Introduction. Today, cardiovascular diseases occupy a leading position in the structure of mortality, both in Russia and throughout the  world. Every year more than 17  million people die from cardiac pathology, according to the World Health Organization, an increase in morbidity and mortality is expected in the future, which is explained, first of all, by an increase in the number of patients with diabetes and obesity.

Aim. Development of optimal approaches to predicting cardiovascular events and unfavorable outcomes in patients with peripheral atherosclerosis during a 3-year prospective follow-up.

Materials and methods. The study included 519  patients with atherosclerotic lesions of  various vascular regions, of  which 360 (69.4%) were men, 159 (30.6%) were women. The average age of the examined patients was 60.0 ± 8.7 years.

Results. In the course of the analysis, it was noted that a factor such as the percentage of table stenosis of the left coronary artery (p = 0.013) influenced the risk of developing non-fatal cases of heart failure in patients with peripheral atherosclerosis. With regard to the end point – fatal cases of heart failure, the following factors demonstrated their statistical significance: age of onset of arterial hypertension, years (p = 0.020); history of chronic heart failure (p = 0.020); left atrial size, mm (p = 0.025); degree of stenosis of the posterior lateral branch, % (p = 0.038); presence of atherosclerotic lesions in the region of the posterior interventricular branch (p = 0.002); number of affected vascular beds (p = 0.044).

Conclusions. Using logistic regression equations, original mathematical tools have been developed to assess the risk of developing both fatal and non-fatal heart failure in patients with peripheral atherosclerosis. 

The leading cause of myocardial ischemia in case of coronary atherosclerosis and coronary vasospasm combination in one patient is difficult to establish. However, it is important to know for optimal treatment strategy: choosing between beta-blockers and calcium channel blockers as a preferred treatment, need for percutaneous coronary intervention. We present a case of a 56-yearold patient who was admitted with acute coronary syndrome without ST-segment elevation, low Killip class, and low GRACE score. Stress echocardiography revealed inducible transmural myocardial ischemia (regional wall motion abnormalities and ST segment elevation on the  ECG) accompanied by polymorphic ventricular tachycardia. The coronary angiography showed single-vessel moderate stenosis in the left anterior descending artery. There were no changes in comparison with previous angiography. The patient was considered to have vasospastic angina. A probable mechanism is coronary artery spasm at the site of the atherosclerotic plaque. The article is discussed the difficulties in diagnosing vasospastic angina, especially in the presence of borderline stenosis in the coronary artery. We reviewed similar cases and discussed the difficulties of a vasospastic angina diagnosis especially in the presence of moderate coronary artery stenosis, the role of the provocative tests, and the pharmacological management. Demonstrating, discussing and analyzing cases of patients with a combined mechanism of myocardial ischemia is substantiated for further improving their diagnosis and treatment. 

Angina pectoris is the most common form of chronic coronary insufficiency, treatment of which consists in reducing the number, duration and severity of anginal pains, as well as improving the prognosis: preventing the development of cardiovascular complications such as acute myocardial infarction, life-threatening rhythm disturbances and congestive heart failure. The treatment of coronary artery disease (CAD) has recently undergone significant changes. This is primarily due to the wide introduction into clinical practice of surgical and endovascular methods of myocardial blood flow restoration, which have moved the use of pharmacological of antianginal agents to the background. Despite this, the clinic continues to feel the need for drugs with anti-ischemic properties. This is due to the fact that there is a group of patients who, for various reasons, cannot undergo revascularization of the heart. This is due to the fact that there is a group of patients who, for various reasons, cannot undergo cardiac revascularization. These include individuals with morphological features of the coronary bed, technical obstacles to surgery, increasing number of cases of diabetic microangiopathy as a cause of myocardial ischemia, frequent recurrence of angina after coronary angioplasty. Finally, today we are not yet able to meet all the needs for myocardial revascularization. Thus, the clinical interest in antianginal therapy remains. The present review shows analysis of usage medications with various pharmacological properties in patients with angina in the historical aspect since the second half of the IX century, evolution of the researchers’ ideas about the mechanism of antianginal action, the amount of drugs used. A brief characteristic of modern antianginal drugs presented in the recommendations of the European Society of Cardiologists last revision (2019) is given. 

