P6323Exercise capacity as predictor for anaemia or iron deficiency in patients with chronic heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Ebner ◽  
G Dinopoulos ◽  
R Evertz ◽  
T Garfias Macedo ◽  
B Godoy ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Iron Deficiency ◽  
Exercise Capacity ◽  
Left Ventricular ◽  
World Health ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Peak Vo2 ◽  
Minute Walk

Abstract Background Anaemia and iron deficiency (ID) are important factors for muscle function and exercise capacity in patients with chronic heart failure (HF). Their interaction in HF remains to be defined. Methods A total of 280 out-patients with stable chronic HF were enrolled with mean age of 67.0±10.7 years, 21%female, mean left ventricular ejection fraction (LVEF) was 38.9±13.4%, mean Body Mass Index (BMI) 29.3±5.5 kg/m2]. Anaemia was defined according to World Health Organization criteria [Haemoglobin (Hb) <13 g/dL in men and <12 g/dL in women]. ID was defined as ferritin <100 μg/L or ferritin <100 <300 μg/L than with transferrin saturation (TSAT) <20%. Exercise capacity was assessed by spiroergometry (peakVO2), 6 minute walk test (6MWT), short physical performance battery test (SPPB), hang grip strength (HGS) and leg force (LF). All patients were followed up for a mean of 8 month. Results A total of 89 (32%) chronic HF patients had anaemia and 142 (51%) had iron deficiency at baseline. Patients with anaemia showed significant lower exercise capacity compared to patients without anaemia (peak VO2: 15.3±4.6 vs. 18.5±4.8 kg/min p<0.0001, 6MWT: 365.2±135.5 vs. 461.6±127.4 m p<0.0001, SPPB: 9.4±2.3 vs. 11.0±1.6 total points p<0.0001, HGS: 32.5±10.0 vs. 38.8±12.4 kg p<0.0001, LF: 31.4±11.0 vs. 41.3±21.6 kg p<0.0001). The same we found in patients with ID compared to patients without ID (peak VO2: 16.3±5.1 vs. 18.6±4.5 kg/min p=0.001, 6MWT: 400.0±140.8 vs. 458.8±128.4 m p=0.0008, SPPB: 10.0±2.1 vs. 10.9±1.7 total points p=0.0003, HGS: 34.5±11.9 vs. 39.3±11.7 kg p=0.001, LF: 35.7±23.4 vs. 40.5±13.6 kg p=0.04). After a Follow up of mean 8 month 53 patients develop a new onset of either anaemia (n=24) or ID (n=29). Logistic regression analysis showed that gender, 6 minute walk distance, SPPB, HGS and presence of diabetes mellitus at baseline are significantly associated with the development of anaemia or ID (all p<0.05). The strongest predictor was lower SPPB (p=0.0008). Interestingly known determinates lower peak VO2, higher age, higher NYHA class, Creatinine, and hsCRP were not predictive in our cohort to develop anaemia or ID after 8 month (all p>0.05). Conclusion Both anaemia and ID are strongly associated with reduced exercise capacity in patients with HF. The effect of anaemia and iron deficiency together is stronger than that of anemia and ID alone. Reduced SPPB, 6MWT, and HGS are important risk factors for the development of anaemia or ID.

scholarly journals PERORAL FERROCORRECTION OF IRON DEFICIENCY IN PATIENTS WITH CHRONIC HEART FAILURE WITH REDUCED LEFT VENTRICULAR EJECTION FRACTION

2019 ◽  
Vol 19 (3) ◽  
pp. 31-36
Author(s):  
V. P. Ivanov ◽  
M. O. Kolesnyk ◽  
O. M. Kolesnуk
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Iron Deficiency ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Latent Iron Deficiency ◽  
Per Oral

