COMPARISON OF 3 INDEPENDENT METHODS AS ESTIMATES OF PLATELET INHIBITION AFTER A SINGLE-DOSE OF ACETYLSALICYLIC-ACID

In order to assess the ability of three different (one in vivo, one ex vivo and one in vitro) methods to estimate platelet function, 10 heal thy volunteers were given a single oral dose of 160mg ASA. Platelet fu nction was assessed before, 4, 24, 48 and 72 h after dosing by urinary excretion of thromboxane B-2, filtragometry and collagen-based whole blood aggregometry. Further, in order to study mechanisms for platelet aggregation in filtragometry, platelet activation was assessed by mea surements of beta-thromboglobulin at three different places within the filtragometer test unit in another nine healthy subjects. Four hours after ASA, the aggregation time during filtragometry increased by 213 +/- 133% (p<0.001) and was parallelled by a decrease in impedance 85 /- 7% (p<0.001) indicating an inhibition of platelet aggregability in both tests. A subsequent gradual recovery was observed with both metho ds. The excretion of thromboxane B-2 followed the aggregability patter n being maximally reduced by 72 +/- 6% (p<0.01) 24h after ASA and then gradually recovering. All three methods indicated that platelet funct ion was still decreased 72h after dosing. The urinary excretion of pro stacyclin did not change significantly. The results of filtragometry a nd impedance aggregometry correlated to the logarithm of thromboxane B -2 excretion (r = 0.60; p<0.01 and r = 0.49; p<0.01, respectively) and to each other (r = 0.70; p<0.001). In filtragometry beta-thromboglobu lin increased significantly (p<0.05) over the filter. Hence, with a de sign where inhibition of thromboxane formation alone accounts for the reduction in platelet aggregation, all three methods employed are comp arable in estimating platelet function. Also, in filtragometry, platel et activation at the filter seems to contribute to the trapping of pla telet aggregates at the filter.