The authors of the article have analyzed the problem of advanced heart failure (AHF). Despite significant and, without exaggeration, revolutionary achievements in clinical pharmacology, cardiac surgery, and implantation arrhythmology, the number of patients with chronic heart failure (CHF) in many countries is not decreasing, and in some states, for example, in Russia, it is increasing. At the same time, unfortunately, immediate and long-term results of the so-called optimal therapy of CHF are often disappointing for both the patient and the doctor. In 2007, experts from The Heart Failure Association of the European Society of Cardiology proposed the term advanced heart failure (AHF) to refer to CHF in which optimal drug therapy, as well as cardiac resynchronization therapy, are not effective, which causes repeated hospitalizations and justifies the need for advanced treatment methods such as heart transplantation and mechanical circulatory support, and/or transition to palliative care. The opinions of experts from the established cardiological communities in the Old and New Worlds on the definition, diagnostic criteria, and treatment of AHF have been changing over time. Unfortunately, this evolution has not yet arrived at a consensus. The lecture consistently addresses the issues of terminology, diagnosis, prognostic stratification, and routing of patients with AHF, as well as short- and long-term strategies for treating these patients. therapy; ICD − implantable cardioverter-defibrillator; LVEF − left ventricular ejection fraction; NYHA − New York Heart Association; RAS – renin- angiotensin system; SBP− systolic blood pressure; SCr − serum creatinine.

The authors of this article have analyzed the problem of diagnostic conclusion unification in patients with chronic heart failure (CHF). The root of this problematic situation in which practitioners find themselves is that, despite the large number of different regulatory documents, there is no consensus on what is considered correct and what is wrong when formulating a diagnostic conclusion in a patient with CHF. The many-faced syndrome is designated differently: CHF, congestive heart failure, chronic circulatory failure. There are difficulties in determining the stage of CHF in patients receiving optimal drug therapy or in those who are in a state of compensation after a successful surgical correction. When assessing the functional status in a patient with CHF, a distinct subjectivity should be taken into account in determining which limited physical activity is slight or, conversely, marked, as well as what kind of physical exertion is normal for the patient. This subjectivity naturally leads to low reproducibility of the assessment results of the CHF functional class in the same patient by different doctors. CHF should also be classified according to the value of a left ventricular ejection fraction. The diagnosis should also take into account the state characteristics of a diastolic function of the left ventricle (especially in patients with CHF and preserved left ventricular ejection fraction). The authors give examples of diagnostic conclusions, including cases of comorbid pathology.

The authors of the study analyze various definitions of chronic heart failure (CHF). CHF, having many faces, despite the consensus concerning the paradigm of its pathogenesis, is given different definitions, using both the syndromic and nosological approaches. Most authors share a view of CHF as the final stage (outcome or complication) of many diseases in which there is impairment of ventricular filling or ejection of blood, i.e. as a syndrome, and not an independent nosological form. Nevertheless, at the beginning of the XXI century leading Russian specialists in heart failure presented a reasoned point of view on CHF not only as the final stage of the cardiovascular continuum, complicating the course of a disease of the cardiovascular system, but also as an independent nosological form. This approach, which contradicts the standard rules for the formulation of the final clinical and pathological diagnoses, as well as the agreed positions of the International Statistical Classification of Diseases and Related Health Problems, has been the subject of reasonable criticism. Since the identification of the underlying cause of heart failure is crucial for therapeutic reasons, the only correct view is that of CHF as a syndrome, the detailed description of which in clinical diagnosis is an important intranosological characteristic that allows building the most effective differentiated therapy and accurately determining the prognosis of the disease.

The authors of the review have analyzed papers published on the problem of pathogenesis chronic kidney disease (CKD), which the experts of the K/DOQI (Kidney Disease Outcomes Quality Initiative) Advisory Board (National Kidney Foundation, USA) is defined as the presence of kidney damage or decreased level of kidney function for three months or more, irrespective of diagnosis. It is shown that the specific mechanisms which result directly from the nature of the disease, completely determine the course of CKD in its initial stage, whereas further reduction in the number of intact nephrons, cascade is initiated univer-sal for all of nephropathy pathological processes, culminating in the formation of nephrosclerosis, often even if the reason that caused the initial damage to the nephrons is eliminated: hyperfiltration, hypercoag-ulability, impaired renal transport protein, changes in the expression of mediators of cell damage, meta-bolic and endocrine mechanisms, polymorphism of genes controlling the expression of nephrotropic bio-logically active substances. Analyzed published data demonstrate that renal protection strategy (complex therapies aimed at the inhibition of the irreversible deterioration of kidney function and affect common to all of nephropathy mechanisms of progression) can slow the progression of CKD.

