Background. Portal hypertension (PH) is one of the leading complications of liver cirrhosis (LC) and determines the risk of developing esophageal varices (EV). Measurement of the hepatic venous pressure gradient is considered a standard indicator of PH; however, this method is invasive and has limited availability. In recent years, spleen elastometry has become a promising non-invasive method for assessing the severity of PH in patients with LC.
Objective: To study the diagnostic value of spleen elastometry in patients with PH associated with LC in the compensation stage and to evaluate the correlation between spleen stiffness (SS) parameters and clinical and instrumental PH features.
Materials and methods. A prospective cross-sectional study included 44 patients (26 male and 18 female individuals) with PH associated with LC and the development of grade 1–2 EVs. All participants underwent liver transient elastography using a FibroScan 502 Touch (Probe M) device and spleen elastometry using a BIOSS ANGIODIN-Sono/P-Ultra ultrasound system. The average age of the participants was 50 (44–60) years. According to the Child–Pugh scale, 26 patients (59.1%) were classified as class A cirrhosis and 18 patients (40.9%) as class B. Esophageal varices (EV) of grade 1 were detected in 20 (45.5%) patients and grade 2 in 24 (54.5%) patients. Spleen size (longitudinal and transverse), liver stiffness (LS) and SS, platelet levels, albumin, international normalized ratio (INR), and EV grade (based on esophagogastroduodenoscopy) were assessed.
Results. In the overall sample, the median SS of the group was 60.5 (IQR 48.0–69.0) kPa, LS – 30.6 (IQR 27.1–48.9) kPa. SS was higher in grade 2 EV than in grade 1 EV: 65.0 (IQR 61.3–69.9) vs. 50.0 (IQR 43.0–62.0) kPa (p = 0.008). The results of determination of SS in patients with LC class A and class B according to Child–Pugh were statistically insignificant (p = 0.48). Correlation analysis revealed a moderate correlation between spleen stiffness and platelet count (ρ = -0.46; p = 0.002), as well as an association with spleen length (ρ = 0.41; p = 0.006), spleen structure (ρ = 0.44; p = 0.003), and the grade of EV (ρ = 0.39; p = 0.009). Correlation between SS and LS, albumin, INR, and Child–Pugh LC class was weak and non-significant. ROC analysis for predicting grade 2 EV using SS parameters yielded the following results: area under the curve (AUC) = 0.74, cutoff value – 58 kPa (sensitivity 75%, specificity 70%).
Conclusion. SS was significantly higher in patients with grade 2 EV comparatively to grade 1 EV, while its association with Child–Pugh cirrhosis class was not found. A spleen stiffness cutoff of 58 kPa allows for a moderate differentiation (AUC = 0.74) of grade 2 EV, which can be used for risk stratification and endoscopic screening planning. Compared with LS measurements, spleen elastometry data better reflects portal hypertension severity, making this method a potential additional noninvasive tool in the management of patients with LC.
Introduction. Hyperuricemia (HU) is a risk factor for a wide spectrum of chronic non-communicable diseases (NCDs). Genetic variants of urate transporters ABCG2 (rs2231142, Q141K) and SLC2A9 (rs1014290) are associated with impaired uric acid (UA) excretion and may modulate the risk of NCDs.
Objective. To investigate the association between NCDs and uric acid metabolism disorders, and to evaluate the role of ABCG2 rs2231142 (c.421C>A, p.Gln141Lys, Q141K) and SLC2A9 rs1014290 urate transporter gene polymorphisms in the development of NCDs.
Materials and methods. A cross-sectional study enrolled 171 metallurgical plant workers with NCDs and HU (serum UA ≥360 µmol/L) and/or urate-lowering therapy: 101 men (59.1%) and 70 women (40.9%), median age 49 [43; 54] years, median BMI 28.0 [25.5; 30.9] kg/m². Biochemical blood analyses, eGFR calculation using the CKD-EPI equation, and genotyping of SLC2A9 rs1014290 and ABCG2 rs2231142 were performed. Multivariable analysis included logistic regression adjusted for age, sex, and eGFR; false discovery rate (FDR) correction was applied using the Benjamini–Hochberg method.
