Progression Of CHF Research Articles

Artificial intelligence systems for predicting disease outcomes in chronic ischemic heart disease patients who have undergone cardiac surgery in respect of anemic syndrome (review).

Materials and methods. The PubMed and RSCI databases were analyzed covering the period of 2000-2023. 906 articles were found using the keywords “artificial intelligence”, “anemia”, coronary artery disease”, “hemoglobin”, “cardiac surgery”, of which 38 met the criteria for inclusion in the analysis. Results. In a number of countries around the world, artificial intelligence (AI) systems have now been created to predict the course of IHD, however, at the moment, data have been published on the single system with AI elements, presented by the developers of the University of Turin (Italy). It has the functionality of predicting the course of IHD and complications of invasive procedures for IHD against the background of anemic syndrome, based on the use of the HAS-BLEED scale. The increase in the number of CABG operations determines the importance of further research into their long-term results and the development of programs for their management, which will take into account such factors that are important for choosing a strategy for their management and the possibility of influencing the risks of an unfavorable prognosis. This review presents published data on the developed and used digital products based on artificial intelligence intended for the management of patients with coronary artery disease, including taking into account basic hematological parameters. Conclusion. Analysis of existing developed AI systems showed a focus on solving prognostic issues. At the same time, in our opinion, the range of analyzed parameters is not wide enough, in particular, taking into account the presence of anemia, which plays one of the key roles in modifying the risk of adverse outcomes (coronary deaths, repeated acute coronary events, progression of CHF).

Depression, anxiety, and quality of life as predictors of rehospitalization in patients with chronic heart failure

BackgroundChronic heart failure (CHF) is a severe condition, often co-occurring with depression and anxiety, that strongly affects the quality of life (QoL) in some patients. Conversely, depressive and anxiety symptoms are associated with a 2–3 fold increase in mortality risk and were shown to act independently of typical risk factors in CHF progression. The aim of this study was to examine the impact of depression, anxiety, and QoL on the occurrence of rehospitalization within one year after discharge in CHF patients.Methods148 CHF patients were enrolled in a 10-center, prospective, observational study. All patients completed two questionnaires, the Hospital Anxiety and Depression Scale (HADS) and the Questionnaire Short Form Health Survey 36 (SF-36) at discharge timepoint.ResultsIt was found that demographic and clinical characteristics are not associated with rehospitalization. Still, the levels of depression correlated with gender (p ≤ 0.027) and marital status (p ≤ 0.001), while the anxiety values ​​were dependent on the occurrence of chronic obstructive pulmonary disease (COPD). However, levels of depression (HADS-Depression) and anxiety (HADS-Anxiety) did not correlate with the risk of rehospitalization. Univariate logistic regression analysis results showed that rehospitalized patients had significantly lower levels of Bodily pain (BP, p = 0.014), Vitality (VT, p = 0.005), Social Functioning (SF, p = 0.007), and General Health (GH, p = 0.002). In the multivariate model, poor GH (OR 0.966, p = 0.005) remained a significant risk factor for rehospitalization, and poor General Health is singled out as the most reliable prognostic parameter for rehospitalization (AUC = 0.665, P = 0.002).ConclusionTaken together, our results suggest that QoL assessment complements clinical prognostic markers to identify CHF patients at high risk for adverse events. Clinical Trial Registration: The study is registered under http://clinicaltrials.gov (NCT01501981, first posted on 30/12/2011), sponsored by Charité – Universitätsmedizin Berlin.

ПЕРСОНИФИЦИРОВАННЫЙ ПОДХОД К ОЦЕНКЕ РИСКА РАЗВИТИЯ ПОВТОРНЫХ СЕРДЕЧНО-СОСУДИСТЫХ СОБЫТИЙ И ХРОНИЧЕСКОЙ БОЛЕЗНИ ПОЧЕК У ПАЦИЕНТОВ С ИНФАРКТОМ МИОКАРДА И ОСТРЫМ ПОВРЕЖДЕНИЕМ ПОЧЕК

