Modern cardiology is entering a phase where improving the prevention, diagnosis, and treatment of cardiovascular diseases (CVD) necessitates a deeper understanding of the underlying biological mechanisms. The traditional clinical model, relying primarily on analysis of risk factors and phenotypic presentation, is limited in its ability to account for the biological heterogeneity and individual progression of CVD. Advancements in systems biology, molecular medicine, and multiomics technologies allow for viewing CVD as a long-term dynamic biological process that begins well before clinical manifestation. Genomic, proteomic, and metabolomic research is uncovering the molecular and metabolic phenotypes that dictate individual vulnerability of the cardiovascular system, disease progression rates, and variability in therapeutic response. Among multiomics approaches, metabolomics is uniquely positioned to reflect the real-time functional state of biological systems, capturing the interplay between genetic, metabolic, and environmental factors. By identifying early biological signals of disease progression, metabolomic profiling enables precise risk stratification and personalized preventive and therapeutic interventions. Integrating these multiomics insights with clinical data, imaging, and digital monitoring establishes a new paradigm in clinical cardiology: biologically-oriented medicine. Given the high complexity of biological data, artificial intelligence and machine learning methods are essential for uncovering latent correlations between molecular and clinical variables, ultimately enhancing personalized clinical decision support. The transition toward biologically-oriented cardiology carries profound scientific, clinical, and socioeconomic implications. By identifying adverse biological traits early and utilizing personalized prevention of complications, we can substantially reduce the burden of CVD on healthcare systems and society. Ultimately, multiomics and metabolomics are establishing the scientific foundation for a new clinical paradigm focused on early detection of biological risk signals, precise patient phenotyping, and personalized treatment of CVD.

Aim        To determine and compare myocardial strain parameters for the left ventricle (LV), left atrium (LA), and right ventricle (RV) in healthy individuals using speckle-tracking echocardiography (STE) across equipment from two different manufacturers.

Material and methods    The study included 30 subjects with no known cardiovascular disease at the time of enrollment. Transthoracic echocardiography (TTE) was performed on all participants on the same day within a single hour by the same experienced clinician, using two ultrasound systems from different manufacturers sequentially. To evaluate chamber strain, dedicated cine loops were recorded for the LV, LA, and RV. The following parameters were analyzed: LV global longitudinal systolic strain and segmental longitudinal strain (17-segment model); LV radial and circumferential strain; RV free wall global and segmental longitudinal strain; and LA strain during the reservoir, conduit, and contractile phases.

Results. The longitudinal strain values for the LV, RV, and LA obtained via STE in healthy individuals using software from two different manufacturers fell within the established normal ranges. A comparison of the strain metrics between the two software packages revealed significant differences in regional longitudinal systolic strain in 6 out of 17 LV segments, 1 out of 3 RV free wall segments, as well as in LV radial and circular strain, and LA global longitudinal strain during the contractile phase. Bland-Altman analysis demonstrated a mean bias exceeding 1 and wide confidence intervals for the metrics across the two software platforms.

Conclusion         The longitudinal strain values for the LV, RV, and LA obtained via STE in healthy individuals fell within the established normal reference ranges, regardless of the software vendor. A comparison of strain parameters calculated using software from different manufacturers revealed significant differences in several metrics. Consequently, strain values obtained from different software manufacturers are not directly comparable.