Results. HU was detected in 30.4% of workers, significantly more frequently in men (43.6% vs. 11.4% in women). The leading NCDs were hypertension (48.5%), obesity (36.3%), gout (21.1%), and urolithiasis (10.5%). In multivariable models, HU was independently associated with hypertension (OR 5.19; 95% CI: 1.87–14.44), urolithiasis (OR 5.38; 95% CI: 1.63–17.79), and gout (OR 3.27; 95% CI: 1.39–7.69). Carriage of the ABCG2 minor allele A was associated with urolithiasis (OR 6.28; 95% CI: 2.19–18.03; padj = 0.032), higher serum UA levels, and reduced eGFR compared to C/C homozygotes (p < 0.001). The protective effect of the SLC2A9 allele G against HU (OR 0.41; 95% CI: 0.23–0.75) did not reach statistical significance after FDR correction (padj = 0.095).
Conclusion. HU is independently associated with hypertension, urolithiasis, and gout. Carriage of the ABCG2 rs2231142 minor allele A increases the risk of urate nephrolithiasis. The SLC2A9 polymorphism demonstrates a trend toward a protective effect. Urate transporter genotyping is warranted for personalized prevention of NCDs in metallurgical workers.
ABSTRACT. Osteoarthritis (OA) was previously considered primarily a degenerative disease associated with joint “wear and tear.” Nevertheless, recent studies indicate that chronic, low-grade inflammation is a central factor in its development. The aim of this review is to characterize the morphology of inflammation in OA, focusing on macrophage polarization mechanisms and the role of obesity. A literature review of the last 5 years was conducted using PubMed, MEDLINE, and eLibrary databases. The analysis focused on pathogenetic mechanisms of joint damage, macrophage polarization, and obesity’s impact on disease progression. The results of the analysis allow us to conclude that the morphology of inflammation in OA reflects a complex network of cellular interactions, in which macrophage polarization plays a pivotal role, and obesity serves as one of the factors precipitating this process.
Introduction. The renal continuum is a pressing issue in clinical practice, and its components – acute kidney injury (AKI), acute kidney disease (AKD), and chronic kidney disease (CKD) – are highly prevalent in elderly patients after stroke. Renal dysfunction and cerebrovascular pathology mutually exacerbate each other’s course, increasing the risk of adverse outcomes.
Objective: to assess the prevalence of renal continuum components in elderly patients after acute cerebrovascular accidents.
Materials and methods. This prospective cohort study included 120 patients, 53,3% of whom were men and 46,7% women, with an average age of 68.2 ± 3.8 years, with a history of strokes of various phenotypes less than 6 months old. The data were described using modern statistical analysis methods; differences were considered significant at p < 0.05.
Results. The obtained data show that in the study group of patients, 36.7% had AKI, 25.8% had AKD, and more than half (56.7%) suffered from CKD. Numerous studies in the literature confirm the high frequency of AKI and CKD in patients with acute cerebrovascular accident, while AKD has been very little studied. The results of our study are consistent with existing scientific data.
Conclusion. Among older patients, components of the renal continuum are significantly more common and require increased attention and up-to-date assessment to modify therapy and improve prognosis.
Background. QRS complex fragmentation (fQRS) is regarded as an electrocardiographic marker of inhomogeneous intraventricular conduction that may reflect ischemic injury, scar formation, and myocardial electrical instability. In patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), the presence of fQRS may be associated with an increased risk of early and long-term adverse cardiovascular outcomes.
Objective: To evaluate the prognostic value of fQRS in patients with STEMI who underwent PCI with respect to in-hospital mortality and major adverse cardiovascular events during long-term follow-up.
