Aim. To determine the associations between adverse pregnancy outcomes (APOs) and the presence of heart failure with preserved ejection fraction (HFpEF) in middleaged women.

Material and methods. The study included 102 women aged 45-59 years with a history of at least one completed pregnancy. The examination protocol involved transthoracic echocardiography, with a diastolic stress test when indicated, measurement of NT-proBNP levels, and structured interviews to obtain a history of APOs. Intergroup differences in cardiac structure and function were analyzed, along with associations between APOs and different HFpEF stages.

Results. More advanced HFpEF stages in middle-aged women are associated with more pronounced alterations in cardiac morphofunctional parameters and a higher prevalence of hypertension and proteinuria in their pregnancy history. The heart failure risk factor stage (Stage A) showed no statistically significant associations with APOs (p>0.05). Pre-heart failure (Stage B) was associated with hypertension (odds ratio, OR 3.57 (1.43-8.88), p=0.006), proteinuria (OR 4.92 (1.29-18.84), p=0.02), and preterm birth (OR 3.65 (1.20-11.11), p=0.022). Stage 1 HFpEF (Stage C) was linked to hypertension (OR 3.81 (1.08-13.39), p=0.037) and smoking (OR 4.46 (1.09-18.2), p=0.038) during pregnancy. Women with a history of hypertension during pregnancy exhibited higher blood pressure, greater prevalence of hypertension, diabetes mellitus, signs/symptoms of heart failure, worse echocardiographic parameters, and a higher rate of diastolic dysfunction (37.9% vs. 14.9%, p=0.03) in middle age compared to those without hypertensive disorders of pregnancy.

Conclusion. A history of hypertension, proteinuria, and smoking during pregnancy is associated with various HFpEF stages in the long term. Middle-aged women with a history of gestational hypertension are characterized by more pronounced alterations in cardiac morphofunctional parameters.

Aim: To identify predictors of acute kidney injury (AKI) after coronary artery bypass grafting (CABG) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS).

Material and methods. The study included patients with NSTE-ACS and multivessel coronary artery disease, for whom the cardiac team determined indications for CABG. Initially, during the first 7 days after CABG and prior to discharge from the hospital, creatinine levels in the blood were measured using the Jaffe method (Synchron CX Systems, USA), and the initial levels of N-terminal pro-brain natriuretic peptide (Nt-proBNP) were examined using an immunochemical method (Elecsys, Roche). Chronic kidney disease (CKD) was diagnosed if the glomerular filtration rate (GFR) was less than 60 ml/min/1,73 m². GFR was calculated using the CKD-EPI formula. CABG was performed either on a "beating heart" or under conditions of artificial circulation. AKI was diagnosed according to KDIGO criteria (2012). In-hospital complications of CABG including AKI, intraoperative myocardial infarction (MI), bleeding, multiple organ failure and cardiac deathwere recorded. The cumulative incidence rate of in-hospital complications, including thoselisted, was calculated, taking into account the first occurrence of the event.

Results. We examined 70 patients with NSTE-ACS, 32,9% of whom had MI. The mean age was 65 years, and 77,1% of the patients were men. They had multivessel coronary artery disease. All patients had arterial hypertension, 31,4% had type 2 diabetes mellitus, and 17,1% had CKD. The initial Nt-proBNP level was 168 (54-902) pg/ml. After CABG, AKI developed in 15 (21,4%) patients, with stage 1 AKI occurring in 17,1%, and stage 2 and 3 in 4,1%. Parameters associated with the development of postoperative AKI included a higher incidence of stages 3 and 4 CKD (p=0,05), an initial left ventricular ejection fraction < 50% (p=0,031), intraoperative MI (p=0,036), the use of adrenaline to stabilize hemodynamics (p=0,001), and a higher initial Nt-proBNP level (909, 278-1394 pg/ml, p=0,011). Nt-proBNP was found to be a predictor of AKI after CABG. A level above the median value of 900 (278-1394) pg/ml increased the likelihood of AKI development by an average factor of 9,0 times. Patients with AKI after CABG showed a tendency toward a higher cumulative incidence of in-hospital complications compared to those without AKI (40% and 16,4%, respectively, p=0,05).