Introduction: AKI (acute kidney injury) is a common comorbid condition in patients with AMI (acute myocardial infarction), complicating its course and treatment. In the future, the prognosis of these patients after discharge from the hospital, as well as the incidence of recurrent cardiovascular events (CVS) and chronic kidney disease (CKD) are not known. The purpose of the study: to study the predictors of the development of recurrent cardiovascular events (CVS) in patients with myocardial infarction (MI) with acute kidney injury (AKI). Develop a calculator - a risk meter for repeated CCC. Materials and methods: the study was performed in the Altai Regional Cardiological Dispensary. 193 patients with MI and PCI (percutaneous coronary intervention) were included, divided into 2 groups: the first - 123 patients aged 62.8±1.1 years with MI and AKI, the second - 70 patients without AKI, age 61.3± 1.6 years. Upon admission and before discharge, the level of the KIM-1 molecule (Kidney Injury Molecule-1) and IL-18 (interleukin-18) was studied by ELISA in the urine. All patients underwent coronary angiography using low-osmolar contrast. One year after discharge, the frequency of development of repeated CCC was assessed. Statistical calculations were carried out using statistical packages STATISTICA 12.0. The level of statistical significance was taken equal to 0.05. Results. The level of KIM-1 (at admission) in the first group was statistically higher than in the second: 1998.9±147.6 versus 1289.8±126.1 pg/ml p=0.001, and IL-18 in the AKI group exceeded the corresponding parameter of the group without AKI: 179.0±12.9 versus 114.9±11.5 pg/ml p=0.007, respectively. A year later, it was found that the frequency of recurrent cardiovascular events was higher in the group with AMI and AKI: unstable angina was diagnosed in 26 (21.1%) patients in the group with AKI and 5 (7.1%) patients without AKI in history, p=0.010; 19 (15.4%) and 2 (2.8%) patients, p=0.006, 20 (16.2%) and 3 (4.2%), p=0.013 patients, respectively, had repeated myocardial infarction and progression of CHF in a year . Progression of renal dysfunction during the year was observed 5 times more often in patients with MI and AKI: CKD C2 was diagnosed in 49 (39.8%) patients of the first group and 16 (22.8%) of the second, p = 0.01; CKD C3a and C3b stages - in 34 (27.6%), p˂0.001 and 19 (15.4%) patients, p=0.002, respectively, CKD stage C4 was detected in 4 (3.2%) patients of the group with AMI and AKI in the early postinfarction period. As a result of constructing a multifactorial logistic regression model, predictors were identified that have a multiplicative effect on the development of recurrent CV events: BMI over 25 kg/m2 increases the risk of recurrent CV events by 0.91 [0.83; 0.99] times, p=0.028, history of prior MI in 3.32 [1.24; 9.86] times, p=0.022. Increase in CRP by 1.01 [1; 1.03] times, p=0.045, troponin I, 0.97 [0.94;1] times, p=0.037, and IMT-1, 1 [1;1] times, p=0.030. On the development of CKD: an increase in age is associated with an increase in the chances of developing CKD by 1.18 [1.1; 1.29], p ˂0.001; troponin I by 0.96 times [0.92; 1], p=0.030; systolic blood pressure in 1.03 [1; 1.07] times, p = 0.029. A calculator has been developed for risk stratification of the development of recurrent CV events and an algorithm for managing this category of patients after discharge from the hospital. Conclusions: thus, the identified predictors make it possible to calculate the risk of developing recurrent CV events and CKD using the developed calculator and allocate these patients to a separate group for personalized observation, taking appropriate measures of secondary prevention.

Systemic inflammatory response in cardiac surgery: possibilities of using colchicine

To evaluate manifestations of systemic inflammatory response (SIR) and the effect of the colchicine therapy on SIR severity in patients with ischemic heart disease (IHD) after coronary artery bypass grafting (CABG) with extracorporeal circulation (EC). This study included 100 patients aged 62+6.3 years with stable IHD and multivessel coronary atherosclerosis scheduled for CABG with EC. Patients of group 1 (n=50) were administered with a single dose of colchicine (Colchicum-Dispert) 500 µg 4 hours before surgery followed by 500 µg twice a day for 10 days after surgery. Patients of group 2 (n=50) received a standard treatment, including nonsteroid anti-inflammatory drugs after surgery. Severity of the inflammatory response was evaluated by measuring blood cytokines. In the postoperative period, patient of group 1 showed a tendency toward a lower incidence of pleurisy and heart rhythm disorders in the form of paroxysmal atrial fibrillation (AF) (p=0.18). Levels of the anti-inflammatory cytokines, interleukin-10 (IL-10) and interleukin-6 (IL-6), were significantly increased in both groups at 6 hours after surgery (p<0.05); at the same time, in group 1, IL-10 remained increased also at 10 days after surgery (р=0.0002). No significant time-related changes in the proinflammatory cytokines, tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), were observed. At 3 days post-CABG, there were significant increases in tissue inhibitors of matrix metalloprotease 1 (TIMP-1) (р<0.0001) and matrix metalloproteinase 9 (MMP-9) (р<0.001); at the same time, patients of group 1 had lower MMP-9 concentrations than patients of group 2 (p<0.05). At 10 days of postoperative period, these values were comparable with the background values. Increases in neopterin compared to preoperative values were found in both groups on days 3 and 10 after surgery (р <0.0001). CABG with EC is associated with the activation of SIR. The colchicine therapy at a dose of 500 µg 4 hours prior to surgery and 500 µg twice a day for 10 days after surgery reduces manifestations of SIR, which is clinically evident as a tendency to reduced incidence of pleurisy and arrhythmias, and does not result in the development of serious complications. The dynamics of matrix metalloproteinases indicates that the colchicine treatment is promising for decreasing the risk of CHF progression and myocardial remodeling in patients with IHD.

