This article analyzes the cardiological aspects of the etiology of cryptogenic stroke, including ESUS (embolic stroke of undetermined source). Special attention is paid to the pathophysiological mechanisms and risk factors for the development of cardioembolism in the absence of instrumentally confirmed atrial fibrillation. Several key areas are considered in detail: atrial cardiopathy as a complex of structural and functional changes in the left atrium, a subclinical form of atrial fibrillation and aorto-arterial embolism caused by non-stenosing atherosclerotic plaques, intracranial atherosclerosis and atheromatosis of the aortic arch. A comprehensive analysis of modern diagnostic biomarkers is presented, including instrumental (P-wave terminal force in lead V1 — PTFV1, supraventricular arrhythmias, indicators of structural changes in the left atrium) and laboratory ones (N-terminal pro-B-type natriuretic peptide, troponin, D-dimer), which identify the hidden embologenic substrate. New diagnostic approaches are highlighted, including advanced electrocardiographic monitoring protocols, echocardiographic techniques, and advanced vascular imaging techniques. The need for a comprehensive early diagnostic protocol implemented as part of a personalized approach is emphasized.

Peripheral blood microvesicles in patients with ischemic stroke are being profoundly investigated. Most works indicate an increase in the level of circulating microvesicles during different periods of stroke. The available data suggest that the level of microvesicles is a potential biomarker of the atherothrombotic subtype of ischemic stroke. Stroke severity, brain lesion volume, and outcome correlate with the level of microvesicles in peripheral blood. In the long term, the detection of microvesicles will help identify patients at high risk of stroke. Further work should determine the diagnostic and prognostic role of different microvesicle phenotypes in relation to stroke outcomes. Microvesicles should be also evaluated as targets for the treatment and prevention of stroke.

Preeclampsia is one of the most significant medical and social problems of modern obstetrics. This complication of pregnancy not only threatens the life of the mother and fetus during pregnancy, but also serves as a predictor of severe cerebrovascular and cardiovascular complications in the long term. Preeclampsia causes both acute and chronic cerebrovascular diseases, which are caused by increased permeability of the blood-brain barrier, impaired cerebral autoregulation, hypercoagulation and inflammation. This literature review analyzes papers published from January 2010 to June 2025 and cited by PubMed, Scopus, MEDLINE, and eLibrary. The features of regulation of cerebral blood flow during normal pregnancy and preeclampsia are described. Cerebrovascular complications of preeclampsia during pregnancy include posterior reversible encephalopathy syndrome, reversible cerebral vasoconstriction syndrome, hemorrhagic and ischemic stroke, and cerebral venous sinus thrombosis. In the long-term postpartum period, women with a history of preeclampsia have an increased risk of neurocognitive disorders, including impaired executive function and memory. There are also significant psychosocial consequences, i.e. decrease in the quality of life and social functioning, increased levels of anxiety, depression, which reduces adaptation to stressful situations of everyday life. Chronic dysfunction of the blood-brain barrier can cause not only functional neurovascular disorders, but also morphological changes. In the long term, preeclampsia is associated with an increased risk of vascular dementia, Alzheimer's disease, and stroke. Offspring born to mothers with preeclampsia have an increased risk of neurological diseases, including cognitive impairment, attention deficit hyperactivity disorder, autism spectrum disorders, depressive disorders, epilepsy, and cerebral palsy.

