scholarly journals The phenomenon of weight loss in patients with chronic heart failure

2021 ◽  
Vol 27 (6) ◽  
pp. 9-18
Author(s):  
К. V. Voitsekhovska ◽  
L. G. Voronkov
Keyword(s):  
Heart Failure ◽  
Weight Loss ◽  
Body Weight ◽  
Chronic Heart Failure ◽  
Nutritional Status ◽  
Body Weight Loss ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cardiac Cachexia ◽  
Body Components

A characteristic sign of chronic heart failure (CHF) is a high frequency of comorbid conditions, one of which is the phenomenon of weight loss. Cardiac cachexia is a systemic metabolic disorder characterized by an unintentional decrease in body weight due to loss of all body components, namely, skeletal muscle, adipose tissue and bone tissue, and identified as a marker of nutritional status, has prognostic value in patients with CHF, regardless of age, NYHA class, left ventricular ejection fraction, and peak oxygen consumption. The article discusses the prevalence, criteria, prognostic significance of cardiac cachexia, as well as immune, metabolic and neurohormonal pathogenetic mechanisms that lead to anabolic-catabolic imbalance and contribute to the progression of CHF. Given the methodological difficulties of proper assessment of unintentional body weight loss over a certain previous period of outpatient follow-up in patients with CHF, it becomes urgent to determine the objective («static») characteristics of the nutritional status of patients, which are associated with an unfavorable clinical prognosis. The article demonstrates the results of our own research to determine prognostic factors based on indicators of the nutritional status of patients the clinical significance of the loss of individual body components is highlighted, preventive and therapeutic approaches to influence body weight loss in patients with CHF are described – nutritional support, neurohormonal blockade, the effect on the intestinal microflora, correction of anemia and iron deficiency, the use of appetite stimulants, immunomodulatory agents, anabolic hormones and physical training.

P786Plasma volume status is associated with the change in nutritional status during hospitalization in acute decompensated heart failure patients with preserved left ventricular ejection fraction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Tamaki ◽  
T Yamada ◽  
T Morita ◽  
Y Furukawa ◽  
M Fukunami ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Weight ◽  
Nutritional Status ◽  
Multivariate Logistic Regression Analysis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Severe Malnutrition ◽  
Operating Characteristics ◽  
Ventricular Ejection Fraction

Abstract Introduction Plasma volume (PV) expansion has an essential role in heart failure (HF). PV can be estimated by a simple formula using hematocrit and body weight, and PV status (PVS) provides prognostic information in patients (pts) with chronic HF. Nutritional status (NS) based on the prognostic nutritional index (PNI) and NS change during hospitalization have been shown to predict prognosis in pts admitted with acute decompensated HF (ADHF). Purpose We sought to assess the hypothesis that PVS is associated with NS change during hospitalization in pts with HF with preserved LVEF (HFpEF) who are admitted with ADHF. Methods We prospectively studied 411 pts who were admitted for ADHF with LVEF ≥50% and survived to discharge. Body weight measurement and venous blood sampling were performed on admission and at discharge. PVS was defined as follows: actual PV = (1 − hematocrit) × [a + (b × body weight)] (a=1530 in males and a=864 in females, b=41.0 in males and b=47.9 in females); ideal PV = c × body weight (c=39 in males and c=40 in females); and PVS = [(actual PV − ideal PV)/ideal PV] × 100 (%). PNI was calculated as 10 × serum albumin (g/dL) + 0.005 × total lymphocyte count (per mm3). The pts were divided into 3 groups by PNI: normal (>38), moderate malnutrition (35–38), and severe malnutrition (<35). During admission, pts who remained in the moderate or severe malnutrition group or whose NS worsened were defined as no improvement in NS. Follow-up data was obtained in 203 cases. They were followed for up to 18 months, and the incidence of all-cause death was evaluated. Results On admission, PVS in the moderate (n=71, 13.3±13.9%) or severe malnutrition group (n=69, 14.8±10.8%) was significantly higher than in the normal PNI group (n=271, 5.4±10.8%, p<0.001). During hospitalization, 123 pts had no NS improvement. Admission PVS was significantly higher in pts with no NS improvement than in pts with improved NS (13.9±11.2% vs 5.9±12.8%, p<0.0001). In multivariate logistic regression analysis, admission PVS was independently associated with no NS improvement during hospitalization (OR 1.06, 95% CI 1.03–1.08, p<0.0001). Receiver operating characteristics curve analysis revealed that the optimal cut-off value of admission PVS for predicting no NS improvement was 9.4% (sensitivity: 72%, specificity: 63%). The area under the curve for predicting no NS improvement using admission PVS was significantly greater than for other independent factors (Figure 1A). During the follow-up period (median 12.4 months), 68 of 203 patients had all-cause death. Kaplan-Meier analysis showed that the patients with no NS improvement had a significantly higher risk of all-cause death (Figure 1B). Figure 1 Conclusions In this multicenter study, admission PVS was shown to be associated with poor improvement in NS during hospitalization in HFpEF pts admitted for ADHF. Acknowledgement/Funding Roche diagnostics, FUJIFILM Toyama Chemical