AIM:To study the effect of eprosartan, an angiotensin II type 1 (AT1) receptor blocker, with sympatholytic activity on the hemostatic system in patients with chronic kidney disease (CKD) associated with hereditary thrombophilia.SUBJECTS AND METHODS:The 12-week open-label uncontrolled trial included 31 patients with Stages I-II CKD: 15 patients with chronic glomerulonephritis and 16 with diabetic nephropathy burdening types 1 and 2 diabetes mellitus (DM) in 10 and 6 cases, respectively. In all the patients, CKD was associated with one of the heterozygous forms of thrombophilia: the polymorphic methylenetetrahydrofolate reductase gene variant C677T was found in 18 patients; the polymorphic coagulation factor V gene variant G1691A was in 9; and the polymorphic coagulation factor II gene variant G20210A in 4. Along with the thorough examination accepted in nephrology and endocrinology clinics, investigations of vascular-thrombocytic and secondary hemostasis and the anticoagulant and fibrinolytic systems were made before and after treatment.RESULTS:Eprosartan therapy caused positive changes in the indicators of vascular-thrombocytic (diminished platelet aggregation, reduced surplus of von Willebrand factor and endothelin-1) and secondary (decreased coagulation factor VII activity, longer activated partial thromboplastin time) hemostasis and the anticoagulant (reduced antithrombin III deficiency) and fibrinolytic (elevated blood plasminogen concentrations) systems.CONCLUSION:The pleiotropic effects of eprosartan may be used to correct hypercoagulability syndrome in patients with CKD associated with hereditary thrombophilia.

Aim. To comprehensively study hemostasis pathology and its association with the laboratory markers and mediators of inflammation in patients with metabolic syndrome (MS).Subjects and methods. One hundred and eleven patients with type 2 diabetes mellitus, who were diagnosed as having MS, were examined. Vascular-platelet and secondary hemostases and anticoagulant and fibrinolytic systems were evaluated, by performing the complete clinical, laboratory, and instrumental study accepted in a specialized endocrinology clinic. The blood concentrations of high-sensitivity C-reactive protein and proinflammatory cytokines were determined in all the patients with MS and control persons (n=50).Results. It was found that in patients with MS, hemostasis pathology that might be classified as the combined form of a prethrombotic state, which was caused by different types of a constellation of vascular-platelet and plasma hemostases, as well as physiological anticoagulant deficiency, was linked to the laboratory markers and mediators of subclinical inflammation.Conclusion. In the patients with MS, subclinical systemic inflammation is of substantial importance for the mechanisms of a prethrombotic state.

The article deals with studying the degree of increase of the von Willebrand factor and the concentration of endothelin-1 in blood plasma in the subgroups of patients with diabetes mellitus formed depending on of type of disease and presence of phenotype with affection of kidneys. The sampling of 176 patients with diabetes mellitus (65 patients with diabetes mellitus type 1, 111 patients with diabetes mellitus type II) was examined. The control group consisted of 30 healthy persons. In the capacity of biochemical markers of endothelium dysfunction the activity of the von Willebrand factor and the concentration of endothelin-1 in blood were considered. In all patients with diabetes mellitus the biochemical characteristics of endothelium dysfunction are present manifesting by increase of concentration of endothelin-1 in blood which is especially expressed under disease phenotype with affection of kidneys. Despite of the apparent lesion of endothelium in patients with diabetes mellitus compromised with diabetic nephropathy the thrombocytes aggregation induced by ristomicine does not undergo natural changes. Hence, to consider in these patients the increasing activity of the von Willebrand factor as a reliable marker of endothelium dysfunction is not seemed possible.

The purpose of the investigation was to study an association of hemostatic disorders in diabetic patients with methylenetetrahydrofolate reductase (MTHFR) (C677T) and coagulation factors II (G20210A) and V (G1691A) gene polymorphism. The investigators examined 90 patients with diabetic nephropathy complicating types 1 and 2 diabetes in 54 and 36 cases, respectively. A control group comprised 100 healthy individuals. A polymerase chain reaction was used to diagnose single-nucleotide substitution of C6777T in the MTHFR gene, a point mutation in the coagulation factor V (FV) gene, and a factor II (FII) G20210A gene mutation in the coagulation factor II (FII) gene. The parameters of platelet and coagulation hemostasis were analyzed. Gene mutations (C677T in the MTHFR gene, G1691A in the FV gene and G20210A in FII gene) are encountered in diabetic patients more frequently than those in healthy individuals. The mutations are associated with increased blood coagulation potential and platelet hyperactivation.