Dosiahnennia kardiolohii u vyvchenni predyktoriv prohnozuvannia hostroi livoshlunochkovoi ta kryteriiv narostannia tiazhkosty khronichnoi sertsevoi nedostatnosty pid chas khvorob sertsia (ohliad literatury; rezultaty vlasnykh doslidzhen)

Introduction. Few works have been published in the literature on the prediction of predictors of acute and chronic heart failure. The aim of the study. Аnalyze the achievements of cardiology in the field of studying the predictors of predicting acute left ventricular failure and the criteria for the progression of CHF with various CVD. Materials and methods. Vikoristani 51 published an article and presented the results of public research in the field of predicting acute respiratory failure and progression of CHF in heart disease. Results. In most patients, the term after the transferred MI is associated with an increase in end-diastolic volume and end-systolic volume, which are prognostically unfavorable signs. In these cases, the development of LV remodeling is of great importance, as well as accepting the same name as MI, stroke, and HF. Predictors of unfavorable cardiovascular diseases dynamics: changes in EDV, ESV and left ventricular ejection fraction. It should be noted that GLS and diastolic dysfunction are important predictors of cardiovascular complications and SCD. The apparent mitral regurgitation increased the risk of death for 5 years of birth. On the basis of our research, we proved for the first time in 1991 that 4 pathogenetically related mechanisms play a leading role in the development of the initial stage of HF in SCD: central, regional pulmonary hemodynamics, microcirculation, and tissue exchange with the development of arteriolar hypoxemia, venous hyperoxia, reduction of ABB by O2 and utilization of oxygen by tissues, reduction of aerobic processes occurring in the H. A. Krebs cycle and replenishment of energy deficit due to increased glycolysis and pentose phosphate shunt (activities of succinate dehydrogenase and cytochrome oxidase). Conclusions. Based on the given data and own results of the study, predictors of predicting acute CHF and progression are: AMI, UA severe form, stable angina pectoris 3-4 FC, cardiac aneurysm, SBP more than 180 mm Hg. and is less than 100 mm Hg, age 70 years and older, AF, TP, VE of 3-5 gradations, “pirouette”-type VT, significant increase in EDV, ESV and decrease in LVEF. The study of predictors of acute progression and criteria for predicting CHF is of primary importance. Key words: predictor of acute left ventricular insufficiency, chronic heart failure

Osteopontin as a Predictor of Adverse Events in Patients with Comorbid Pathology

Information about the results of the examination of 78 women aged 50 to 65 years is given. The nature of comorbid pathology was studied: chronic heart failure, type 2 diabetes mellitus and osteoporosis. It has been established that osteopontin is an independent risk factor for the development of adverse cardiovascular events and bone fractures in women with comorbid pathology. During 36 months of prospective follow-up, patients with comorbid pathology and OPN level >21.4 ng/ml were significantly more likely to have adverse cardiovascular events and osteoporotic fractures. In patients of the 2nd group with an AKI level of >21.4 ng/ml compared with the group with an AKI concentration of ≤21.4 ng/ml, the risk of cumulative (combined frequency of the combined end point of cardiovascular events) was increased (OR = 6.200 [95% CI 2.258-17.024; p=0.001]). Separate analysis showed a significant increase in the risk of adverse events within 36 months at an AKI concentration of >21.4 ng/ml: progression of CHF (OR=4.073 [95% CI 1.575–10.531; p=0.023]) and osteoporotic bone fractures (OR=0 .81 [95% CI 0.72-0.90; p=0.01]); risks of MI (OR=4.343 [95% CI 0.463-40.751; p=0.162]), stroke (OR=1.178 [95% CI 0.315-31.860; p=0.498]), and decompensation of CHF (OR=1.938 [95% CI 0.696-5.391; p=0.083]) increased insignificantly. The level of acute renal failure >21.4 ng/ml (sensitivity-83%, specificity-62%) makes it possible to predict the onset of adverse cardiovascular events in patients with coronary artery disease with type 2 diabetes and osteoporosis with a high probability.

Barriers and enablers to the diagnosis and treatment of obstructive sleep apnoea in chronic heart failure from patients' and clinicians' perspectives.