In guidelines of the European Society of Cardiology (ESC) for the diagnosis and treatment of chronic and acute heart failure 2021 authors have written necessity of regular checkup of all patients with chronic heart failure (CHF) to identify anemia or iron deficiency. The prevalence of anemia in patients with CHF varies significantly depending on the clinical characteristics of the studied population and the criteria for the diagnosis of anemia from 4 to 75%. Frequency of iron deficiency without anemia, according to various studies, achieve 55% of cases. In the literature, data are increasingly appearing that even mild anemia and iron deficiency are associated with worsening symptoms, decreased exercise tolerance. They can provoke increasing of numbers of hospitalizations of patients with CHF, and decreasing of their quality of life and increasing rate of mortality. In this paper a number of factors determining iron deficiency in patients with CHF are analyzed. The article also assesses the current state of the problem of the dependence of the presence of anemic syndrome and the gender-age characteristics of patients with CHF, observed in  a  number of  studies, which remains quite contradictory to date. The results of  the study of  the mechanisms of development of secondary erythrocytosis and the course of CHF against the background of anemic syndrome, iron deficiency conditions, relative erythrocytosis are presented, promising directions of drug correction are reflected. Data from randomized controlled trials (RCTs) on the possibility of using iron supplementation as part of the management of patients with CHF and iron deficiency status are presented. It was noted that using of an injectable form of iron carboxymaltosate in patients with CHF and low EF improves the functional class of CHF according to NYHA, quality of life, tolerance to physical activity, as well as contributes to an increase in the left ventricular ejection fraction and its final systolic volume. 

Chronic heart failure (CHF) is one of the most important problems in clinical cardiology due to high morbidity, frequent hospitalizations and poor prognosis of patients. Quite unexpectedly, sodium-glucose cotransporter type 2 (SGLT2i) inhibitors dapagliflozin and empagliflozin, which were created for the treatment of diabetes mellitus, proved to be effective means of reducing the risk of an adverse outcome in patients with CHF, they were included in a new four-component therapy for CHF with a reduced left ventricular ejection fraction with a class of recommendations I and level of evidence A. The basis for changing the clinical guidelines for CHF was the results of large randomized trials of DAPA-HF and EMPEROR-Reduced. Despite the obvious clinical benefit of using SGLT2i in CHF, the mechanisms of the observed effects remain speculative and continue to be actively studied. In particular, the literature discusses the role of osmotic diuresis, lowering blood pressure and body weight, increasing erythropoietin production, influencing myocardial remodeling, modifying the energy metabolism of the heart, inhibiting the sodium-hydrogen exchanger, autophagy, and influencing leptin and adiponectin levels. SGLT2i has many of the qualities of an ideal agent for the treatment of CHF with reduced left ventricular ejection fraction, including a single dose without the need for titration, once daily administration, early positive effects on clinical outcomes and quality of life, a favorable safety and tolerability profile with a frequency of serious side effects not different from placebo. At the same time, the choice of medical tactics may be influenced by the features of the evidence base of SGLT2i, in particular, the reduction in cardiovascular mortality and death from any cause in a randomized trial of dapagliflozin.