Materials and methods. A systematic search was conducted in the PubMed and Cochrane Library databases covering the period from January 1, 2010, to May 1, 2026. Prospective and retrospective observational studies of STEMI patients who underwent primary PCI were included if they reported data on in-hospital mortality and/or long-term adverse cardiovascular outcomes stratified by fQRS status. The quality of included studies was assessed using the Newcastle–Ottawa Scale. Quantitative synthesis was performed using a random-effects model to calculate the pooled odds ratio (OR) for in-hospital mortality and risk ratio (RR) for long-term outcomes. Heterogeneity was assessed using the I² statistic; the robustness of the findings was assessed by sequential leave-one-out sensitivity analysis.
Results. Nine studies comprising a total of 3,834 patients were included in the analysis. The presence of QRS complex fragmentation on ECG was associated with an increased risk of in-hospital mortality (OR 3.15; 95% CI: 1.70–5.84; p = 0.0003; I² = 65%) and adverse long-term cardiovascular outcomes (RR 3.43; 95% CI: 1.78–6.61; p = 0.0002; I² = 61%) in STEMI patients after primary PCI. Following exclusion of two outlier studies, heterogeneity for the in-hospital mortality outcome decreased (I² = 27%) while the statistical significance of the effect was maintained.
Conclusion. The results of this meta-analysis indicate an association between QRS complex fragmentation and an increased risk of in-hospital mortality and adverse long-term cardiovascular outcomes in STEMI patients who underwent primary PCI. However, the heterogeneity of results and the predominantly observational nature of the included studies necessitate cautious interpretation of the findings. Further prospective studies are warranted to clarify the prognostic value of fQRS.
ABSTRACT. Historically, the use of anticoagulant therapy (ACT) in liver cirrhosis (LC) was limited by the concept of “autoanticoagulation”. Current data support the “rebalanced hemostasis” paradigm, which posits that patients with LC are in a latent prothrombotic state and exhibit an increased incidence of venous thromboembolic complications. The practical use of ACT remains associated with altered drug pharmacokinetics, bleeding risk, and a lack of large, randomized trials. The aim of this review is to examine the evidence base, pharmacokinetic characteristics, and safety profiles of the main classes of anticoagulants, and propose algorithms for personalized ACT administration based on Child–Pugh score stratification. This article analyzes the potential use of ACT according to the degree of liver dysfunction and specifies the indications for ACT in thrombotic complications of LC. Particular attention is paid to new data (CIRROXABAN study) that indicate the potential role of factor Xa inhibitors in reducing the incidence of decompensation and modulating fibrogenesis. The choice of anticoagulant should be based on rigorous stratification using the Child–Pugh score, an assessment of clinical benefits, and comprehensive management of portal hypertension.
ABSTRACT. Influenza is a disease with systemic effects that extend beyond the respiratory tract and contribute to a wide range of extrapulmonary complications. Cardiovascular events, neurological manifestations, functional decline, progression of frailty, and metabolic disturbances are increasingly recognized as significant contributors to influenza-related morbidity and mortality, particularly among older adults and individuals with chronic medical conditions. Vaccination remains a key element of influenza prevention and is consistently associated with reductions in influenza-related morbidity, hospitalization, and mortality rates. Beyond its direct protective effects against infection, accumulating evidence suggests that the administration of seasonal influenza vaccine can provide broader health benefits, including cardiovascular protection, reduction of chronic disease exacerbations, preservation of functional status, support of healthy aging, and reduction of antibiotic use. Ongoing advances in vaccine development, including broadly protective influenza vaccines, mRNA-based platforms, improved vaccine formulations for older adults, and novel mucosal vaccination strategies, have the potential to improve protection against seasonal and emerging pandemic influenza viruses. Meanwhile, seasonal influenza vaccination coverage rates among older adults and people with chronic conditions are still much below the targeted 75%; hence increasing influenza vaccination rates remains a global public health priority. Recognizing that influenza is a multi-systemic disease and understanding the broader benefits of the vaccination against influenza in adults can help strengthen prevention strategies and reduce the global influenza burden.
Background. Glucosamine and chondroitin sulfate are widely used symptomatic slow-acting drugs for osteoarthritis; however, their efficacy remains controversial.
Objective: to evaluate the efficacy of combined glucosamine and chondroitin sulfate therapy in knee osteoarthritis through a systematic review and meta-analysis of randomized controlled trials.