Conclusion. The incidence of AKI after CABG in patients with NSTE-ACS was 24,1%. On average, the likelihood of developing AKI after CABG was 9,0 times higher for patients with an initial Nt-proBNP level above the median value (900, 278-1394 pg/ml). Patients who developed AKI after CABG were more likely to experience adverse in-hospital complications than those without postoperative AKI.

Aim. To develop a software package that predicts the presence of significant stenosis of the left main coronary artery (LMCA) in patients with stable coronary artery disease (CАD) based on clinical and instrumental signs using machine learning (ML) methods.

Material and methods. The study included 208 patients with stable CAD, hospitalized for planned invasive coronary angiography (ICA). Based on the results of ICA, two groups of patients were identified: the main group - 104 patients with hemodynamically significant stenosis of the LMCA and the control group - 104 patients without obstructive lesions of the coronary arteries. Stenosis of the LMCA of more than 50% was considered significant. Based on the study of case histories, an Excel database was created containing information on 107 clinical and instrumental features of all patients. Based on the results of a preliminary significance analysis, 63 potentially important features were selected for further use in the classifier model. Then, 59 of the most important features from the point of view of ML were identified. Given the nature of the features under consideration, gradient boosting was chosen as the ML algorithm. The programs developed during the study were written in the Python programming language in the PyCharm integrated programming environment.

Results. Based on the most informative features, models for predicting LMCA damage in patients with CAD were constructed. Gradient boosting was determined as the optimal ML algorithm. Three of its implementations were considered: LightGBM (Light Gradient Boosting Machine), XGBoost (Extreme Gradient Boosting) and CatBoost (Categorical Boosting). The CatBoost model turned out to be the most effective for classifying the presented objects. The software package using the CatBoost model demonstrated the accuracy of the classifier prediction of 86.2% on the test data set with a sensitivity and specificity of 77% and 76.9%, respectively. According to the constructed learning curves, it was found that further expansion of the training data volume will improve the quality of the model.

Conclusion. The developed software package for identifying hemodynamically significant stenosis of the LMCA in patients with CAD has good prognostic accuracy with the prospect of further training. The obtained solution can be integrated into the diagnostic process as part of an application for a personal computer or a web interface in order to provide support for medical decision-making.

Aim. To evaluate the impact of arterial stiffness and targeted therapy (biologic drugs and Janus kinase inhibitor) during the acute phase of coronavirus disease 2019 (COVID-19) on the risk of post-COVID syndrome (PCS). The rationale for the study is the high prevalence of PCS and the insufficient knowledge of factors influencing its development, especially in the context of using modern biologic drugs.

Material and methods. The prospective observational study included 129 adult patients (55% women) hospitalised with a confirmed diagnosis of COVID-19. The mean age was 59.16±13.38 years. Upon admission, all participants underwent measurement of the cardio-ankle vascular index (CAVI) to assess arterial stiffness. Data on the acute course of illness and clinical status during the 6-month follow-up after discharge were obtained from electronic medical records. PCS was diagnosed according to WHO criteria. Univariable and multivariable logistic regression analyses were performed to identify independent predictors of PCS, with odds ratios (ORs) and 95% confidence intervals (CI) calculated. Results. PCS was diagnosed in 33.3% of patients. The most common PCS symptoms were fatigue (20.2%), headache (10.9%), shortness of breath (10.1%), palpitations (9.3%), and dizziness (8.5%). Univariate analysis revealed significant association with PCS development for age, arterial hypertension (AH), level of systolic blood pressure (SBP) at admission, elevated CAVI index (≥ 9.5), and glomerular filtration rate (GFR). The multivariate regression model confirmed the independent status of three predictors: elevated CAVI index (OR 3.533; 95% CI 1.242-10.047; p=0.018) and SBP level at hospitalization (OR 1.053; 95% CI 1.016-1.091; p=0.004) were associated with an increased risk of PCS. At the same time, the use of targeted drugs (levilimab, olokizumab, baricitinib) during the acute phase of COVID-19 significantly reduced the likelihood of developing PCS (OR 0.276; 95% CI 0.104-0.734; p=0.010), which corresponds to a 3.62-fold reduction in odds.