Cardiovascular disease is the most common cause of death in the world. For almost 60 years vitamin K antagonists (VKAs) have been the mainstay of anticoagulant therapy, but in recent years direct oral anticoagulants (DAACs) have become the anticoagulant of choice, as they have many well-known advantages: more predictable anticoagulant effect, no need for dose selection (there is  a  need for  dose adjustment only for  renal dysfunction), routine laboratory monitoring of  pharmacodynamic effect  (except in special clinical situations), less frequency of clinically significant drug interactions compared with warfarin, and less dependence on patient genetic characteristics. The main indications for POAC are: prevention of venous thromboembolism in patients who have undergone endoprosthesis of lower limbs, prevention of stroke and systemic embolism in patients with atrial fibrillation, treatment and prevention of recurrent deep vein thrombosis (DVT) and pulmonary embolism. The administration of direct oral anticoagulants (DOACs) has long been considered a major therapeutic advance, mainly because they do not require therapeutic monitoring. Despite this, POACs, like vitamin K antagonists, can still cause major and clinically significant minor bleeding, even when used correctly. Considering that POAC patients are often older and have multiple comorbidities, polypragmasy is widespread. Drug interactions involving POACs are important contributors to the increased risk of bleeding. Awareness of these drug interactions and how to address them is critical to optimizing treatment while reducing the risk of bleeding. This review provides an overview of POAC metabolism, the most common drugs that may interact with POACs, and ways to eliminate these interactions. 

Introduction. Fibroblast growth factor type 23 (FGF-23) inhibits phosphate reabsorption and vitamin D hormone synthesis in the kidneys. There is a known relationship between FGF-23 levels and serum phosphate, as well as a direct correlation between hyperphosphatemia and the risk of cardiovascular events.

Aim. To evaluate associations between serum FGF-23 levels and bone and mineral metabolism in patients on renal replacement therapy (RRT) with hemo- and peritoneal dialysis, receiving and not receiving phosphate binders.

Materials and methods. The study included 65 patients, of which 43 received maintenance hemodialysis tratment (HD), and  22 – peritoneal dialysis (PD). The control group consisted of 28 healthy volunteers.

Results. The increase in the concentration of FGF-23 in the blood serum in patients on maintenance HD correlated with the vintage of dialysis treatment (rs = 0,765; p = 0,04). The positive correlation was found between the serum concentrations of FGF-23 and inorganic phosphorus (rs = 0,54; p = 0,03). The serum level of FGF-23 positively correlated with the serum PTH level (rs =  0,5; p = 0,01). In patients receiving sevelamer carbonate levels of  FGF-23  was lower, than in  control group (12.4 ± 5.9, and 23 ± 7.3, respectively; p = 0.003), as well as PTH (110 ± 27 ng/mL, and 340 ± 15, respectively; p = 0.01).

Conclusions. The level of FGF-23 in dialysis patients directly correlated with the serum level of PTH and “dialysis vintage”. The use of phosphate binders, in particular sevelamer carbonate, positively affects the expression of FGF-23 and PTH in dialysis patients. 

Introduction. Patients with chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD) are increasingly found in the clinical practice. The comorbidity of CHF and COPD promotes high mortality in such patients. Therapy that is prescribed to patients with CHF and COPD may not always have a positive effect on the condition of blood vessels. In this regard, researchers began to pay attention to drugs that have a beneficial effect on blood vessels, without worsening the course of CHF and COPD, one of which is meldonium.

The purpose of the study. To study the effect of meldonium as part of complex therapy on arterial stiffness and microcirculation in patients with CHF and COPD.

Materials and methods. The open randomized study included 60 patients with CHF IIA stage, II–III functional class (clinical recommendations of RKO, OSSN 2020) and COPD of the I–III degree of airflow restriction (classification GОLD 2021) without exacerbation. The patients were divided into 2 groups: the 1st group – the main group (n = 30) with CHF and COPD, which was prescribed meldonium as part of complex therapy at a dosage of 1000 mg/day, the 2nd group – the control group (n = 30) was on therapy only with basic drugs of CHF and COPD. The observation period is 12 weeks.

Results. As a  result of  12  weeks of  therapy with the  inclusion of  meldonium in  the complex therapy of  patients with CHF and COPD, a decrease in the stiffness of the main arteries, an improvement in the regulation and parameters of microcirculation, an increase in the frequency of occurrence of the normocirculatory type of microcirculation were noted.

Conclusions. A significant useful effect of complex therapy with the inclusion of meldonium on the condition of arterial stiffness and microcirculation in  patients with CHF and COPD has been established, which makes it possible to recommend the  use of meldonium in this category of patients. 

