Aim. To identify factors and develop a clinical risk model (nomogram) for in-hospital mortality in patients with acute myocardial infarction (AMI) after timely early invasive diagnosis and revascularization of infarct-related artery (IRA).

Material and methods: We conducted a prospective, single-center observational study that included 712 consecutive patients with AMI [median age 65 (interquartile range 56-74 years), 61% were male, 47.8% with ST-elevation] who underwent coronary angiography <24 hours after symptom onset and successful endovascular revascularization of IRA. The primary endpoint was in-hospital mortality. Logistic regression analysis was used to identify independent prognostic risk factors for in-hospital mortality. Based on the multivariate analysis, a nomogram was developed to predict outcome. The discriminative ability of the nomogram was assessed by calculating the area under the receiver operating characteristic (ROC) curve.

Results. The in-hospital mortality rate was 5.06%. The most common cause of in-hospital mortality was acute heart failure (AHF, 75%), followed by myocardial rupture with cardiac tamponade (11.1%). Multivariate analysis revealed that age (odds ratio (OR) 1.07, 95% confidence intervals (CI) 1.01-1.14, p=0.027), Killip class (OR 2.95, 95% CI 1.67-5.23, p<0.001), hemoglobin at admission (OR 0.97, 95% CI 0.95-0.99, p=0.006), and left ventricular ejection fraction (LVEF) ≤36% (OR 8.87, 95% CI 2.95-26.69, p<0.001), were independent predictors of adverse outcome. The identified predictors were included a nomogram, which demonstrated excellent discrimination in predicting in-hospital mortality (area under the ROC curve = 0.949, 95% CI: 0.925-0.972, p<0.001, sensitivity: 91.3%, specificity: 89.9%) and good calibration (Hosmer-Lemeshow test, p=0.93).

Conclusions. Age, hemoglobin at admission, Killip class and left ventricular ejection fraction were independent predictors of in-hospital mortality in acute MI. The most common etiology of in-hospital mortality was AHF. The nomogram for prediction of in-hospital mortality demonstrated high prognostic potential, allowing for the identification of patients at high-risk of adverse outcome, and targeted therapeutic strategies may be needed to improve the survival of patients with acute MI.

Aim. To study the relationship and predictive value of integral metabolic indices of obesity in the identification of ectopic obesity.

Material and methods. The study included 326 patients (146 men and 180 women, mean age 61±9 years). Anthropometric data, degree of obesity, body mass index (BMI), waist circumference (WC), sagittal abdominal diameter (SAD), body obesity index (BAI), visceral obesity index (VAI), lipid accumulation index (LAP), triglycerides-glucose index (TyG) was assessed. Perivascular adipose tissue (PVAT) volume, pericardial adipose tissue (PAT) volume and thickness of perirenal fat tissue (PRF) were assessed with CT.

Results. Patients were divided into groups: with isolated ectopic obesity (iEO) (n=17); with isolated abdominal obesity (iAO) (n=74); with EO variants: pericardial (PCO) (n=31), perivascular (PVO) (n=22) or perirenal (PRO) (n=33) with AO; with mixed ectopic obesity and AO (mEO+AO) (n=117), and patients without obesity (n=32). Significantly higher BMI, WC, SAD, and BAI indices were found in individuals with PCO+AO, PRO+AO and mEO+AO. The highest values of LAP were found in groups: PCO+AO, PVO+AO, PRO+AO. There was a correlation between ectopic fat depots and WC (r=0,62 for PAT, r=0,55 for PVAT and r=0,39 for PRF, p=0,01) and SAD (0,429, 0,329 and 0,435, respectively, p=0,01). Correlation was established between PAT, PRF and LAP (0,425 and 0,319, respectively, p=0,01). The highest AUC values>0,8 had models of WC and SAD in identification of PCO (0,801 and 0,801, respectively) and PRO (0,826 and 0,826, respectively). For PCO, the cut-off point of WC was 100,5 cm (specificity 72,9%, sensitivity 70,2%, p=0,000), SAD — 25 cm (specificity 73%, sensitivity 70,2%, p=0,000). For PRO, the cut-off of WC was 101 cm (specificity 71,4%, sensitivity 72,7%, p=0,000), SAD — 25 cm (specificity 71,4%, sensitivity 72,7%, p=0,000).

