One of the manifestations of ischemic cardiomyopathy is remodeling of left ventricular (LV), which can manifest itself both globally and as a result of an aneurysm. In the vast majority of cases, LV aneurysm location is the apex and the anterior septal region; very rarely, aneurysms are localized in the area of the posterior LV wall and are large. Due to the relative rarity of the given localization surgical treatment tactics of this pathology is not well-established and standardized. The work presents a clinical case of surgical treatment of an aneurysm of the LV posterior wall, demonstrates the stages of diagnosis, and also identifies the features of surgical intervention with the results of treatment in 6 months after surgery.

Aim: To access frailty and its impact on 10-year survival in patients with implanted devices for cardiac resynchronization therapy (CRT).

Methods: 77 patients with congestive heart failure (74% men, 26% women; mean age of 58.7 ± 10.7 years) with NYHA class II–IV were enrolled. Frailty Index was calculated using 31 parameters (the ability to perform daily activities, clinical status, laboratory markers, comorbidities). Based on the frailty index patients were identified as not frail (< 0.375; n = 41; 53%), and frail (≥ 0.375; n = 36; 47%).

Results: The mean follow-up period was 49.0 ± 34.2 months. Survival at 10-year follow-up was 87.5% for non-frail patients, compared to 47.2% for frail patients (log-rank test p < 0.001). In univariate analysis, frailty associated with 10-year mortality (OR 7.824; 95% CI 2.495 – 24.533; p < 0.001). After adjustment for age, gender, rhythm, NYHA class, left ventricular ejection fraction, left bundle branch block, and QRS width, frailty remained a significant prognostic factor associated with 10-year mortality (OR 9.528; 95% CI 2.720 – 33.368; p < 0.001). Also, according to logistic regression, the presence of frailty reduced the chance of superresponse (decrease of left-ventricular end -systolic volume ≥ 30%) to CRT (OR 0.278; 95% CI 0.100–0.770; p = 0.014).

Conclusion: Frailty is widespread in patients with heart failure and implanted devices for CRT. In these patients frailty is associated with a more than seven-fold increased risk of death during 10-year follow-up and with a lower chance of superresponse to CRT.

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, had a profound impact on global health, and society and become one of the deadliest in history. Knowledge of risk factors for mortality is critically important in the formation of organizational, methodological and clinical decisions to limit disease progression and reduce the number of fatal outcomes. However, it is still unclear whether generally accepted risk factors can be equally useful in identifying risk groups in a diverse population of patients in small cities.

Aim: To evaluate the utility of demographic, clinical, and laboratory characteristics in the prediction of negative outcome of patients with COVID-19 admitted to the intensive care unit (ICU) of the multidisciplinary COVID-19 hospital in the city of Saransk.

Material and Methods. Medical records of 153 patients (including 134 recovered and 19 dead) with laboratory-confirmed SARS-CoV-2 infection treated in the intensive care unit of the S.V. Katkov Republican Clinical Hospital between March and December of 2020 were included in this retrospective, single-center, clinical trial. Demographic, clinical, and laboratory characteristics, complications and therapeutic interventions were compared between deceased and recovered patients. The primary endpoint was in-hospital all-cause mortality. Risk factors for mortality were analyzed using logistic regression.

Results. Multivariate regression analysis showed that in the population studied, included both therapeutic and surgical patients, a history of coronary artery disease, chronic non-specific lung disease, acute surgical conditions, plasma creatinine at ICU admission ≥ 106 µmol/L had a negative effect on in-hospital mortality, whereas fever at admission had a protective effect. Patients who died had lower oxygen saturation upon the admission to ICU and were more likely to receive invasive mechanical ventilation and higher doses of dexamethasone in treatment.

Conclusion. The present study identified predictors to mortality of patients with COVID-19, treated in the ICU of a Mordovia Republic hospital (Russia), which were somewhat different from those previously reported for larger cities and indicate a large contribution of concomitant diseases to the negative outcome. We did not identify a significant contribution of many proposed laboratory markers to predicting mortality. These findings may help authorities and clinicians optimize organizational, methodological, and clinical approaches to medical care of patients to reduce the risk of a negative outcome from COVID-19.

