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Abstract BackgroundAntiplatelet agents are a cornerstone of therapy in myeloproliferative neoplasms (MPN) for reduction of thrombotic risk. While indications for their use are established in both polycythemia vera (PV) and essential thrombocytosis (ET), the therapeutic role of aspirin (ASA) in myelofibrosis (MF) remains poorly defined. Furthermore, evidence-based data to guide clinical practice are lacking (Br J Haematol, 2024). This study aimed to characterize ASA utilization: 1) practice patterns; 2) impact on thrombotic and hemorrhagic events; and 3) influence on disease-related symptoms in a population-based MF cohort. MethodsThis multicenter retrospective/prospective study recruited consecutive patients diagnosed with WHO/ICC-defined primary or secondary MF from the Quebec MPN Research Group registry (13 academic/community centers) between 2015 and 2024. Clinical and laboratory data were abstracted from medical records. Thrombosis endpoints were per convention and confirmed through imaging; hemorrhage outcomes were reported per treating physician (clinically relevant), encompassing all event grades. Self-reported patient symptoms were analyzed according to the validated MPN-Symptom Assessment Form Total Symptom Score (MPN-SAF TSS) (JCO, 2012) completed between 04/2013-08/2022 with >20/100 considered significant. Conventional statistical methods were used (SAS version 9.4, Cary, NC, USA); all tests were two-sided with p<0.05 defined as significant. ResultsOf 215 patients, 105 were primary (PMF) and 110 were secondary MF (SMF) (44 post-PV; 66 post-ET). Exposure to ASA was documented in 58 (55.2%) PMF and 82 (77.3%) SMF cases (p=0.013). Of note, ASA was prescribed as frequently in JAK2V617F-mutatedas in calreticulin-mutated patients (p=0.82). Analyzed in aggregate, patients receiving ASA vs no ASA presented similar clinical characteristics including demographics, risk scores, JAK2V617F allele burdens, cardiovascular risk factors, and thromboembolic antecedents. Baseline laboratory results, including complete blood counts, were comparable across ASA-exposed vs non-exposed cohorts, except for platelet count (median 446 vs 324 x 109/L; p=0.0004) and MCV (91.9 vs 88.4 fL; p=0.0185), both discernibly higher in those initiated on ASA. Thrombosis and Hemorrhage: After a median follow-up of 46.8 months (range 22.3-94.6), 11 (7.85%) vs 7 (9.33%) thrombotic (p=0.71) and 10 (7.14%) vs 11 (14.7%) hemorrhagic events (p=0.09) were recorded in patients exposed vs not exposed to ASA, respectively. When association of ASA with thrombo-hemorrhagic events was analyzed, adjusting for gender, disease status, and previous thrombosis, ASA conferred an overall protective effect against thrombosis (HR=0.63 (0.18-2.23 CI); p=0.48), though not reaching statistical significance, without appreciable increase in hemorrhage (p=0.13). Symptom Burden: A sub-analysis of 130 MF patients having completed at least one MPN-SAF TSS survey (median 5/patient) since diagnosis disclosed a significant salutary effect of ASA therapy on symptom burden. MF patients on ASA had markedly lower average MPN-SAF TSS scores vs those not on ASA (13.7 vs 21.3; p=0.0023), less frequent elevated mean scores i.e. >20/100 (17 (30%) vs 39 (53%); p=0.0065), and fewer had a maximal score above 20 at any time (33 (58%) vs 54 (74%); p=0.05). When individual sub-items were appraised, significantly lower scores for early satiety (p=0.036), abdominal pain (p=0.024), inactivity (p=0.036), difficulty concentration (0.014), pruritus (p=0.035), and bone pain (p=0.01), as well as tendencies towards lower fatigue and fever (p=0.09; 0.06) were recorded in patients on ASA therapy vs no ASA. Conclusion There are currently no recommendations for ASA use in MF. This broad registry-based study provides data confirming more frequent ASA use in secondary vs primary MF, reflecting near-universal use in PV and ET and frequent continuation post-MF transformation. Furthermore, a tendency towards thrombosis risk reduction is demonstrated, suggesting a possible benefit for ASA in the global MF population, requiring validation from prospective studies. Finally, a substantial symptom benefit of ASA in MF is exposed, saliently improving not only average symptom burden scores but the vast majority of sub-item scores. Further studies are necessary to clarify the effects of ASA in MF to help guide clinical decision-making, especially in primary myelofibrosis.