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): This study was co-funded by the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care East Midlands (CLAHRC EM), now recommissioned as NIHR Applied Research Collaboration East Midlands (ARC EM) and Leicestershire Partnership NHS Trust - Raising Health Charitable Funds Award and supported by the NIHR Leicester Biomedical Research Centre. The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care. Background Chronic Heart Failure (CHF) is associated with a considerable burden of disability. Despite the impact of evidence-based therapies on CHF related deaths and disability, many patients continue to experience persistent symptoms and will die from progressive CHF. This may be exacerbated by the presence of co-morbidities that contribute to both the development and progression of CHF. The identification and management of co-morbidities, such as obstructive sleep apnoea (OSA), may provide an additional strategy for the management of CHF, leading to improved survival, symptoms, and health care cost. OSA remains largely under diagnosed and under treated with a negative impact on the patient and health care systems as complications develop. To bridge this gap and to develop targeted interventions, the identification of possible barriers to, and enablers of, the diagnosis and treatment of OSA in CHF, is essential. Purpose To investigate the barriers to, and enablers of, the diagnosis and treatment of OSA from CHF patients’ and clinicians’ perspectives. Methods A qualitative study design was utilised to elicit and describe perceived barriers and enablers associated with the diagnosis and treatment of OSA in CHF. CHF patients (n=10) and clinicians (n=20) took part in semi-structured interviews that were analysed using thematic analysis. Results Findings from both patients’ and clinicians’ interviews reported barriers and enablers at all stages of the diagnostic pathway. Patient-reported barriers comprised poor recognition of symptoms, lack of understanding, insufficient information provided by health care professionals, poorly tolerated treatment, and poor access to sleep services. Patient enablers were partner-reported symptoms, awareness of others with OSA, confidence in their heart failure clinician, outcome expectancy, and support from a partner and the sleep disorders service. Clinician-reported barriers were that patients perceived OSA as a low priority compared to their diagnosis of CHF, lack of awareness, knowledge, and skills in the assessment of OSA, variable levels of confidence and low clinical priority of OSA, variable access to sleep services and poor patient uptake and adherence to OSA treatment. Key enablers were perceived outcomes expectancy, education, high confidence, and prompts built into their assessment template. Conclusion Findings identified several key barriers and enablers across the OSA diagnostic pathway and associated with both CHF patients and clinicians. Targeted interventions based on the study findings are likely to significantly influence the OSA diagnostic pathway, effective clinical recognition, diagnosis of OSA and treatment of OSA. Development of co-designed and co-produced targeted interventions for clinician upskilling is essential.

THE COURSE OF CHRONIC HEART FAILURE IN PERSONS WITH POST-INFARCTION CARDIOSCLEROSIS AND TYPE 2 DIABETES MELLITUS AND OBESITY ACCORDING TO A NUMBER OF METABOLIC AND HORMONAL INDICATORS

The aim of the study is to investigate the effect of lipid metabolism, biomarkers of fractalkin and clusterin inflammation on the development and progression of chronic heart failure in patients with post-infarction cardiosclerosis, type 2 diabetes and obesity. A retrospective analysis of a comprehensive examination of 67 patients with postinfarction cardiosclerosis with concomitant type 2 diabetes and obesity. All patients were divided into 3 groups depending on the functional class (FC) of CHF: 1 group (n = 22) - patients with CHF II FC; Group 2 (n = 23) - patients with CHF III FC; Group 3 (n = 22) - patients with CHF IV FC. All patients were examined clinically, they were instrumental, biochemical and hormonal examination. With the progression of CHF from FC II to FC III there is a deterioration of lipid metabolism: a significant increase in cholesterol levels by 5.5%, TG - by 15.7%, LDL cholesterol - by 74.4%, VLDL cholesterol - by 15 , 9%, reduction of HDL cholesterol - by 27.6% (p <0,05). An analysis of the fractal equation showing that ailing on CHF is advised by FC; rіven clusterin –decrease. Classical changes in patients with postinfarction cardiosclerosis with CHF and concomitant type 2 diabetes mellitus and obesity , which are the formation of atherogenic lipid metabolism disorders associated with body weight, as well as changes in the latest indicators such as fractalkin and clusterin , indicating the role of these molecules in the progression of CHF.

Commentary on the Article "Multiple Hormonal and Metabolic Deficiency Syndrome Predicts Outcome in Heart Failure: The T.O.S.CA. Registry", Antonio Cittadini et al. Eur. J. Prev. Cardiol. 2021.

Chronic heart failure represents a relevant concern for public health. The endocrine system is heavily involved in the induction and progression of chronic heart failure. Among endocrine disorders, the most relevant alterations are related to the growth hormone-insulin like growth factor 1 axis, serum testosterone, dehydroepiandrosterone sulfate, triiodothyronine levels, insulin resistance, and type 2 diabetes mellitus. It is currently debated whether these changes might be simple adaptive mechanisms or, instead, they may deteriorate myocardial pump function over time. In this commentary on a recently published paper by Antonio Cittadini et al. (Eur J Prev Cardiol. 2021), we briefly presented and discussed data form the "Trattamento Ormonale nello Scompenso CArdiaco; Hormone Treatment in Heart Failure (TOSCA) Registry". One or more hormonal deficiencies or metabolic disorders, including insulin resistance and diabetes mellitus, were more commonly diagnosed in patients with heart failure (358 patients, 75% of study group). The presence of multiple hormone deficiency identified a subset of patients at increased risk of hospitalization and death, with a graded relation between the number of deficiencies and total events. This finding suggests a possible causal role of hormone deficiencies in CHF progression. Screening of hormonal and metabolic imbalances in CHF patients would be an interesting opportunity for improving the prognosis of patients with heart failure as it would identify high-risk patients requiring an additional medical management of the underlying endocrine and metabolic disorders.

METABOLIC AND HORMONAL FEATURES OF CHRONIC HEART FAILURE IN PERSONS WITH POST-INFARCTION CARDIOSCLEROSIS WITH TYPE 2 DIABETES MELLITUS AND OBESITY.