Conclusion. Increased arterial stiffness (CAVI ≥9.5) and elevated systolic blood pressure at hospitalisation are independent predictors of PCS, supporting a key role of vascular dysfunction in its pathogenesis. Targeted therapy administered during the acute phase of COVID-19 was associated with a protective effect against PCS, possibly through attenuation of cytokine-driven inflammation and prevention of prolonged endothelial injury. These findings support the potential value of targeted therapy not only for improving acute COVID-19 outcomes but also for reducing long-term adverse outcome, and underscore the importance of monitoring and managing vascular risk factors in COVID-19 survivors.

Aim. To study the clinical phenotypes of the right ventricular-pulmonary artery coupling (RV-PA coupling) and prognostic features in patients with pulmonary hypertension associated with ischemic chronic heart failure (PH-iCHF).

Material and methods. A total of 69 stable patients with PH-iCHF and different left ventricular ejection fractions (LVEF) were examined. PH was defined as an increase in systolic pulmonary artery pressure (sPAP) above 30 mm Hg according to transthoracic echocardiography. The probability of PH was compared to the number of confirmed PH cases. The prevalence of PH-iCHF among CHF patients was established. Correlation between RV-PA coupling and LVEF was assessed. Clinical phenotypes were based on RV-PA coupling values as the tricuspid annular plane systolic excursion (TAPSE) and sPAP ratio. Adverse outcomes such as all-cause mortality and hospitalizations due to CHF decompensation over a follow-up period of 13.2±0.9 months were analyzed.

Results. PH-iCHF occurred in 3.3% of CHF cases. sPAP above 30 mm Hg corresponded to 34.8% of patients with high probability of PH. For every 10% increase in LVEF, there was a corresponding increase in RV-PA coupling by 0.096 mm/mmHg. Based on the severity of RV-PA dissociation, three clinical phenotypes were formed: severe (<0.28 mm/mmHg), moderate (≥0.28 and ≤0.47 mm/mmHg) and mild (>0.47 mm/mmHg). Severe RV-PA dissociation was more frequently characterized by significant clinical manifestations (lower limb edema in 53%, ascites in 21% of cases), poor functional state (PH functional class III in 79% of cases), low exercise tolerance (six-minute walk test distance 267.2±107.4 m) and prolonged hospital stays (9.9±4.9 bed-days). High probability of PH was present in 67% of cases with severe RV-PA dissociation. There was no difference in time-to-adverse-outcome across clinical phenotypes. Predictors of adverse prognosis included RV-PA coupling ≤0.47 and ≤0.28 mm/mmHg, sPAP ≥40 mmHg, TAPSE ≤18 mm, right atrial area ≥18 cm², and transverse diameter of right ventricle ≥3.5 cm.

Conclusion. The RV-PA coupling provides additional characteristics of clinical and functional status and identifies early adverse outcomes in patients with PH-iCHF.

Aim. To assess the prevalence of inappropriate prescribing (IP) in patients with cardiovascular diseases and concomitant non-cardiac multimorbidity using data from an outpatient registry.

Material and methods. The study sequentially included patients aged over 50 years with cardiovascular diseases and at least one concomitant non-cardiac condition requiring drug therapy. Patients completed original questionnaires regarding their medication therapy. Prescriptions were evaluated for inappropriateness based on their compliance with the official Summary of Product Characteristics (SmPC), clinical practice guidelines, and contemporary criteria for inappropriate prescribing.

Results. The study included 300 patients (120 men and 180 women). Patients had 2 to 11 comorbidities, with a median (Me) of 5 [4;6]. A total of 2961 medications were prescribed; 2071 prescriptions (69.9%) were classified as IP. At least one IP was identified in 99% of patients, Me 6 [4;9] per patient. The most common categories of IP were: misprescribing — 32% (of which more than half were combinations with potentially harmful drug-drug interactions), underprescribing — 20.1%, and overprescribing — 14%. Two additional types of IP were identified: “careless prescribing” (prescriptions lacking essential information such as dosage, frequency, or administration instructions), accounting for 18.5% of IPs, and “delegated prescribing” (cases where the physician transferred the responsibility for therapeutic decisions to the patient), accounting for 13.9% of IPs. The proportion of IP increased significantly with the total number of prescribed drugs. Of the 103 identified inappropriate drug combinations, 61% were prescribed by a single physician, while 38.4% resulted from uncoordinated prescribing by multiple physicians.