Materials and methods. A systematic search of Medline, EMBASE, Cochrane Library, and PubMed databases was conducted covering 2000–2024. Eligible studies were randomized controlled trials of duration ≥8 weeks comparing glucosamine and/or chondroitin sulfate with placebo in symptomatic knee osteoarthritis. Quality was assessed with Cochrane RoB 2.0 and Newcastle–Ottawa tools. Random-effects meta-analysis (DerSimonian–Laird method) was used to calculate pooled standardized mean differences (SMD) with 95% confidence intervals.
Results. Seventeen studies (n = 6,198) were included. The mean age of participants was 60.5 ± 10.1 years; 68.6% were women. The mean treatment duration was 34.7 ± 33.3 weeks. Combined therapy was associated with statistically significant improvements versus placebo in visual analogue scale pain (SMD -0.180; 95% CI: from -0.271 to -0.089; p < 0.001; I² = 81.7%) and WOMAC function (SMD -0.170; 95% CI: from -0.254 to -0.086; p < 0.001; I² = 78.1%). The safety profile was similar to placebo. Egger’s test did not detect publication bias (p >0.10).
Conclusion. Combined glucosamine and chondroitin sulfate therapy provides statistically significant but clinically small improvements in pain and function for knee osteoarthritis. The effect size is small (SMD <0.2) but may be clinically relevant for selected patients given the favorable safety profile.
ABSTRACT. Early osteoarthritis (OA) developing in young individuals is increasingly recognized as one of the clinical manifestations of heritable disorders of connective tissue (HDCTs). In contrast to age-associated osteoarthritis, degenerative joint changes in HDCTs arise in the context of primary defects of the extracellular matrix, impaired mechanotransduction, and dysregulation of tissue-remodeling signaling pathways, particularly transforming growth factor-β (TGF-β). This review discusses the hypothesis of distinct endophenotypes of early OA in HDCTs, including a fibrotic endophenotype (predominantly associated with Marfan syndrome), and osteopenic and mixed endophenotypes, more commonly observed in hypermobility-related conditions such as the hypermobile type of Ehlers–Danlos syndrome. Particular emphasis is placed on the role of subchondral bone as an active pathogenic compartment and on TGF-β-mediated transdifferentiation of resident fibroblasts into α-smooth muscle actin (α-SMA)-positive myofibroblasts, which may promote the formation of a functionally compromised collagen matrix. Phenotypic stratification of early OA in HDCTs is considered a prerequisite for a personalized approach to diagnosis and management in this patient population.
Introduction. Long‑term outcomes after acute pulmonary embolism (PE) remain insufficiently studied. Early identification of patients at high risk for adverse events is an unresolved clinical problem.
Objective: To evaluate the dynamics of clinical, laboratory, and echocardiographic parameters in the patients at 3 months after acute PE and to identify independent predictors of adverse outcome (AO) – all‑cause death, recurrent venous thromboembolism (VTE), or chronic thromboembolic pulmonary hypertension (CTEPH) – within 12 months of follow‑up.
Materials and methods. This retrospective‑prospective observational study included 212 consecutive patients with confirmed acute PE (median age 64 years, 56.6% male). Clinical, laboratory, and echocardiographic assessments were performed at hospital discharge and after 3 months of follow‑up. Multivariable logistic regression analysis was used to identify independent predictors.
Results. An adverse outcome occurred in 47 patients (22.2%): death – 10.8%, recurrent VTE – 11.8%, CTEPH – 7.5%. In patients with a favorable outcome, the prevalence of weakness decreased from 66.9% to 33.8% at 3 months (p <0.001), whereas in the AO group weakness persisted in 75% (p < 0.001 for between‑group difference). Over the 3‑month period, the AO group showed a decrease in estimated glomerular filtration rate (Δ -9.5 ml/min/1.73 m², p = 0.007), no increase in haemoglobin (p = 0.044), an increase in right ventricular size (Δ +2.1 mm, p = 0.037), and no reduction in systolic pulmonary artery pressure (SPAP) (between‑group p <0.001). Independent predictors of adverse outcome were: persistence of weakness at 3 months (OR 3.63, 95% CI: 1.41–9.38, p = 0.008), an increase in right ventricular size per 1 mm (OR 1.15, 95% CI: 1.05–1.26, p = 0.004), and lack of SPAP reduction per 1 mmHg (OR 1.05, 95% CI: 1.01–1.10, p = 0.010). Weakness persisting at 3 months likely reflects reduced exercise tolerance. The identified predictors make it possible to identify a high‑risk group already at an early stage of outpatient follow‑up.
