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BACKGROUND. Patients with type 2 diabetes mellitus (DM2) have disorders of cellular and plasma hemostasis independent of the level of glycemia, increased platelet activation, combined with microvascular angiopathy. The study of the role of genetic markers of hemostasis disorders in the formation and progression of chronic heart failure (CHF) in patients with type 2 diabetes will allow for prevention, possibly optimize treatment and improve prognosis.AIM. To reveal polymorphisms of genes of the hemostasis system in patients with type 2 diabetes mellitus and chronic heart failure with preserved ejection fraction.MATERIALS AND METHODS. The frequency of coagulation factor genetic polymorphisms was studied in patients with CHF-pEF and DM2 (52 people), CHF with reduced ejection fraction (CHF-rEF) and DM2 (49) and healthy volunteers (66), mean age 69.9±10.1 years old. DNA was isolated from venous blood according to the method of the manufacturer. Genetic polymorphisms were determined by real-time polymerase chain reaction.RESULTS. The frequencies of polymorphisms rs1799963 and rs6025 of the genes of blood coagulation factors F2 (prothrombin) and F5 (factor V of blood coagulation) in all three groups were insignificant and comparable in magnitude. In patients with CHF and DM2, the frequencies of the rs6046 polymorphism of the factor F7 gene in the heterozygous form were slightly higher (by 2.6 and 1.7 times, respectively) than in the control group, but the result was not statistically significant. The CHF-pEF and CHF-rEF groups differ in the frequencies of F13 (rs5985) and fibrinogen (rs1800790) genetic polymorphisms, but are more common in patients with CHF-rEF and DM2.CONCLUSION. Based on the results of the study, it follows that the groups of CHF-pEF and CHF-rEF differ significantly in the frequencies of polymorphisms of the studied genes, both among themselves and with the control group. The highest frequency of polymorphisms of genes, the products of which are involved in the coagulation and cellular components of hemostasis, is observed in the group of patients with DM2 and CHF-rEF.

Left ventricular hypertrophy, atrial fibrillation and chronic heart failure are often in the practice of a cardiologist. The etiology of these conditions is very important because the correct early treatment. We are presenting a case of a late diagnosis of amyloidosis in a 53-year-old man. Despite the complex therapy, the course of the disease was complicated by the development of bilateral pneumonia, sepsis, disseminated intravascular coagulation and the patient died. Autopsy confirmed the diagnosis of systemic AL-amyloidosis (type Kappa) with massive damage to the heart, kidneys, lungs, liver, spleen, adrenal glands, thyroid gland, pancreas, gastrointestinal tract, subcutaneous fatty tissue and arterial vessels of the bone marrow. Thus, screening for amyloidosis is necessary in idiopathic LV thickening, atrial fibrillation, and heart failure for timely intravital diagnosis and therapy.

Cardiac amyloidosis (amyloid cardiomyopathy) is a disease damage to the heart caused by extracellular amyloid deposition. In some cases, there may be local damage to the structures of the heart, for example, the atria; more often, heart damage is part of a systemic (generalized) pathology. Depending on the amyloid precursor protein, 36 types of amyloidosis are described, among which hereditary and acquired forms are distinguished. Cardiac amyloidosis is diagnosed 1) in the case of the amyloid infiltration in the myocardial bioptates or 2) in the case of non-cardiac amyloid deposition and the left ventricular wall thickening >12 mm without arterial hypertension and other reasons. The heart is most often affected in AL-, ATTR-, AA-, AANF-types of amyloidosis. Cardiac amyloidosis should be considered in patients with a heart failure with an unclear etiology, especially with preserved left ventricular ejection fraction, refractory to treatment, with proteinuria and CKD 4-5, in patients with idiopathic atrial fibrillation and conduction disturbances, in patients with left ventricular wall thickening of unclear etiology, low ECG voltage, unexplained arterial hypotension and pulmonary hypertension. Screening for cardiac amyloidosis should include non-invasive methods such as electrophoresis and immunofixation of blood and urine proteins, the free light lambda and kappa chains of immunoglobulins, 99Tc-DPD scintigraphy, genetic testing (if hereditary variants of amyloidosis are suspected), as well as a histological examination of biopsy samples stained with Congo red and polarizing microscopy.

Aim. To determine the impact of polymorphic variant rs1739843 of the HSPB7 gene on clinical profile and outcomes in patients with hypertrophic cardiomyopathy (HCM).Material and methods. The study population consisted of 108 patients with HCM ≥45 years old. The control group included 192 healthy donors. The design of the study included an assessment of the clinical course, determining the outcome of HCM using a new methodological approach proposed by Rowin EJ, et al. (2017). Polymorphic variant rs1739843 of the HSPB7 gene was genotyped by allele-specific real-time polymerase chain reaction (PCR) assay.Results. It was found a significant increase in frequency of TT genotype of rs1739843 of the HSPB7 gene in patients with HCM — 20,4%, compared with control group — 4,2% (ТТ: ТС+СС, odds ratio (OR) =5,88, 95% confidence interval (CI) =2,52-13,75, p

