Abstract P323: Waon Therapy, a Form of Thermal Therapy, Reduces Oxidative Stress Systemically and Inhibits the Progression of Cardiac Dysfunction in TO-2 Cardiomyopathic Hamsters with Heart Failure

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Yoshiyuki Ikeda ◽  
Masaaki Miyata ◽  
Yuichi Akasaki ◽  
Takahiro Miyauchi ◽  
Yuko Furusho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiac Dysfunction ◽  
Therapy Group ◽  
Left Ventricular ◽  
Thermal Therapy ◽  
Control Group ◽  
Vascular Endothelial ◽  
Cardiac Apoptosis ◽  
Cardiomyopathic Hamsters

Background: Oxidative stress is one of the most crucial factors that develop chronic heart failure (CHF), leading to cardiac apoptosis and fibrosis and vascular endothelial dysfunction. We have reported that Waon therapy, which is a form of thermal therapy using a far infrared-ray dry sauna at 60 degrees centigrade, improves cardiac and vascular endothelial functions and prognosis in patients with CHF. The aim of this study is to investigate whether Waon therapy reduces oxidative stress and prevents from developing cardiac dysfunction in CHF. Methods: Thirty-week old male TO-2 cardiomyopathic hamsters with CHF were divided into Waon therapy or control group. Waon therapy group underwent Waon therapy daily for 4 weeks. Control hamsters did not take any treatment. We examined the amounts of reactive oxygen species of serum, hearts and aortas using ELISA and immunohistochemistry. We measured left ventricular % fractional shortening (LV%FS), and performed TUNEL and Azan staining of hearts to assess cardiac function, apoptosis and fibrosis, respectively. Anti-oxidants and apoptotic and angiogenetic factors were assessed by Western blot. All examinations were performed after 4 weeks of treatment. Results: Four-week Waon therapy significantly decreased oxidative stress of serum, hearts and aortas compared to those of controls. Waon therapy significantly increased LV%FS and decreased cardiac apoptosis and fibrosis (LV%FS, Waon therapy: 23.3±4.3 vs. control: 16.5±4.2%, P<0.01, TUNEL positive nuclei, 22.0±2.6 vs. 49.3±7.2%, P<0.01, % fibrosis, 20.6±5.3 vs. 47.6±4.8%, P<0.01). Waon therapy significantly increased the expressions of manganese superoxide dismutase, heat shock protein 27 (HSP27) and HSP32 of hearts and aortas, which negatively modulate oxidative stress, compared to those of controls. Waon therapy significantly increased endothelial nitric oxide synthase and decreased plasminogen activator inhibitor-1 of aortas. In addition, Waon therapy significantly decreased Bax, cleaved caspase 3 and cytochrome c and increased Bcl-2 and hypoxia-inducible factor-1α of the failing hearts. Conclusions: Waon therapy reduces oxidative stress systemically and inhibits the progression of cardiac dysfuntion in TO-2 cardiomyopathic hamsters.

The Pattern of Ventricular Remodeling Influences the Level of Oxidative Stress in Heart Failure Patients

2017 ◽  
Vol 68 (7) ◽  
pp. 1506-1511
Author(s):  
Cerasela Mihaela Goidescu ◽  
Anca Daniela Farcas ◽  
Florin Petru Anton ◽  
Luminita Animarie Vida Simiti
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Clinical Laboratory ◽  
Left Ventricular ◽  
Control Group ◽  
Reactive Protein ◽  
Lv Mass ◽  
Few Data

Oxidative stress (OS) is increased in chronic diseases, including cardiovascular (CV), but there are few data on its effects on the heart and vessels. The isoprostanes (IsoP) are bioactive compounds, with 8-iso-PGF25a being the most representative in vivo marker of OS. They correlate with the severity of heart failure (HF), but because data regarding OS levels in different types of HF are scarce, our study was aimed to evaluate it by assessing the urinary levels of 8-iso-PGF2aand its correlations with various biomarkers and parameters. Our prospective study included 53 consecutive patients with HF secondary to ischemic heart disease or dilative cardiomyopathy, divided according to the type of HF (acute, chronic decompensated or chronic compensated HF). The control group included 13 hypertensive patients, effectively treated. They underwent clinical, laboratory - serum NT-proBNP, creatinine, uric acid, lipids, C reactive protein (CRP) and urinary 8-iso-PGF2a and echocardiographic assessment. HF patients, regardless the type of HF, had higher 8-iso-PGF2a than controls (267.32pg/�mol vs. 19.82pg/�mol, p[0.001). The IsoP level was directly correlated with ejection fraction (EF) (r=-0.31, p=0.01) and NT-proBNP level (r=0.29, p=0.019). The relative wall thickness (RWT) was negatively correlated with IsoP (r=-0.55, p[0.001). Also 8-iso-PGF25a was higher by 213.59pg/�mol in the eccentric left ventricular (LV) hypertrophy subgroup comparing with the concentric subgroup (p=0.014), and the subgroups with severe mitral regurgitation (MR) and moderate/severe pulmonary hypertension (PAH) had the highest 8-iso-PGF2a levels. Male sex, severe MR, moderate/severe PAH, high LV mass and low RWT values were predictive for high OS level in HF patients.Eccentric cardiac remodeling, MR severity and PAH severity are independent predictors of OS in HF patients.

