Atherosclerosis is a chronic inflammatory vascular disease caused by various risk factors, in particular smoking, obesity, high blood pressure, and dyslipidemia. In addition, such signaling pathways as NLRP3 inflammasome, toll-like receptors, proprotein convertase subtilisin/kexin type 9, Notch and Wnt, which are associated with the inflammatory response in the human body, are involved in the pathogenesis of atherosclerosis. Therapeutic targeting of inflammatory pathways, especially the NLRP3 inflammasome pathway and the cascade of reactions regulated by it leading to the production of inflammatory interleukin-1β, may represent a new avenue for the treatment of atherosclerotic diseases. This article summarizes knowledge of the cellular participants and key inflammatory signaling pathways in atherosclerosis, discusses preclinical studies targeting these key pathways in atherosclerosis, clinical trials that will target some of these processes, and the effects of suppressing inflammation and atherosclerosis.

Alcoholic cardiomyopathy is the most common form of myocardial damage caused by ethanol. Ethanol and its main active metabolite acetaldehyde have a direct toxic effect on the myocardium. The mechanisms of the cardiotoxic effect of ethanol are diverse and include membranotropic action, damage to cellular organelles, activation of lipid peroxidation, and a number of others. Dissolving in the lipids of biological membranes, ethanol changes their physico-chemical properties, disrupts the activity of membrane receptors, eventually disconnecting the connection of excitation with the contraction of cardiomyocytes. Particular importance in the pathogenesis of alcoholic cardiomyopathy is attached to the ability of ethanol to cause structural and functional changes in mitochondria, which is directly related to the violation of oxidative processes and energy supply of the myocardium as a whole. Under the influence of alcohol, free-radical lipid oxidation products content increases and antioxidants activity decreases, which indicates oxidative stress development. The deterioration of myocardial contractility due to chronic alcohol intoxication triggers a cascade of compensatory mechanisms in the form of cardiomyocyte hypertrophy and progressive fibrosis, while adaptive reactions become a factor in further pathological changes. Ethanol causes myocardial damage in a dose-dependent manner.

The probability of alcoholic cardiomyopathy occurrence is a derivative of the total accumulated dose of alcohol and individual predisposition. Alcoholic cardiomyopathy is considered as a variant of secondary dilated cardiomyopathy with all its clinical manifestations and consequences: dilation of the heart chambers, low left ventricular ejection fraction, progressive circulatory insufficiency, and cardiac arrhythmias. A relatively favorable prognosis in alcoholic cardiomyopathy is provided due to partial reversibility of myocardial damage under the condition of abstinence from alcohol consumption. Specific drugs for the treatment of alcoholic cardiomyopathy have not been developed. New treatment strategies include the use of myocardial growth and regulation factors synthesized by cardiomyocytes, as well as the stimulation of heart muscle regeneration and repair processes.

Introduction. Intervertebral disc (IVD) degeneration is defined as a multifactorial degenerative disease of the spine, starting from the structures of the nucleus pulposus of the IVD, spreading to the fibrous ring and other elements of the spinal motion segment. Unlike natural aging, a pathological degenerative process that occurs in IVDs as a result of the additive effect of genetic predisposition and external environmental factors leads to the formation of chronic back pain and reduces the patient’s quality of life. Despite many years of studying the problem of the pathogenesis of IVD degeneration, it is far from being resolved, which encourages us to further study the pathogenetic mechanisms of the development of this pathology.

Aim. To update the knowledge of practicing neurologists about the results of modern studies of the leading mechanisms of development of IVD degeneration in humans and their role in the development of promising biomarkers of this pathology and new strategies for pathogenetic therapy.

Materials and methods. A search and analysis of publications was carried out in Russian-language (e-Library) and Englishlanguage databases (PubMed, Oxford Press, Clinical Keys, Springer, Elsevier, Google Scholar). Search depth – 5 years (2018–2023).

Results. The analyzed and generalized results of studies of the molecular mechanisms influencing the development and progression of this pathology are presented. The leading pathogenetic mechanisms for the development of IVD degeneration, such as oxidative stress and the NO system, cytokine imbalance, increased activity of matrix metalloproteinases, dysfunction of fibrillar collagens and proteoglycan, as well as their relationship with each other, were considered.

