Fetal stem cells in combined treatment of chronic heart failure and their effect on morphofunctional parameters of the left ventricle myocardium

2014 ◽  
Vol 2 (1) ◽  
pp. 20-24
Author(s):  
M. Klunnyk ◽  
N. Sych ◽  
I. Matiyaschuk ◽  
O. Ivankova ◽  
M. Demchuk ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Chronic Heart Failure ◽  
Left Ventricle ◽  
Combined Treatment ◽  
Left Ventricular ◽  
Walking Distance ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Fetal Stem Cells

Fetal stem cells treatment (FSCT) is assumed to be a new direction in a combined therapy for the patients with the severe chronic heart failure (CHF).Material and methods. 20 patients (average age of 50.1 ± 1.1 yrs.) with CHF functional class III-IV (FC) undergoing the transplantation of the cryopreserved cells of the fetal liver and heart obtained from 5-8 weeks gestation embryos were examined. The control group (CG) of 20 patients was compared by gender and age with the main group (MG).Results. Within 6 months after FSC therapy CHF patients reported a significant improvement of the contractile activity of the left ventricle (LV) heart muscle in echocardiography (EchoCG) findings (left ventricular ejection fraction (LVEF) increased by 20.9 % being 2-fold higher than in patients without FSCT, p<0.05) and in features of LV remodeling (left ventricle end diastolic volume (LV EDV) decreased by 20.5 %, p < 0.05). Serum NT-proBNP significantly raised within 1 month after FSCT by 33.8 %, 50 % and 65.1 % in 1, 3 and 6 months respectively (p<0.001) and was significantly lower after a month of treatment compared with CG (р<0.05).As a result of general condition improvement in CHF patients significant elevation in 6 minute walking distance (6MWD) test was observed and the distance walked increased 7.3-fold (p<0.001), 10.3-fold (p<0.001) and 12.5-fold (p<0.001) vs. the baseline in 1, 3 and 6 months, respectively, which was generally 2-fold higher than in patients of the CG. DASI score increased by 54.6 %, after 3 months — by 63.2 %, after 6 months — by 66.4 %, which is significantly higher than the baseline (p<0.05 vs. baseline).Conclusion. It has been proven that combined treatment of CHF patients using FSCs along with the standard therapy increases the LV myocardial contractility, lowering the blood serum NT-proBNP level and results in overall life quality improvement among the patients.

scholarly journals Features of structural and geometric remodeling of the heart and changes in heart diastolic filling in patients with chronic heart failure of ischemic genesis with reduced left ventricular ejection fraction

2021 ◽  
Vol 23 (1) ◽  
pp. 17-23
Author(s):  
V. A. Lysenko
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Diastolic Filling ◽  
Ventricular Ejection Fraction ◽  
Lv Mass