Conclusion. Еctopic fat depots are related to the risk of metabolic disorders. Potential informative value of simple and accessible integral metabolic indices was established. WC>100,5 cm, SAD>25 cm may indicate to the presence of PCO; WC>101 cm, SAD>25 cm — to the presence of PRO.

Aim. To compare the relative expression levels of circulating microRNAs associated with cardiovascular diseases, selected according to the literature review, in the blood plasma samples of patients with two variants of chronic vascular wall injury: coronary artery atherosclerosis (CAA) and thoracic aortic aneurysm (TAA).

Material and methods. Patients admitted to the Clinical Center of the I. M. Sechenov First Moscow State Medical University (University Clinical Hospital No. 1) with CAA (n=45), TAA (n=38), as well as a control group (n=17) were included. Standard clinical and demographic, laboratory and instrumental data were collected in accordance with Russian clinical guidelines, and additional sampling and preparation of blood plasma of patients was carried out with further quantitative determination of the circulating microRNAs level via real-time polymerase chain reaction with reverse transcription. A comprehensive comparative analysis of the profiles of circulating microRNAs in the blood plasma of patients with two different variants of arterial pathology: atherosclerosis and aneurysmal changes, as well as with the control group was carried out. The levels of 12 circulating microRNAs were studied: miR-21-5p, -23a-3p, -29b-3p, -92a-3p, -126-5p, -143-3p, -145-5p, -146a-5p, -150-5p, -181b-5p, 2-23-3p and -451a.

Results. The strongest difference with the control group in patients with CAA and TAA was observed for miR-21-5p, -29b-3p and -126-3p. Most of the circulating microRNAs studied were higher in the TAA group compared with CAA and controls these include miR-21-5p, -23a-3p, -29b-3p, -92a-3p, -126-3p, -126-5p, -146a-5p, -150-5p, -181b-5p. Significant differences between the pathology groups were noted for miR-126-3p and miR-205-5p. Some microRNAs (­miR-143-3p, -92 a3, -195-5 p) can be used to diagnose coronary artery atherosclerosis, other microRNAs (miR-21-5p, -23a-3p, -126-3p, -126-5p, -451a) are TAA-specific.

Conclusion. The present study showed significant differences in the circulating microRNAs in patients with atherosclerotic and aneurysmal lesions of the arteries in comparison with the control group. The most significant difference between norm and pathology was found for miR-21-5p, -29b-5p and -126-3p. The levels of miR-126-3p and -205-5p can be used to differentiate CAA and TAA.

Aim. To develop a diagnostic complex (DC) of ultrasound markers characterizing carotid arteries (CA) atherosclerotic load, and to evaluate its association with breast arterial calcification (BAC) in women.

Material and methods. The cross-sectional case-control study included 198 women aged 40-74 years, who made up of 2 groups of 99 participates in each, with or without BAC, who underwent diagnostic digital mammography. The study protocol included physical examination, medical history, questionnaires, laboratory tests, electrocardiography, carotid ultrasound. BAC severity was assessed on a 12-point scale. Ultrasound parameters of CA atherosclerotic load were assessed: the number of atherosclerotic plaques, maximum, total and average stenosis. All patients signed informed consent to participate in the study.

Results. Atherosclerotic plaques were detected in 79.9% of women with BAC and in 60.6% of women without BAC. The best statistically significant difference in both groups was found in the "number of atherosclerotic plaques", "average stenosis" and "maximum stenosis", on the basis of which the DC in points was formed. When comparing the average DC value, it was found that the degree of atherosclerotic load is statistically significantly higher in women with calcification (p=0.001). There was a significantly higher proportion of people with BAC in the groups of women with both DC values >2 points (p<0.001) and DC >0 points (p=0.022). Univariate analysis showed that with a DC >2 points, the probability of having BAC in women increases by 4.06 times (95% CI: 1.92-9.25; p<0.001). Menopause (p=0.024), osteoporosis (p=0.013), glomerular filtration rate <90 ml/min/1.73 m2 (p=0.004), thyroid disease (p=0.041) and hormone replacement therapy for hypothyroidism (p=0.015) were associated with BAC. As a result of multivariate analysis, significant associations of BAC with DC >2 points (OR=2.87; p=0.012) and hormone replacement therapy for hypothyroidism (OR=0.31; p=0.017) were found. There was no statistically significant relationship between DC and the severity of BAC on a 12-point scale.

