Objective: To assess renal function and renal hemodynamics in obese individuals at various stages of the cardiometabolic continuum, including metabolically healthy abdominal obesity (MНАО) without metabolic syndrome (MS), MS, and type 2 diabetes mellitus (DM).

Materials and methods: The sample (n = 156) consisting of individuals with abdominal obesity (AO) aged 18-45 years. Study methods included anthropometric measurements, laboratory (total cholesterol, triglycerides, HDL, LDL, uric acid, creatinine, cystatin C, glucose, insulin, with calculation of HOMA-IR, adiponectin, leptin, glomerular filtration rate) and instrumental examinations (renal ultrasound and renal artery duplex scaning, CT with determination of fat depots).

Results: Renal function (GFR) and renal blood flow were to be strongly related to fat depot sizes, both systemic (intraabdominal fat) and local (perirenal fat and renal sinus fat) depot. In persons with MHAO, there is a slight decrease in GFR compared to healthy persons and an increase in the pulse index (PI), which indicates an increase in peripheral vascular resistance to blood flow. In individuals with MS and type 2 DM, these changes are even more pronounced.

Conclusions: Thus, the identification of renal hemodynamic disorders at the early stages of the cardiometabolic continuum will allow highlighting persons with high renal and cardiovascular risk

Adipose tissue is considered as an endocrine organ that affects the metabolic health of a person. Unified quantitative indicators of fat depots according to computed tomography have not been determined. Determination the critical level of intraabdominal, subcutaneous, epicardial, perivascular fat depots associated with metabolic syndrome in young adults is of scientific and practical interest.

The aim of the study was to evaluate the distribution and relationship of fat depots with metabolic profile in young adults with different metabolic phenotypes, and to determine the critical level associated with metabolic syndrome (MS).

Materials and methods: the study included 132 people (average age 37,59 ± 6,35 years). 3 groups were formed: 0 group – 16 healthy volunteers (median age 32 [27; 35); 1 group – 46 people with MSAO (40 years [34; 43); 2 group – 70 people with MS 40 years [35; 44. All the subjects were assessed for height, weight, waist circumference (WC), BMI. The following were evaluated: lipid profile, glucose, 2-hour glucose tolerance test, insulin, leptin, adiponectin, HOMA-IR. Performed by BPM. The volumes of subcutaneous, intraabdominal, perivascular, epicardial fats, the ratio of subcutaneous to intraabdominal fat were determined using computed tomography.

Results: The maximum values of intraabdominal, epicardial and periportal fat were in individuals with MS – with an unhealthy metabolic phenotype. There was a significant association of the periaortic fat depot with the maximum number of MS indicators: lipid profile (p < 0,01), glucose (p < 0,01), systolic and diastolic blood pressure (p < 0,01), WC (p < 0,01). Intraabdominal and epicardial fat depots were significantly associated with the level of TG, HDL, glucose, with the level of pressure and WC (p < 0,01). Subcutaneous fat had few reliable correlations, and was associated only with TG and WC (p < 0,01). The critical level of periaortic fat associated  with metabolic syndrome was < 12,2 cm³ (AuROC 0,72, p < 0,01), epicardial < 88,5 cm³ (AuROC 0,69, p < 0,01), intraabdominal < 129,9 cm² (AuROC 0,78, p < 0,01), subcutaneous < 330,0 cm² (AuROC 0,61, p < 0,01), the ratio of subcutaneous to intraabdominal < 1,6 (AuROC 0,70, p < 0,01).

Conclusion: Critical values of periportal, epicardial, intraabdominal, subcutaneous and the ratio of subcutaneous to intraabdominal associated with the presence of metabolic syndrome were identified in young adults. The level of periportal fat < 12,2 ml can be considered as a predictor of MS in young adults, but further studies are required.

Аim: to assess the influence of the patient's psychotype on the degree of nighttime reduction in blood pressure (BP) to determine predictors of an unfavorable daily BP profile.

Materials and methods. The study involved 80 patients with newly diagnosed or untreated arterial hypertension (AH), with various stages, severity, risk of developing cardiovascular complications, in the absence of concomitant severe somatic pathology, who independently consulted a local therapist. All patients underwent 24-hour blood pressure monitoring in the absence of antihypertensive therapy and the psychological profile was assessed using the SMOL  questionnaire.

Results. The psychopathological profile of the examined AH patients corresponded to the social and psychological adaptation. Our analysis of the indices of   the averaged profile of the SMOL test, depending on the degree of reduction in nocturnal systolic blood pressure (between dipper and non-dipper profiles) and diastolic blood pressure (between dipper, non-dipper and extreme dipper patterns profiles) did not reveal statistically significant differences (p > 0,05). Patients with a riser daily blood pressure profile, due to the small size of the group, were not included in the comparative analysis. The average profile of SMOL of the examined patients was noted by an increase in indicators on the scales 1 – hypochondria and 3 – emotional lability.

