The spread of cardiovascular disease is epidemic, driven by lipid profile abnormalities. High levels of atherogenic lipoproteins are a risk factor for stroke, myocardial infarction, and peripheral arterial complications. These diseases are leading causes of disability, premature death, and healthcare costs worldwide. Statins are the “gold standard” for controlling cholesterol levels and reducing the risks associated with atherosclerosis; however, patients often fail to adhere to therapy and may discontinue medications due to statin-associated muscle symptoms or fear of other adverse drug effects. In the search for optimal lipid-lowering therapy, many pharmacological solutions other than statin drugs have been proposed, ranging from the use of trivial nutraceuticals to high-tech vaccines against PCSK9. This article analyzes the past trends, current status, and future development vectors of non-statin lipid-lowering therapy.

Acute coronary syndrome is traditionally classified based on the presence of ST-segment elevation, which is considered a marker of acute coronary artery occlusion. This established paradigm, however, does not always reflect the pathophysiological reality. Current data show that up to 34% of patients with non-ST-segment elevation myocardial infarction have total occlusion of the infarction-related artery, which is associated with an increased risk of mortality. This emphasizes that the absence of ST-segment elevation does not exclude the presence of an occlusive lesion. In addition to the well-known electrocardiographic equivalents of ST-segment elevation myocardial infarction, numerous rare and subtle patterns have been described in the literature that suggest acute coronary occlusion. To systematize these data, a literature review was conducted. It revealed that rare electrocardiographic phenomena such as hyperacute T waves, terminal QRS distortion, precordial swirl, Aslanger patterns, and northern myocardial infarction patterns may potentially have high diagnostic value. The analysis demonstrates that in most cases, the presence of these patterns is highly specific for occlusion and is associated with more extensive myocardial damage and a worse prognosis. However, their widespread adoption in routine practice is limited by low sensitivity and the complexity of visual assessment, which requires specialized training and the use of automated electrocardiogram analysis systems. These issues necessitate further prospective studies to confirm the clinical significance of these patterns and the development of artificial intelligence algorithms for their accurate interpretation in clinical practice.

Undifferentiated connective tissue dysplasia (uCTD) is characterized by a high prevalence of autonomic disturbances; however, the optimal method for assessing autonomic status in this patient population has not been established. Existing indices (Robinson index, Baevsky index, minute blood volume) predominantly reflect hemodynamic parameters and may not account for the specifics of autonomic dysregulation in uCTD. Objective. To justify the selection of the Kerdo Vegetative Index as the most informative parameter for assessing autonomic status in female patients with undifferentiated connective tissue dysplasia. Materials and Methods. A single-center observational cross-sectional study was conducted involving 24 female patients with verified uCTD aged 20–31 years (mean age 24.12 ± 2.66 years). The following indices were calculated: Kerdo Vegetative Index (KVI), minute blood volume (MBV), and the Index of Functional Changes (IFC). Correlation analysis with clinical parameters (dysplasia scores, autonomic dysfunction scores, anxiety) was performed. Statistical analysis was carried out using SPSS 26.0. Results. KVI demonstrated the strongest correlations with clinical manifestations of uCTD: with autonomic dysfunction scores (r = 0.715; p < 0.001), anxiety (r = 0.773; p 0.05). When comparing groups, KVI significantly differed between patients with and without anxiety (+9.99 vs −9.02; p = 0.0009), as well as between groups with and without autonomic dysfunction (+10.09 vs −11.98; p = 0.0002). Conclusion. The Kerdo Vegetative Index is the most informative parameter for assessing autonomic status in female patients with uCTD, owing to its strong correlations with clinical disease manifestations and its ability to differentiate patients based on the presence of psychovegetative disturbances.