Introduction. Association of left ventricular hypertrophy (LVH) in obesity and accompanying metabolic risks with adipokines levels at the different stage of heart failure (HF) is still debatable.

The aim of study was to investigate the relationship of circulating adipokines levels with LVH in obese patients at preclinical stage of HF.

Materials and methods. The study included 74 obese patients: 43% had no markers of LVH (stage A HF, group 1); 57% had LVH (stage B HF, group 2). Transthoracic echocardiography, laboratory assessment of N-terminal fragment of the brain natriuretic peptide, soluble suppression of tumorigenesis-2 (sST2), circulating leptin and adiponectin levels, homeostasis model assessment of insulin resistance (IR) (HOMA-IR) were done. Matched-pairs analysis was applied.

Results. Negative correlations of LVH with leptin levels in group 1 (stage A HF) and with adiponectin levels in group 2 (stage B HF) were detected (all p < 0.05). Positive correlations of the sST2 / adiponectin ratio and HOMA-IR with the parameters of LVH were detected in group 2 (all p >< 0.05). Conclusion. The direction of the associations between circulating adipokines and LVH varies with the preclinical stage of HF. The data obtained may reflect a relationship between heart remodeling in response to molecular mechanisms of inflammation and IR in obese patients at the certain stage of cardiovascular continuum. Keywords: leptin, adiponectin, insulin resistance, HOMA-IR, inflammation, sST2, left ventricular hypertrophy>˂ 0.05). Positive correlations of the sST2 / adiponectin ratio and HOMA-IR with the parameters of LVH were detected in group 2 (all p ˂ 0.05).

Conclusion. The direction of the associations between circulating adipokines and LVH varies with the preclinical stage of HF. The data obtained may reflect a relationship between heart remodeling in response to molecular mechanisms of inflammation and IR in obese patients at the certain stage of cardiovascular continuum. 

Introduction. In the treatment of stable angina in patients with concomitant bronchial asthma (BA), the bronchopulmonary system may be adversely affected by a number of drugs. Diltiazem may be the drug of choice when antianginal therapy with a pulseslowing effect is required, but β-blockers are contraindicated.

Aim of the study. To compare the antianginal, pulse-slowing and vasoprotective effects of the calcium antagonist (CA) diltiazem, the calcium antagonist verapamil and the cardioselective beta-adrenoblocker (BAB) bisoprolol in the treatment of stable angina (SA) patients with concomitant BA.

Materials and methods. The study included 60 patients with stable angina II-III FC with concomitant mild or moderate persistent BA. The patients were divided into three groups of 20 patients depending on antianginal drugs: Group 1 received betaadrenoblocker bisoprolol, Group 2 – calcium antagonist verapamil, Group 3 – calcium antagonist diltiazem. All patients underwent cardiography (Doppler EchoCG), external respiration function (ERF), endothelium-dependent vasodilation (EDVD) study at baseline and after 2, 4, 6 weeks of treatment.

Results. No negative dynamics of FEV1 was found in patients of all groups during the study of ERF after 6 weeks of treatment. There was a statistically significant increase in FEV1 after 6 weeks of treatment in group 3 patients receiving diltiazem (p = 0.032). There was a statistically significant decrease in HR in all three groups during treatment, but in group 2 the dynamics were significantly lower when treated with verapamil. Analysis of mPAP of patients showed that it decreased in all groups after 6 weeks of treatment, but significant dynamics was noted only in Group 3. EDVD test after 6 weeks of treatment revealed positive dynamics, with a statistically significant increase in the index registered in patients of groups 1 and 3.

Conclusions. In treatment of patients with stable angina with mild and intermediate persistent disease without exacerbation, antianginal therapy with the calcium antagonist diltiazem has marked antianginal, pulse-slowing action, has vasoprotective effect on the small and large circulatory vessels, improves the parameters of bronchial permeability. 

