PS1481 PLATELET REACTIVITY AND RESPONSE TO ANTIPLATELET DRUGS IN THROMBOCYTOPENIA AND THROMBOCYTOSIS
Authors: W. Kuliczkowski, J. Dębski, E. Żurawska‐Płaksej, B. Karolko, M. Cielecka‐Prynda, K. Kaaz, M. Podolak‐Dawidziak, L. Usnarska‐Zubkiewicz
Journal: HemaSphere (2019)

Background: Antiplatelet therapy for coronary artery disease (CAD) in patients with quantitative platelet disorders is still a matter of debate. Possible changes in platelet reactivity may also influence the response to these treatment. But platelet response to the antiplatelet drugs is not routinely examined, and the relevant evidence is scarce. Aims: The aim of the study was to assess the platelet reactivity and response to antiplatelet drugs (aspirin with and without clopidogrel) in patients with CAD and platelet disorders. Methods: We measured platelet aggregation in whole blood (Multiplate aggregometer, Roche, Switzerland) using as agonists arachidonic acid (AA), adenosine 5‘‐diphosphate (ADP) and thrombin receptor agonist peptide‐6 (TRAP). AA was used as a measure of response to aspirin (ASA) with a cut‐off above 30 AUC (area under curve of aggregation) showing high on‐treatment platelet reactivity to aspirin (HTPR‐A). ADP induced aggregation measured response to clopidogrel with a cut‐off above 48 AUC for high on‐treatment platelet reactivity to clopidogrel (HTPR‐C). TRAP induced aggregation shows baseline platelet reactivity not affected by oral antiplatelet drugs. Results: Overall, 174 patients (115 M, 59 F, median age 64 yrs) with stable coronary artery disease and history of recent coronary angioplasty were included into the study: 64 with chronic trombocytopenia (PLT &lt; 140 G/L), 30 with thrombocytosis due to myeloproliferative neoplasms (PLT &gt; 450 G/L), and 80 with normal platelet count served as controls. All patients were on ASA (75 mg), and 55 of them on dual antiplatelet treatment (ASA 75 mg + clopidogrel 75 mg). AA and ADP induced aggregation was comparable between thrombocytopenic patients and controls (AA aggregation 17.4 ± 10.3 vs 28.2 ± 21.1, and ADP aggregation 28.3 ± 12.0 vs 40.7 ± 27.3, respectively), while it was significantly increased ( p &lt; 0.0001) in patients with thrombocytosis (AA aggregation 80.1 ± 52.6 vs 28.2 ± 21.1, and ADP aggregation 105.6 ± 48.1 vs 40.7 ± 27.3, respectively). TRAP induced aggregation proved significant gradient ( p &lt; 0.005) with lowest aggregation in patients with trombocytopenia (60.2 ± 33.8) and highest with those thrombocytosis (119.2 ± 15.9). HTPR‐A was significantly more frequent ( p &lt; 0.0002) in patients with thrombocytosis (60 %), but there was no significant difference between patients with trombocytopenia (4 %) and controls (15 %). HTPR‐C frequency showed a significant gradient ( p &lt; 0.001) with lowest frequency in patients with trombocytopenia (8 %), the highest in thrombocytosis (100 %), whereas in control 40 %. Summary/Conclusion: Our results imply, that platelet count can influence the platelet reactivity and its response to antiplatelet therapy in patients with CAD. In comparison to controls effect of aspirin is attenuated in patients with thrombocytosis, but not in those with trombocytopenia. Baseline platelet reactivity, and response to clopidogrel showed the lowest aggregation in patients with thrombocytopenia and the highest with thrombocytosis. Our study provides an evidence for a need of personalized approach to antiplatelet therapy in patients with CAD and platelet disorders.