Aim    To evaluate the impact of digital remote monitoring on the effectiveness of intensive dose titration for guideline-directed medical therapy (GDMT) in patients with heart failure with reduced ejection fraction (HFrEF) for the achievement of target doses and the reduction of decompensated heart failure rate and all-cause mortality.
Materials and methods    The study utilized vital sign monitoring via a personal messenger-based questionnaire (chatbot) and weekly therapy optimization recommendations for 6 weeks following hospital discharge. The control group received standard outpatient care. The study is registered at ClinicalTrials.gov (NCT06304753). Between October 27, 2023, and December 27, 2024, 66 HFrEF patients were enrolled and randomized into a remote monitoring (RM) group (n=33) and a standard care (SC) group (n=33). The 6-week observation period was completed by 26 patients in the RM group and all 33 patients in the SC group.
Results    The RM group showed a statistically significant increase in the dosages of GDMT and a higher number of patients reaching target doses. In contrast, the SC group showed either no changes in therapy or a decrease in dosages of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor-neprilysin inhibitor (87.5 [50; 100]% vs. 25 [12.5; 25]%, p<0.001); beta-blockers (100 [50; 100]% vs. 50 [25; 50]%, p<0.001); and mineralocorticoid receptor antagonists (100 [100; 100]% vs. 50 [50; 100]%, p=0.005). Diuretic doses were reduced in the RM group (2 adjusted doses (AD) [1; 2] at baseline vs. 1 AD [0.5; 2] at 6 weeks; p=0.010) but remained unchanged in the SC group (2 [2; 2] AD at baseline vs. 2 [2; 2] AD at 6 weeks; p=0.9). The incidence of decompensated CHF and death was significantly higher in the SC group compared to the RM group, 16 cases (2 deaths, 14 decompensations) vs. 2 cases (0 deaths, 2 decompensations; p<0.001). Intensive titration proved safe, with no statistically significant differences observed between groups at 6 weeks regarding systolic blood pressure (119 [110-130] mm Hg vs. 120 [110-130] mm Hg; p=0.9), heart rate (70.5 [62-80] bpm vs. 78 [73-91.5] bpm; p=0.062), glomerular filtration rate (65.9 [49.2-77] mL/min/1.73 m² vs. 49.6 [45.8-71.9] mL/min/1.73 m²; p=0.22), or serum potassium levels (4.39 ± 0.48 mmol/L vs. 4.218 ± 0.37 mmol/L; p=0.33).
Conclusion    The study confirmed the feasibility, efficacy, and safety of intensive titration of guideline-directed medical therapy for chronic heart failure using remote monitoring.

Aim        To evaluate the dynamic impact of an 8-month glucagon-like peptide-1 receptor agonist (GLP-1 RA) therapy with semaglutide on anthropometric metrics, blood lipid profiles, and adipokine status in obese patients, with and without type 2 diabetes mellitus (T2DM).

Material and methods    The study included 65 patients with obesity, 26 of whom had T2DM. All participants were prescribed semaglutide, with dose titration up to 1 mg once weekly over 8 months. Before and after the treatment period, the following variables were assessed: anthropometric data (body weight, body weight index, waist circumference), biochemical parameters (lipid profile, glucose, aspartate aminotransferase, alanine aminotransferase, creatinine), and adipokine concentrations (leptin, adiponectin, resistin) via immunofluorescence assay.

Results  Semaglutide therapy was associated with a statistically significant reduction in body weight (p<0.001), body mass index (p<0.001), and waist circumference (p<0.001). Improvements in the lipid profile were observed over time, including decreased concentrations of low-density lipoprotein cholesterol (p=0.001), triglycerides (p<0.001), and total cholesterol (p=0.001), alongside an increase in high-density lipoprotein cholesterol (p<0.01). Therapy significantly impacted adipokine status: a statistically significant increase in anti-atherogenic adiponectin (p<0.001) and a decrease in leptin levels (p<0.001) were recorded, indicating improved adipose tissue metabolic function. However, no significant changes in resistin concentrations were found. Additionally, positive effects on liver and kidney function markers were noted, manifested by reductions in aspartate aminotransferase and alanine aminotransferase activity, as well as creatinine levels. In the subgroup of patients with T2DM, a statistically significant improvement in glycemic control was observed.

Conclusion         Semaglutide therapy for 8 months in obese patients yielded a robust cardiometabolic impact, characterized by significant weight reduction, optimized lipid profiles, and improved liver and kidney function markers, alongside a favorable restructuring of adipokine status. These results support the use of GLP-1 RAs not only for glycemic and weight control but also as a multifaceted cardioprotective therapy for obese patients.

Aim        A comprehensive assessment of retinal microcirculation in patients with stable ischemic heart disease (IHD) exhibiting obstructive and non-obstructive coronary artery (CA) lesions.

Materials and methods  This observational comparative study included 35 patients with stable IHD, divided into those with CA obstructive lesions (n=25) and those with ischemia with non-obstructive coronary arteries (INOCA) (n=10). A control group consisted of 30 healthy volunteers with no cardiovascular risk factors. The groups were matched for age and body mass index. All participants underwent coronary angiography or CT coronary angiography. Tissue perfusion and the amplitude-frequency spectrum of blood flow fluctuations (endothelial component) were assessed via laser Doppler flowmetry (LDF) of the bulbar conjunctiva, and optical coherence tomography angiography (OCT-A) of the macular region was performed using the SOLIX platform (Optovue, USA).