The aim: To determine the role of lipid metabolism and fractalkin and clusterin in the progression of chronic heart failure in patients with postinfarction cardiosclerosis with concomitant type 2 diabetes and obesity. Materials and methods: A retrospective analysis of a comprehensive examination of 67 patients with postinfarction cardiosclerosis with concomitant type 2 diabetes and obesity. All patients were divided into 3 groups depending on the functional class (FC) of CHF: 1 group (n = 22) - patients with CHF II FC; Group 2 (n = 23) - patients with CHF III FC; Group 3 (n = 22) - patients with CHF IV FC. All patients were examined clinically, they were instrumental, biochemical and hormonal examination. Results: With the progression of CHF from FC II to FC III there is a deterioration of lipid metabolism: a significant increase in cholesterol levels by 5.5%, TG - by 15.7%, LDL cholesterol - by 74.4%, VLDL cholesterol - by 15 , 9%, reduction of HDL cholesterol - by 27.6% (p <0,05). An analysis of the fractal equation showing that ailing on CHF is advised by FC; rіven clusterin -decrease. Conclusions: Classical changes in patients with postinfarction cardiosclerosis with CHF and concomitant type 2 diabetes mellitus and obesity , which are the formation of atherogenic lipid metabolism disorders associated with body weight, as well as changes in the latest indicators such as fractalkin and clusterin , indicating the role of these molecules in the progression of CHF.

Abstract 9084: Selective Beta3-Adrenergic Receptor Antagonist Therapy Causes Regression of Cardiac Dysfunction in a Rat Model of Progressive Heart Failure: Insights into Molecular and Cellular Mechanisms

Background: Heart failure (CHF) causes cardiac β 3 -adrenergic receptor (AR) upregulation with resultant enhanced β 3 -AR-stimulated-G i -coupled negative modulation on cardiac function. This suggests a direct and contributing role of β 3 -AR activation on CHF progression. However, its precise role is unclear. We hypothesize that up-regulation of cardiac β 3 -AR promotes CHF progression. Chronic β 3 -AR antagonist (ANT) may improve Left ventricular (LV) myocyte function, and β-adrenergic reserve, thus preventing the progression of CHF. Methods: LV and myocyte functional response and β 1 - and β 3 -AR expression were compared in 3 groups of SD male rats (8 each) during 3 months: 1) CHF, 3 months after receiving Isoproterenol (ISO, 170 mg/kg, sq, for 2 days); 2) CHF/β 3 -ANT, 2 months after receiving ISO, L-748,337, a selective β 3 -AR antagonist (β 3 -ANT) (10 -7 M/kg/day, mini pump) was initiated and was given for 1 month; and 3) sham controls. Results: Versus controls, ISO-treated rats had CHF onset at 1 month after ISO and progressed to severe CHF at 3 months. Plasma norepinephrine (NE, 1298 vs 261 pg/ml) increased 4-fold; whereas, stroke volume (SV) and ejection fraction (EF, 34 vs 62%) decreased more than 45%. These changes were parallel with significant reductions in cell contraction (dL/dt max , 95 vs 189 μm/s), relaxation (dR/dt max ,75 vs 158 μm/s) and [Ca 2+ ] i transient ([Ca 2+ ] iT ) (0.17 vs 0.26). Acute superfusion of ISO (10 -8 M) caused much less increases in dL/dt max (34 vs 74%), dR/dt max and [Ca 2+ ] IT (14 vs 28%). These changes were associated with significantly decreased β 1 -AR mRNA (52%, 0.30 vs 0.62), but increased β 3 -AR mRNA (119%, 1.25 vs 0.57) expression. CHF with β 3 -ANT treatment, significantly decreased plasma NE (197 pg/ml). EF (59%) and SV returned to normal control values. The signal ratios of β 1 -AR mRNA (0.59) and β 3 -AR mRNA (0.66) recovered to control levels. ISO-induced increases in dL/dt max (75%), dR/dt max and [Ca 2+ ] iT were also significantly augmented. Conclusion: Chronic β 3 -ANT leads to normalization of LV myocyte β 1 - and β 3 -AR gene expression, restores normal LV myocyte β-AR reserve, and leads to regression of LV and myocyte dysfunction in a rat model of progressive CHF. Thus, β 3 -AR blocker may provide a new therapeutic strategy for the treatment of CHF.

Whether inflammatory disorders matter for long-term prognosis after myocardial infarction?