Conclusion. A DC was developed to assess the degree of CA atherosclerotic load. Differences in DC parameters were revealed between groups of women with and without BAC: DC>2 points increase the chance of having BAC. The demonstrated connection between BAC and asymptomatic CA atherosclerosis indicates the prospects for using this form of vascular calcification as a gender-specific marker of cardiovascular diseases in women.

Aim. Development and external validation of a risk prediction model for acute decompensated heart failure (ADHF) in patients with low left ventricular ejection fraction.

Material and methods. The model development group was represented by patients with heart failure with reduced ejection fraction (HFrEF) included in a registry observational study from 2015 to 2019, a total of 260 patients, age 59 (53; 66) years, 214 (82.3%) — men. External validation of the model was carried out in a cohort of independent prospective observation of 94 patients with HFrEF from the same registry for the period from 2020 to 2021, median age 66 (52;73) years, of which 73 (77.6%) were men. The prospective follow-up period was 4.6 (2.3; 4.9) years in the internal validation group, 2.5 (1.7; 2.9) years in the external validation group. Data were obtained on the status of patients, causes of death, and the frequency of hospitalizations for ADHF. The actual and predicted incidence of ADHF using the evaluated prognostic model was compared.

Results. During the observation period in the internal validation group, ADHF developed in 69 (26.5%) patients, and 47 (18.1%) died due to ADHF. The prognostic regression model included LA enlargement of more than 45 mm, male gender, left ventricular ejection fraction less than 35%, absence of renin-angiotensin system blocker and amiodarone. When performing ROC analysis, the area under the ROC curve (AUC) of the created model was 0.8, sensitivity model — 69.2%, specificity — 80%, accuracy — 75.3%. In the external validation group, 34 (36.2%) cases of ADHF were registered; mortality from ADHF in the external validation group was 15.9%, which is comparable to the development group (p > 0.05). The diagnostic value of the developed model during external validation showed to be high and was comparable to the results obtained in the development group: the area under the ROC curve (AUC) was 0.8, sensitivity — 73.3%, specificity — 82.5%, accuracy 76.1%, (p=0.102, McNeil test).

Conclusion. The developed regression model has sufficient statistical power to predict the risk of ADHF in patients with low left ventricular ejection fraction in the long term, which is confirmed by external validation.

Aim. To study the long-term prognosis of patients’ life who have suffered cerebrovascular accident (CVA), and to determine the role of diabetes mellitus (DM) as a possible negative prognostic factor, according to the outpatient follow-up stage in the REGION-M registry.

Material and methods. The outpatient part of the REGION-M registry included 684 patients assigned to the Moscow City Polyclinic No. 64, discharged from the hospital in the period from 01.01.2012 to 30.04.2017 with a confirmed diagnosis of CVA, of which 122 patients (17.8%) were diagnosed with DM. The polyclinic stage included three observation points: 2017, 2020, and 2022. Data on the life status of all patients were obtained by telephone survey, if it was impossible to establish contact with the patient or his relatives, a unified medical information and analytical system was used to determine the life status of patients. The study patients were observed on an outpatient basis for more than 5 years (ME 1958 (751; 2555) days), the primary endpoint was death from any cause.

Results. Information about the life status was obtained for all 684 patients. By the end of the observation, 415 cohort members had died, and 269 were alive. The average age of patients with DM was significantly higher than that of patients without DM: 71.5±10.9 years vs 68.0±14.7 years (p<0.05). The proportion of women in the cohort of DM patients was significantly higher than in the cohort of patients without DM: 72.1% vs 55.2% (p<0.05). Patients with DM were statistically significantly more likely to have a history of comorbid diseases (coronary heart disease, myocardial infarction, arterial hypertension, kidney disease and chronic lung disease, chronic heart failure). Obesity occurs with the same frequency in patients with and without DM. The studied groups of patients did not differ in types of CVA (transient ischemic attack, ischemic, hemorrhagic stroke). According to Cox Proportional Hazards Regression Analysis at the outpatient stage of follow-up, no significant negative effect of DM on patients’ mortality with CVA was confirmed (relative risk =1.239 (95% CI: 0.975; 1.574), p=0.079).

Conclusion. In the long-term follow-up of patients with CVA, there was no statistically significant adverse effect of DM on long-term survival.