Introduction. The presence of obstructive sleep apnea (OSAS) in patients with chronic heart failure (CHF) increases cardiovascular and overall mortality in comparison with patients without breathing disorders during sleep.

Aim of study. Assessment of prevalence and dynamics of OSAS in patients with CHF due to rheumatic heart disease (RHD).

Materials and methods. The study included 172  patients with RHD. OSAS was assessed using a  cardiorespiratory monitor “Kardiotekhnika-04-3Р (M)”.

Results and discussion. Analysis of echocardiography results of showed a significant increase in the linear dimensions of the LV: for LVED B = 0.020 (0.013; 0.027), p = 0.001, R2  = 0.087; for LVES B = 0.017 (0.010; 0.024), p = 0.001, R2  = 0.073. An increase in the indices of  hypertrophy was also revealed  – LVPW and IVS: for  IVS B  = 0.008  (0.006; 0.010), p  = 0.001, R2   = 0.148; for  LVPW B = 0.006 (0.004; 0.08), p = 0.001, R2  = 0.087. The highest values of echocardiography indicators were achieved in the group with OSAS III, in comparison with patients without OSAS. significantly differed: for LVED – 0.86 cm, for LVES – 0.56 cm, for IVS – 0.41 cm, for  LVPW  – 0.34  cm. but there was also the  maximum distance of  the 6-minute walk test  – 390.02  (360.15; 419.88) meters. Assessment of the quality of life according to the summary scales of the questionnaires showed a higher level of quality of life in the group without OSAS according to the physical health SF-36 (B = -0.100 (-0.169; -0.031), p = 0.005, R2  = 0.029), mental health SF-36 B = 0.120 (-0.091; 0.115), p = 0.821) and according to overall summary score KCCQ (B = -0.289 (-0.473; -0.105), p = 0.002, R2  = 0.036).

Conclusion. In the dynamics over 10 years, in patients with RHD, there was an increase in the number of episodes of obstructive and central apnea, an increase in the frequency of episodes of apnea / hypopnea with desaturation and snoring. However, a significant increase was achieved only in the case of obstructive sleep apnea episodes – by 14.60 episodes. 

Introduction. Frequent comorbidity of chronic obstructive pulmonary disease and myocardial infarction is due to the commonality of a number of etiopathogenetic links and the development of endogenous intoxication syndrome. The convincing markers of endogenous intoxication syndrome are medium and low molecular weight molecules including medium and low molecular weight substances and oligopeptides.

Aim. To study the levels of medium and low molecular weight substances in patients with myocardial infarction against the background of chronic obstructive pulmonary disease.

Materials and methods. 225 patients with myocardial infarction were examined. In 195 patients the infarction developed against the background of COPD, in 130 patients – without COPD. The comparison group consisted of 110 somatically healthy individuals. Substances of medium and low molecular weight (MLMWS) and oligopeptides (OP) were determined by direct spectrometry (according to M.Y. Malakhova, 1995) in plasma, erythrocytes and urine. Endogenous intoxication indices and intoxication coefficient were calculated on the basis of these indices. Statistical processing of the data was performed using SPSS 26.0 software package.

Results. In blood plasma and erythrocytes, the levels of average molecules in both studied groups were statistically significantly higher compared to controls. The highest levels were detected in comorbid patients. In the group of patients with myocardial infarction without chronic obstructive pulmonary disease 60% of the examined patients had phase I endogenous intoxication. Phase III intoxication prevailed among comorbid patients with myocardial infarction against chronic obstructive pulmonary disease – 62,6%.

Conclusions. Molecules of average mass have proven to be informative indices of endogenous intoxication syndrome in patients with myocardial infarction accompanied by chronic obstructive pulmonary disease. This opens the prospect of using these indices in the development of assessment scales and the creation of prognostic algorithms in patients with cardiorespiratory comorbidity. 

