Platelet reactivity clinical and biochemical markers when taking acetylsalicylic acid as part of dual antiplatelet therapy in the myocardial infarction subacute period

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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Journal
Rational Pharmacotherapy in Cardiology
Published
2024-11-28
DOI
https://doi.org/10.20996/1819-6446-2024-3037
Primary Topic
Antiplatelet Therapy and Cardiovascular Diseases
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article
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article

Platelet reactivity clinical and biochemical markers when taking acetylsalicylic acid as part of dual antiplatelet therapy in the myocardial infarction subacute period

T. P. Pronko, V. А. Snezhitskiy, А. V. Kapytski
Rational Pharmacotherapy in Cardiology
Antiplatelet Therapy and Cardiovascular Diseases
article

Platelet reactivity clinical and biochemical markers when taking acetylsalicylic acid as part of dual antiplatelet therapy in the myocardial infarction subacute period

T. P. Pronko, V. А. Snezhitskiy, А. V. Kapytski
article en

Abstract

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.

Rational Pharmacotherapy in CardiologyVol. 20(6)
Grodno State Medical University (BY)
Openalex Percentile: Top 55%
Antiplatelet Therapy and Cardiovascular Diseases
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