The article describes the history of the discovery of aldosterone and the creation of its antagonist, spironolactone. The effects of aldosterone associated with the stimulation of two types of receptors.  Long-term effect (nuclear or genomic) and fast - term (membrane). They are manifested not only by the influence on the water-salt metabolism and the volume of extracellular fluid, but also in the regulation of vascular tone and elasticity of the vascular wall and, most interestingly, the effect on cardiac remodeling. Early after its development  Spironolactone was considered as a medicine for water-salt metabolism regulation, diuresis and normalization of blood pressure. In the following period,  Spironolactone embraced a new area - systolic heart failure. The drug was considered not only to enhance safe diuresis, but also to eliminate the phenomenon of escape of the antialdosterone effect angiotensin-converting enzyme inhibitors. The change in the paradigm of heart failure towards the prevailing changes in her diastolic phenotype, which is based on excessive diffuse myocardial fibrosis, changed role of spironolactone in the treatment of heart failure. Currently, it is considered as an independent drug, due to its powerful antifibrotic effect, blocking which controls the whole complex of endo- and paracrine effects of aldosterone.

Aim      To study the prevalence of hyperlipidemia in patients with myocardial infarction (MI) in the Russian Federation; to assess the compliance with clinical practice guidelines of the lipid-lowering therapy prescribed upon discharge from the hospital; and to determine the number of patients who are indicated for the combination lipid-lowering therapy to achieve the low-density lipoprotein cholesterol (LDL-C) goal.

Material and methods  REGION-MI is Russian rEGIstry Of acute myocardial iNfarction, a multicenter, retrospective and prospective observational study. The observation period was divided into 3 stages: observation during the stay in the hospital and at 6 and 12 months after the inclusion in the registry. Plasma total cholesterol (TC) and LDL-C were measured in all patients on admission. Evaluation of the prescribed lipid-lowering therapy included the intensity of the treatment.

Results The study included 3 620 patients; 62.4 of them had hyperlipidemia on admission. Mean TC on admission was 5.29 mmol/l and LDl-C level was 3.35 mmol/l. Upon discharge, 95.4% of patients after myocardial infarction continued on or were prescribed statin therapy; ezetimibe was prescribed to 1.22% of patients. Patients with an extremely high level of LDL-C >5 mmol/l accounted for 10.7% of patients with hyperlipidemia. The target level of LDL-C ≤1.4 mmol/l cannot be achieved with the statin and ezetimibe combination therapy in these patients; drugs from the group of PCSK9 inhibitors are indicated for them.

Conclusion      According to the data of the Russian registry of acute myocardial infarction, REGION-MI, a high incidence of hyperlipidemia is observed in patients with acute MI. Despite multiple studies that have proven the importance of achieving a low LDL-C level and good tolerance and safety of ezetimibe and PCSK9 inhibitors, the prescription frequency of combination therapy remains unreasonably low. Results of a simulation study that was conducted in Sweden and the data of the REGION-MI registry showed that PCSK9 inhibitors as a part of the combination therapy are indicated for many patients. The combination therapy is presently the most powerful type of lipid-lowering treatment that allows, in most cases, achievement of the LDL-C goal.

Aim      To study the relationship between monomeric C-reactive protein (mCRP) and the progression of asymptomatic carotid atherosclerosis in patients with a moderate risk for cardiovascular diseases (CVD) as assessed with the SCORE model.

Material and methods  The study included 80 men and women aged 53.1±5.8 years assigned to the category of a moderate risk for CVDs by the SCORE model with a low-density lipoprotein cholesterol (LDL-C) level of 2.7–4.8 mmol/l and asymptomatic, hemodynamically insignificant (<50% luminal narrowing) carotid atherosclerosis according to ultrasonic data. All patients were prescribed atorvastatin to achieve a LDL-C level <2.6 mmol/l. After 7 years of follow-up, ultrasonic examination of carotid arteries was performed, and concentrations of high-sensitivity C-reactive protein (hsCRP) and mCRP were measured.