scholarly journals PREDICTORS OF WEIGHT LOSS IN PATIENTS WITH CHRONIC HEART FAILURE AND REDUSED LEFT VENTRICULAR EJECTION FRACTION

2019 ◽  
Vol 5 ◽  
pp. 3-11
Author(s):  
Kateryna Voitsekhovska ◽  
Leonid Voronkov
Keyword(s):  
Heart Failure ◽  
Weight Loss ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Nyha Class ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Vasodilator Response

Chronic heart failure (CHF) is a heterogeneous syndrome with a poor prognosis. Aim of the work – to define predictors of body weight (BW) loss in patients with CHF and a reduced left ventricular ejection fraction (LVEF). Materials and methods. 120 patients with stable CHF and LVEF ≤35 %, II-IV NYHA class were examined. Patients were divided into two groups according to the value of BW loss for 6 months: the first group - loss of BW <6 %, the second - ≥ 6 %. Results. Out of the 120 patients who were studied, a BW loss of ≥ 6 % occurred in 59 (49.2 %) patients. According to the results of binary logistic regression, predictors of BW loss of ≥6 % in patients with CHF and LVEF ≤ 35 % were: age, coronary heart disease, anaemia, and the number of hospitalizations over the last year. People with poorer quality of life, bigger number of points on the Beck depression scale and DEFS, with lower levels of physical activity and worse endothelium-dependent vasodilator response; higher sizes of the right atrium, right ventricle, and pulmonary artery systolic pressure, E / E '. Higher levels of C-reactive protein (CRP), uric acid are associated with a risk of losing BW≥6 %. Conclusions. Weight loss ≥ 6 % is observed in 49.2 % of patients with CHF and LVEF≤35 %. According to multivariate analysis, independent predictors of BW loss of ≥6 % in patients with CHF and LVEF≤35 % are age, CRP level, III-IV NYHA class, lower cholesterol levels, as well as lower rates of flow-dependent vasodilator response and hip circumference.

Efficacy of Vitamin D on Chronic Heart Failure Among Adults

2020 ◽  
Vol 90 (1-2) ◽  
pp. 49-58 ◽  
Author(s):  
Wang Chunbin ◽  
Wang Han ◽  
Cai Lin
Keyword(s):  
Heart Failure ◽  
Vitamin D ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Confidence Interval ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Controlled Trials ◽  
Ventricular Ejection Fraction ◽  
Randomized Controlled

