Why the study?
About 20–40% of patients experience low effectiveness of antiplatelet therapy, predisposing to thrombosis, stent thrombosis, and thromboembolic complications.
This review highlights the significant prevalence of clinical and laboratory resistance to antiplatelet therapy, emphasizing the need for personalized antithrombotic strategies based on genetic and modifiable risk factors.
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Antiplatelet use in CHD thrombosis needs individualized caution; leaves open optimal mono- versus dual-therapy choices.
In recent years, significant advances in the diagnosis and treatment of cardiovascular diseases have been achieved in the healthcare of most countries. However, among the causes of mortality in patients with coronary heart disease, arterial thrombosis takes one of the leading positions. Antiplatelet drugs are prescribed to prevent thrombotic complications, which can be used as mono- or two-component therapy. In case of atherosclerosis in arteries, acetyl-salicylic acid (ASA) or clopidogrel can be used as monotherapy; treatment of acute coronary syndrome (ACS) and percutaneous coronary interventions (PCI) required using of double antiplatelet therapy (DAT), including acetylsalicylic acid drugs together with one antiplatelet agent from the group of thienopyridine derivatives — blockers of P2Y12 platelet receptors (clopidogrel, ticagrelor, prasugrel). In patients with ACS who underwent primary PCI or thrombolysis followed by PCI, the duration of DAT is 12 months, and clopidogrel is the drug of choice [16, 30]. According to various literature sources about 20–40% of patients have low effectiveness of antiplatelet therapy, which can lead to thrombosis, stent thrombosis and thromboembolic complications. This review provides an analysis of modifiable and nonmodifiable factors contribution to the development of clinical and laboratory resistance of antiplatelet agents.
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Кантемирова et al. (2022) studied this question.
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