Results  Compared to the control group, patients with INOCA exhibited significantly higher vascular resistance (σ) and coefficient of variation (Kv), indicating more pronounced perfusion fluctuations. Both obstructive IHD and INOCA groups showed reduced endothelial flow amplitudes, a marker of endothelial dysfunction. OCT-A revealed that while macular vessel density remained stable, all IHD patients had increased foveal avascular zone (FAZ) area and perimeter. Specifically, the FAZ area was more significantly enlarged in obstructive IHD, whereas the FAZ perimeter was greater in INOCA (p<0.05). The left eye FAZ perimeter showed moderate diagnostic accuracy in differentiating stable IHD patients from healthy volunteers (AUC=0.632).

Conclusion         LDF of the bulbar conjunctiva effectively captures systemic vascular alterations in IHD and differentiates between obstructive and non-obstructive IHD. The integration of LDF and OCT-A provides a promising multimodal approach for the early detection of microvascular impairment, including in IHD patients.

Background    Heart failure (HF) patients with type 2 diabetes mellitus (T2DM) are at high risk of hospital readmission due to cardiovascular events. Glycemic control may play a key role in reducing this risk, but the optimal glycemic control threshold for preventing readmissions remains unclear.
Material and methods     This single-center, retrospective cohort study included 160 adult patients with HF and type 2 diabetes mellitus (T2DM). Patients were classified into two groups based on HbA1c measured 3 months after discharge: poor glycemic control (HbA1c ≥ 7.0 %) and good glycemic control (HbA1c < 7.0 %). Data were collected from electronic medical records, and cardiovascular event readmissions were tracked over a one-year follow-up period. Kaplan–Meier event-free survival (EFS) analysis and Cox regression models were used to examine the relationship between the three-month HbA1c and cardiovascular event readmission. A Fine–Gray competing-risk model was additionally applied to provide a more robust estimate of the cumulative incidence of cardiovascular readmission.
Results         Among the 160 patients, 56 (35 %) were readmitted due to cardiovascular events, including HF exacerbation (39.3 %), myocardial infarction (25.0 %), arrhythmias (14.3 %), and coronary artery disease (8.9 %). Their median EFS time was 121 days. The readmission rate was significantly higher in patients with poor glycemic control (HbA1c ≥7.0 %), with 58.8 % of the patients being readmitted compared to 17.4 % in the group with good glycemic control (HbA1c <7.0 %, p<0.001). Kaplan–Meier EFS analysis confirmed a significantly shorter EFS in patients with poor glycemic control. Cox regression analysis identified the three-month HbA1c value as an independent predictor of cardiovascular event readmission (HR=3.41, 95 % CI 2.15–5.29, p<0.001), which was consistent with the Fine–Gray competing-risk analysis (sub-distribution HR = 3.12, 95 % CI 1.95–4.98, p<0.001).
Conclusion    Early glycemic control, particularly the three-month HbA1c value, is a strong predictor of cardiovascular event readmission in HF patients with DM. Optimizing glycemic control within the first three months post-discharge may significantly reduce readmission risk and improve clinical outcomes.

Objective    To evaluate the diagnostic efficacy of exercise stress echocardiography in patients with suspected coronary artery disease (CAD) without typical angina symptoms, and to explore its predictive value for intermediate-term prognosis.
Material and methods    A total of 643 patients aged 45–76 yrs (mean age 58.4±9.7 yrs) with suspected CAD but without typical angina symptoms were retrospectively enrolled in this study. All patients underwent treadmill exercise stress echocardiography using the modified Bruce protocol. Left ventricular wall motion was assessed using the 17 segment scoring method, with coronary angiography or coronary computed tomography angiography (CCTA) as the reference standard for evaluating diagnostic efficacy. The median follow-up time was 36.2 mos. The primary endpoint was a major adverse cardiovascular event (MACE) including cardiac death, non-fatal myocardial infarction, elective revascularization based on objective evidence of myocardial ischemia, and hospitalization for unstable angina. ROC curve analysis was used to evaluate diagnostic efficacy, the Kaplan-Meier method for survival analysis, and a Cox proportional hazards regression model to analyze risk factors for occurrence of MACE.
Results    Of the 643 patients, 253 (39.3 %) were diagnosed with severe obstructive CAD (stenosis ≥70 %), and 246 (38.3 %) had positive results of exercise stress echocardiography. The sensitivity of exercise stress echocardiography for diagnosing severe obstructive CAD was 76.3 %, specificity was 88.5 %, AUC was 0.824, and diagnostic accuracy was 83.5 %. During follow-up, there were 89 cases (13.8 %) of MACE. The 3 yr MACE-free survival rate was 72.8 % in the positive exercise stress echocardiography group and 94.2 % in the negative group (p<0.001). Multivariate Cox regression analysis showed that positive exercise stress echocardiography immediately post-stress, wall motion score index, N-terminal pro-B-type natriuretic peptide concentration, and age were independent risk factors for MACE (all p<0.01).
Conclusion    Exercise stress echocardiography demonstrated good diagnostic accuracy in patients with suspected CAD but without typical angina symptoms. It had significant predictive value for intermediate-term adverse cardiovascular events. Exercise stress echocardiography can be used for risk stratification and clinical decision-making in this population.