Abstract Funding Acknowledgements Type of funding sources: None. Introduction In the acute period of myocardial infarction (MI) inflammatory disorders of blood are registered, but data of prognostic significance of these disorders is multiple-valued. Purpose Research of manifestation of the inflammatory response in patients who suffered MI, and estimation of its prognostic significance. Materials and methods 772 patients with myocardial infarction were examined. Prospective follow-up from 1 to 7 years was performed. Results The death rate during all years of follow-up was 14,2 % of all included in the study. 61% of patients died suddenly, but 26% of them died as a consequence of the progression of chronic cardiac insufficiency. In patients died suddenly lower level of lymphocytes in the first 24 hours: 1,30 ± 0,47 * 109/l vs 1,80 ± 0,73*109/l, (p = 0,03) was registered. In patients who died due to heart failure progression, authentically registered higher leukocytosis in the first 24 hours, in comparison to survived ones, reached 13,83 ± 6,00*109/l (vs 11,9 ± 3,12*109/l; p = 0,005), but to 5th day in the compared groups leukocytes levels had practically the same values (7,36 ± 1,89*109/l vs 7,47 ± 1,99*109/l; accordingly p = 0,8). In the compared groups the number of lymphocytes, expressing CD 95 did not differ authentically, but in died abruptly patients this index was rather lower. There were not authentic differences detected among groups of dead and survived patients, in terms of interleukins 1β,2, and 6, whereas TNF-α was almost twice as high in patients who died due to CHF progression. Studying inflammatory markers were not included in the number of independent indexes, connected with the risk of death when conducting multivariate regressive Cox-analysis. Conclusion In our opinion, inflammatory factors were displaced from the prognostic model for assessing the risk of death, both sudden and due to heart progression, by more powerful structural-functional predictors.

Значение определения адренореактивности организма у пациентов с хронической сердечной недостаточностью

The article provides an overview of the studies of sympathoadrenal system activity in the patients of cardiovascular continuum. The analyzed publications show an excess of β-APM in patients with arterial hypertension, ischemic heart disease, rhythm disturbances, and heart failure in comparison with healthy individuals. The features of the course and development of cardiovascular system complications in patients with myocardial infarction at various β-APM levels are shown. The dynamics of β-APM level was demonstrated in patients with resistant hypertension after renal denervation and patients with myocardial infarction during a year. The level of β-ARM ≥ 49,53 conv. units is revealed at which the risk of CHF progression increases in patients with MI (OR 5,48; 95% CI 1,28–23,37; p = 0,024). Correlations of β-APM value with SHORC, heart rate, data of a 6-minute walking test in CHF patients are presented. The data of the β-APM and polymorphism of the ADRB1 and ADRB2 genes studies are presented. The prognostic significance of determining the adrenergic reactivity by the value of β-adrenergic reception of cell membranes for determining the individual sensitivity of the organism to β-adrenergic blockers is shown. The associations obtained suggest a genetic predisposition to SAS hyperactivation and β-APM use for personalized selection of the β-adrenergic blocker dosage.

Personalized algorithm for formation of risk groups for progression and development of complications of atrial fibrillation in hypertension in combination with extracardial diseases

Aim . To develop a personalized algorithm for predicting the progression of atrial fibrillation and its complications in hypertension in combination with extracardial diseases. Methods . The observational cohort study observed 308 men aged 45–60 years with AF and AH in combination with extracardial pathology: diabetes mellitus (DM; n = 40), diffuse toxic goiter (TTZ; n = 42); hypothyroidism (GT; n = 59), abdominal obesity (AO; n = 64) and chronic obstructive pulmonary disease (COPD; n = 47). The comparison group consisted of 56 patients without extracardial pathology. Clinical, laboratory, anthropometric data, results of daily ECG monitoring and echocardiography were evaluated. All statistical calculations were performed in Rstudio program. Results . Found significant predictors of progression of atrial fibrillation: indicators of remodeling: galectin-3, which increase by 1 ng/l increases the risk of progression to 1.0030 (1.0006; 1.0050) times (p = 0.016); PL (p < 0.001), with an increase of 1 cm, the risk increases to 2.67 (1.58; 4.65) times; KDR (p = 0.025), with the increase of 1 cm decrease the chance of atrial fibrillation recurrence in 0.13 (0.02; 0.65) and LVMWI, where the increase LVMWI 1 g/m 2 increases the risk of progression of AF at 0.9 times; also, the inflammation index-with an increase in IL-6 by 1 PG/l, the risk increases by 0.6 times, and the vascular stiffness marker MMP-9 – an increase by 1 ng/ml increases the risk of progression by 0.16 times. It was determined that emergency hospitalization for the progression of CHF during the year in patients with atrial fibrillation was significantly more common in all clinical groups, except for patients with hypothyroidism. Statistically significant predictors of hospitalization for CHF progression were revealed: increase of LP size by 1 cm increases CHF risk by 5.04 (1.80; 16.10) times; an increase in NT-proBNP by 1 pg/l increases the risk of CHF by 1.01 (1.00; 1.02) times. The comparative assessment of the incidence of cardioembolism in these groups, although not showed a statistically significant difference, but in percentage terms was higher in patients with atrial fibrillation – 11.2 vs. 6.0 % in patients without atrial fibrillation, the relative risk of confidence interval – 3.736 (0.500; 26.900). Conclusion . The developed personalized algorithm can be used to assess the prognosis of progression of atrial fibrillation and the development of its complications in hypertension in combination with extracardial diseases

Роль метаболического синдрома в ремоделировании миокарда и прогрессировании хронической сердечной недостаточности