Aim. To study prevalence, clinical and prognostic significance of prothrombotic genotypes pre-dominant in inborn thrombophilia in patients with diabeticnephropathy (DN). Materials and methods. A total of 90 patients with DN were examined; 54 and 36 cases suffered DM1 and DM2 respectively. Control group comprised100 healthy subjects. PCR was used to iden-tify single nucleotide substitution (C677T) in the methylene tetrahydrofolate reductase gene (MTHFR),point mutation in coagulation factor V gene (FV), and G202210A mutation in factor II gene (FII). Results. The probability of DN in patients with DM1 increases in the presence of Leiden mutation and in DM2 patients in the presence of single nucleotidesubstitu-tion (C677T) in MTHFR gene and G202210A mutation in the 3-untranslated region of FII. Conclusion. The prevalence of the above mutations associated with blood coagulation potential in DN patients is higher than in healthy subjects.Key words: diabetes mellitus, diabetic nephropathy, gene polymorphism, methylenetetrahydrofolate reductase

AIM:to study the activity of free radical processes in patients with alcoholism and renal lesion (A+RL) and the implication of depressed efficiency of the regulatory mechanisms limiting the accumulation of highly toxic products of lipid free radical oxidation (LFRO) in the development of secondary nephropathy.SUBJECTS AND METHODS:Fifty-seven patients (mean age 31 +/- 2.8 years) with a 5-10 history of alcoholism who had been admitted to hospital for uncomplicated alcohol withdrawal syndrome were examined. Alcoholic renal lesion was detected in 17 (29.8%) patients. A control group comprised 20 healthy individuals. The activity of LFRO and antioxidative defense (AOD) was studied.RESULTS:In patients with alcoholism, the study indicators reflecting the activity of LFRO statistically significantly exceeded those in the group of healthy individuals. These patients were found to have also suppressed mechanisms of first- and second-line AOD in the A+RL group.CONCLUSION:LFRO activation developing in the presence of suppressed AOD seems to contribute to the development of secondary nephropathy in patients with alcoholism.

The aim of the investigation was to study the prevalence, clinical and prognostic values of polymorphism of genes II, V factors of blood coagulation and methylenetetrahydrofolate reductase in patients with chronic kidney disease. Examination was performed on 90 patients with diabetic nephropathy (DN) and 180 patients with chronic glomerulonephritis (CG). In addition to complete clinical and instrumental examination accepted in specialised clinic, with the help of polymerase chain reaction diagnostics of polymorphism of the referred above genes (samples of genomic DNA were obtained from peripheral blood leukocytes) was conducted. It was found that the protrombogenic mutations under investigation which are detected in patients with DN and CG more often than in healthy subjects are associated with development of hypercoagulation syndrome and higher risk of renal failure.

The aim of the investigation was to study the prevalence, clinical and prognostic values of polymorphism of genes II, V factors of blood coagulation and methylenetetrahydrofolate reductase in patients with chronic kidney disease. Examination was performed on 90 patients with diabetic nephropathy (DN) and 180 patients with chronic glomerulonephritis (CG). In addition to complete clinical and instrumental examination accepted in specialised clinic, with the help of polymerase chain reaction diagnostics of polymorphism of the referred above genes (samples of genomic DNA were obtained from peripheral blood leukocytes) was conducted. It was found that the protrombogenic mutations under investigation which are detected in patients with DN and CG more often than in healthy subjects are associated with development of hypercoagulation syndrome and higher risk of renal failure.

THE AIM. To investigate the activity of free radical processes in alcoholic patients (A), associated with renal damage (A with RD), and the role of depression of effectiveness of regulatory mechanisms, restricting the accumulation of high toxicity products of free radical lipid oxidation (FrLO), in the formation of the nephropathy in these patients. PATIENTS AND METHODS . Were evaluated 57 male patients (mean age of 31 ± 2,8 years), suffering from A during 5-10 years and admitted to the hospital in the state of urgent alcohol abstinence. The renal damage was discovered in 17 (29,8 %) patients. The control group included 20 healthy patients. The activity of FrLO and antioxidant defense was studied. RESULTS . In patients A the values of studied features, showing the activity of FrLO, were statistically higher than those in the healthy group patients. In these patients was discovered the depression of the first and second line mechanisms of AOD. Showed deviation was more obvious in the group of patients A with RD. CONCLUSION . The activation of FrLO developing on the phone of AOD depression, probably, played a role in the development of nephropathy in A patients.