BACKGROUND: Antiplatelet drugs play an important role in the prevention and treatment of coronary artery diseases. Triflusal, an antiplatelet drug structually related to acetylsalicylic acid, selectively inhibits the cyclooxygenase of platelet and thromboxane A2 formation. However there is a controversy about the clinical dosage and the quantitative evaluation of the platelet antiaggregatory effect of triflusal. In this study we have evaluated the platelet antiaggregatory effect and cost-effective dosage of triflusal in the whole blood of healthy volunteers. METHODS: Using the whole blood of 50 healthy people, we performed a baseline platelet aggregation function test induced by adenosine diphosphate (ADP) and collagen. The subjects were subdivided into 3 treated groups (300 mg, 600 mg, 900 mg). We compared the platelet aggregation effect between the baseline results and 2 weeks after triflusal administration. RESULTS: Triflusal inhibited the platelet aggregation induced by ADP and collagen in the 600 mg administration group most effectively. The platelet aggregation induced by collagen was inhibited dose-dependently. The definite inhibitory responders (% inhibition > or = 25) for platelet aggregation induced by collagen were more common than those induced by ADP (33% vs 27% in 300 mg, 71% vs 53% in 600 mg, 78% vs 39% in 900 mg). There were no serious clinical side-effects except gastrointestinal trouble. One volunteer in the 900 mg treated group discontinued the treatment due to epigastric pain. CONCLUSION: We conclude that triflusal has a dose-dependent inhibitory effect on platelet aggregation induced by collagen and that the most effective dosage for platelet antiaggregation effect is 600 mg per day.
Adenosine Diphosphate ; Aspirin ; Blood Platelets* ; Collagen ; Coronary Artery Disease ; Electric Impedance* ; Evaluation Studies as Topic ; Healthy Volunteers* ; Platelet Aggregation Inhibitors ; Platelet Aggregation* ; Prostaglandin-Endoperoxide Synthases ; Thromboxane A2 ; Volunteers

BACKGROUND: Antiplatelet drugs play an important role in the prevention and treatment of coronary artery diseases. Triflusal, an antiplatelet drug structually related to acetylsalicylic acid, selectively inhibits the cyclooxygenase of platelet and thromboxane A2 formation. However there is a controversy about the clinical dosage and the quantitative evaluation of the platelet antiaggregatory effect of triflusal. In this study we have evaluated the platelet antiaggregatory effect and cost-effective dosage of triflusal in the whole blood of healthy volunteers. METHODS: Using the whole blood of 50 healthy people, we performed a baseline platelet aggregation function test induced by adenosine diphosphate (ADP) and collagen. The subjects were subdivided into 3 treated groups (300 mg, 600 mg, 900 mg). We compared the platelet aggregation effect between the baseline results and 2 weeks after triflusal administration. RESULTS: Triflusal inhibited the platelet aggregation induced by ADP and collagen in the 600 mg administration group most effectively. The platelet aggregation induced by collagen was inhibited dose-dependently. The definite inhibitory responders (% inhibition > or = 25) for platelet aggregation induced by collagen were more common than those induced by ADP (33% vs 27% in 300 mg, 71% vs 53% in 600 mg, 78% vs 39% in 900 mg). There were no serious clinical side-effects except gastrointestinal trouble. One volunteer in the 900 mg treated group discontinued the treatment due to epigastric pain. CONCLUSION: We conclude that triflusal has a dose-dependent inhibitory effect on platelet aggregation induced by collagen and that the most effective dosage for platelet antiaggregation effect is 600 mg per day.
Adenosine Diphosphate ; Aspirin ; Blood Platelets* ; Collagen ; Coronary Artery Disease ; Electric Impedance* ; Evaluation Studies as Topic ; Healthy Volunteers* ; Platelet Aggregation Inhibitors ; Platelet Aggregation* ; Prostaglandin-Endoperoxide Synthases ; Thromboxane A2 ; Volunteers