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Features of the reactive oxygen species production by platelets and neutrophils in the formation of an insufficient response to acetylsalicylic acid in patients with coronary heart disease after coronary bypass surgery
Author(s) -
Maxim Goncharov,
Yu. I. Grinshtein,
А. А. Савченко
Publication year - 2022
Publication title -
translâcionnaâ medicina
Language(s) - English
Resource type - Journals
eISSN - 2410-5155
pISSN - 2311-4495
DOI - 10.18705/2311-449-2022-9-1-12-28
Subject(s) - platelet , medicine , aspirin , clopidogrel , cardiology , coronary artery disease , reactive oxygen species , p2y12 , platelet activation , pharmacology , chemistry , biochemistry
Background. Aspirin resistance can lead to thrombosis. Platelets interact with neutrophils in the focus of atherosclerotic damage. The levels of synthesis of reactive oxygen species (ROS) characterize their functional potential. Platelet resistance to acetylsalicylic acid (ASA) can affect the synthesis of ROS. Objective. To reveal the features of ROS synthesis by platelets and neutrophils in patients with coronary heart disease (CHD) after coronary artery bypass grafting (CABG) depending on sensitivity to ASA and antiplatelet therapy. Design and methods. There were 104 patients with CHD and 36 healthy donors. Patients stopped receiving antiplatelet agents 5 days before CABG, ASA was prescribed after surgery, patients on dual antiplatelet therapy (DAT) clopidogrel were added to ASA for 2–3 days. Resistance to ASA was determined at a level of platelet aggregation with arachidonic acid ≥ 20 %. The ROS synthesis levels were examined by the chemiluminescent method (CL). Results. 31.7 % of patients were resistant to ASA (rASA). In ASA-sensitive patients (sASA), CL values were increased. In rASA on DAT, CL parameters were increased, but did not differ from sASA. In the sASA and rASA groups on ASA therapy, correlations between neutrophil and platelet CL parameters were revealed. Conclusion. The presence or absence of interaction between platelets and neutrophils at the level of receptors and/or microvesicles can lead to platelet resistance to ASA in patients with coronary artery disease. Sometimes, this effect could be compensated by DAT.

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