Conclusion. Patients with persistent weakness, absence of regression of pulmonary hypertension, and right ventricular enlargement require dynamic follow‑up.
Background. As is known, the issue of maintaining a balance between the efficacy and safety of anticoagulant therapy in patients with atrial fibrillation causes a number of difficulties in real clinical practice. In recent years, the development and clinical validation of sensitive and selective methods for quantitative determination of direct oral anticoagulant levels in the blood have demonstrated their relevance for optimizing drug monitoring in patient groups at increased risk of thromboembolic and hemorrhagic complications.
Objective: To develop a method for determining the concentration of apixaban (APX) in peripheral blood using a voltammetric sensor based on phenyl-modified graphite.
Materials and methods. The experimental basis of this study was the development of a new method for modifying a graphite electrode for the voltammetric determination of APX using domestic equipment and readily available reagents. A graphite electrode modified with phenyl groups using arenediazonium tosylates was used. The degree of modification was monitored instrumentally. The electrode surface was characterized using the ζ-potential (streaming potential) method. Electrode process characteristics (adsorption stage, electron fraction in the rate-limiting stage, and the αn factor) were determined using voltammetric peak shape analysis and the Laviron equation. Operating conditions for APX determination were selected.
Results. It was established that the anodic oxidation of APX on the surface of phenylated graphite is adsorption-based. The αn factors were calculated for the rate-limiting step (≈1.5) and for the overall electrode process (≈2). The flow potential method revealed an increase in the cathodic ζ-potential of the modified electrode, indicating an increase in its adsorption capacity. The following parameters were selected: analyte accumulation conditions; voltammogram recording mode; background electrolyte composition.
Conclusion. A new method for modifying a graphite electrode has been developed, enabling reliable monitoring of its properties. The modification has been shown to increase the surface’s adsorption capacity for APX. Operating parameters for its voltammetric determination have been selected. The method utilizes domestically produced equipment and readily available reagents, making it promising for clinical monitoring of anticoagulant therapy.
ABSTRACT. Systemic sclerosis (SSc) is a rare systemic autoimmune disease of connective tissue characterized by a markedly heterogeneous clinical course and multiorgan involvement. The etiology of the disease is considered the result of a complex interaction between exogenous trigger factors and a genetic predisposition. Viral and bacterial infections, occupational hazards (exposure to silica dust, chemicals), and exposure to cold are discussed in the current literature as potential triggers. Along with studying these external factors, in recent years, scientists have focused on identifying new genetic markers for the development of SSc. An analysis of current data on the genetic basis of predisposition to SSс and the mechanisms of its development was conducted based on a review of literature data for the period from 2010 to 2026. A search for relevant sources was conducted in the international databases PubMed, Scopus, Web of Science, as well as in the Russian scientific electronic library eLibrary.ru.
Introduction. Chronic kidney disease (CKD) develops as an outcome both of immune-mediated glomerulonephritides and predominantly metabolic or hemodynamic nephropathies. Despite differences in etiology, common pathogenetic mechanisms are involved in CKD progression, including metabolic disturbances, immune inflammation, and development of glomerulosclerosis.
Objective: To determine the contribution of immune and non-immune (hemodynamic and metabolic) mechanisms to the development of chronic kidney disease (CKD).
Materials and methods. A single-center retrospective analysis of 119 patients with CKD who underwent kidney biopsy was performed. Based on the totality of clinicopathological features (type of glomerulopathy, pattern of immune deposits), patients were divided into two groups: predominantly immune-mediated lesions (n = 72) and predominantly non-immune lesions (n = 47). Clinical and laboratory parameters, 24-hour proteinuria, urinalysis data, as well as morphological indices of inflammatory activity and glomerulosclerosis were analyzed.