Aim. To analyze the frequency, indications, and outcomes of using glycoprotein IIb/IIIa inhibitors in patients with acute myocardial infarction (AMI) in Russia based on data from a multicenter registry.

Material and methods. This work is part of the REGION-MI (Russian Registry of Acute Myocardial Infarction) multicenter retrospective-prospective observational study, which included patients admitted to hospitals in 45 regions of Russia with a diagnosis of AMI from 2020 to 2023. The decision to prescribe glycoprotein IIb/IIIa inhibitors was made by physicians. The observation period was 12 months, the following outcomes were recorded: cardiovascular events (relapse/repeated AMI, stent thrombosis, revascularisation), hemorrhagic complications, and in-hospital and all-cause mortality during the entire observation period. The study is conducted on the "Quinta" platform. Statistical data processing was performed using IBM SPSS Statistics ver.24.

Results. A total of 10,884 patients were included in the registry, glycoprotein IIb/IIIa inhibitors were prescribed to 114 patients (1%), all of whom underwent percutaneous coronary intervention (PCI), while among patients with non-ST elevation myocardial infarction, the frequency of IIb/IIIa inhibitors was 0.5%, among ST-segment elevation myocardial infarction patients — 1.3%. Eptifibatide was used most often (67.5%), tirofiban was prescribed in 28.9% of cases, abciximab — 2.6%, framon — 0.9%. The most common indication for prescribing drugs were complications of PCI, in particular — distal embolism. There was a higher incidence of cardiogenic shock and multivessel revascularization in the glycoprotein IIb/IIIa inhibitor group. In-hospital mortality and adverse events within 180 days (death, cardiovascular events) did not differ between patients who did and did not receive glycoprotein IIb/IIIa inhibitors. The use of glycoprotein IIb/IIIa inhibitors in this study was associated with an increased risk of all in-hospital bleeding (odds ratio 9.656, confidence interval 2.859-3,894, p <0.001). Other predictors of in-hospital bleeding were: prescription of glycoprotein IIb/IIIa inhibitors, chronic kidney disease with glomerular filtration rate <60 ml/min/1.73 m², body weight less than 60 kg.

Conclusion. We observed a very low frequency of glycoprotein IIb/IIIa inhibitors usage in Russia, while these drugs are used mainly for complications of PCI in the group of patients with the highest risk — with cardiogenic shock, multivessel revascularisation, and complications of the procedure, which can have impact on the outcomes. Further research is needed to develop an optimal protocol for glycoprotein IIb/IIIa inhibitors administration in AMI.

From modern perspective, hyperuricemia should be considered as a trigger of inflammatory activity in tissues and organs, leading to the formation of tophi, arthropathy, kidneys and cardiovascular system damage. Similarly, hypercholesterolemia, a proven factor in atherogenesis-far from all patients leads to the development of relevant clinical events. This commonality may be explained by the involvement of universal inflammatory mechanism. The key mediator of gout attacks is recognized as IL-1β, a product of NLRP3 (NLR family pyrin domain containing 3) inflammasome activation (complex multiprotein), responsible for local inflammatory response in synovial membrane and periarticular tissues with participation of macrophages and neutrophils. NLRP3 inflammasome activation is carried out by uric acid crystals, cholesterol exclusively after priming by lipopolysaccharides, peroxidation products and other damage factors associated with aging and comorbid conditions typical for gout and cardiovascular diseases. In addition, NLRP3 inflammasome activity is genetically determined and determines the frequency of these conditions. The discussed mechanism explains why the impact on factors associated with comorbidity is able to reduce the frequency of gout attacks along with cardiovascular outcomes. New clinically relevant pleotorpic effects of statins, sodium-glucose cotransporter-2 inhibitors, which have advantages over urates-lowering therapy in patients with asymptomatic hyperuricemia and can modify the course of gout, are demonstrated. Their anti-inflammatory properties, cardio and renoprotective effects, and tolerability advantages are emphasized. Blocking the activity of inflammasome is considered as a new universal therapeutic target for rheumatology and cardiology.

