PO030 | PLATELET AGGREGOMETRY AS POTENTIAL TOOL TO EVALUATE ANTI-PLATELET RESPONSE IN MYELOPROLIFERATIVE NEOPLASMS: COMPARISON OF DIFFERENT TECHNIQUES AND INITIAL RESULTS
Abstract
Background and aims. Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders associated with increased thrombotic risk. The prothrombotic phenotype of MPNs is multifactorial, involving not only an increased mass of circulating cells, but also qualitative alterations in their activation and function. Interactions among blood cells, endothelium, and coagulation promote a hypercoagulable state in which activated platelets play a central role. Low-dose acetylsalicylic acid (ASA) is a cornerstone of thromboprophylaxis in MPNs, but its antiplatelet effect has been reported to be heterogeneous, possibly due to increased platelet turnover and/or expanded platelet mass. Available data on ASA effect in MPN often lack healthy controls, ASA-naïve patients, baseline aggregometry or comparison of different techniques. This study aimed to compare multiple electrode aggregometry (MEA) and light transmission aggregometry (LTA) in assessing platelet function in MPN patients and controls, before and during ASA therapy. Methods. Nineteen patients with MPN (15 Essential Thrombocythemia, 4 Polycythemia Vera; 6 M, 13 F; median age at diagnosis 39 y) diagnosed and followed in our Department, were enrolled. Platelet function was assessed using both MEA (Multiplate®) and LTA (CN3000). MEA included TRAP, ADP, and ASPI tests, while LTA was performed using ADP, collagen, arachidonic acid, ristocetin, and adrenaline as agonists. All assays were conducted both before and during ASA therapy. Results were compared with 19 couples of non-MPN subjects (22 males, 16 females; median age 68 years) matched for sex, age, and platelet count; half of them were on ASA therapy for other indications and the other half was ASA-naïve. Results. In the absence of ASA, MPN patients showed significantly higher baseline platelet aggregation compared with non-MPN across all agonists, as assessed by both MEA and LTA. During ASA therapy, MPN patients had higher residual platelet aggregation than non-MPN when assessed by MEA using the ASPI test (median 59 vs 13, p<0.001; Figure 1), whereas no significant differences were observed with other MEA assays or with LTA across all agonists. To reduce bias connected to significant differences in platelet count, an ASA/non-ASA aggregation ratio was calculated for every MPN patient and couple of controls, for each test and agonist. This ratio was significantly higher in MPN patients in the ASPI test (0.5 vs 0.2, p=0.011), while no relevant differences were observed with other MEA parameters or with LTA. Conclusions. Our study shows that MPNs exhibit increased platelet aggregation compared with controls both at baseline and during antiplatelet therapy. Both MEA and LTA can detect this hyper-aggregation in not treated/naïve patients. During ASA, only MEA, particularly the ASPI test, was able to identify residual aggregation, while this heterogeneous pharmacodynamic response seems to be not captured by LTA. To reduce thrombocytosis-related bias, we calculated the ASA/non-ASA ratio both for MPN and controls. Comparison of the ratios confirmed a persistent higher aggregation in MPN patients. For clinical purposes, MEA may represent a potential tool to evaluate the effect of ASA in MPN patients leading to individualized antiplatelet management, including dose adjustment or alternative regimens, with the ultimate goal of improving thrombotic risk prevention in this high-risk population.
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BibTeX
@article{galbiati2026po030,
title = {{PO030 | PLATELET AGGREGOMETRY AS POTENTIAL TOOL TO EVALUATE ANTI-PLATELET RESPONSE IN MYELOPROLIFERATIVE NEOPLASMS: COMPARISON OF DIFFERENT TECHNIQUES AND INITIAL RESULTS}},
author = {Alessandro Galbiati},
journal = {Bleeding, Thrombosis and Vascular Biology},
year = {2026},
month = oct,
url = {https://www.btvb.org/btvb/article/view/846},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - PO030 | PLATELET AGGREGOMETRY AS POTENTIAL TOOL TO EVALUATE ANTI-PLATELET RESPONSE IN MYELOPROLIFERATIVE NEOPLASMS: COMPARISON OF DIFFERENT TECHNIQUES AND INITIAL RESULTS
AU - Alessandro Galbiati
PY - 2026
DA - 2026/10/26
JO - Bleeding, Thrombosis and Vascular Biology
UR - https://www.btvb.org/btvb/article/view/846
AB - Background and aims. Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders associated with increased thrombotic risk. The prothrombotic phenotype of MPNs is multifactorial, involving not only an increased mass of circulating cells, but also qualitative alterations in their activation and function. Interactions among blood cells, endothelium, and coagulation promote a hypercoagulable state in which activated platelets play a central role. Low-dose acetylsalicylic acid (ASA) is a cornerstone of thromboprophylaxis in MPNs, but its antiplatelet effect has been reported to be heterogeneous, possibly due to increased platelet turnover and/or expanded platelet mass. Available data on ASA effect in MPN often lack healthy controls, ASA-naïve patients, baseline aggregometry or comparison of different techniques. This study aimed to compare multiple electrode aggregometry (MEA) and light transmission aggregometry (LTA) in assessing platelet function in MPN patients and controls, before and during ASA therapy. Methods. Nineteen patients with MPN (15 Essential Thrombocythemia, 4 Polycythemia Vera; 6 M, 13 F; median age at diagnosis 39 y) diagnosed and followed in our Department, were enrolled. Platelet function was assessed using both MEA (Multiplate®) and LTA (CN3000). MEA included TRAP, ADP, and ASPI tests, while LTA was performed using ADP, collagen, arachidonic acid, ristocetin, and adrenaline as agonists. All assays were conducted both before and during ASA therapy. Results were compared with 19 couples of non-MPN subjects (22 males, 16 females; median age 68 years) matched for sex, age, and platelet count; half of them were on ASA therapy for other indications and the other half was ASA-naïve. Results. In the absence of ASA, MPN patients showed significantly higher baseline platelet aggregation compared with non-MPN across all agonists, as assessed by both MEA and LTA. During ASA therapy, MPN patients had higher residual platelet aggregation than non-MPN when assessed by MEA using the ASPI test (median 59 vs 13, p<0.001; Figure 1), whereas no significant differences were observed with other MEA assays or with LTA across all agonists. To reduce bias connected to significant differences in platelet count, an ASA/non-ASA aggregation ratio was calculated for every MPN patient and couple of controls, for each test and agonist. This ratio was significantly higher in MPN patients in the ASPI test (0.5 vs 0.2, p=0.011), while no relevant differences were observed with other MEA parameters or with LTA. Conclusions. Our study shows that MPNs exhibit increased platelet aggregation compared with controls both at baseline and during antiplatelet therapy. Both MEA and LTA can detect this hyper-aggregation in not treated/naïve patients. During ASA, only MEA, particularly the ASPI test, was able to identify residual aggregation, while this heterogeneous pharmacodynamic response seems to be not captured by LTA. To reduce thrombocytosis-related bias, we calculated the ASA/non-ASA ratio both for MPN and controls. Comparison of the ratios confirmed a persistent higher aggregation in MPN patients. For clinical purposes, MEA may represent a potential tool to evaluate the effect of ASA in MPN patients leading to individualized antiplatelet management, including dose adjustment or alternative regimens, with the ultimate goal of improving thrombotic risk prevention in this high-risk population.
SN - 2785-5309
ER -