Abstract. Vitamin D deficiency commonly occurs in chronic heart failure. Whether additional vitamin D supplementation can be beneficial to adults with chronic heart failure remains unclear. We conducted a meta-analysis to derive a more precise estimation. PubMed, Embase, and Cochrane databases were searched on September 8, 2016. Seven randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in adults with chronic heart failure, and comprised 592 patients, were included in the analysis. Compared to placebo, vitamin D, at doses ranging from 2,000 IU/day to 50,000 IU/week, could not improve left ventricular ejection fraction (Weighted mean difference, WMD = 3.31, 95% confidence interval, CL = −0.93 to 7.55, P < 0.001, I2 = 92.1%); it also exerts no beneficial effects on the 6 minute walk distance (WMD = 18.84, 95% CL = −24.85 to 62.52, P = 0.276, I2 = 22.4%) and natriuretic peptide (Standardized mean difference, SMD = −0.39, 95% confidence interval CL = −0.48 to 0.69, P < 0.001, I2 = 92.4%). However, a dose-response analysis from two studies demonstrated an improved left ventricular ejection fraction with vitamin D at a dose of 4,000 IU/day (WMD = 6.58, 95% confidence interval CL = −4.04 to 9.13, P = 0.134, I2 = 55.4%). The results showed that high dose vitamin D treatment could potentially benefit adults with chronic heart failure, but more randomized controlled trials are required to confirm this result.

A translational model of chronic heart failure in rats

2018 ◽  
pp. 136-148
Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Experimental Myocardial Infarction ◽  
Left Ventricular Ejection ◽  
Translational Model ◽  
Innovative Drug ◽  
Ventricular Ejection Fraction

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.

Abstract 3791: Improved Ventricular-Arterial Coupling After 4 Weeks of Exercise Training in Patients with Chronic Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Marcus Sandri ◽  
Stephan Gielen ◽  
Norman Mangner ◽  
Volker Adams ◽  
Sandra Erbs ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Endothelial Function ◽  
Training Group ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Lv Function ◽  
Ventricular Ejection Fraction

Background: The concept of ventricular-arterial coupling implies that LV-function is determined by the three factors left ventricular diastolic, left ventricular systolic and arterial elastance. We have previously documented an improvement in endothelial function and systolic LV-function in patients with chronic heart failure (CHF) after 6 months of exercise training (ET). It remains, however, unclear, how shorter ET periods may affect endothelial, systolic and diastolic ventricular function as echocardiographic parameters related to ventricular arterial coupling in patients with CHF. METHODS: In this ongoing study we randomised 43 patients with stable CHF (age 60.3 ± 2.9 years, EF 27.4 ± 1.7%, VO 2 max 14.7 ± 4.3ml/kg*min) to a training or a control group (C). Patients in the training group exercised 4 times daily at 70% of the individual heart rate reserve for 4 weeks under supervision. At baseline and after 4 weeks the E/A ratio and septal/lateral E’/A’ velocities were determined by echocardiography with tissue Doppler. Exercise capacity was measured by ergospirometry and flow-mediated dilatation (FMD) was assessed by high-resolution radial ultrasound. RESULTS: After only 4 weeks of ET oxygen uptake at peak exercise increased from 14.9 ± 3.3 to 18.1 ± 4.7 ml/min/kg, (p<0.01 vs. C) in training subjects. Left ventricular ejection fraction improved from 26.8 ± 4.6 to 33.1 ± 5.5% (p<0.05 vs. C) in patients of the training group while it remained unchanged in the control group. E/A-ratio mended from 0.63 ± 0.12 to 0.81 ± 0.22 (p<0.01 vs. C) in training patients. Septal E’ velocities increased from 5.5 ± 0.5 to 7.8 ± 1.4 cm/s in training patients (p<0.05 vs. C). FMD of the radial artery improved from 8.2 ± 2.1 to 15.2 ± 3.8% (p<0.01 vs. C) as a result of ET. CONCLUSIONS: Only 4 weeks of endurance training are highly effective with significantly improved FMD accompanied by an emended systolic and diastolic LV-function. We hypothesise that the improvement in LV-EF in training patients may be caused by a corrected ventricular-arterial coupling: ventricular diastolic relaxation and effective endothelial function are ameliorated resulting in an augmentation of stroke volume.

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