Introduction. The increase of morbidity results from both an increase of life expectancy of the population, and influence of various risk factors contributing to development and increase of heart failure. The combination of several atherogenic mechanisms (abdominal obesity (AO), insulin resistance (IR), arterial hypertension (AH), hyperglycemia, dyslipidemia), combined as «metabolic syndrome» (MS), causes a more rapid development of CHF. Material and methods. The research finding of 74 patients with class II–III of CHF, including 37 patients (50%) with MS, are presented. The age structure of the pathology, severity of clinical course, data of laboratory and instrumental examination in various groups of patients were evaluated. A special program included an echocardiographic test with an assessment of various myocardial parameters. Results. Research materials find out a number of characteristics of CHF clinical course (its earlier development and severe course) in patients with MS. Echocardiographic tests reveal an increase of heart chambers sizes, thickness of left and right ventricle, pulmonary hypertension. Myocardium morpho-functional changes are more significant in patients with CHF and MS than in those without MS. An increase in leptin levels, a marker of obesity, fibrosis and inflammation, has been found. Leptin, CRP and high-sensitive troponin in patients with MS significantly exceeded those in patients with CHF. Correlations of leptin levels, adiponectin, CRP and left ventricular mass, thickness of epicardial fat (TEF), ejection fraction were established. Conclusion. Materials of the research indicate the important role of inflammatory and dysmetabolic processes in development and progression of CHF in patients with MS.

Myocardial 123I-mIBG scintigraphy in relation to markers of inflammation and long-term clinical outcome in patients with stable chronic heart failure

AimChronic heart failure (CHF) results in both increased cardiac sympathetic activity and myocardial inflammation. The aim of this study was to identify the relationship between severity of heart failure (i.e., NT-proBNP and LVEF), cardiac sympathetic activity (123I-mIBG scintigraphy), and measures of inflammation in subjects with stable, optimally treated CHF. In addition, the predictive value for cardiac events (i.e., ventricular arrhythmia, progression of CHF and cardiac death) of 123I-mIBG parameters and these inflammatory markers was evaluated. Materials and MethodsFifty-five CHF patients (age 66.3 ± 8.0 years, 78% male, LVEF 22.4 ± 6.3) referred for cardiac 123I-mIBG imaging were included. At 15 minutes (early) and 4 hours (late) after i.v. administration of 123I-mIBG (185 MBq), planar images were acquired. Early Heart/Mediastinum (H/M) ratio, late H/M ratio, and 123I-mIBG washout (WO) were calculated. NT-proBNP and markers of inflammation (i.e., C-reactive protein (CRP), IL-1β, IL-6, IL-8, IL-10, IL-12p40, tumor necrosis factor-α (TNF-α), soluble (s)E-selectin, myeloperoxidase (MPO), plasminogen activator inhibitor-1 (PAI-1), tPA, tumor necrosis factor receptor (TNFR) 1 and 2, and interferon (IFN) α and β) were measured in blood plasma samples, taken just before 123I-mIBG administration. ResultsMean early H/M ratio was 2.12 ± 0.39, late H/M ratio was 1.84 ± 0.40, and 123I-mIBG WO was 13.0 ± 10.9. LVEF was the only independent predictor of late H/M ratio (adjusted R2 = 0.100, p = 0.011). NT-proBNP was an independent predictor of 123I-mIBG WO (adjusted R2 = 0.090, p = 0.015). CRP, IL12p40, TNF-α, sE-selectin, MPO, PAI-1, tPA, and TNFR2 were not related to late H/M ratio and 123I-mIBG WO. During a median follow-up of 34 months (2–58 months), 13 patients experienced a cardiac event [ventricular arrhythmia (4), progression of CHF (4), and cardiac death (5)]. Univariate Cox regression analysis showed that the risk of a cardiac event was associated with CRP (HR 1.047 [1.013–1.081]), NT-proBNP (HR 1.141 [1.011–1.288]), MPO (HR 0.998 [0.996–1.000]), and late H/M ratio (HR 0.182 [0.035–0.946]). Multivariate Cox regression analysis showed that only CRP, NT-proBNP, MPO, and IL-12p40 were predictors of a cardiac event. ConclusionInflammation and cardiac sympathetic activity seem not to be related in stable CHF patients. This is corroborated by the finding that they both provide prognostic information in this specific CHF population. The current findings should be regarded as insightful but preliminary.

PROGNOSTIC SIGNIFICANCE OF THE VNTR POLYMORPHISM INTRON 4 OF THE GENE OF NITRIC OXIDE ENDOTHELIAL SYNTHASE IN CHRONIC HEART FAILURE PATIENTS

Aim. To analyze the prevalence of VNTR-polymorphism intron 4 (4b/4b and 4a/4b) carriage of the gene of endothelial nitric oxide synthase (eNOS) in chronic heart failure patients (CHF) of ischemic origin according to ejection fraction of the left ventricle (LVEF) and the disease stage. Material and methods. Totally, 280 CHF patients studied, selected to groups in accordance with LVEF (by echocardiography) and the disease stage. Then, within the study, genetic test specimens were collected with further typing of the gene alleles 4b/4b and 4a/4b of eNOS gene polymorphism. Results. By the prevalence analysis, 4b/4b and 4a/4b polymorphism of eNOS gene and the rate of various CHF stages in carriers, the predominance was found of 4a/4b carriers in IIА to III stages of the disease in both preserved and low LVEF. The increase of absolute risk was found, and of odds ratio of carriage of genotype 4а/4b in CHF patients with IIB-III stages. Conclusion. Genetically associated predisposition revealed to CHF progression in all patients with 4а/4b polymorphism of eNOS gene carriage and protective role of the carriage of 4b/4b eNOS polymorphism.