Conclusion. The prevalence of IP in patients with cardiovascular diseases and non-cardiac multimorbidity was substantial, at 70% of all prescriptions, consistent with rates in comparable international studies. Misprescribing was the predominant type of IP, with potentially harmful drug-drug interactions being the most common issue, accounting for 19.0% of all inappropriate prescriptions.

The objective of this review is to analyze publications about biochemical studies of inflammasome profile proteins in patients with heart failure as diagnostic markers and promising therapeutic targets. Inflammasomes are cytoplasmic high-molecular protein complexes, which activation leads to the development of inflammation through the release of proinflammatory cytokines. The most studied types of inflammasomes are NLRP3 inflammasomes, which contribute to the development of systemic and local inflammation, including in the myocardium. The NLRP3 inflammasome comprises the receptor/sensor protein NLRP3 (nucleotide-binding leucine-rich repeat receptor pyrin domain-containing-3), the adaptor protein ASC (apoptosis-associated speck-like protein containing CARD), and the effector protein caspase-1. The NLRP3 receptor protein, as a structural component of the NLRP3 inflammasome, functions as an intracellular pattern-recognition receptor that detects pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs, molecules from damaged cells). Activation of this receptor triggers the assembly of the NLRP3 inflammasome, leading to the release of interleukin-1β and interleukin-18. The article presents data on studies of inflammasome profile biomarkers and the possibility of their use in order to improve diagnostics, prognosis and personalisation of treatment of heart failure. The accumulated data of clinical and experimental studies convincingly indicate the necessity for further comprehensive analysis of inflammasome profile proteins in patients with heart failure.

Aim. To analyze published clinical trials, to assess the effectiveness of early initiation of sodium-glucose cotransporter 2 (SGLT-2) inhibitors in preventing cardiovascular events and all-cause mortality in patients with acute coronary syndrome.

Material and methods. The meta-analysis was performed in accordance with PRISMA guidelines based on a literature search of the PubMed/MEDLINE database for the period from 2021 to July 7, 2025. Keywords included the MeSH terms “sodium–glucose co-transporter 2 inhibitors” OR “SGLT2” OR “empagliflozin” OR “dapagliflozin” OR “canagliflozin” OR “sotagliflozin” AND “myocardial infarction” OR “acute coronary syndrome”. The ROBIS-I and RoB2 tools were used to assess the risk of bias in the included studies.

Results. The initial search strategy identified 13,879 publications. After excluding records that did not meet the inclusion criteria, 15 studies with no exclusion criteria were included in the analysis. The meta-analysis included 118,332 patients from 15 studies (54,853 patients received SGLT-2 inhibitors, 63479 were included in the control group). The results showed that patients with acute coronary syndrome treated with SGLT-2 inhibitors had a 39% lower rate of all-cause mortality (OR=0.61, 95% CI=0.46-0.81, p=0.006) and a 32% lower rate of hospitalisation for heart failure (HR=0.68, 95% CI=0.54-0.86, p=0.001) compared with patients who did not receive this group of drugs. When divided into groups that included only patients with type 2 diabetes mellitus and patients with and without type 2 diabetes mellitus, a decrease in all-cause mortality and the number of hospitalizations due to heart failure was achieved only in the group of patients with type 2 diabetes mellitus (OR=0.43, 95% CI=0.31-0.59, p<0.001 and HR=0.63, 95% CI=0.48-0.82, p<0.001, respectively). While in studies in which type 2 diabetes was not a mandatory inclusion criterion or was an exclusion criterion, SGLT-2 inhibitors were not associated with a decrease in both deaths from all causes (OR=0.77, 95% CI=0.55-1.09, p=0.14) and the number of hospitalisations due to the cause of heart failure (HR=0.77, 95% CI=0.52-1.14, p=0.19). Patients who received SGLT-2 inhibitors for one reason or another before the onset of acute coronary syndrome had a more pronounced reduction in both the risk of death from all causes (OR=0.36, 95% CI=0.29-0.45, p<0.001) and hospitalisation due to heart failure (HR=0.47, 95% CI=0.24-0.89, p=0.02) than patients who started SGLT-2 inhibitors during hospitalisation due to acute coronary syndrome (OR=0.73, 95% CI=0.55–0.97, p=0.03 and HR=0.67, 95% CI=0.53-0.86, p=0.001, respectively). SGLT-2 inhibitors did not reduce the risk of death from cardiovascular causes (HR=0.98, 95% CI=0.80-1.21, p=0.86), nonfatal stroke (HR=0.98, 95% CI=0.93-1.03, p=0.44).