A review of domestic and foreign scientific publications from 2018 to 2023 was conducted. The search was carried out using the Pubmed biomedical research database and the Russian Science Citation Index. 1673 articles were found, using keywords. Various etiological and pathogenetic variants of gastroduodenitis (GD) are considered. One of the most common pathogens of gastroduodenal pathology is Helicobacter pylori (Hp), which, due to its virulence factors, can persist for a long time on the mucous membrane of the stomach and duodenum, thereby causing its inflammation, subsequently leading to gross damage to the mucosa and complications of gastrointestinal tract. Today, despite the prevalence of Hp, many new etiological agents are found: cytomegalovirus, Epstein - Barr viruses, Lamblia intestinalis, Blastocystis spp., Entamoeba spp. and various factors contributing to the development of this disease. For example, such as human constitution, environment, gender differences, age, genetics, drug exposure, stress, the relationship of perinatal brain lesions, endothelial dysfunction and immunity with the detection of GD has also been described. Every year the range of etiological agents expands, which leads to changes in the pathogenesis of GD.

Relevance. For almost six decades, in right ventricular outflow tract reconstruction the choice of a conduit has been and remains a chelleging task for cardiac surgeons. Among the vast number of valve prostheses offered, the choice of its material is still controversial. There are various allografts, xenografts, a combination of Dacron linear prostheses with an implanted locking element made of biological tissue and mechanical materials. Synthetic prostheses with handmade valves made of expanded polytetrafluoroethylene (ePTFE) and bioresorbable tissue-engineered conduits are also being popularized. The constant search for the best conduit is associated with unsatisfactory long-term performance results. The main problem relates to the inevitable biodegradation of the material from which the prosthesis is made. Durability is the main and most important indicator of the quality of conduits.

Aim: To review conduits for right ventricular outflow tract reconstruction based on the analysis of literature data.  

Material and Methods. The research was carried out in the databases Medline (PubMed) and the Russian Science Citation Index (RSCI) using search queries, keywords and logical operators.

Results. According to a systematic literature analysis, the aspects of choosing a conduit for implantation in the pulmonary position were studied. The main complications, immediate and long-term postoperative results were highlighted.

Conclusion. Currently, there is no consensus on the choice of conduit. Quantaty of adult patients previously underwent interventions is increasing. Biodegradation has led to obstruction of the prosthesis, insufficiency of the locking element, or a combination of both situations.

Background. Chronic ischemic heart disease (IHD) is characterized by progressive myocardial remodeling caused by the combined effects of persistent ischemia and hemodynamic overload. Sustained activation of the sympathetic nervous system leads to alterations in β-adrenergic signaling, which may influence both the extent and spatial distribution of myocardial fibrosis.

Aim: To evaluate the association between β1- and β2-adrenergic receptor expression in cardiomyocytes and topographic patterns of myocardial fibrosis in patients with chronic IHD, and to determine the modifying effect of concomitant arterial hypertension on myocardial remodeling.

Material and Methods. This pilot study included 29 patients with chronic IHD undergoing elective coronary artery bypass grafting. According to the presence of hypertension, patients were stratified into an IHD group (n = 17) and an IHD with hypertension group (n = 12). Right atrial appendage specimens were analyzed. The extent and distribution of fibrosis were assessed using Van Gieson staining. Immunohistochemistry was performed to determine ADRB1 and ADRB2 expression intensity in cardiomyocytes. Associations were evaluated using Spearman’s rank correlation and proportional odds regression adjusted for arterial hypertension.

Results. Myocardial fibrosis was present in all cases. Although the overall burden of fibrosis did not differ between groups, patients with concomitant arterial hypertension demonstrated a distinct distribution of subepicardial fibrosis (p = 0.008). In the pooled cohort, lower ADRB1 expression intensity was significantly associated with greater subendocardial fibrosis severity (ρ = −0.49; p = 0.007), and this relationship remained independent after arterial hypertension (OR = 0.17; p = 0.014). ADRB2 expression intensity showed an inverse correlation with subepicardial fibrosis (ρ = −0.43; p = 0.020); however, statistical significance was attenuated after adjustment for arterial hypertension (p = 0.074).

Conclusions. These findings support the concept of spatial heterogeneity in myocardial fibrotic remodeling in chronic IHD. Reduced β1-adrenergic receptor expression is independently associated with subendocardial remodeling, consistent with an ischemia-driven pattern of injury. In contrast, the relationship between β2- adrenergic receptor expression and subepicardial fibrosis appears less robust and partially influenced by clinical phenotype. Arterial hypertension modifies the topographic distribution of fibrosis without increasing its overall burden.