Conclusion. The review provides a broader look at the pathogenetic mechanisms of IVD degeneration, which makes it possible to set new goals for future development of promising therapeutic strategies.

Aim. To determine the features of hemostasis system disorders and the possibility of their correction in patients with arterial hypertension (AH) and multifocal atherosclerotic lesions (MFA) with risk factors indicated.

Materials and methods. The study included 135 patients (mean age 53.7 ± 7.76 years), including 80 patients with controlled AH stage and II (group 1) and 55 patients with controlled AH stage III who had ischemic stroke (group 2). Among all patients studied, 33 patients (24.4 %) were smokers. All 135 patients received comparable antihypertensive, antiplatelettherapy (acetylsalicylic acid at a dose of 100 mg/day), had MFA and target lipid spectrum values.

Results. Procoagulant shifts are noted already in patients with AH stage I and II, especially in the presence of smoking. Such indices of global thrombodynamics test as initial clot growth rate, average clot growth rate, clot size significantly exceed the reference values and indicate high prothrombogenic potential in patient with AH and MFA. Prescription of dual antiplatelet therapy allows normalization of identified disorders. Presence of risk factors (smoking) aggravates existing hemostasis disorders in patients with AH and MFA.

Conclusion. Smoking cessation, optimization of risk factors and complex antihypertensive, hypolipidemic and antithrombotic therapy are the basis of treatment of patients with AH and MFA and can be considered as priority measures to reduce morbidity and mortality in this patient population.

Objectives. The purpose of this work is to provide a clinical case study of Lemierre’s syndrome (LS) in order to raise awareness amongst doctors of various medical specialties regarding this rare cause of septic pulmonary embolism (SPE).

Materials and methods. The patient in clinical case is a 25-year-old female who was hospitalized due to SPE, which had been complicated by respiratory distress, pneumothorax and septic shock. The initial source of embolus lung damage was the septic thrombosis of both the internal and external jugular veins. This thrombosis occurred against the backdrop of a carbuncle of the lower lip, an inflammatory infiltrate at the bottom of the mouth, an abscess in the soft tissue of the chin and neck cellulitis, which correspond to the diagnostic criteria for Lemierre Syndrome.

Results. The literature data of the epidemiology, etiology, pathogenic mechanisms of the venous thrombosis, embolic and septic complications among patients with LS are presented. The article discusses the clinical features and course of the disease, as well as key aspects of diagnosis, including current diagnostic criteria, with regard to the typical and atypical variants of LS. The principles of antibiotic therapy and the possibility of anticoagulation therapy in cases of septic pulmonary emboli associated with head and neck vein thrombosis are also considered.

Conclusion. LS is a rare, but clinically significant condition characterized by the development of septic thrombosis in the internal jugular vein in response to acute suppurative inflammation of the head and neck. In typical cases, the causative organism is Fusobacterium necrophorum, or other anaerobic bacteria. This pathological condition is often accompanied by multiple other septic complications, with the most significant being the development of septic pulmonary embolism. Clinical observation indicates the necessity for including LS in the differential diagnosis among causes of the septic pulmonary embolism, and for adopting a multidisciplinary approach in the treatment of these patients in a specialized multifield hospital. Identification and diagnosis of Lemierre Syndrome can be challenging due to its low incidence and variable clinical presentation. Although the condition is not widely recognized among physicians, an understanding of the basic principles of its diagnosis and management can significantly improve treatment outcomes and patients prognosis.

Aim. To report a clinical case of autoimmune/inflammatory syndrome, induced by adjuvants in patient after polypropylene mesh implantation for inguinal hernia repair.

Materials and methods. Patient Z., male, 68 years old, was admitted to the hospital presenting muscle weakness and progressive dyspnoea. Interview and physical exam revealed signs of cognitive impairment and memory loss, proximal muscle weakness. Differential diagnosis was made to clarify genesis of symptoms, to rule out polymyositis, other systemic connective tissue diseases, oncologic diseases, hypothyroidism, infectious diseases.