Results. In the overall cohort, the presence of arterial hypertension was associated with higher 24-hour proteinuria, increased blood urea and creatinine levels, and reduced estimated glomerular filtration rate (eGFR); patients also had more pronounced interstitial infiltration and a higher degree of glomerulosclerosis. Metabolic syndrome, diabetes mellitus, and obesity were accompanied by increased 24-hour proteinuria and thickening of the glomerular basement membranes, but were not associated with eGFR. In patients with predominantly non-immune lesions, the presence of immune deposits on immunofluorescence and high morphological inflammatory activity were associated with more pronounced eGFR decline, azotemia, electrolyte disturbances, greater proteinuria, and anemia. In the group with predominantly immune-mediated lesions, CKD severity was determined mainly by the degree of glomerulosclerosis and the presence of arterial hypertension, whereas indices of morphological inflammatory activity were not associated with nitrogen-excreting kidney function.
Conclusion. In the progression of CKD in patients with biopsy-proven nephropathies, arterial hypertension, the extent of glomerulosclerosis, and inflammatory activity in renal tissue play a key role. For predominantly non-immune nephropathies, immune deposits and high morphological inflammatory activity are of greatest importance, whereas in predominantly immune glomerulopathies CKD severity is largely determined by chronic changes (glomerulosclerosis) and the presence of hypertension.
ABSTRACT. This article presents a clinical observation illustrating the differential diagnosis between the true combination of B12-deficiency pernicious anemia (PA) and autoimmune hemolytic anemia and the phenomenon of “pseudo-hemolysis.” A 71-year-old female patient with verified PA against a background of autoimmune atrophic gastritis and concomitant autoimmune thyroiditis was found to have macrocytic anemia, hyperbilirubinemia, elevated lactate dehydrogenase (LDH), and a positive direct Coombs test (DAT) with negative anti-erythrocyte antibodies. The key criterion was the reticulocyte production index (RPI = 1.38), indicating ineffective erythropoiesis characteristic of PA rather than true hemolysis. Cyanocobalamin monotherapy caused a reticulocyte crisis, decreased LDH and bilirubin, and increased hemoglobin, confirming the false-positive nature of the DAT. The authors conclude that a positive Coombs test in PA does not require the administration of glucocorticosteroids; correct interpretation allows avoiding unnecessary immunosuppression.
Introduction. The theory of mucosal development of rheumatoid arthritis (RA) is of considerable interest in relation to the search for unconventional predictors of RA progression, among which Chlamydia trachomatis (C. trachomatis) occupies a special place.
Objective: To study the effect of C. trachomatis on early and late outcomes of RA, as a potentially unfavorable predictor of the disease course.
Materials and methods. The study included 106 patients with a confirmed diagnosis of RA, lasting up to one year, without basic therapy. Patients were examined for the presence of C. trachomatis by PCR and ELISA and divided into two groups. The first (n = 69) included patients with C. trachomatis, the second (n = 37), patients without it. Clinical and laboratory parameters and markers of disease activity were assessed in the groups. The control group consisted of 34 healthy volunteers. The group of C. trachomatis+ patients was divided into two subgroups. The first consisted of patients (n = 30) with a course of antibacterial therapy (AB); the second, without AB therapy (n = 39). In both subgroups, the chances of development/non-development of short-term (12 months) and long-term (5; 10; 15 years) outcomes were assessed.
Results. Patients with RA with C. trachomatis were characterized by longer morning stiffness (49.1 [0.0; 102.0] vs. 14.9 [0.0; 27.2]; p = 0.043), CRP level (14.0 [0.5; 17.0] vs. 9.0 [5.0; 16.0]; p = 0.046). Eradication of C. trachomatis increased the chance of clinical and laboratory remission / low activity at 12 months of follow-up by 3.9 time (OR 3.9; 95% CI: 1.4–10.9; p = 0.009); and functional remission according to HAQ-DI by 4.3 times (OR 4.3; 95% CI: 1.4–13.5; p = 0.011) after 10 years; 8.1 times higher chance of not developing hand/foot deformities by the 5th year of observation (OR 8.1; 95% CI: 1.1–59.1; p = 0.039).
