin will effectively prevent future thrombo-embolic events.
- 社団法人 日本老年医学会の論文