Background. Cognitive impairment in acute ischemic stroke has a negative impact on patients’ adaptability and quality life. They can result from acute ischemic brain damage affecting areas responsible for cognitive functions, or they can precede stroke. In the latter case, chronic cerebrovascular pathology and neurodegenerative process are the most common clinical variants. Their combination is considered within the concept of mixed cognitive impairment. In routine practice, magnetic resonance imaging (MRI) plays an important role, and visual semi-quantitative MR scales have been developed for the assessment of brain damage. Objective. To assess changes in white and gray matter in patients with lacunar and cardioembolic stroke using visual MR scales and to compare these data with the results of neuropsychological examination. Design and methods. We included 42 patients with cardioembolic and 52 patients with lacunar stroke and assessed changes in white and gray matter using 6 visual MR scales. A comprehensive neuropsychological examination was also performed. A correlation analysis was applied to assess the associations between the results of MR scales and impaired cognitive functions. Results. Patients with both lacunar and cardioembolic stroke subtypes, were characterized by a moderate degree of white matter damage. At the same time, patients with cardioembolic stroke tend to have more severe changes. In lacunar stroke, minor and moderate changes in gray predominate, while cardioembolic stroke is characterized by moderate and severe atrophy, which is reflected by the Koedam scales (0,000004) and atrophy of medial temporal lobe (0,000002). However, the results of the global cortical atrophy scale did not differ in these groups (0,902). Neuropsychological examination demonstrated that mild (44,2 % and 16,7 %, respectively) and moderate (46,2 % and 59,5 %, respectively) cognitive impairment predominates in both lacunar and cardioembolic stroke, and dementia is less common. Correlation analysis showed reliable links between structural brain damage and clinical features of cognitive impairment. Conclusion. Cardioembolic and lacunar strokes are characterized by moderate diffuse damage of white matter. The Wahlund and Scheltens scales are the most efficient for their detection. The greatest of degree gray matter damage was recorded in frontal lobes, in mediobasal regions of temporal lobes and parietal lobes in cardioembolic stroke and infratentorially and in basal ganglia in lacunar stroke. Both stroke subtypes are characterized by mild and moderate cognitive disorders, and dementia is registered only in isolated cases. The development of cognitive impairment correlates with topography and degree of white and gray matter damage.

Objective. To investigate the associations of polymorphic variants rs662799 of the APOA5 gene with the development of acute cerebrovascular accident in patients with cardiovascular pathology. Design and methods. The main group of our study included 260 patients with acute cerebrovascular accident on the background of cardiovascular diseases and 272 volunteers without cardiovascular diseases (control group). The age range of patients with acute cerebrovascular accident was from 32 to 69 years [57,0 (51,0–62,0) years], and the age range of the control group was from 37 to 68 years [55,0 (51,0–62,0) years]. There were 157 men (age 56,5 (51,0–62,0 years) and 103 women (age 57,0 (51,0–62,0) years) in the main group. The control group included 170 men (age 55,0 (51,0–62,0) years) and 102 women (age 55,0 (51,0–62,0) years). All patients with acute cerebrovascular accident underwent the following examinations: collection of complaints and medical history, clinical examination, brain computed tomography, electrocardiography, echocardiography, and ultrasound doppler. The control group represents a population sample of residents of Novosibirsk who were examined as part of the international HAPIEE project in Novosibirsk. The results of the molecular genetic analysis were obtained from 254 patients in the main group and 272 patients in the control group. Statistical analysis was carried out using the SPSS v. 23. Results. The heterozygous AG genotype and the G allele of the APOA5 gene were more prevalent in the stroke cohort compared to control group. Among patients with acute cerebrovascular accident, a statistically significant decrease in the number of carriers of the common AA genotype and the A allele of the APOA5 gene was confirmed compared to the control group. Conclusion. The results of our study proved associations of single-nucleotide polymorphism rs662799 (A > G) with the development of acute cerebrovascular accident. The AG genotype and the G allele of the APOA5 gene showed significant associations with acute cerebrovascular accident in the main group of patients, in the subgroup of men and in the subgroup of patients with hypertension. 

Objective. The aim of the study was to identify clinical, demographic, laboratory and instrumental predictors of the functional outcome of primary intracerebral hemorrhage (ICH) after 90 days among the parameters available within the first hour after the patient's admission to the hospital. Design and methods. A retrospective analysis of the medical records of all patients with primary ICH admitted to the primary vascular department of the Dyurtyulinskaya Central District Hospital of the Republic of Bashkortostan from 2015 to 2021 was performed. Clinical, demographic data and the results of standard laboratory and instrumental examinations were recorded, as well as functional outcomes after 90 days according to the modified Rankin scale (mRs). Results. Data from 120 patients were analyzed. The following predictors of unfavorable functional outcome (mRs 3 points or more) of primary ICH after 90 days were identified: high blood sodium level (p = 0,014), stroke severity according to the NIHSS scale (p = 0,0001), longer QT interval duration (p = 0,05). Conclusion. Thus, early predictors of unfavorable functional outcome of primary ICH after 90 days, along with the initial severity of neurological deficit, were electrolytes level, as well as signs of myocardial repolarization disorders. These results allow for an early (at admission to the hospital) identification of the risk group for the unfavorable functional outcome, as well as for the optimal management of patients with primary ICH due to early correction of the identified factors.