Conclusion. C. trachomatis can be considered an additional unconventional predictor of an unfavorable course of RA, the effect of which is apparently carried out indirectly through other arthritogenic factors.
Background. Psychosocial factors, including anxiety and depressive symptoms, significantly influence the risk of developing cardiometabolic diseases and treatment adherence. The early diagnosis of these conditions in young individuals is a promising direction for primary prevention programs.
Objective: To evaluate the association among anxiety, depression, and behavioral cardiometabolic risk factors among university students.
Materials and methods. A cross-sectional study (survey) was conducted on 3296 students (22.7% male, 77.3% female; median age 21.0 years) from 19 universities across 16 Russian cities. The HADS scale was used to assess psychosocial status, while the CINDI (smoking, nutrition and alcohol) and IPAQ (physical activity) questionnaires were used to evaluate lifestyle factors.
Results. The prevalence rates of anxiety and depression were 48.3% and 32.6%, respectively. Anxiety was significantly more frequent in women (52.4% vs. 34.6% in men; p < 0.001). Multivariate analysis showed that the risk of anxiety was associated with active smoking (odds ratio [OR] 1.53; 95% confidence interval [CI]: 1.24–1.88), alcohol consumption (OR 1.66), low physical activity (OR 1.22), and suboptimal nutrition (OR 1.39). The risk of depression was associated with low physical activity (OR 1.47) and suboptimal nutrition (OR 1.44).
Conclusion. A high prevalence of anxiety and depression was identified in the youth population, showing independent associations with modifiable cardiometabolic risk factors.
ABSTRACT. Early, adequate cardiovascular risk stratification as part of primary prevention is most justified in young and middle-aged individuals due to its maximum clinical benefits. An analysis of the main actual risk assessment tools designed to identify and correct cardiovascular risk factors in the 20–59 age group is performed. The majority of existing risk assessment systems are most effective within the population groups for which they were developed; their informativeness decreases when used in other populations, even after calibration based on current morbidity and mortality rates. Furthermore, significant differences can be observed in the structure and predictive value of cardiovascular risk factors in age cohorts under and over 40 years. Despite the potential of artificial intelligence and machine learning to improve the accuracy of risk stratification for any age group, the widespread implementation of these methods is limited by the lack of sufficient evidence of their clinical superiority over traditional approaches to personalized prognosis in primary prevention. A solution to this problem may lie in validating existing risk stratification models for target patient groups, as well as increasing their informativeness by expanding the set or varying the range of cardiovascular risk markers. It is also important to consider the availability of assessment methods in clinical practice, particularly in primary healthcare.
ABSTRACT. The present clinical case demonstrates a rare variant of acute coronary syndrome, in which the most likely mechanism of myocardial ischemia was extrinsic compression of a coronary artery by an intrapericardial mass with magnetic resonance imaging features of a teratodermoid tumor. A 47-year-old woman was admitted with clinical signs of acute coronary syndrome with ST-segment elevation. Echocardiography revealed regional left ventricular wall motion abnormalities and a mass in the pericardial cavity adjacent to the anterior and anterolateral walls of the left ventricle. Contrast-enhanced cardiac magnetic resonance imaging showed a well-defined heterogeneous mass measuring 33 × 43 × 41 mm with features consistent with a teratodermoid lesion. The differential diagnosis included cardiac and pericardial tumors, metastatic disease, and visceral syphilis. The patient refused biopsy for morphological verification of the mass, as well as surgical treatment. During four years of follow-up, clinical deterioration associated with progression of chronic heart failure was observed. Thus, this case demonstrates a rare “non-classical” cause of the clinical presentation of “classical” acute coronary syndrome and is intended to broaden physicians’ understanding of the etiology of myocardial ischemia.