Conclusion. The variant of the daily blood pressure profile does not depend on the psychotype of the patient; it is likely that functional and structural changes that occur during the formation of hypertension affect the type of the degree of nighttime decrease in blood pressure.

The management of patients with uncontrolled arterial hypertension in real clinical practice remains a difficult task, despite the impressive arsenal of  antihypertensive drugs. In most cases, correction of medical therapy and lifestyle modification in this group of patients can achieve success in treatment, but in some cases, the target levels of blood pressure (AH) cannot be achieved.

Aim. To assess the incidence of true resistant arterial hypertension in patients with hypertension, to identify the main causes of uncontrolled hypertension and to determine the main methods of modification of therapy.

Materials and methods. The study included 70 patients with uncontrolled hypertension who received antihypertensive therapy previously. All patients underwent office measurement of blood pressure at the initial visit and after correction of therapy, 24-hour blood pressure monitoring (ABPM) was performed. Correction of therapy included the prescription of a standard three-component regimen «RAAS blocker + calcium antagonist + thiazide diuretic». In case of failure to achieve     the target BP levels, the measurement of aldosterone/renin in the blood was carried out to exclude primary hyperaldosteronism (PHA). In all patients, the body mass index (BMI) was calculated, echocardiography was performed to determine the target organ damage, complete blood count, biochemical blood tests were performed (to detect existing kidney damage).

Results. In 86% of patients, target BP levels were achieved through lifestyle modification (weight loss) and correction of previous therapy. In 24% of the study subjects, low adherence to therapy (non-compliance) due to polypharmacy was revealed, in connection with which patients were recommended to switch to    fixed combinations of drugs, which made it possible to significantly reduce blood pressure below 140/90 mm Hg. according to the results of ABPM in all patients.   In 8% of patients, amlodipine/lercanidipine was replaced with long-acting nifedipine, which also led to a decrease in blood pressure (−5,5 mm Hg mean blood pressure according to ABPM). In two cases, the diagnosis of PHA was established, the tumor form of this disease was excluded using computed tomography of the adrenal glands, and treatment with aldosterone antagonists was prescribed. In 10% of patients, the diagnosis of «Resistant arterial hypertension» was confirmed, spironolactone in low doses (25-50 mg), doxazosin 1 mg, moxonidine 0,4 mg, bisoprolol 5 mg were sequentially added to the treatment. Spironolactone and doxazosin showed similar efficacy (−7,1 mmHg and −6,9 mmHg in mean BP, respectively), moxonidine and bisoprolol were less effective (−4,8 and −5,2 mmHg,

respectively). In two patients, the addition of spironolactone or doxazosin did not lead to the achievement of the target BP level, a loop diuretic (furosemide 40 mg) was added to the treatment.

Conclusion. The incidence of resistant hypertension among patients in the study was 10%. All patients with uncontrolled hypertension, if it is impossible to achieve the target values of blood pressure, provided that the treatment is correctly prescribed, it is necessary to exclude symptomatic hypertension, in particular, PHA. In case of confirmation of true RAH, it is necessary to prescribe aldosterone antagonists (spironolactone) in small doses, and doxazosin is also acceptable.

SARS-CoV-2, a novel coronavirus infection that primarily affects the lungs, can induce multi-organ involvement. Arterial hypertension (AH), diabetes mellitus (DM), and obesity increase the risk of severe COVID-19, up to and including the development of a fatal cytokine storm. The risk of severe SARS-CoV-2 infection in persons with obesity and DM is associated with baseline systemic inflammation and immune system dysfunction. In addition, this category of patients is more likely to have post-COVID-19 syndrome and worsen the course of chronic diseases. Endothelial damage – direct (SARS-CoV-2 infection) and indirect (systemic inflammation) may play a crucial role in the development of COVID-19 complications. Angiotensin-converting enzyme 2 (ACE-2) expressed in human endothelium plays a fundamental role in the new coronavirus infection. SARS-CoV-2 uses it as a receptor to enter the cell, which leads to a decrease in the bioavailability of ACE-2 on the endotheliocytes surface. Once inside, the virus induces its apoptosis, leading to the development of a proinflammatory and procoagulant state and, as a result, vascular damage. Drugs including ACE inhibitors, ARB, beta-blockers, and statins are widely prescribed to patients with DM, AH, and CHD, the groups most at risk for COVID-19, and their effects on the endothelium are well known. New classes of hypoglycemic drugs, particularly glucagon-like peptide 1 (GLP-1) receptor agonists, have demonstrated the ability to affect systemic inflammation and improve prognosis in DM and CHD patients. In addition, they have a positive effect on BP and metabolic profile. The proven reduction in weight on the background of the use of GLP-1 may be an additional factor in determining the choice of this class of drugs. These effects can be used in COVID-19 patients with a high risk of severe course, as well as in persons with obesity in the post-COVID-19 condition.