Conclusion. Our meta-analysis shows that in patients with acute coronary syndrome, SGLT-2 inhibitors treatment is associated with a reduced risk of death from all causes and hospitalisation due to heart failure, mainly in the group of patients with type 2 diabetes mellitus, but does not affect death from cardiovascular causes.

Among the important psychosocial risk factors (RFs) for cardiovascular disease (CVD), loneliness and social isolation hold a special place. The prevalence of these RFs is increasing among people of all ages due to social, cognitive, and behavioral factors. However, in clinical practice, there is a lack of a thorough understanding of the distinctive characteristics of loneliness and social isolation, their causes, and their negative consequences for the development of CVDs, such as hypertension, atherosclerosis, and many others, including endothelial dysfunction.

Loneliness and social isolation are associated with a higher risk of CVD regardless of sex, as confirmed by various meta-analyses. There are conflicting data regarding the impact on mortality. Some national cohorts have shown an increased risk of cardiovascular mortality in conditions of loneliness, while in others this relationship has not been confirmed due to cultural differences. Social isolation increases the risk of death from coronary heart disease and stroke indirectly through sympathetic nervous system activation, chronic inflammation, and unhealthy behaviour (smoking, sedentary lifestyle and poor diet).

Loneliness and social isolation are significant underlying psychosocial risk factors, requiring regular screening using validated scales.

This review examines the role of programmed cell death in the pathogenesis of obesity and associated conditions. It provides the comprehensive examination of the key mechanisms of apoptosis and NETosis in the context of the pathogenesis of obesity and associated metabolic diseases, particularly type 2 diabetes mellitus, dyslipidemia, and metabolic dysfunction-associated steatotic liver disease (MASLD). One of the key consequences of excessive adipose tissue accumulation in obesity is chronic low-grade inflammation. The development of a proinflammatory state, the resulting cellular stress, and mitochondrial dysfunction contribute to the activation of signaling pathways that trigger programmed cell death. Apoptosis of adipocytes, cardiomyocytes, endothelial cells, pancreatic β-cells, and hepatocytes is mediated by an imbalance of proand antiapoptotic proteins of the Bcl-2 family and caspase activation and is implicated in the development of MASLD, type 2 diabetes mellitus, diabetic cardiomyopathy, and endothelial dysfunction. Studies of potentially protective molecules (apelin-13, agomelatine) and triggers are described. NETosis plays a key role in maintaining inflammation, endothelial dysfunction, and the development of thrombotic complications in obesity. Increased activity of NETosis markers, myeloperoxidase and neutrophil elastase, correlates with the severity of obesity, MASLD, and microvascular complications, while their inhibition restores endothelial function in preclinical models. Thus, key molecular factors and signaling pathways of apoptosis and NETosis are significant components in the pathogenesis of obesity and associated diseases. Studying the mechanisms of programmed cell death is a promising area in the context of the search for potential therapeutic targets for these diseases.

Aim. To summarize the available data on the effects of first-line antihypertensive agents – angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) – on serum uric acid (UA) levels in adults with (arterial hypertension) AH, with the goal of optimizing pharmacotherapy in patients with AH and asymptomatic hyperuricemia.