Relevance. Despite the high effectiveness of spa treatment in patients with bronchial asthma (BA), not all comorbid conditions can be eliminated by this treatment method, which necessitates the search for new methods of influencing various aspects of BA pathogenesis. Goal. To study the effect of grape polyphenols (GP) on the relationship between lipid profile parameters and markers of endotoxin-binding systems in post-COVID patients with BA during sanatorium treatment. Materials and methods. The study involved 105 BA patients treated at the Sechenov Sanatorium (Yalta). Group 1 (n=60) received GP, group 2 (n=45) did not. Body mass index (BMI), lipid profile, and markers of endotoxin-binding systems (BPI, LSB, LPS, sCD14, zonulin) were evaluated. Results. Significant changes in BPI, sCD14, and zonulin levels were observed in both groups during treatment. However, significant dynamics in BMI, HDL, LDL, and triglycerides were noted only in Group 1: BMI decreased from 29.4 kg/m² (23.5-33.9) to 29.0 kg/m² (23.2- 33.1) (p=0.04); HDL increased from 1.4 mmol/L (1.2-1.8) to 1.9 mmol/L (1.4-2.4) (p=0.01); LDL decreased from 3.5 mmol/L (2.7-4.3) to 3.0 mmol/L (2.5-3.4) (p=0.03); TG decreased from 1.1 mmol/L (0.9-1.6) to 0.9 mmol/L (0.7-0.9) (p=0.04). By the end of follow-up, intergroup comparison revealed significant differences in BMI (p=0.04), LDL (p=0.02), triglycerides (p=0.04), and LSB (p=0.03) levels. In Group 1, numerous correlations between lipid profile and endotoxin-binding system markers were identified before and after treatment. Conclusion. The prospects of using GP as an additional tool for correcting metabolic disorders in post-COVID patients with BA during sanatorium treatment have been confirmed.

Objective. To assess the pathogenetic role of metabolic and inflammatory biomarkers in the development of alcoholic liver disease and determine the relationship between their concentrations and disease progression. Materials and methods. An observational case-control study was conducted with the formation of a study group of 1 out of 36 patients with ALD at the stage of hepatosis and chronic hepatitis, a study group of 2 out of 92 patients with ALD at the stage of liver cirrhosis (LC) and a control group of 71 healthy volunteers. Metabolic and inflammatory markers (adiponectin, leptin, copeptin, autotaxin, interleukin-6 (IL-6), C-reactive protein (CRP), procalcitonin (FCT), ferritin, and serum ceruloplasmin were determined by enzymelinked immunosorbent assay (ELISA). Results. During the development of the initial stages of ALD, serum levels of copeptin, adiponectin, leptin, CRP, PCT, IL-6 and RF increased (p < 0.001), and autotaxin was — added during the formation of alcoholic LC (p < 0.04). According to Child-Pugh classification, the progression of alcoholic LC was accompanied by an increase in adiponectin, IL-6, PCT, CRP and RF values (p < 0.05), the MELD scale — an increase in adiponectin, IL-6, CRP and PCT concentrations (p < 0.05) , and a decrease in leptin values (p = 0.02). The most informative markers in detecting complications of LC were adiponectin, PCT and IL-6. Adiponectin and IL-6 were associated with ascites (AUC = 0.72; 95%CI: 0.62-0.81; AUC = 0.71; 95%CI: 0.61-0.80, respectively; p < 0.05) and renal impairment (AUC = 0.69; 95%CI: 0.59-0.79; AUC = 0.68; 95%CI: 0.57-0.77, respectively; p < 0.05), PCT — ascites, esophageal varices and encephalopathy (AUC: 0.77; 95%CI: 0.67-0.85; AUC = 0.68; 95%CI: 0.57-0.77; AUC = 0.74; 95%CI: 0.64-0.83, respectively; p < 0.01). Conclusion. This study confirmed the relationship of the formation and progression of ALD with the levels of metabolic and inflammatory parameters. This allows metabolic imbalance and chronic inflammation to be considered as key components of disease pathogenesis. Based on the data obtained, the proposed parameters can be used as surrogate screening markers to predict the risk of development and severity of the course of ALD.

Infective endocarditis caused by Gram-negative bacteria is a relatively rare form of endocarditis with distinct diagnostic and therapeutic features. We present a clinical case of infective endocarditis of the aortic valve, whose etiological agent (Klebsiella pneumoniae) was identified only by highthroughput metagenomic sequencing. This case demonstrates the importance of using advanced technologies to identify the causative agents of infective endocarditis.

