Dmitrii O. Dragunov

Chronic heart failure (CHF) remains one of the leading causes of hospitalization, disability, and mortality among older patients. In this context, sarcopenia is becoming increasingly important, as it is associated with reduced physical functioning, impaired quality of life, and an unfavorable prognosis. The aim of this review was to analyze current evidence on the impact of long-term diuretic therapy, disturbances of sodium and osmotic homeostasis, and the phenomenon of metabolic aestivation on the development of sarcopenia in patients with CHF. The review was conducted in accordance with PRISMA recommendations; the literature search was performed in PubMed, Scopus, eLIBRARY.ru, Google Scholar, WHO IRIS, and other scientific resources. Current evidence suggests that long-term diuretic therapy, osmotic stress, activation of protein catabolism, and increased urea production may be involved in the pathogenesis of sarcopenia. Diuretic-associated sarcopenia has both clinical and organizational significance, as it is associated with increased hospitalization rates, functional dependence, and healthcare costs, supporting the need for sarcopenia screening in patients with CHF receiving long-term diuretic therapy.

The article discusses digital technologies as an integral part of the modern higher medical education system. Attention is focused on electronic educational platforms, virtual patients, interactive clinical scenarios, multimedia simulators, and other tools that expand access to educational materials, standardize specific elements of training, and ensure the monitoring of academic performance. We analyzed the role of the digital educational event and the potential of its design within the pedagogical process, as well as the necessity of developing clinical AI literacy among students. Special attention is given to the use of electronic learning management systems at the final stage of training to build the practical readiness of General Medicine graduates. An example of using a digital educational environment as a tool for developing follow-up care skills in future physicians is presented.

Physician training requires a unified approach to the content of educational programs across the country’s various medical universities in order to standardize the vo­lume of knowledge that underlies professional skills, abilities, and competencies. To improve the preparation of medical students for practice, creation of a unified educational program for studying the interdisciplinary concept of cardiovascular-renal-hepatic-metabolic (CRHM) syndrome within the General Medicine program is discussed. This article presents methodological materials allowing pedagogical explanation of the concept, pathogenesis, characteristics of cardiometabolic risk factors, and individual components of CHRM syndrome in fundamental and clinical departments using the end-to-end learning principle. In this regard, the role of fundamental disciplines lies in shaping the curriculum in accordance with the needs of clinical practice. Special attention is given to teaching diagnostic criteria for the syndrome and a set of personalized preventive measures depending on the stage and phenotype of CHRM syndrome. It is proposed to emphasize the transition from target organs to a unified metabolic phenotype, taking into account the multi-vector nature of CHRM syndrome processes. The inclusion of the CHRM syndrome in the curricula of the Oncology, Neurology, Rheumatology, and Obstetrics and Gynecology disciplines appears promising, allowing future practicing physicians to perceive this concept holistically and systemically.

Aim. To evaluate the effects of fluid deficit, diuretic therapy, and osmotic stress on changes in the plasma osmolyte profile (osmolarity, sodium, and urea concentrations) and their association with clinical outcomes, including muscle catabolism. Material and methods . This systematic review was conducted in accordance with PRISMA-2020. The search was conducted in October 2025 in SciSpace, PubMed, EMBASE, Google Scholar, the Cochrane Library, Web of Science, and the ClinicalTrials.gov, WHO ICTRP, and EU-CTR registries (1680 records + 124 registries + 45 additional sources). After removing duplicates (n=118) and a two-stage screening, 18 following studies (2017-2025) were included: 7 clinical studies, 6 experimental studies, 3 review studies, and 2 mixed studies. Adults aged 18 years or older with markers of dehydration or osmotic stress were included in the analysis. Key parameters included plasma osmolarity, the proportion of Na+ and urea in eOSM, copeptin/vasopressin levels, amino acid profile, muscle catabolism, hemodynamics, and renal function. Risk of bias was assessed using ROB 2.0 and ROBINS-I. Results . The systematic review included 18 studies, of which 6 clinical studies were included in the quantitative meta-analysis. A meta-analysis showed that fluid deficit, diuretic therapy, and SGLT2 inhibitor therapy were associated with an increase in plasma osmolarity (SMD 0,63 [0,19; 1,07], random-effects model; I2=93,8%). An increase in urea concentration (SMD 0,44 [0,12; 0,75]) and a decrease in sodium concentration (SMD -0,17 [-0,27; -0,06], p=0,0029) were observed. Analysis of the relative contribution of urea to plasma osmolarity, available in 2 studies, revealed an increase in its share (SMD 1,00 [0,64; 1,36]). Conclusion. Metabolic aestivation is a universal adaptive water-saving program in humans, activated by dehydration, high salt load, and diuretic therapy. Osmolyte redistribution in favor of urea is accompanied by muscle catabolism, increased blood pressure, myocardial remodeling, and may contribute to HF progression and sarcopenia. Systematic review indicates the need to monitor osmolarity, Na ⁺ and urea contribution, and vigilance when restricting fluid intake in patients recei­ving diuretics. Monitoring for metabolic aestivation signs can improve therapy safety and prognosis in cardiovascular and cardiorenal diseases.