Therapy of iron deficiency as a common comorbidity in chronic heart failure is being paid much attention. It plays contributory role in the morbidity and mortality of heart failure. However, there are some questions requiring future research to answer them. Nowadays, the parenteral administration of iron supplements has been considered as one of the effective approaches for the correction of the above-mentioned disorders, although per oral rout of ferrum administration is playing the leading role. Among the disputable questions there is duration of peroral ferrocorrection course for patients with latent iron deficiency. Taking into account some disadvantages of per oral ferrocorrection, e.g. slow absorption in the gastrointestinal tract or reduced absorption in conditions of even minimal inflammation or blood congestion, in order to improve the condition of the patients with chronic heart failure and concomitant latent iron deficiency, we decided to prolong the course of therapy in our study. The purpose of the study was to determine the effectiveness of 6-month per oral ferrotherapy in patients with heart failure with reduced left ventricular ejection fraction and concomitant latent iron deficiency. Material and methods. We examined 60 patients, 41 (68.3%) men and 19 (37.1%) women, aged 68.3 ± 0.63 years with chronic heart failure with reduced left ventricular ejection fraction functional class II-III according to NYHA, who were also diagnosed to have concomitant latent iron deficiency. Two study groups were formed: the patients of the 1st group (n=30) received only the standard therapy for chronic heart failure according to the European recommendations (2016); the patients of the 2nd group (n=30) were prescribed to take ferrous sulphate per orally in a dose of 320 mg, equivalent to 100 mg of bivalent iron and 60 mg of ascorbic acid 2 tablets per day for 6 months. Results and discussion. By the study’s end, anaemia was observed in 76.5% of patients. However, among these patients, 84.6% had latent iron deficiency and only 15.4% had complete cure of the iron deficiency. Thus, it was found out that without supportive therapy with iron medicines for 32.8±0.7 months after the end of iron deficiency, patients with chronic heart failure had negative laboratory dynamics. Analysis of the dynamics of haematological indices as markers of the ferrocorrection effectiveness in the patients who received the 6-month ferrotherapy demonstrated an increase of all parameters and normalization of iron metabolism indices. Moreover, 96.7% of the patients, who took standard therapy and ferrum medicines, demonstrated the elimination of iron deficiency signs. Conclusion. Thus, the study showed that per oral therapy with iron sulphate at the stage of latent iron deficiency in patients with heart failure with reduced left ventricular ejection fraction for a period of 6 months has been found out as effective.

Abstract 2424: Improvement Of Cardiopulmonary Exercise Capacity In Patients With Chronic Post-infarction Heart Failure (CHF) After Intracoronary Infusion Of Bone Marrow-derived Progenitor Cells (BMC)

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Joerg Honold ◽  
Lenka Geiger ◽  
Ulrich Fischer-Rasokat ◽  
Birgit Assmus ◽  
Volker Schaechinger ◽  
...  
Keyword(s):  
Heart Failure ◽  
Oxygen Uptake ◽  
Exercise Capacity ◽  
Serum Levels ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Cardiopulmonary Exercise ◽  
Cardiopulmonary Exercise Capacity ◽  
Peak Vo2

Intracoronary (i.c.) infusion of BMC in patients (pts.) with CHF is associated with improvements in left ventricular ejection fraction (LVEF) and reduction of NT-proBNP serum-levels, especially in pts. with more severe heart failure. However, ist is unknown whether the modest improvements in cardiac function translate into an increase in cardiopulmonary exercise capacity. A total of 52 CHF-pts. performed cardiopulmonary exercise tests (CPET) according to a modified Bruce protocol before and 3 months after i.c. infusion of BMC into the infarct-related artery. Anaerobic threshold (AT) was determined by the v-slope method. Overall, pts. were 58±12 years old with a moderately impaired LVEF (mean 42±11%) and a median NYHA-class 2±0.75. NT-proBNP-serum levels were elevated (1007±154 pmol/ml). All pts. received chronic optimized medical therapy with betablockers, ACE-inhibitors and combined diuretics, which was kept constant during the study duration. Initial CPET revealed reduced peak oxygen uptake (peak VO2: 14.0 ml/min/kg), maximal oxygen Pulse (O2Pmax: 11.4 ml/beat) and oxygen uptake at AT (VO2AT: 10.9 ml/min/kg), whereas CO2-equivalents (EqCO2) were elevated (29.7). 3 months after therapy, repeated CPET showed an increase in peak VO2 (14.0±3.9 to 15.3±4.3 ml/min/kg, p=0.07), whereas VO2 AT (10.8±2.5 to 10.8±2.5 ml/min/kg, p= n.s.), O2Pmax (11.2 ± 3.1 to 12.0±3.3 ml/beat, p= n.s.) or EqCO2 (29.7±6.4 to 29.8±6.8, p= n.s.) remained unchanged. However, after dichotomizating the patient cohort according to the median of VO2max at baseline, pts. with lower initial VO2max showed a significant improvement in VO2max (12.8±1.5 to 13.5±2.7ml/min/kg, p= 0.03) and an improvement in VO2AT (9.1±1.8 to 9.5±2.2 ml/min/kg, p= ns), as well as a reduction of EqCO2 (34.7±7.1 to 33.8±8.0, p= ns). In contrast, pts. with initial VO2max > median did not show any significant improvements. These findings indicate that intracoronary BMC-therapy improves exercise capacity in CHF-patients with more advanced heart failure. Therefore, cardiopulmonary exercise testing might help to identify pts. more likely to derive functional benefit from intracoronary BMC administration.

scholarly journals Effect of ferrotherapy on clinical and instrumental indices in patients with chronic heart failure with reduced left ventricular ejection fraction and concomitant latent iron deficiency

2019 ◽  
Vol 23 (3) ◽  
pp. 382-388
Author(s):  
V.P. Ivanov ◽  
M.O. Kolesnyk ◽  
O.M. Kolesnуk
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Iron Deficiency ◽  
Ejection Fraction ◽  
Stress Test ◽  
Transferrin Saturation ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Latent Iron Deficiency

