24-hour antiplatelet effect of aspirin in patients with previous definite stent thrombosis

Once-daily aspirin is standard treatment, but recent studies point towards increased platelet function at the end of the dosing interval. Stent thrombosis (ST) has been linked with reduced antiplatelet effect of aspirin, so we investigated if platelet inhibition by aspirin declines through 24 h in patients with previous definite ST. Furthermore, we explored whether increased levels of immature platelets and thrombopoietin are associated with a particularly rapid recovery of platelet function.

This case-control study included 50 patients with previous definite ST matched with 100 patients with stable coronary artery disease and 50 healthy volunteers. All participants were on aspirin 75 mg/day mono antiplatelet therapy. Platelet aggregation was measured 1 and 24 h after aspirin intake using platelet aggregometry (Multiplate® Analyzer). Cyclooxygenase-1 activity, platelet activation, immature platelets, and thrombopoietin were measured.

Platelet aggregation increased by 109±150 (arachidonic acid) and 47±155 (collagen) aggregation units per minute from 1 to 24 h after aspirin intake (p-values <0.0001) with corresponding increases in thromboxane B2 (5.6±5.1 ng/ml, p<0.0001) and soluble P-selectin (6.2±15.5 ng/ml, p<0.0001). Platelet aggregation increased equally in all groups, but patients with previous ST displayed the highest levels of platelet aggregation at 24 h (p-values≤0.05) and the highest levels of immature platelets (p<0.01) and thrombopoietin (p<0.0001).

Platelet inhibition declined significantly during the 24-hour dosing interval in aspirin-treated patients with previous definite ST or stable coronary artery disease and in healthy individuals. Increased levels of immature platelets and thrombopoietin were observed in patients with previous definite ST.