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.