TICAGRELOR VERSUS CLOPIDOGREL IS ASSOCIATED WITH BETTER RECOVERY OF LV FUNCTION AFTER ACUTE MYOCARDIAL INFARCTION

Background: Recovery of LV function following AMI is associated with the risk of long-term CV mortality and CHF progression. We sought to evaluate the predictors of recovery of LV function in AMI patients. Methods: AMI patients treated with uneventful PCI were prospectively enrolled (n=224). At 30-

Factors associated with levels of interleukins -18, -8, and -6 in hypertensive patients at high and very high cardiovascular risk

To identify the most significant factor influencing blood levels of cytokines in patients at high and very high cardiovascular risk. A patient base from the "Management of chronic patients with multiple diseases" project was analyzed. 523 patients (mean age, 87±17.8) were included. Plasma samples were analyzed for concentrations of sodium, creatinine, IL-1, IL-2, IL-4, IL-6, IL-8, IL-10, IL-18, and NT-proBNP. GFR was calculated using the CKD-EPI formula. Time-related CHF progression was assessed in one year; the time-related progression was considered an increase in CHF stage. Salt consumption was determined using the Charlton: SaltScreener questionnaire at the baseline visit and at one year. Low-salt diet containing 5 g of salt per day was recommended to all patients; 3.5 g of salt per day was recommended to patients with a documented diagnosis of CHF. Statistical analysis was performed using the Statistica 10.0 software. 52.2 % of included patients consumed 6-10 g of salt per day; 43.4 % of patients consumed 10 g of salt or more per day; and only 4.4 % of patients consumed 5 g of salt or less per day. 21 % of included patients were at high risk of cardiovascular complications whereas for the vast majority of patients (79 %), the risk was stratified as very high. Two clusters of patients were formed based on the grade of hypertension, one-year CHF progression, and plasma levels of IL-6, -8, and -18. The one-year progression of CHF most significantly influenced the levels of IL-18, -8, and -6. The IL-6 level was correlated with the NT-proBNP level; an approximately similar degree of correlation was found for NT-proBNP and BP. Therefore, the performed statistical analysis determined correlations between the following factors: IL-6 level, NTproBNP level, and one-year CHF progression.

Treatment method by correcting of purine metabolism in case of cardiovascular disease in the elderly patients

&lt;p&gt;A large number of metabolic diseases are the cause of their particular violation. One of these conditions is a&lt;br /&gt;violation of purine metabolism substances. Meaning of purine bases in metabolizme is large since they are part of&lt;br /&gt;purine nucleotides forming the nucleid acid (DNA and RNA). Purine nucleotides also have a part-energy compounds&lt;br /&gt;(ATP, ADP) and certain regulatory coenzymes monophosphate (cAMP, cGMP and others). Normal flow of purine&lt;br /&gt;metabolism underlies the optimum level update nucleic acids and proteins, stability in energy metabolism. Violation&lt;br /&gt;of the synthesis of purine nucleotides leads to decreased tissue growth. Uric acid (UA) is the end product of purine&lt;br /&gt;metabolism substances. Level of UA, which is formed during the reaction hypoxanthine qsantinoqsidase reaction&lt;br /&gt;is a marker of activity of free radical processes – endotoxicoses that trigger damaging processes in the vessels&lt;br /&gt;and myocardium. Thus, the UA is the main derivative of purine metabolism and an important mediator of catabolic&lt;br /&gt;processes in stress and cardiovascular disease. Most studies have confirmed the role of UA as a risk factor for&lt;br /&gt;cardiovascular disease. In fact, it turned out that the UA stronger predictor of results than the ejection fraction or&lt;br /&gt;the oxygen uptake. Uric acid can be inserted in the adhesion and aggregation of platelets. This gave birth to the&lt;br /&gt;hypothesis that hyperuricemia increases the risk of coronary thrombosis. It is believed that the increase of the UA&lt;br /&gt;displays endothelial damage. An important mechanism of rapid progression of CHF in elderly patients who have&lt;br /&gt;suffered myocardial infarction, there are systemic activation of apoptosis – cell death. A correlation revealed a high&lt;br /&gt;index values between apoptosis and severity of CHF. An interesting fact is, that the use of pentoxifylline, a corrector&lt;br /&gt;of the purine metabolism in patients with CHF improves the left ventricular function and prognosis of patients. Correction&lt;br /&gt;of purine metabolism then acts as a correction of endotoxemia and apoptosis.&lt;/p&gt;