Background. Currently, there has been an increase in the number of reported cases of hypertrophic cardiomyopathy, probably due to improvements in diagnostic techniques, examination methods, and an increase in the total number of patients. The gold standard for surgical treatment remains open transaortic myectomy, which has a number of disadvantages, such as limited visualization, in some cases leading to the inability to perform radical resection of hypertrophied muscles. The need to expand the scope of resection, improve the quality of visualization, and reduce the frequency of disease recurrence determines the relevance of developing a new technique for accessing the interventricular septum.

Objective. To investigate the possibilities of new extended access to the interventricular septum with effective repair of the aortic and mitral valves in the surgical treatment of hypertrophic cardiomyopathy in an experimental setting.

Design and methods. From March 2017 to May 2023, two series of experiments have been conducted at the Center for Preclinical and Translational Research of the Almazov National Medical Research Centre to investigate extended access to the interventricular septum with repair of the aortic and mitral valves.

Results. The developed extended access to the interventricular septum demonstrated its effectiveness on experimental anatomic models. The possibility of effective repair of the aortic valve commissure and the anterior mitral valve leaflet after the extended access without a significant impact on the geometry of the fibrous annuli and the function of these valves has been proven.

Conclusion. The developed extended access allows for improved visualization of the interventricular septum in patients with a narrow fibrous ring of the aortic valve, mid-ventricular and apical forms of hypertrophic cardiomyopathy. Restoration of the valve apparatus (mitral and aortic valves) using the new access is possible and effective. Based on the results of this study it seems promising to conduct preclinical studies (in vivo on animals). And in the future — implementation in clinical practice in certain groups of patients.

Background. Transformation of the morphology of the post-infarction myocardium changes the electrical characteristics of the heart muscle, increasing the risk of life-threatening arrhythmias.

Objective. The aim of the study was to compare the structural and electrical features of the heart muscle in post-infarction patients.

Design and methods. The study participants were 105 (85.4 %) patients who had suffered an MI, aged 56.7±8.4 years. Six months after the MI, the patients underwent cardiac magnetic resonance imaging (MRI) (GE SIGNA Voyager tomograph, GE HealthCare, USA) with the introduction of a contrast agent — gadoteric acid. Six and 12 months after the MI, the patients underwent multi-day electrocardiogram monitoring (MMEKG) for 72 hours.

Results. According to MMEKG, unstable paroxysms of VT were registered in 9 (6.8 %) patients. Frequent (>30/h) ventricular extrasystoles (VE) were correlated with the percentage of scar zone — r=0.679 (p=0.0101), the mass of the heterogeneous zone — r=0.721 (p=0.00951). An association was established between polymorphic VE with the presence of areas of microvascular obstruction r=0.812 (p=0.0095) and intramyocardial hemorrhage r=0.798 (p=0.0114). Most parameters of autonomic regulation and heart rate turbulence showed a moderate negative relationship with the scar mass. According to the data of univariate regression analysis, risk markers of unstable VT were established: scar zone mass, end-diastolic size, turbulence slope, SDNN variability parameter.

Conclusion. Predictors of unstable runs of ventricular tachycardias within 12 months after myocardial infarction are the mass of the scar zone, the values of the left ventricular end-diastolic diameter, the values of the turbulence slope and the SDNN variability parameter.

Background. Standard HLA typing and simple allele mismatch counts do not always provide an objective assessment of rejection risk. Platforms PIRCHE (Predicted Indirectly ReCognizable HLA Epitopes) and HLAEMMA (HLA Epitope MisMatch Algorithm) estimate donor–recipient HLA incompatibility at the epitope level, based on low-resolution HLA typing.

Objective: To evaluate the predictive ability of PIRCHE and HLA-EMMA for stratifying the risk of heart allograft rejection within the first year after orthotopic heart transplantation.

Materials and Methods. This retrospective study included 160 heart recipients. During the first-year post-transplantation 77 recipients (control group) showed no rejection (ACR 0R–1R and/or pAMR 0–1). Eighty-three recipients experienced an adverse event: a rejection episode (ACR 2R–3R and/or pAMR 2–3) or death from any cause without preceding rejection. HLA incompatibility was calculated using the PIRCHE-T2, PIRCHE-B, and six HLA-EMMA algorithms. The prognostic significance was assessed using the Kaplan-Meier method.

Results. Statistically significant differences between groups were observed for five algorithms: Allele-MM-L2, AA-MM-L1, AA-MM-L2, SA-L2, and PIRCHE-T2. PIRCHE-T2 demonstrated the strongest predictive value with a threshold >80: adverse events occurred in 73.7 % (28/38) of recipients with PIRCHE-T2 >80 versus 45 % (55/122) with PIRCHE-T2 ≤80.

Conclusion. The obtained results indicate the potential utility of the PIRCHE-T2 with a threshold value of >80 for risk stratification during the first post-transplant year.

Background. Tumor immune evasion plays a key role in the progression of colorectal cancer (CRC). β-galactoside-binding proteins galectin-1 and galectin-3 may be important mediators of this process; however, their specific immunomodulatory effects in CRC require further investigation.

Objective. To study the in vitro effects of galectin-1 and galectin-3, expressed by colon adenocarcinoma cells, on the secretion of IFNγ, IL-17A, and TGFβ1 by peripheral blood mononuclear cells (PBMCs) from CRC patients and healthy donors.