Introduction. The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was declared a pandemic by the World Health Organization (WHO) in March 2020. New waves of different virus genotypes regularly roll across the globe. Recent studies show the most serious prognosis for patients with known cardiovascular disease, indicating a possible relationship between SARS-CoV-2 infection and an increase in new cases of cardiovascular diseases and diabetes regardless of the severity of the pathology. If this trend is true, with hundreds of millions of infected patients the disease burden might presage a potentially alarming rise of cardiovascular diseases and diabetes in the future.

The aim is to study the laboratory test results of patients with novel coronavirus infection COVID-19 with underlying type 2 diabetes mellitus (DM) and chronic heart failure.

Materials and methods. A  total of  51  patients with a  verified diagnosis of  moderately severe novel coronovirus infection COVID-19 with underlying type 2 diabetes and chronic heart failure were included in the study. All patients underwent quantitative laboratory blood tests. Correlation analysis was carried out using the Spearman’s rank correlation coefficient.

Results and discussion. In our opinion, the most interesting were numerous correlations between glucose levels and internal organs and systems dysfunction markers: with bilirubin levels, international normalized ratios, creatinine levels, with carbon dioxide (ctCO2 ) levels, bases (BE) levels, with the bicarbonate (HCO3  act) levels. The most pronounced (rs  = 0.74) was the correlation between glucose levels and basophil counts, which may suggest a  possible effect of  hypersensitivity mechanisms on the severity of hyperglycemia in patients with COVID-19.

Conclusions. The hyperglycemia level indicates the severity of not only metabolic acidosis, but also the internal organs and systems dysfunction in patients with novel coronavirus infection COVID-19 with underlying type 2 diabetes and heart failure. 

Peripartum cardiomyopathy (PPCM) is a diagnosis of exclusion in women presenting with heart failure due to left ventricular (LV) systolic dysfunction. PPCM should be considered in case of unknown etiology of heart failure during pregnancy or after childbirth. Long QT syndrome is a primary electrical heart disease associated with a prolonged QT interval on the ECG, recurrent paroxysms of ventricular tachycardia, and a high risk of sudden death. Our aim was to demonstrate a case of cardiomyopathy in combination with long QT syndrome in a patient with a mutation in the FLNC gene. A 38-years-old woman was hospitalized 4,5 months after childbirth after sudden cardiac arrest and successful cardiopulmonary resuscitation. Long QT interval was revealed on the electrocardiogram. Echocardiography registered an akinesis of the apical and middle segments of the anterior wall of the left ventricle and interventricular septum, apex, left ventricular ejection fraction – 32%. Coronary angiography revealed no stenotic lesion of the coronary arteries. N-terminal precursor of brain natriuretic peptide (NTproBNP) was 33300 mg/l. Mass parallel sequencing of 17 genes revealed the nucleotide variant c.1609T>G (chr7:128480661T>G, NM_001488.4; rs760471547) in a heterozygous state in exon 10 of the FLNC gene (OMIM 102565), leading to the amino acid variant p.Y537D.The combination of peripartum cardiomyopathy and long QT syndrome may increase the likelihood of sudden cardiac death, especially in individuals with a genetic mutation of cardiomyopathy. Timely diagnosis of the described conditions is necessary to prevent complications and increase the life expectancy of patients. 