Chronic heart failure (CHF) does not lose its leading position among the problems of cardiovascular disease. Pathological cardiac remodeling combines the processes of hypertrophy and dilatation of cavities and is the main cause of heart failure progression, and consequently results in high cardiac mortality, especially in CHF patients with reduced left ventricular ejection fraction (LV EF). Despite a substantial range of studies on the features of structural and geometric remodeling of the heart, changes in systolic and diastolic function of the ventricles in CHF patients, this issue still presents a challenge and needs to be improved. The aim of the work – to examine changes in structural and geometric parameters and diastolic function of the heart in patients with CHF of ischemic genesis with reduced LV EF. Materials and methods. The study included 79 patients (men – n = 49; women – n = 30) with CHF of ischemic origin with reduced LV EF, sinus rhythm, stage II AB, NYHA II-IV FC (the main group), and 90 patients with coronary heart disease without signs of CHF (men – n = 40, 44.5 %; women – n = 50, 55.5 %), (the comparison group). The patient groups were age-, sex-, height-, weight-, body surface area-matched. Doppler echocardiographic examination was performed on the device Esaote MyLab Eight (Italy). Results. In CHF patients with reduced LV EF, the following indicators prevailed: EDD LV by 18 % (P = 0.001), LV EDV by 45.8 % (P = 0.001), LV EDV index by 44.6 % (P = 0.001), LV ESD by 44.9 % (P = 0.001), PW by 17.7 % (P = 0.001), LV mass index by 66.6 % (P = 0.001) according to the Penn Convention, and by 62.1 % (P = 0.001) according to the ASE; 16.1 % (P = 0.010) increased RV cavity without changes in its wall thickness. In patients with CHF of ischemic origin with reduced LV EF, the main types of LV geometry were: eccentric (70 %) and concentric (24 %) LV hypertrophy. More than half of the CHF patients with reduced LV EF had significant disorders of LV diastolic filling (25 % – “restrictive” and 28 % “pseudonormal”), a 2.3 times increase (P = 0.001) in E/e’ ratio, a 35 % (P = 0.014) increase in the left atrial volume index and 32 % (P = 0.0001) – in pulmonary capillary wedge pressure (PCWP), increased mean and systolic pressure in the pulmonary artery by 1.5 times (P = 0.002) and 1.6 times (P = 0.0001), respectively. Conclusions. Structural and geometric remodeling of the left ventricle in patients with CHF of ischemic origin with reduced LV EF occurs due to an increase in LV myocardial mass via thickening of its walls and cavity dilatation (44.6 % (P = 0.001) increase in the LV EDV index), as well as 66.6 % (P = 0.001) increase in LV mass index with the predominance of eccentric (70 %) and concentric hypertrophy (24 %) over other types of LV geometry. Severe disorders of LV diastolic filling (25 % – “restrictive” and 28 % “pseudonormal”) are attributable to the significant increase in end-diastolic pressure in the left ventricle (2.3 times increase (P = 0.001) in E/e´) with the development of postcapillary pulmonary hypertension (1.5 times increase (P = 0.002) in the mean and 1.6 times (P = 0.0001) – in systolic pressure in the pulmonary artery).

Effect of Diabetes on the Assessment Role of 2-Oxoglutarate to the Severity of Chronic Heart Failure

2017 ◽  
Vol 126 (08) ◽  
pp. 478-486
Author(s):  
Pingan Chen ◽  
Lina Hou ◽  
Yishan Luo ◽  
Lushan Chen ◽  
Shaonan Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mass Spectrometry ◽  
Chronic Heart Failure ◽  
Left Ventricle ◽  
Left Ventricular ◽  
Clinical Severity ◽  
Volume Index ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Predictive Role

Abstract Background Serum 2-oxoglutarate can reflect the severity of chronic heart failure (CHF) in patients without diabetes. Whether this predictive role persists in type 2 diabetes mellitus (T2DM) patients is unclear. In this study, we investigated this predictive role in T2DM patients and whether 2-oxoglutarate can indicate the diastolic or systolic function of left ventricle. Methods One hundred eighty CHF patients (76 with T2DM) and 66 healthy controls were studied. 2-Oxoglutarate was assayed by liquid chromatography-mass spectrometry/mass spectrometry. Echocardiographic parameters, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and other parameters were measured. Results 2-Oxoglutarate was increased in CHF patients with or without T2DM compared with controls (both P<0.01). Patients with a lower left ventricular ejection fraction or a higher NT-proBNP or left ventricular end-diastolic volume index had higher levels of 2-oxoglutarate (median, 18.77 μg/mL versus 11.25 μg/mL; median, 14.06 µg/ml versus 9.39 µg/ml; median, 18.06 µg/mL versus 11.60 µg/mL, all P<0.05) in nondiabetic patients but not in T2DM patients. In multiple logistic regression analysis, NT-proBNP (OR=3.445, 95% CI=1.098 to 10.816, P=0.034) and left ventricular end-diastolic diameter (OR=2.544, 95% CI=1.033 to 6.268, P=0.042) were independently associated with increased 2-oxoglutarate in nondiabetic patients. Conclusions The levels of 2-oxoglutarate can reflect the clinical severity of CHF in nondiabetic patients but not in those with T2DM, and it can be used as a potential indicator of the systolic dysfunction of the left ventricle.

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.

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