Material and methods. A comprehensive search was conducted in PubMed, the Cochrane Central Register of Controlled Trials (CENTRAL) within the Cochrane Library, eLIBRARY, Google Scholar, and the National Institutes of Health clinical trials registry ClinicalTrials.gov. The systematic review was prepared in accordance with PRISMA guidelines. No restrictions were placed on the year of publication during the search and analysis.

Results. Analysis of nine randomized controlled trials of ACEIs showed that enalapril, captopril, and fosinopril demonstrated neutrality with respect to UA levels, whereas other drugs in this class may increase UA concentrations. Analysis of eleven randomized controlled trials of ARBs showed that only losartan exhibits a uricosuric effect, while irbesartan, valsartan, and eprosartan are metabolically neutral.

Conclusion. Among ACEIs, enalapril, low-dose ramipril, and fosinopril exhibit the most favorable safety profile and the greatest neutrality regarding UA levels. ARBs are generally metabolically neutral with respect to UA, with the exception of losartan, which possesses a uricosuric effect.

The simultaneous detection of atrial fibrillation (AF) and left ventricular (LV) dysfunction raises questions about their relationship and necessitates a nosological diagnosis. This case study presents a 39-year-old patient who has had recurrent AF and moderate LV systolic dysfunction. Concomitantly, the patient has experienced sinus bradycardia, a transient left bundle branch block (LBBB), and prolonged QTc, which precluded the use of antiarrhythmic medication. In 2018, successful radiofrequency ablation (RFA) for paroxysmal AF was performed. However, in 2023, the patient experienced anginal pain, with a reduced ejection fraction to 26%, and persistent AF. After cardioversion, LV dysfunction persisted, and a myocardial biopsy revealed active, virus-negative, lymphocytic myocarditis (LM). The patient was prescribed immunosuppressive therapy, including corticosteroids and azathioprine. Despite recurrent tachyarrhythmic AF, LV dysfunction regressed. A epeat RFA was performed in 2024 but was clinically unsuccessful. Whole-exome sequencing revealed a variant in the RBM20 gene, suggesting that investigating the etiology of AF in patients with LV dysfunction may improve the efficacy of AF treatment and influence the course and outcomes of the underlying disease, which can be obscured by the diagnosis of «idiopathic» AF.

Obesity and dyslipidemia are the most important components of cardiometabolic risk, formed against the background of complex pathophysiological interactions between visceral adipose tissue, lipid and carbohydrate metabolism, as well as endocrine regulation. In this review, we present current data on the relationship between obesity and atherogenic dyslipidemia, as well as systematic information on the clinical and metabolic efficacy of glucagon-like peptide-1 (arGPP-1) receptor agonists, in particular semaglutide, in overweight, obese and associated lipid metabolism disorders. The mechanisms of action of arGPP-1 in the correction of dyslipidemia are considered, the effect on lipid profile parameters and the potential of the drug in managing the risk of cardiovascular diseases are evaluated. Data from randomized controlled trials (including SELECT, SUSTAIN, STEP, PIONEER), meta-analyses, retrospective observational studies, and experimental studies were analyzed. It should be noted that long-term use of the drug semaglutide contributes to a decrease in body weight by 10-15% over 68 weeks of therapy. Based on the presented data, a significant positive effect of the use of semaglutide in relation to the correction of lipid profile parameters was noted. The mechanisms include suppression of lipogenesis, activation of lipolysis, and slowing gastric emptying. The drug reduces the levels of atherogenic lipid fractions — triglycerides (TG) by 12-18%, low-density lipoprotein cholesterol (LDL) by 5-7% and very low-density lipoprotein cholesterol (VLDL) by 21% — both on an empty stomach and in the postprandial period. In addition, the use of arGPP-1 is associated with a 20% reduction in the risk of serious adverse cardiovascular events in patients with obesity and cardiovascular diseases. The advantage of arGPP-1 use is not only in reducing body weight, but also in correcting dyslipidemia was shown, with prospects for its use as part of comprehensive, personalized strategies for the prevention and treatment of cardiometabolic disorders.