Key result
Clinical and biochemical markers including platelet count, PLCR, fibrinogen, endothelin-1, and von Willebrand factor predicted high residual platelet reactivity to ASA (AUC 0.79; 95% CI 0.696-0.883).
Why the study?
To identify markers that determine residual platelet reactivity in the subacute period of MI during the administration of acetylsalicylic acid as part of dual antiplatelet therapy.
Cross-Sectional (n=405)
Effect estimate: AUC 0.79 (95% CI 0.696-0.883)
A significant proportion (39.0%) of patients exhibit high residual platelet reactivity to acetylsalicylic acid in the subacute phase of myocardial infarction, which can be predicted using specific clinical and biochemical markers.
Potential markers of residual platelet reactivity post-MI on ASA identified; leaves open their role in guiding therapy pending validation.
Aim. To study markers that determine residual platelet reactivity in the subacute period of myocardial infarction (MI) during the administration of acetylsalicylic acid (ASA) as part of dual antiplatelet therapy. Material and methods. 405 patients with MI (79.5% men and 20.5% women, average age 58.0 years) were divided into groups based on aggregometry results. Group 1 — 11 patients with low residual platelet reactivity, group 2 — 236 patients with optimal platelet reactivity, group 3 — 158 patients with high residual platelet reactivity (HRPR). All studies were performed on days 12-14 after MI: aggregometry on a Multiplate aggregometer (Germany) with several aggregation inducers, a blood test and a study of platelet indices, determination of endothelin-1, von Willebrand factor, sP-selectin and soluble CD40 ligand levels. Results. Parameters influencing the ASPItest value according to univariate linear regression analysis: body mass index (β=0.53, 95% CI: 0.11-0.96; p=0.013); waist circumference (β=0.31, 95% CI: 0.14-0.49; p=0.0004); erythrocyte sedimentation rate (β=0.27, 95% CI: 0.12-0.42; p=0.0004); white blood cells count (β=1.47, 95% CI: 0.51-2.42; p=0.0027); platelets count (β=0.042, 95% CI: 0.019-0.064; p=0.00025); thrombocrit (β=36.8, 95% CI: 14.6-59.1; p=0.0012); mean platelet volume (β=1.94, 95% CI: 0.06-3.84; p=0.043); platelet distribution width (β=1.36, 95% CI: 0.22-2.51; p=0.02); creatinine (β=0.11, 95% CI: 0.011-0.21; p=0.03); C-reactive protein (β=0.18, 95% CI: 0.05-0.32; p=0.007); TRAP-test (β=0.18, 95% CI: 0.11-0.24; p=0.000001); fibrinogen (β=2.6, 95% CI: 1.17-4.02; p=0.0004). The binary logistic regression model to calculate the probability of developing HRPR to ASA included the following factors: platelet count, percentage of large platelet volume (PLCR), fibrinogen, endothelin-1 and von Willebrand factor. With a probability cutoff p₀=0.5412 for this model: sensitivity — 81.08%, specificity — 73.21%, classification accuracy — 76.34%, area under the ROC curve — 0.79 (CI: 0.696 - 0.883). Conclusion. There are 2.7% of patients with an excessive response to ASA and 39.0% with an insufficient response to ASA on days 12-14 of MI. Clinical and biochemical markers of HRPR to ASA in the subacute period of MI are the number of platelets, PLCR, fibrinogen, endothelin-1 and von Willebrand factor.
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Pronko et al. (2024) conducted a cross-sectional in Myocardial infarction (n=405). Clinical and biochemical markers (platelet count, PLCR, fibrinogen, endothelin-1, von Willebrand factor) was evaluated on High residual platelet reactivity (HRPR) to acetylsalicylic acid (AUC 0.79, 95% CI 0.696-0.883). Clinical and biochemical markers including platelet count, PLCR, fibrinogen, endothelin-1, and von Willebrand factor predicted high residual platelet reactivity to ASA (AUC 0.79; 95% CI 0.696-0.883).
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