Results A concentration of LDL-C <2.6 mmol/l was achieved in all patients. The progression of atherosclerosis as determined by an increased number of atherosclerotic plaques (ASPs), was observed in 45 (56 %) patients. At 7 months of follow-up, concentrations of cCRP were higher in the group of patients with progressive carotid atherosclerosis, while the levels of hsCRP did not differ between the groups. Increased mCRP concentrations were associated with changes in variables of the “atherosclerotic load”, including the number of ASPs, total ASP height, and the intima-media thickness (IMT). In patients with a median mCRP concentration of 5.2 [3.3; 7.1] µg/l and more, the increases in mean ACP number and total ASP height were considerably higher than in patients with mCRP concentrations lower than the median (3.9 and 2.7 times, respectively), whereas the odds ratio for the progression of asymptomatic carotid atherosclerosis was 5.5 (95 % confidence interval, CI: 2.1–14.6; p=0.001). ROC analysis showed that the concentration of hsCRP had no predictive value for prognosis of asymptomatic carotid atherosclerosis (p=0.16), while the area under the ROC curve (AUC) for mCRP was 0.75±0.056 (95 % CI: 0.64–0.86; p=0.001).

Conclusion      According to the results of 7-year follow-up, the plasma concentration of mCRP was significantly higher in patients with an increased number of ASPs than in patients without this increase. An increased level of mCRP may indicate a higher inflammatory risk of CVD.

Aim      To study the relationship of the platelet function and plasma homeostasis with the blood flow in the infarct-related artery (IRA) and with the course of acute myocardial infarction (AMI).

Material and methods  This study included 93 patients with AMI (75 patients with ST-elevation AMI and 18 patients without ST segment elevation). 63 patients had TIMI 0-1 blood flow in the IRA and 30 patients had TIMI 2–3. Rotational thromboelastometry, impedance aggregometry, the endothelium-dependent vasodilation (EDVD) test, and the thrombodynamics test were performed for all patients. The primary clinical endpoint included the totality of in-hospital complications of AMI, and the secondary endpoint included the totality of out-of-hospital complications of AMI. Major bleedings (BARC 3-5) and minor bleedings (BARC 1-2) were evaluated separately.

Results Patients with IRA TIMI 0–1 flow were characterized by a shorter blood clotting time (BCT), larger thrombus size and density, more intense platelet aggregation induced by arachidonic acid and ADP, and lower values of the EDVD test. It was found that the parameters of platelet aggregation induced by arachidonic acid (AUC Asa) in combination with BCT allowed assessment of the severity of IRA blood flow disorder (sensitivity 76 %, specificity 71 %) in patients with AMI, regardless of the presence of ST segment elevation on the ECG. In addition, the incidence of the primary endpoint was greater in patients with IRA TIMI 0–1 flow (41.3% and 16.7%, respectively; p=0.015). In patients with TIMI 2–3 flow in the long-term period of the disease, the incidence of minor bleedings was significantly higher (8.5% and 30.4 %, respectively; p=0.045).

Conclusion      Compared to patients with preserved blood flow, patients with AMI and IRA TIMI 0–1 flow are characterized by endothelial dysfunction and more intense processes of thrombogenesis and platelet aggregation. It has been shown for the first time that the combination of two simple criteria for assessing hemostasis (AUC Asa; BCT) allows assessment of the degree of IRA blood flow disorder in patients with AMI.