In this paper the information about a comparatively rare form of cardiomyopathy – noncompaction of the left ventricular myocardium is showed. As a result of genetical changes on the early stages of embryogenesis a disability of myocardial fibres develops, and two-layer myocardial structure is formed: thin compact layer and remaining more voluminous non-compact layer with significant trabeculation and deep intratrabecular cavities communicated with ventricular cavity. Mutations in  genes which encode sarcomeric, structural and regulatory proteins and proteins, which are responsible for ion channels functioning, are considered to be one of the main reasons of non-compact myocardium. There is a theory that considers a non-compact myocardium as a result of an exposure of various factors during lifetime – so-called non-embryonal (acquired) noncompaction myocardium. “Non-embryonal” hypothesis views non-compact myocardium as a sign of functional maladaptation, possible stage in cardiomyopathy development. By way of illustration the clinical case of 32-year-old female patient is presented in the article. The noncompaction of  the left ventricular myocardium in  conjunction with restrictive cardiomyopathy was first diagnosed in  her. The  diagnosis was confirmed by main diagnostic methods for  this pathology such as echocardiography and MRI of  a  heart. This clinical observation is interesting due to formation of disease patterns by two rare combined pathological conditions: noncompaction of the myocardium syndrome and restrictive cardiomyopathy. Changes of heart hemodynamics occurs in interaction between these pathologies. Diastolic filling of left ventricular decreases as a result of restrictive cardiomyopathy, which leads to decreasing of its myocardium load. Therefore, systolic disfunction, which is specific to non-compact myocardium, doesn’t occur. Generally, prognosis for this patient is poor due to presence of two serious pathologies. 

Statins represent an important class of cardiovascular drugs for the prevention of atherogenic complications. However, despite the effectiveness of statins, non-adherence and discontinuation of therapy with these drugs is a problem worldwide. Reasons for not using statins in patients at high CV risk include statin-associated muscle symptoms (SAMS), which are not usually associated with significant elevations of serum creatine kinase. SAMS are the most common side effects of statins: 3–5% in RCTs, 15–20% in observational studies, and 60% in patient surveys. This range is possibly due to misinterpretation of symptoms, as well as patients’ expectation of harm from statin treatment (“statin fear”). The article highlights the problem of studying the role of nocebo and drusebo effects for SAMS, presents differences in definitions and methods of detection. The concept of the drucebo effect was proposed by the International Lipid Expert Group (ILEP, 2018) as a harm to the patient, unrelated to the pharmacological action of the drug (negative effect of the drucebo). The results of studies and meta-analyses evaluating the effects of nocebo and drusebo for SAMS are presented, in which no difference was found in the frequency and severity of muscle symptoms between statin and placebo; the nocebo rate was 90% of the statin effect, and the contribution of the drusebo effect to SAMS and statin discontinuation ranged from 38 to 78%. Also presented are current international guidelines and principles of patient management aimed at preventing discontinuation of statin use in connection with SAMS. 

Introduction. A special position among the structural changes of the heart is occupied by left ventricular myocardial hypertrophy (LVH), which refers to the subclinical signs of heart damage in arterial hypertension (AH). Currently, the role of not only demographic, neuroendocrine, but also genetic factors in the development and progression of LVH is no longer in doubt.

Aim. To assess the role of clinical and genetic factors in the progression of LVH in patients with hypertension based on the results of a dynamic 5-year follow-up of a cohort of Shors.

Materials and methods. The survey of the indigenous population in Gornaya Shoria was carried out in two time periods: onetime (from 2013 to 2017) and prospective (from 2018 to 2020). The study included the adult population (18 years and older) – a total of 901 people – by continuous method. A group of patients with hypertension was identified – 367 people (40.7%). LVH was assessed by electrocardiography and/or echocardiography. The prospective stage of the study included patients with hypertension who had not previously received antihypertensive therapy (263 people). The control and correction of blood pressure numbers was carried out annually, the dynamics of LVH was assessed after five years.

Results. Clinical predictors of negative dynamics of LVH were established: obesity (OR = 3.61), abdominal obesity (OR = 4.11), impaired carbohydrate metabolism (OR = 2.83), low high-density lipoprotein cholesterol (OR = 2.05). Genetic markers also demonstrated their involvement in the progression of LVH: allele D of the ACE gene, allele C of the AGTR1 gene, and 4a of the eNOS gene (OR = 9.69; OR = 6.72; OR = 6.37, respectively).

Conclusion. The associations of clinical and genetic factors with LVH identified in the Shor cohort can be considered as predictors of myocardial remodeling in hypertension. The data obtained support the hypothesis that polymorphisms of the renin-angiotensin-aldosterone system and endothelial function can influence the phenotype, creating new approaches to the possible prediction of unfavorable outcomes.