This study investigates the molecular and mechanical effects of sodium accumulation in myocardial tissue using a combination of physiological measurements and Raman spectroscopy. Male Wistar rats were maintained on normal- and high-salt diets to induce differential sodium loading in cardiac tissue. Hemodynamic and mechanical analyses revealed increased myocardial stiffness and altered contractile parameters in the high-salt group. Raman microspectroscopy of myocardial sections demonstrated distinct spectral changes, particularly in regions corresponding to glycosaminoglycan (GAG), collagen, and its component, proline. Enhanced Raman signals near 1640 cm⁻¹ in the Amide I range, 1246 cm⁻¹ in the Amide III range, and in the 1030–1070 cm⁻¹ range indicated structural modifications of the GAG–collagen complex and an increased contribution of proline-rich collagen, consistent with elevated tissue rigidity. These findings support the concept that sodium deposition in the myocardium alters its molecular architecture and mechanical properties through GAG-mediated binding and collagen remodeling. This study provides new insights into the biophysical mechanisms linking sodium homeostasis to myocardial stiffness and diastolic dysfunction.

Sarcopenia is highly prevalent among patients with chronic kidney disease (CKD) and chronic heart failure (CHF), yet the underlying immunometabolic mechanisms remain insufficiently understood. Short-chain fatty acids (SCFAs), inflammatory cytokines, and body-composition alterations may jointly contribute to the development of muscle dysfunction in this population. In this cross-sectional study, 80 patients with CKD and CHF underwent comprehensive clinical, biochemical, bioimpedance, inflammatory, and SCFA profiling. Sarcopenia was diagnosed according to EWGSOP2 criteria. Multivariable logistic regression, LASSO feature selection, correlation analysis, PCA, and Random Forest modeling were used to identify key determinants of sarcopenia. Sarcopenia was present in 39 (49%) participants. Patients with sarcopenia exhibited significantly lower body fat percentage, reduced ASM, and slower gait speed. Hexanoic acid (C6) showed an independent positive association with sarcopenia (OR = 2.24, 95% CI: 1.08–5.37), while IL-8 showed an inverse association with sarcopenia (OR = 0.38, 95% CI: 0.13–0.94), indicating that lower IL-8 levels were more frequently observed in individuals with sarcopenia. Correlation heatmaps revealed distinct SCFA–cytokine coupling patterns depending on sarcopenia status, with stronger pro-inflammatory clustering in C6-associated networks. The final multivariable model integrating SCFAs, cytokines, and body-composition metrics achieved excellent discrimination (AUC = 0.911) and good calibration. Sarcopenia in CKD–CHF patients represents a systemic immunometabolic disorder characterized by altered body composition, chronic inflammation, and dysregulated SCFA signaling. Hexanoic acid (C6) and IL-8 may serve as informative biomarkers of muscle decline. These findings support the use of multidimensional assessment and highlight potential targets for personalized nutritional, microbiota-modulating, and rehabilitative interventions.

Objective To identify clinical, laboratory, and imaging predictors of myocardial sodium accumulation in patients with chronic heart failure (CHF). Methods This was a prospective two-center observational study including 15 patients with decompensated CHF on a high-salt diet and 5 healthy volunteers on a low-salt diet. All participants underwent dual-energy computed tomography (DECT) with generation of material decomposition maps (H₂O|Na, H₂O|NaCl) for quantitative assessment of myocardial sodium and NaCl. Estimated plasma osmolarity (eOSM) was calculated as 2[Na⁺] + 2[K⁺] + [Urea] + [Glucose], followed by calculation of osmolyte fractions (PropNa/eOSM, PropUrea/eOSM, etc.). Between-group comparisons, correlation analysis, ROC analysis, and regression modeling (univariate and multivariate models with FDR correction; internal bootstrap validation of the multivariate model) were performed. Results Compared with healthy controls, CHF patients had higher myocardial relative density (HU: 51.69 ± 5.67 vs. 38.65 ± 4.72; p = 0.004) and sodium concentration (72.24 ± 26.38 vs. 25.49 ± 44.04 mmol/kg; p = 0.025). Myocardial sodium concentration correlated inversely with the sodium fraction of eOSM (R=–0.63; p = 0.0027) and positively with the urea fraction (R = 0.66; p = 0.0014). Similar associations were observed for NaCl (R=–0.54; p = 0.015 and R = 0.66; p = 0.0015, respectively). In ROC analysis, sodium and urea fractions of eOSM demonstrated comparable discrimination for low myocardial sodium (AUC = 0.829 and 0.843; Youden thresholds 45.6% and 2.25%, respectively). In a multivariate linear model, myocardial sodium accumulation was associated with reduced sodium (β=–54; p < 0.001) and glucose fractions of eOSM (β=–27; p = 0.014), as well as increased absolute monocyte count (β = 21; p = 0.047). Internal validation confirmed acceptable calibration of the model. Conclusion Patients with decompensated CHF demonstrate increased myocardial sodium content and higher HU on DECT. The plasma osmometric profile—particularly sodium and urea fractions of eOSM—together with inflammatory markers, are associated with myocardial sodium accumulation and may serve as predictors for risk stratification and personalized therapy.