Background. Pediatric hypertrophic cardiomyopathy (HCM) is a major cause of sudden cardiac death in children and represents a clinically and genetically heterogeneous condition distinct from adult disease. Although advances in adult HCM have informed management strategies, pediatric-specific evidence remains comparatively limited, particularly regarding imaging-based risk assessment and validation of pediatric risk prediction models.

Aim: To assess current diagnostic approaches, genetic insights, and current challenges in risk stratification in pediatric HCM.

Methods. A structured narrative review of studies published from 1997 through early 2025 was conducted using major biomedical databases and guideline references. Priority was given to pediatric cohort studies, population-based registries, contemporary clinical guidelines, and genetic investigations addressing epidemiology, etiologic classification, diagnostic evaluation, and risk prediction.

Key Content and Findings. Recent evidence confirms the predominant role of sarcomeric gene variants beyond infancy, while underscoring the importance of syndromic and metabolic etiologies in early childhood. Advances in electrocardiographic risk markers, multimodal imaging including cardiac magnetic resonance imaging assessment of myocardial fibrosis and next generation genetic testing have enhanced diagnostic precision and family screening. However, phenotypic variability, age-dependent penetrance, and limitations in external validation of pediatric risk prediction tools, including HCM Risk-Kids, continue to challenge individualized management.

Conclusion. Pediatric HCM remains a prognostically complex and biologically diverse disease. Refinement of pediatric-specific risk stratification models, improved integration of imaging and genetic data, and international collaborative research are essential to optimize early diagnosis and personalized care in affected children.

Background. Amiodarone remains one of the most effective antiarrhythmic drugs; however, its use is associated with a risk of amiodarone-induced thyroid dysfunction, including thyrotoxicosis and hypothyroidism. Thyroid dysfunction may worsen the course of cardiovascular disease and affect in-hospital prognosis. Despite the availability of clinical guidelines, data on the real-world incidence of amiodarone-induced thyroid dysfunction and its association with in-hospital outcomes remain limited. Aim: To evaluate the incidence of amiodarone-induced thyroid dysfunction, identify factors related to its presence, assess the relationship between thyroid dysfunction and cardiovascular complications and hospital mortality.

Material and Methods. A retrospective analysis was performed in 340 patients receiving amiodarone therapy during hospitalization. Age, sex, primary cardiac diagnosis, left ventricular ejection fraction, amiodarone dose, duration of therapy, thyroid status parameters, and in-hospital outcomes were evaluated. The presence of amiodarone-induced thyroid dysfunction was determined on the basis of a clinical diagnosis documented in the medical records. Group comparisons of quantitative and categorical variables, an additional Welch t-test, contingency table analysis, and binomial logistic regression were used.

Results. Amiodarone-induced thyroidopathy was detected in 40 out of 340 patients (11.8%). Age was associated with a higher odds ratio for thyroid disease (OR=1.12; 95% CI for OR 1.07–1.17; p < 0.001; approximately a threefold increase in the odds of developing thyroid disease over 10 years). A maintenance dose of amiodarone doubled the odds of a thyroid disorder diagnosis (OR=1.01 per 1 mg; 95% CI for OR 1.007–1.014; p=0.031); the dose of amiodarone received during hospitalization was not statistically significant. Left ventricular ejection fraction showed no association with the development of thyroidopathy. The presence of amiodarone-induced thyroidopathy was associated with a threefold increase in the odds of cardiac complications (OR=3.47; 95% CI 1.61–7.47; p=0.001). The association between thyroid dysfunction and in-hospital mortality was not assessed due to the low incidence of the event (1.18%, n=4).

Conclusion. Amiodarone-induced thyroid dysfunction develops in approximately one in nine patients receiving amiodarone therapy and is related to an adverse in-hospital course. Older age and a higher maintenance dose of the drug were related to a higher probability of detecting amiodarone-induced thyroid dysfunction. Differences in the dynamics of hormonal normalization confirm the heterogeneity of the pathogenesis of thyroidopathy, given that its development is not associated with systolic myocardial dysfunction. These data may serve as a basis for revising the management guidelines for patients taking amiodarone. The study results can be used to personalize thyroid function monitoring in older patients and when higher maintenance doses of amiodarone are used.