Results. Creatine kinase, thyroxine, thyreothropic hormone levels were normal. Clinical and immunological investigation revealed no data on polymyositis or any other systemic connective tissue disease. Yersiniosis, salmonellosis, malaria were ruled out. Chest CT scan, abdomen CT scan, gastroscopy, colonoscopy no data on the presence of malignant neoplasms. PSA level were normal. Electroneuromyography revealed signs of symmetrical axonal type damage to the motor portion of the ulnar nerves on both sides, and demyelinating type damage to the sensory portion. Prednisolone therapy was started at a dose of 40 mg per 24 hour (0.5 mg per kg), which lead to a significant clinical improvement. Based on the therapy response and positive diagnostic criteria (clinical manifestation after polypropylene mesh implantation, typical clinical manifestation – muscle weakness, chronic fatigue, cognitive impairment, neurological manifestations associated with demyelination) patient was diagnosed with autoimmune/inflammatory syndrome, induced by adjuvants (ASIA) after polypropylene mesh implantation for inguinal hernia repair.

Conclusion. This clinical case report demonstrates possibility of a persistent course of the disease (symptoms were present for 15 years). Feature of this case is partial clinical improvement due to long-term uncontrolled dexamethasone use, which was prescribed empirically.

Antiphospholipid syndrome (APS) is a systemic autoimmune pathology characterized by thrombotic manifestation associated with antiphospholipid antibodies (aPL) and phospholipid-binding proteins circulation. Long-term anticoagulant therapy is a cornerstone in the treatment and prevention of relapses and manifestations of APS-associated For high-risk APS phenotypes with arterial thrombosis, microthrombosis and triple aPL-positivity VKA use is the only possible option for anticoagulant therapy. The need for constant monitoring of international normalized relations (INR) for achievement and control of target values, intolerance and variability of INR reduce patient compliance in a certain category of patients, which limits their use in some clinical situations. Use of direct oral anticoagulants (DOAC) is an alternative option for anticoagulant therapy. Despite the benefits of using DOAC according to current international recommendations and guidelines their use is limited by the phenotype of APS with venous thrombosis and monoand double aPL-positivity if the patient is unable or unwilling to take VKA due to need for constant INR monitoring. In the obstetric version of APS during gestation, antithrombotic therapy is performed with aspirin and low molecular-weight heparins. The intensity and duration of antithrombotic prophylaxis determining at high-risk APS is a real challenge for the clinician due to the lack of tools for risk stratification and should be carried out depending on the individual characteristics of the patient and the course of APS.

Traumatic brain injury (TBI) is one of the most common causes of neurological disability in young and middle-aged people. Cognitive impairment is the most persistent and universal brain injury syndrome in cases of TBI and, moreover, the best indicator of TBI severity to predict its outcome. Cognitive impairment can persist persistently even after mild TBI, which accounts for 70–90 % of the total number of trauma patients. This may be due to the fact that in cases of mild TBI, the most fragile functions of integrative structures of the frontal and temporal lobes are slowly and not always completely recovered and the dominant clinical manifestation become complex neuropsychological disorders. Individuals with repeated mild TBI are characterized by development of chronic post-traumatic encephalopathy, that is a kind of neurodegenerative disease manifested by slowly increasing cognitive impairment, parkinsonism and a number of other neurological syndromes. Early detection and adequate correction of the cognitive impairments may improve the outcome of injury of diverging severity. Due to the fact that the pathogenesis of TBI is based on disorder of cholinergic system, the patients have predominance of regulatory disorders in the neuropsychological profile, as well as a combination of cognitive and affective disorders. Administration of acetylcholine precursors leads to rapid increase of free choline levels in plasma that penetrates the blood-brain barrier well and enhances cholinergic activity by increasing acetylcholine synthesis and release. The article considers the possibilities of using acetylcholine precursors in connection with their potential to block the progressive impairment of cognitive functions induced by trauma as well as to reduce severity of behavioral and affective disorders.