Design and method. The human colorectal adenocarcinoma cell line COLO 201 was co-cultured with PBMCs from CRC patients and healthy donors in the presence or absence of selective galectin-1 (OTX 008) and galectin-3 (GB1107) inhibitors. The concentrations of IFNγ, IL-17A, and TGFβ1 in the culture supernatants were measured by enzyme-linked immunosorbent assay.

Results. Inhibition of galectin-1 in COLO 201-PBMC co-cultures significantly increased IFNγ and IL-17A production and decreased TGFβ1 secretion by PBMCs from both CRC patients and healthy donors. In co-cultures with patient-derived PBMCs, galectin-3 inhibition had a similar effect. However, in co-cultures with healthy donor cells, it was accompanied by suppressed IL-17A production and an increased TGFβ1 level. Combined galectin-1,3 blockade in co-cultures containing PBMCs from CRC patients caused a more pronounced reduction in TGFβ1 levels than individual inhibition; at the same time, changes in IFNγ and IL-17A levels mirrored the effects of single inhibitors.

Conclusion. Colorectal cancer cell-derived galectin-1 and galectin-3 mediate in vitro disruption of the cytokine profile in peripheral blood mononuclear cells. Galectin-1 exhibits tolerogenic properties, while the effect of galectin-3 depends on the source of the target immune cells (PBMCs from CRC patients or healthy donors).

This clinical case report describes the surgical management of a shrapnel wound to the thigh with associated vascular damage. A 55-year-old male soldier sustained a shrapnel injury to his left thigh during a combat mission. A tourniquet was applied immediately at the point of injury to control life-threatening bleeding. Upon evacuation to the nearest military field hospital (MFH), ultrasound examination revealed a rupture of the superficial femoral artery (SFA) and superficial femoral vein (SFV), along with an embolism of the posterior tibial artery and anterior tibial artery. Acute ischemia of the left lower limb, classified as grade 2b according to the Fontaine-Pokrovsky classification, was diagnosed. The case was complicated by a multi-level vascular injury, combining a proximal rupture of major vessels and distal embolism, which posed a significant threat of irreversible ischemia. Given the imminent risk of limb loss and the impossibility of evacuation to a higher-level multi-specialty military hospital, a decision was made to perform emergency surgery at the MFH. The surgical strategy involved a comprehensive set of reconstructive procedures on both the arteries and the vein. The intervention included resection of the SFA with an end-to-end anastomosis, repair of the SFV wall defect, removal of a thromboembolus from the popliteal artery bifurcation, and popliteal-to-distal posterior tibial artery bypass grafting using a reversed great saphenous vein. The postoperative course was uneventful, with complete resolution of acute ischemic symptoms and primary healing of the surgical wounds. The successful outcome demonstrates the feasibility of performing complex revascularization procedures in a military field hospital setting, even without on-site angiographic support. The surgical care provided at the MFH stage ultimately prevented limb amputation and subsequent disability.

Certain autoimmune diseases (AIDs) are grouped into autoimmune polyglandular syndromes (APS), characterized by pathological reactivity of T and B lymphocytes to the body’s own normal components. These include both the monogenic APS type 1, caused by an AIRE gene mutation with an autosomal recessive inheritance pattern, and the polygenic APS types 2, 3, and 4, which follow an autosomal dominant pattern. The most prevalent combination is primary adrenal insufficiency (PAI), autoimmune thyroiditis (AIT) or Graves’ disease, and type 1 diabetes mellitus, constituting APS-2. Consequently, a diagnosis of one AID increases the risk of developing others. Therefore, patients with an established AID require targeted screening for other syndrome components, particularly for life-threatening conditions like PAI. The highly variable initial clinical presentations, coupled with insufficient awareness of PAI among physicians, often lead to delayed diagnosis of this critical condition. The presented clinical case illustrates a prolonged development of various autoimmune pathologies, involving multiple medical specialists, culminating in the diagnosis of PAI during an Addisonian crisis. A key aspect of managing such patients is educating them about early signs of adrenal insufficiency, such as severe weakness and hypotension. The treatment and follow-up are detailed in accordance with the latest clinical guidelines. The report underscores the critical importance of interdisciplinary collaboration and adherence to modern screening recommendations to prevent life-threatening complications.

Background. Carpal tunnel syndrome (CTS) is the most common compression-ischemic neuropathy of the upper extremities, with significant medical and social significance due to the significant reduction in work capacity of patients of various age groups.

Study Objective. To evaluate the outcomes of surgical treatment of patients with CTS using minimally invasive open decompression of the median nerve in the carpal tunnel.

Materials and Methods. The study included 107 patients diagnosed with CTS, aged 33 to 88 years. All surgical procedures were performed on an outpatient basis under local anesthesia. Clinical outcomes were assessed using an objective examination and patient questionnaires using the Boston Symptom Severity Questionnaire (BSS) and the Functional Disability Questionnaire (FSS).

Results. In the vast majority of cases, regression of clinical symptoms was noted as early as 14 days after surgery. Before surgery, the mean SSS and FSS values were 3.61±0.56 and 3.75±0.56, respectively. Postoperatively, a statistically significant reduction in these values was observed: the mean SSS decreased to 1.16±0.04, and the FSS decreased to 1.07±0.07 (p<0.05).Conclusion. Surgical treatment remains the most effective method for treating carpal tunnel syndrome. Despite the variety of surgical techniques, minimizing surgical trauma while ensuring adequate decompression of the median nerve is key to optimizing clinical outcomes and improving patients’ quality of life.