This article describes a clinical case of the detection of primary hyperaldosteronism (PA) a 37-years-old female patient has. The patient was urgently hospitalized at the Cardiology department because of stable polymorphic ventricular tachycardis (V-tach) episode. The feature of the disease in her case is a sudden manifestation of PA in the form of ventricular arrhythmias compared with the long period of essential hypertension (EH) without symptomatic origin signs. The detailing of diagnostic steps confirms the importance of potassium level determining for patients with arrhythmia when they are taken to hospitals. Electrolyte analysis is an important aspect of the diagnostic search with a persistent elevated blood pressure and without traditional risk factors EH. In the present case the persistent hypokalemia without anamnestic preconditions for likelihood of electrolyte disturbances has been detected. Primary hyperaldosteronism has a wide range of clinical manifestations described in the medical literature. Present observation confirms the possibility of an atypical clinical course of PA, and it shows objective suitability of searching of adrenal tumors as a reason for letal arrhythmias occurrence. Ventricular rhythm disturbances in the PA are probable option of electrical instability of the myocardium that occurs against the background of grave electrolyte disorders. In this observation medication-assisted treatment with amiodaron, aldosteron antagonists stabilizided the patient`s condition during the preoperative period. This clinical case demonstrates continuity between physicians of various specialties (cardiologist, endocrinologist, surgeon-urologist) during diagnosis and treatment with aldosteronism, as well it considers the peculiarities of cardiologic support for patients with rhythm disturbances, in need surgery of adrenal tumors.

Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder with multisystem involvement, in which vascular abnormalities are rare but potentially life-threatening. NF1-associated vasculopathy may lead to aneurysm formation due to arterial wall fragility, and spontaneous rupture can result in catastrophic hemorrhage. Massive upper gastrointestinal hemorrhage secondary to aneurysmal rupture in NF1 is extremely uncommon and poses significant diagnostic and therapeutic challenges.

Here we report a case of a 54-year-old man with NF1 who presented with massive recurrent upper gastrointestinal bleeding. Imaging revealed a left gastric artery aneurysm secondary to NF-1-associated vasculopathy with active contrast extravasation into the stomach. The patient subsequently developed tachycardia and hypotension consistent with hemodynamic deterioration. Digital subtraction angiography confirmed that the source of upper gastrointestinal bleeding was active extravasation from a ruptured left gastric artery aneurysm. Subsequently, successful coil embolization of the ruptured left gastric artery aneurysm was performed for the patient. Following the intervention, hemostasis was achieved with stabilization of vital parameters.

The case indicates the need to consider vascular causes in NF-1 patients presenting with massive gastrointestinal bleeding to ensure timely endovascular management and favorable outcomes.

Introduction. A clinical case of the use of a cardiac myosin ATPase inhibitor in a female patient with hypertrophic cardiomyopathy (HCM) characterized by critical obstruction and pulmonary hypertension (PH) is presented. Case summary. A 50-year-old female patient with obstructive HCM (pathogenic nucleotide variant p.R1420Q in the MYH7 gene) was hospitalized with paroxysmal atrial fibrillation (heart rate up to 170 bpm) and pulmonary edema. Sinus rhythm was restored by electrical cardioversion. The peak left ventricular outflow tract (LVOT) obstruction gradient was 112 mmHg, and systolic pulmonary artery pressure (sPAP) was 114 mmHg. Surgical treatment was declined due to severe pulmonary hypertension. The patient began treatment with the cardiac myosin ATPase inhibitor mavacamten at a dose of 2.5 mg, with follow-up assessments after 3.5 weeks and after 3 months of the therapy starting. As a result of treatment sPAP decreased to 71 mmHg and the peak LVOT pressure gradient (Pg max) dropped to 73 mmHg; consequently, the patient successfully underwent an extended septal myectomy. Treatment with mavacamten was discontinued. Conclusion: Treatment with the cardiac myosin ATPase inhibitor mavacamten (2.5 mg) for 3.5 months in a patient with severe obstructive HCM and significant pulmonary hypertension resulted in a reduction of systolic pulmonary artery pressure, enabling successful surgery.