Activation of the sympathetic nervous system plays an important role in arterial hypertension (AH) development. Antihypertensive drugs of central action contribute to the elimination of sympathetic activation. The selective imidazoline receptor agonist moxonidine has been successfully used in the treatment of patients with hypertension. The review article presents data on the antihypertensive efficacy of moxonidine, the possibility of its use in combination therapy to reduce elevated blood pressure (BP). The effectiveness of moxonidine in overweight patients, metabolic syndrome, diabetes mellitus, and postmenopausal women is shown. In addition to lowering blood pressure in obese patients, moxonidine reduces plasma leptin levels and weakens sympathetic overactivity, which contributes to weight loss. In patients with metabolic syndrome — obesity, type 2 diabetes mellitus, the use of moxonidine, along with the antihypertensive effect, was accompanied by an additional positive effect on increased variability in blood pressure levels, contributing to the normalization of the daily blood pressure profile, eliminating the morning rise in blood pressure levels. The beneficial effect of moxonidine on carbohydrate metabolism and tissue sensitivity to insulin was noted. The administration of moxonidine to patients with hypertension and menopausal syndrome in peri- and postmenopause, along with effective level control, was accompanied by a significant improvement in the quality of life. In patients with hypertension and osteopenia during menopause, moxonidine led to increased bone formation processes, which helps reduce the risk of developing or progressing osteopenia and osteoporosis. The article focuses on additional indications for the use of moxonidine. In the presence of concomitant pathology — chronic obstructive pulmonary disease, chronic kidney disease, dementia in elderly patients, the use of moxonidine, along with antihypertensive action, led to an improvement in the quality of life.

The most common causes of death in acromegaly are cardiovascular diseases (about 60%). Heart arrhythmias and conduction disorders lead to sudden cardiac death (SCD). In this article, we described a clinical case about preventing SCD in a patient with acromegaly. We identified in this patient predictors of SCD: severe left ventricular hypertrophy, the signs of myocardial fibrosis, decreased systolic function of the left ventricular myocardium, ventricular rhythm disturbances, and heart failure. Patients with acromegaly have higher risk of heart arrhythmias due to development acromegalic cardiomyopathy with includes: left ventricular hypertrophy, diastolic and systolic dysfunction, myocardial fibrosis and electrical disturbances of the myocardium. The main limitation is the lack of special clinical recommendations for the management of this group of patients. Current recommendations based on a standard algorithm and do not consider specificity of acromegalic cardiomyopathy.

Progress in instrumental diagnostics, as well as increased awareness among doctors about rare diseases, is steadily leading to an increased number of patients diagnosed with cardiac amyloidosis. Regardless of amyloid formation route, cardiac damage is the main cause of mortality in systemic amyloidosis. The article presents a unique clinical observation of hereditary transthyretin (ATTR) amyloidosis mixed phenotype detection during skeletal scintigraphy. In the patient with severe shortness of breath, based on the results of radiological research, an oncological process in the lungs was suspected. The patient underwent skeletal scintigraphy to exclude metastatic lesions, during which a scintigraphy pattern characteristic of ATTR amyloidosis (Grade 3) was revealed. Subsequently, the oncological diagnosis was removed. An independent disease of hematopoietic system was excluded, and mutation in TTR gene was additionally confirmed. This clinical case illustrates the possibility of making a diagnosis of cardiac amyloidosis without resorting to myocardial biopsy, when the patient still has slight limitations in physical activity (NYHA class II) and there is no late gadolinium enhancement on magnetic resonance imaging.

The article describes a clinical case of BRASH syndrome in patient M., born in 1938, suffering from hypertension and diabetes mellitus. The patient took bisoprolol, eplerenone, azilsartan medoxomil, lercanidipine hydrochloride daily. She was admitted to the hospital complaining of weakness, eyes darkening, nausea, short-term loss of consciousness, rare pulse, diarrhea the day before. During the examination, she was diagnosed with severe sinus bradycardia (38 beats/min) and transient first-degree atrioventricular (AV) block, stage 4 chronic kidney disease of with hyperkalemia (potassium 5.53-6.12 mmol/l). Pulse-reducing drugs, blockers of the renin-angiotensin-aldosterone system were canceled for the patient, 0.9% sodium chloride solution and furosemide were prescribed. The patient was discharged in a satisfactory condition. This clinical example meets the criteria of BRASH syndrome, since against the background of taking an AV node blocker in a small dose, a patient with chronic kidney disease with mild to moderate hyperkalemia developed severe sinus bradycardia and transient grade 1 AV block. The trigger factors for BRASH syndrome development of were azilsartan medoxomil and eplerenone intake, as well as hypovolemia due to diarrhea.