Timing of anti-platelet effect after oral aspirin administration in patients with sympathetic excitement.

Aspirin is used in percutaneous coronary interventions (PCI) for acute myocardial infarction (AMI) to prevent thrombosis. It is reported that the aspirin concentration in blood reaches its peak approximately 20 min after oral administration in healthy volunteers, but the absorption and bioavailability of aspirin in AMI may be quite different. In the present study patients undergoing coronary angiogram for the first time were enrolled as a model of sympathetic excitement and the timing of the antiplatelet effect after oral aspirin administration was investigated. Aspirin (162 mg) was administered to the patients in a catheter laboratory. Platelet count, aspirin concentration, and platelet aggregation were measured at scheduled timepoints before and up to 120 min. Ticlopidine was administered in the same procedure, and platelet count and platelet aggregation were evaluated at 0 and 120 min. There was no significant change in the platelet count. Aspirin concentration in blood had not reached its peak by 120 min. Platelet aggregation induced by collagen or ADP began to be inhibited 45 min after aspirin administration. No significant inhibition of platelet aggregation was observed up to 120 min following ticlopidine administration. During sympathetic excitement, aspirin absorption and its antiplatelet effect were significantly delayed in these patients. Ticlopidine did not show any antiplatelet effect by 120 min. For PCI performed in a patient with a high level of sympathetic excitement, aspirin should be administered at least 45 min before the first balloon dilatation.