Rationale: More than half of patients with chronic heart failure have a preserved left ventricular ejection fraction. It has been found that sudden cardiac death is more frequent in this patient category. A reliable and easily available marker is needed that would predict the death outcome with a high probability. The use of the late ventricular potentials for this purpose could be reasonable.Aim: To assess the prevalence of the late ventricular potential and their association with the structural and functional parameters of the myocardium in patients with early stages of chronic heart failure with preserved ejection fraction.Materials and methods: We examined 77 patients with chronic heart failure (grade I to IIА, functional class I to III) with preserved ejection fraction (> 50%), aged 47 to 77 years (mean ± SD, 59.7 ± 7.8 years). Echocardiography (SonoScape 8000 and Vivid 3) at М-, В- and Doppler modes was performed in all patients. Ventricular ectopic activity and late ventricular potentials were registered during 24- hour ECG monitoring (Cardiotekhnika, INKART, St. Petersburg).Results: Late ventricular potentials were found in 13% (10 of 77) of patients. The following correlations were found in patients with concentric hypertrophy (n = 53): between the duration of the filtered QRS (TotORSF) and the left ventricular end diastolic diameter (r = 0.27, p = 0.049), TotORSF and the interventricular septum thickness (r = 0.28, p = 0.04), TotORSF and the left ventricular myocardial mass (r = 0.35, p = 0.01), mean square magnitude of fluctuations within the last 40 ms of ORS (RMS40) and the left ventricular end diastolic diameter (r = -0.42, p < 0.01), RMS40 and the left ventricular end-systolic diameter (r = -0.37, p < 0.01). In the patients with eccentric hypertrophy (n = 14), the following correlations were found: between RMS40 and the left ventricular myocardial mass index (r = -0.77, p < 0.01), between duration of the low amplitude signal (< 40 μV) at the end of QRS (LAS40) and the left ventricular myocardial mass index (r = 0.76, p < 0.01), as well as between LAS40 and RMS40 with the end diastolic diameter of the left ventricle adjusted to the body surface area (r = 0.76, p < 0.01 and r = -0.83, p < 0.01, respectively). The patients with a pseudo normal type of diastolic dysfunction (n = 27) showed an association between their NT-proBNP levels and TotORSF (r = 0.56, p < 0.01).Conclusion: The prevalence of late ventricular potentials among patients with early stage chronic heart failure and preserved left ventricular ejection fraction is not high. The parameters of electrophysiological myocardial instability in patients with concentric hypertrophy are mostly influenced by the size of heart chambers, whereas in those with the eccentric one, by the myocardial mass and volume parameters. The risk of sudden cardiac death is higher in patients with a pseudo normal type of diastolic dysfunction.

The paper reviews major biomarkers for determining the prognosis in patients with chronic heart failure and preserved ejection fraction. It also considers cystatin C, one of the novel and probably the most practically important biomarkers.

For the long time the systolic myocardial dysfunction was traditionally associated with the severity of chronic heart failure (CHF). Increasing number of patients with symptoms of CHF but without systolic dysfunction has drawn the attention of specialists to so-called CHF with preserved ejection fraction. Prognosis in CHF with preserved ejection fraction may be as bad as in CHF with reduced ejection fraction. Significant changes in views on the pathogenesis of CHF led to the creation of new therapeutic approaches in the treatment of this disease. However, at present, convincing evidence base of mortality reduction in patients with CHF with preserved ejection fraction using well-known therapeutic agents is unavailable. It makes conduct active searches for new biological markers of diastolic heart function. Participation of proinflammatory cytokines, in particular GDF-15, in the process of elasticity reduction and relaxation disorders of left ventricular myocardium, may be of great importance in the development of new medical agents designed to delay the progression of CHF with preserved ejection fraction.

Purpose: to evaluate interaction of obesity, inflammation and myocardial dysfunction in senile myocardial infarction survivors. Material and Methods. Patients aged 70 and older were involved in the study (n=108) and divided into 2 groups according to the history of myocardial infarction (Ml) — 5 years before involvement: senile Ml survivors (n=26) vs senile patients without history of Ml (n=82). Measurements of serum levels of adipokines (leptin, adiponectin), myocardial dysfunction markers (BNP, NT proBNP, proANP, galectin 3) and inflammatory cytokines (TNF, interleukin 6) were performed. Results. Both groups were comparable by age and major clinical characteristics. Ejection fraction was preserved in both groups under the study (67 (64; 70) %vs67 (64; 68) %, p=0,655). Frequency of diastolic dysfunction was comparable in both groups. However it was more severe in Ml survivors. BNP and NT proBNP levels were significantly lower in patients without the history of Ml (p=0,021; 0,004, respectively). On the contrary serum levels of proANP had tendency to increase in patients with the history of Ml, but not significantly: p=0,821. Adiponectin and galectin-3 were significantly higher in patients with the history of Ml (p=0,019and p=0,011). Conclusion. Pathogenetic peculiarities of chronic heart failure with preserved ejection fraction in senile patients with and without myocardial infarction history were revealed. More expedient biomarker panel appropriate for senile patients with probable heart failure should include NT-proBNP, galectin-3 and adiponectin.