Objectives    Myocardial ischemia-reperfusion (I / R) injury is a major clinical challenge, largely caused by oxidative stress-induced cardiomyocyte death. Ferroptosis, an iron-dependent form of regulated cell death, plays a key role in this process, but its upstream modulators remain unclear. This study aimed to investigate the role of PEX10, a peroxisomal biogenesis factor, in ferroptosis during myocardial I / R injury.
Material and methods        Peroxisome biogenesis factor 10 (PEX10) expression was analyzed in the GSE4105 dataset and validated in H9c2 cells subjected to oxygen-glucose deprivation / reoxygenation (OGD / R). PEX10 was silenced using siRNA, and cell viability, oxidative stress, iron accumulation, and ferroptosis-related markers were measured. Glutathione peroxidase 4 (GPX4) transcriptional regulation was examined, and rescue experiments were conducted using the GPX4 inhibitor RSL3. Ferrostatin-1 was used to pharmacologically inhibit ferroptosis.
Results     PEX10 was significantly upregulated in I / R-injured myocardium and OGD / R-treated cardiomyocytes. PEX10 knockdown improved cell viability and reduced oxidative stress, iron accumulation, and ferroptosis markers. Mechanistically, PEX10 suppressed GPX4 transcription, and the protective effects of its silencing were partially reversed by RSL3 (RAS-selective lethal). Ferrostatin-1 mimicked the protective effects of PEX10 knockdown.
Conclusion    PEX10 acts as a previously unrecognized mediator of ferroptosis by repressing GPX4 transcription. Targeting the PEX10–GPX4 axis may provide a promising therapeutic strategy for mitigating myocardial I / R injury.

The development of new drugs for cardiovascular diseases based on endogenous peptide hormones is a field of significant interest, driving intensive experimental research. One promising direction is the synthesis of short bioactive peptides that mimic the effects of larger peptide molecules while offering superior physicochemical properties. Recent studies have shown that C-terminal fragments of the peptide apelin mitigate metabolic and functional impairments following cardiac injury. This review summarizes current literature alongside our own experimental findings regarding the effects of apelin-13, [Pyr1]apelin-13, apelin-12, and its chemically modified analogs on the heart during in vitro and in vivo pathophysiological modeling. The therapeutic spectrum of apelin-12 analogs in the damaged myocardium includes reduced cardiomyocyte death, decreased membrane damage, improved myocardial metabolic status, and the suppression of reactive oxygen species and lipid peroxidation products. These findings highlight the potential of molecular construction of apelin receptor (APJ) agonists with enhanced proteolytic resistance and shelf-life stability as a foundation for a new class of cardiovascular drugs.

Patients with end-stage renal disease (ESRD) have a very high risk of cardiovascular disease (CVD). Addressing lipid metabolism disorders for both primary and secondary prevention of cardiovascular complications (CVC) is a critical priority for this population. However, patients with ESRD or organ transplants are frequently excluded from major randomized trials. The lack of large-scale evidence-based studies on lipid-lowering therapy and the risk of drug-drug interactions limit the use of intensive lipid-lowering treatment in this patient cohort. Furthermore, international consensus documents have not been updated to reflect the latest evidence. Consequently, target low-density lipoprotein cholesterol (LDL-C) levels are often not achieved following coronary complications, even with combination therapy (statins + ezetimibe).
This article presents a clinical case of the successful use of inclisiran in a female patient with ESRD and confirmed multifocal atherosclerosis, both prior to and following a planned kidney transplant.