Aspirin’s effects on platelet function outcomes
Eighty-six participants completed a baseline visit, 81 exposed to low-dose aspirin, and 79 exposed to high-dose (Figure 1A). To assess the extent to which platelet COX-1 was inhibited we used serum thromboxane B2 (TXB2), and arachidonic acid (AA) induced platelet aggregation. After 4 weeks of daily dosing, both 81mg and 325mg equivalently suppressed platelet COX-1 as assessed by (AA) induced platelet aggregation (Figure 1B) and TXB2 (Figure 1B). To assess non-COX1 dependent assays of platelet function, we used a previously described platelet function score (PFS, see Supplemental Methods) that aggregates nine different, non-COX1 dependent assays of platelet function into a single score. Higher PFS values reflect greater platelet function. After 4-weeks of daily aspirin, both 81 and 325mg doses reduced PFS (p < 0.001) with slightly greater reduction with 325mg vs. 81mg (p = 0.07) (Figure 1D). Therefore, daily doses of low- and high dose aspirin reduce COX-1 and non COX-1 measures of platelet function. Compared to low-dose aspirin, high dose aspirin produces equivalent COX-1 suppression and slightly greater non-COX 1 inhibition of platelet function.