Among the forms of precapillary pulmonary hypertension (PH) are pulmonary arterial hypertension (PAH) and chronic thromboembolic PH (CTEPH) with a diagnostic triad of hemodynamic parameters: mean pulmonary artery pressure > 25 mm Hg (> 20 mm Hg according to the new version of European guidelines 2022), pulmonary artery wedge pressure ≥ 15 mm Hg; pulmonary vascular resistance > 3 Wood units (> 2 Wood units in the new version of European guidelines 2022) by right heart catheterization at rest. The leading factors in the pathogenesis of PAH are an endothelial dysfunction with an imbalance between vasodilating and vasoconstrictor substances, activation of endothelial/smooth muscle cell proliferation and the blood coagulation system, which lead to remodeling of the vessels of the pulmonary circulation. In CTEPH there is a morphological substrate as a chronic obstruction of large and medium branches of pulmonary arteries, as well as secondary changes in the microcirculatory bed of the lungs, and chronic/organized thrombi/emboli in the elastic type of pulmonary arteries are detected after three months of effective anticoagulant therapy.

As a result of a significant progress in the study of the pathophysiological aspects of PAH in recent years, specific therapy has been introduced into clinical practice with an impact on key targets of the pathogenesis of the disease. In CTEPH pulmonary endarterectomy remains the treatment of choice for all operable patients.  In case of inoperable and residual forms of CTEPH, if technically feasible, pulmonary artery balloon angioplasty is performed while taking PAH-specific drugs, in particular, the only officially approved stimulator of soluble guanylate cyclase (sGC) riociguat.

The most important aspects of PAH-specific therapy of patients with PAH, inoperable and residual forms of CTEPH; the targets of therapy are indicated, promising approaches to therapy with a focus on the sGC stimulator riociguat, the possibilities of combination therapy and switching strategies are discussed in the article. The optimal safety and efficacy profile of riociguat, demonstrated in large international studies and routine clinical practice, allows the drug to be widely used in the treatment of patients with PAH and CTEPH. Switching from phosphodiesterase type 5 (PDE5) inhibitors to riociguat is safe and appropriate, which is emphasized in the Eurasian and Russian clinical guidelines, in 2022. the strategy of switching to riociguat is approved in case of failure of PDE5 inhibitors as part of combination therapy with endothelin receptor antagonists in the new version of the European document.The originality of riociguat due to the presence of a dual mechanism of action by direct stimulation of sGC and sensitization of the enzyme to endogenous NO, allows its use not only as a long-term monotherapy, but also as part of a combination therapy, with the implementation of a switching strategy in case of clinical failure of PDE5 inhibitors.

This article describes a clinical case of a patient suffering from ulcerative colitis and cardiovascular pathology for a long time. In the clinical case, a patient with a late onset of ulcerative colitis and a sharp deterioration in cardiovascular pathology is presented. This combination of diseases is of clinical interest, because according to existing data, inflammatory bowel diseases (IBD) are predictors of increased cardiovascular risk. The clinical case describes the therapy of inflammatory bowel diseases, which can stop the symptoms of the disease and thereby reduce the risk of progression of cardiovascular pathology, describes the hypotensive, hypolipidemic therapy received by the patient. Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), affect not only the gastrointestinal tract, but also have extra-intestinal manifestations. For example, IBD develops chronic inflammation syndrome, which leads to the development of endothelial dysfunction and accelerated growth of atherosclerotic plaques. Given that inflammation triggers the early stages of atherogenesis, and an increase in inflammatory cytokines is accompanied by a higher cardiovascular risk, today there is an assumption that patients suffering from IBD have a higher risk of developing cardiovascular events than healthy ones. In our clinical case, the latest data on IBD as a risk factor for cardiovascular diseases are presented. Infl mmation plays a key role in the development of IBD and cardiovascular pathology. Understanding the main mechanisms underlying these diseases and leading to increased cardiovascular risk and worsening prognosis in patients with IBD will optimize treatment tactics and, thus, reduce the number of adverse events and mortality in this cohort of patients. The purpose of our clinical case is to attract special attention to this cohort of patients from cardiologists, gastroenterologists and therapists in order to be able to consider starting preventive prevention as early as possible.