The role of platelet in the pathogenesis of acute coronary syndrome and cerebral thrombosis is well known and the platelet inhibitors are used widely for primary and sccondary prevention of cardiovascular disease. Aspirin is the least expensive and most widely used antiplatelet agent and its effect is associated with its ability to inhibit plateletthromboxane A2 synthesis. The effectiveness of aspirin is dependent on its ability to block the formation of thromboxane A2. Ticlopidine is another popular antiplatelet agent used today in the era of stent implantation for treating coronary artery obstructive disease(CAOD) with aspirin. The mechanism of action of ticlopidine is clearly different from that of aspirin. It is concluded recently that ticlopidine is an inhibitor of ADP binding to platelets. The inhibition of ADP binding to platelets by ticlopidine is very nicely correlated with its does and the inhibition of platelet aggregation. Therefore, in this study, antiplatelet effect of low dose enteric-coated aspirin in place of aspirin and combined therapy with low does enteric-coated aspirin plus ticlopidine were evaluated in the normal subjects.

In twenty normal subjects, platelet aggregation tests with adenosine diphosphate(ADP) and collagen were performed baseline, after I week adminisrtation of enteric-coated aspirin, and in randomly selected ten among twenty normal subjects, I week administration of enteric-coated aspirin and ticlopidine. The maximal aggregation rate was calculated by measuring the maximal change of the light transmittance after addition of aggregating agents.

Low does enteric-coated aspirin inhibited platelet aggregation in response to collagen significantly. Less than 25% of antiaggregation effect was noted in about 50% of subjects with low dose enteric-coated aspirin when platelet aggregation was induced by ADP. Ticlopidine in combination with low does enteric-coated aspirin potentiated the inhibitory effect significantly on platelet aggregation in response to ADP.

Effect of low dose enteric-coated aspirin alone on platelet aggregation in response to ADP stimulation was weak and showed variablity, comparing to collagen stimulation. The combined treatment of ticlopidine plus aspirin was synergistically inhibited platelet aggregation responding to ADP stimulation. Therefore to achieve the synergistic inhibition of platelet aggregation to ADP and collagen stimulation, combination theraphy might be a effective regimen.