Aim    Endothelial progenitor cells (EPCs) play important roles in heart valve replacement surgery. Up-regulation of Grb2‑associated binder 1 (Gab1) promotes hepatocyte growth factor (HGF) – induced endothelial progenitor cell proliferation and migration. This study aimed to investigate the effects of up-regulation of Gab1 in hepatocyte growth factor-induced EPCs in tissue-engineered heart valves (TEHV).
Material and methods    Fresh porcine aortic valves were placed in 1 % Triton X-100 and trypsin buffer for decellularization. EPCs in the control group were cultured normally, whereas those in the experimental group were both HGF stimulated and transfected with adenovirus containing the Gab1 gene. Cells in the two groups were seeded onto the decellularized valve scaffolds and cultured for 3 or 7 days. TEHV were analyzed by HE and AB-PAS staining.
Results    By day 3, the experimental group had formed confluent endothelial monolayers on top of the decellularized valves, on the basis of by HE staining and AB-PAS staining. One week later, the control group showed a imperfect endothelial layer.
Conclusion    HGF-induced EPCs overexpressing Gab1 can endothelialize the decellularized matrix and create functional TEHV, which may then be preconditioned in a bioreactor before clinical implantation.

The article discusses the problem of improving the effectiveness of treatment of heart failure with preserved left ventricular ejection fraction (HFpEF). The relative "failure" of early studies with renin-angiotensin-aldosterone system inhibitors was largely due to the lack of understanding that patients with HFpEF represent a heterogeneous group with various etiological factors and pathogenetic mechanisms of the disease. Therefore, the so-called personalized approach should be used in the treatment of these patients. This approach is based on the identification of clearly defined disease phenotypes, each characterized by a set of demographic, pathogenetic, and clinical characteristics. Based on the literature and own experience, the authors consider four main phenotypes of HFpEF: 1) phenotype with brain natriuretic peptide “deficiency” syndrome associated with moderate/severe left ventricular hypertrophy; 2) cardiometabolic phenotype; 3) phenotype with mixed pulmonary hypertension and right ventricular failure; and 4) cardiac amyloidosis phenotype. In the treatment of patients with phenotype 1, it seems preferable to use the valsartan + sacubitril (possibly in combination with spironolactone) combination treatment; with phenotype 2, the empagliflozin treatment is the best; with phenotype 3, the phosphodiesterase type 5 inhibitor sildenafil; and with phenotype 4, transthyretin stabilizers. Certain features of different phenotypes overlap and may change as the disease progresses. Nevertheless, the isolation of these phenotypes is advisable to prioritize the choice of drug therapy. Thus, the diuretic treatment (preferably torasemide) should be considered in the presence of congestion, regardless of the HFpEF phenotype; the valsartan + sacubitril and spironolactone treatment is appropriate not only in the shortage of brain natriuretic peptide but also in the presence of concentric left ventricular hypertrophy (except for the amyloidosis phenotype); and the treatment with empagliflozin and statins may be considered in all situations where pro-inflammatory mechanisms are involved.

This review focuses on the participation of von Willebrand factor (VWF), that considerably contributes to thrombogenesis in damaged blood vessels, in the pathogenesis of atherosclerosis-induced cardiovascular pathology. Excessive formation and dysfunction of VWF leads to intravascular thrombosis and facilitates the development of endothelial dysfunction, vascular inflammation, and, thereby, the initiation and progression of atherosclerosis. The review presents information based on the analysis of full-text publications from PubMed that address the role of VWF in the development of atherosclerosis and its complications as well as the potential for influencing this index.

This article summarizes current information about the interrelation between testosterone concentrations and chronic heart failure (CHF). The authors described key publications that address the prevalence of testosterone deficiency in patients with CHF, the effect of endogenous and exogenous testosterone on the cardiovascular system, the relationship between testosterone levels and the severity and prognosis of CHF, and the efficacy of interventional treatments for CHF.

This article presents two clinical cases of patients with myocardial infarction and stage A (at risk) and B (beginning) cardiogenic shock who underwent intra-aortic balloon counterpulsation (IABP). In patients with a high risk of classic cardiogenic shock and/or the no-reflow phenomenon, stenting of the infarct-related coronary artery during this type of mechanical circulatory support was performed without complications. Theoretical and practical aspects of using IABP at different stages of cardiogenic shock are discussed.