Response to aspirin therapy in patients with myeloproliferative neoplasms depends on the platelet count.

Patients with myeloproliferative neoplasms (MPN) are at an increased risk of thrombotic events even during antiplatelet therapy with aspirin. In the current study, we sought to investigate the association of the platelet count with the inhibitory potential of antiplatelet therapy in MPN. We determined arachidonic acid (AA)- and adenosine diphosphate (ADP)-inducible platelet reactivity by multiple electrode aggregometry in 93 patients with essential thrombocythemia, polycythemia vera or primary myelofibrosis. In patients without aspirin therapy (n = 44), the platelet count did not correlate with platelet aggregation. In aspirin-treated patients (n = 49), we observed a moderate correlation of residual AA-inducible platelet aggregation with the platelet count (r = 0.49; P < 0.001). Further, patients with high on-treatment residual platelet reactivity to AA (HRPR AA) had a significantly higher platelet count than patients without HRPR AA (547 × 109 /L [340 - 644 × 109 /L] vs 358 × 109 /L [242 - 501 × 109 /L], P = 0.01). Receiver-operating characteristic curve analysis revealed a platelet count of ≥317 × 109 /L as best threshold to distinguish between patients without and with HRPR AA (area under the curve: 0.73). After adding the direct ADP P2Y12 inhibitor cangrelor to blood samples from all 93 patients in vitro, residual ADP-inducible platelet reactivity correlated weakly with the platelet count (r = 0.26, P = 0.01), but the platelet count did not differ significantly between patients with and without HRPR ADP (396 × 109 /L [316 - 644 × 109 /L] vs 340 × 109 /L [241 - 489 × 109 /L]; P = 0.2). In conclusion, our findings suggest that the extent of platelet inhibition by aspirin in patients with MPN at least in part depends on their individual platelet count.