Objective. To determine the predictors of the development of cognitive impairment in patients with hypertension (HTN) with long-term post-COVID syndrome. Design and methods. A single-stage screening clinical study was conducted. Over a period of 3 years, 205 patients (23,4 %) with long-term post-COVID syndrome according to the NICE criteria were recruited among eligible 878 patients with HTN. The patients were divided taking into account the presence of cognitive impairment using the SEMOGRAPH information system: the first group included 80 patients (39,0 %) with cognitive impairment, the second group included 125 patients (61,0 %) without cognitive impairment. Results. The predictors of the development of cognitive impairment in patients with long-term post-COVID syndrome and their cut-off points were chosen using ROC curve: for body mass index values, a cut-off point of 28,36 kg/m² was set, > 26,0 mm/h — for erythrocyte sedimentation rate, < 126,0 g/l — for hemoglobin level, > 3,9 mg/l — for C-reactive protein serum concentration, > 101,9 pg/ml — for serum N-terminal fragment of brain natriuretic propeptide, > 171,1 μg/l — for ferritin, > 0,016 pg/ml — for serum tumor necrosis factor alpha, > 28,8 pg/ml — for serum caspase-6. In HTN patients with long-term post-COVID syndrome after hospitalization due to COVID-19-related pneumonia, the relative risk of cognitive impairment is increased by 2,8 times (95 % confidence interval (95 % CI) 1,63–4,92); the risk of concentration problems — by 8,1 times (95 % CI 4,84–13,99); “brain fog” symptom — by 2,5 times (95 % CI 1,75–3,50), abnormal blood pressure (BP) circadian profile “Non-dipper / Night-peaker systolic BP” — by 1,9 times (95 % CI 1,37–2,68); “Over-dipper systolic BP” — by 18,8 times (95 % CI 2,67–390,89); masked nocturnal hypertension — by 5,1 times (95 % CI 1,61–18,13). Conclusion. More severe forms of COVID-19, long-term post-COVID syndrome manifested by symptoms such as “brain fog”, impaired concentration, as well as abnormal patterns of circadian BP rhythm, obesity, ferrokinetic disorders, the development of myocardial stress, the presence of low-intensity non-specific inflammation, and signs of apoptosis were predictors of the development of cognitive impairment in COVID-19 survivors with HTN.

Objective. To evaluate the effect of escitalopram on heart rate (HR) in patients with anxiety disorder. Design and methods. A retrospective study included 38 patients (24 women, 14 men) with anxiety disorder (Hospital anxiety and depression scale, HADS anxiety subscale ≥ 8 score) treated with escitalopram for at least 6 months. Patients receiving beta-blockers, with arrhythmias, or severe comorbidities were excluded. HR was measured at rest using the ri-fox N pulse oximeter before and 1 month after initiating therapy. Statistical analysis was performed using paired t-test and ANOVA (R, version 4.3.2). Results. Baseline HR was 88 ± 10; 91 ± 12, and 82 ± 9 beats/min in women aged 23–60 years (n = 16), women aged 60–78 years (n = 8), and men aged 26–56 years (n=14), respectively. After 1 month of therapy, HR decreased to 69 ± 8; 73 ± 9, and 68 ± 7 beats/min, respectively (p < 0,001). HR reduction was observed in 73,7 % of patients; 21,1 % maintained HR > 80 beats/ min. No significant differences were found by age (p = 0,15) or sex (p = 0,11). Conclusion. Escitalopram reduces HR, mitigating tachycardia associated with anxiety disorder, but monitoring is required due to variable treatment responses.

Objective. To analyse the clinical features of posterior reversible encephalopathy syndrome. Design and methods. We carried out analysis and systematisation of national and international literature on the pathogenesis, clinical manifestations and treatment of posterior reversible encephalopathy. Results. The main risk factors, etiology and differential diagnosis of this syndrome are considered. A clinical case of posterior reversible encephalopathy manifested in a patient with hypertension is presented. Conclusions. Due to its rare occurrence, the information on the pathogenesis, clinical manifestations, differential diagnosis and treatment of posterior reversible encephalopathy remains scarce. Advancements in diagnostic methods, in particular magnetic resonance imaging, contribute to better detection and differentiation of this disease. Spontaneous regression of clinical manifestations of the disease is often observed, but irreversible cases can occur.