The objective of the study was to assess changes of clinical and instrumental indices in patients with chronic heart failure (CHF) with reduced left ventricular (LV) ejection fraction (EF) and concomitant latent iron deficiency (ID) on the background of the standard treatment in combination with 6-months oral ferrotherapy. 60 patients with CHF with reduced LV EF functional class (FC) II-III according to NYHA with concomitant latent ID were examined. Among them were 41 (68.3%) men and 19 (37.1%) women aged 68.3±0.63 years. Two groups of patients with CHF and latent iron deficiency were formed: the 1st group (n=30) received a standard therapy, the patients in the 2nd group (n=30) were additionally prescribed oral ferrous sulfate in a dose of 320 mg, equivalent to 100 mg of bivalent iron and 60 mg of ascorbic acid per day for 6 months. Number of red blood cells (Rbc), hemoglobin (Hb) level, serum iron (SI), ferritin, transferrin saturation (ТS), 6-minute walk stress test (6MWT), MLHFQ and MOS SF36 questionnaire and LV morpho-functional parameters by echocardiography were determined. The studied values are presented as a median (upper, lower quartile). After the therapy the values of Hb, Rbc, SI, ferritin and TS have significantly increased in the 2nd group. But in the 1st group due to the lack of ferrocorrection, in most cases, the values have reduced. An increase of the covered 6MWT distance, MLHFQ points, physical (PH) and mental (MH) components of health of MOS SF36 was observed in both groups: in the first group only by 5.3 (р=0.06), 1.2 (р=0.46), 6.9 (р=0.31) and 7.2% (р=0.02), respectively. Whereas in the second group by 13.8 (p<0.001), 13.6 (p<0.001), 24% (p<0.001) and 15% (p<0.001), respectively. EDD (end-diastolic dimension) decreased by 2.1% (p<0.001), EDV (end-diastolic volume) — by 4.8% (p<0.001), ESD (end-systolic dimension) — by 3.9% (p<0.001), ESV (end-systolic volume) — by 13.3% (p<0.0001), EF has increased by 12.7% (p<0.001) in the first group. No difference in the dynamics of the Echo-CG indices between two groups of patients over 6 months of observation was detected (р>0.18). EDD decreased by 2.7% (p<0.001), EDV — by 3.9% (p<0.0001), ESD — by 3.9%, ESV — by 10.9% (p<0.0001), EF has increased by 16.3% (p<0.0001).Thus, the positive hematological changes in case of latent ID correction in patients with CHF with reduced LV EF, despite the similar dynamics of myocardium morpho-functional indices in case of absent ferrocorrection, are accompanied by more significant positive dynamics of effort tolerance and quality of life.

scholarly journals Does physical training increase insulin sensitivity in chronic heart failure patients?

2004 ◽  
Vol 106 (5) ◽  
pp. 459-466 ◽  
Author(s):  
L. W. E. SABELIS ◽  
P. J. SENDEN ◽  
B. C. M. TE BOEKHORST ◽  
H. J. HULZEBOS ◽  
A. VAN DE WIEL ◽  
...  
Keyword(s):  
Heart Failure ◽  
Insulin Sensitivity ◽  
Chronic Heart Failure ◽  
Physical Training ◽  
Heart Association ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Ventricular Ejection Fraction ◽  
Peak Vo2

To determine the effect of training on insulin sensitivity (IS) and how this relates to peak VO2 (peak oxygen uptake) in CHF (chronic heart failure), 77 CHF patients (New York Heart Association class, II/III; men/women, 59/18; age, 60±9 years; body mass index, 26.7±3.9 kg/m2; left ventricular ejection fraction, 26.9±8.1%; expressed as means±S.D.) participated in the study. Patients were randomly assigned to a training or control group (TrG or CG respectively). Sixty-one patients completed the study. Patients participated in training (combined strength and endurance exercises) four times per week, two times supervised and two times at home. Before and after intervention, anthropometry, IS (euglycaemic hyperinsulinaemic clamp) and peak VO2 (incremental cycle ergometry) were assessed. Intervention did not affect IS significantly, even though IS increased by 20% in TrG and 11% in CG (not significant). Peak VO2 increased as a result of training (6% increase in TrG; 2% decrease in CG; P<0.05). In both groups (TrG and CG), the change in IS correlated positively with the change in peak VO2 (r=0.30, P<0.05). Training resulted in an increase in peak VO2, but not in IS. Whether physical training actually increases IS in CHF patients remains unclear.

scholarly journals Iron Deficiency Predictors in Patients with Chronic Heart Failure and Reduced Left Ventricular Ejection Fraction

2018 ◽  
Vol 0 (4) ◽  
pp. 45-49
Author(s):  
Л. Г. Воронков ◽  
В. В. Горбачова ◽  
А. В. Ляшенко ◽  
Т. І. Гавриленко ◽  
Л. С. Мхітарян
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Iron Deficiency ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

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.

Sign in / Sign up

Export Citation Format

Share Document