Laboratory Resistance to Antiplatelet Therapy as Part of Secondary Prevention of Ischemic Stroke in a Young Patient (Clinical Case)

In recent years, the incidence of ischemic strokes in young people worldwide has been increasing, leading to early disability, loss of work capacity, and reduced quality of life. Platelets play an active role in the pathogenesis of ischemic stroke. The main drugs for secondary prevention of ischemic stroke are acetylsalicylic acid (ASA) and clopidogrel (CL). ASA inhibits cyclooxygenase-1 (COX-1), which prevents the production of thromboxane A2 (TXA2), thereby inhibiting platelets, while CL acts by inhibiting ADP, which binds to two protein receptors on platelets (P2Y1 and P2Y12) and leads to platelet aggregation. Effective antiplatelet therapy can significantly reduce the risk of recurrent ischemic stroke. Aim . To identify clinical and genetic factors contributing to the development of laboratory resistance to antiplatelet agents in a patient with a previous ischemic stroke. Materials and methods . The medical history of a patient who had a previous ischemic stroke of unknown origin was studied In Sverdlovsk Regional Clinical Hospital No 1 (SOKB 1). To identify laboratory resistance, we used the optical aggregometry method and a set of genes ( ABCB1, CYP2C19*2, CYP2C19*3, CYP2C19*17, ITGA2, ITGB3, PAI-1 ) that affect the development of high residual platelet reactivity. Results . For the first time, the patient was examined 3 months after the development of an ischemic stroke, against the background of regular ASA intake. Laboratory resistance to this antiplatelet agent was detected using optical aggregometry. Subsequently, against the background of ASA correction, the introduction of clopidogrel (CL) was repeatedly revealed ineffective disaggregation. When analyzing anamnestic data, it was revealed that the development of high residual platelet reactivity could be influenced by the presence of obesity, hypertension, which are present in this patient. Genetic studies have identified mutations in two genes (ABCB1, CYP2C19*2) that may also contribute to the development of laboratory resistance. Conclusions . Conclusions. Effective disaggregation against the background of ASA and CL intake is an important factor in the secondary prevention of ischemic stroke. The study and identification of clinical and genetic risk factors that may affect the development of high residual platelet reactivity remains an important clinical task that requires further study.