scholarly journals THERMAL THERAPY, NAMED WAON THERAPY, REDUCES CARDIAC OXIDATIVE STRESS, APOPTOSIS AND FIBROSIS OF TO-2 CARDIOMYOPATHIC HAMSTERS WITH HEART FAILURE

2011 ◽  
Vol 57 (14) ◽  
pp. E239
Author(s):  
Yoshiyuki Ikeda ◽  
Masaaki Miyata ◽  
Yuichi Akasaki ◽  
Takahiro Miyauchi ◽  
Yuko Furusho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Thermal Therapy ◽  
Cardiomyopathic Hamsters

Erythropoietin protects against doxorubicin-induced heart failure

2011 ◽  
Vol 301 (6) ◽  
pp. H2413-H2421 ◽  
Author(s):  
Hania Ibrahim Ammar ◽  
Soliman Saba ◽  
Rasha Ibrahim Ammar ◽  
Laila Ahmed Elsayed ◽  
Wael Botros Abu-Alyamin Ghaly ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Control Group ◽  
Maximal Increase ◽  
Male Wistar Rats ◽  
Developed Pressure

The hormone erythropoietin (EPO) has been demonstrated to have cardioprotective properties. The present study investigates the role of EPO to prevent heart failure following cancer treatment with doxorubicin [adriamycin (AD)]. Male Wistar rats (150 ± 10 g) were treated with saline (vehicle control group); with EPO, subcutaneously at 1,000 IU/kg body wt, three times per week for 4 wk (EPO group); with adriamycin, intraperitoneally at 2.5 mg/kg body wt, three times per week for 2 wk (AD group); and with adriamycin and EPO (EPO-AD group). Echocardiographic measurements showed that EPO-AD treatment prevented the AD-induced decline in cardiac function. Each of the hearts was then exposed to ischemia and reperfusion during Langendorff perfusion. The percentage of recovery after ischemia-reperfusion was significantly greater in EPO-AD than the AD-treated group for left ventricular developed pressure, maximal increase in pressure, and rate pressure product. The level of oxidative stress was significantly higher in AD (5 μM for 24 h)-exposed isolated cardiomyocytes; EPO (5 U/ml for 48 h) treatment prevented this. EPO treatment also decreased AD-induced cardiomyocyte apoptosis, which was associated with the decrease in the Bax-to-Bcl2 ratio and caspase-3 activation. Immunostaining of myocardial tissue for CD31 showed a significant decrease in the number of capillaries in AD-treated animals. EPO-AD treatment restored the number of capillaries. In conclusion, EPO treatment effectively prevented AD-induced heart failure. The protective effect of EPO was associated with a decreased level of oxidative stress and apoptosis in cardiomyocytes as well as improved myocardial angiogenesis.

scholarly journals Analysis of levels of oxidative stress markers depending on the left ventricular ejection fraction in patients with chronic heart failure

2018 ◽  
Vol 17 (5) ◽  
pp. 34-39
Author(s):  
E. A. Polunina ◽  
L. P. Voronina ◽  
E. A. Popov ◽  
O. S. Polunina
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Sod Activity ◽  
Ventricular Ejection Fraction

Aim.To study and analyze the levels of oxidative stress (OS) markers (malondialdehyde (MDA), superoxide dismutase (SOD), advanced oxidation protein products (AOPPs)) depending on the left ventricular ejection fraction (LVEF) and functional class (FC) in patients with chronic heart failure (CHF).Material and methods.We examined 60 somatically healthy individuals and 345 patients with CHF, which were divided into three main groups depending on the LVEF and subgroups depending on FC. The levels of OS markers were determined in blood serum — MDA, SOD and AOPPs.Results.In the group of patients with preserved LVEF and FC II-IV CHF, levels of MDA and AOPPs were statistically significantly higher, and the SOD level was lower compared to the control group. In the group of patients with moderately reduced and reduced LVEF, the levels of MDA and AOPPs were statistically significantly higher, and SOD activity was lower compared with the control group and the group of patients with CHF and preserved LVEF. In patients with CHF with higher FC, there was a statistically significant increase of MDA and AOPPs levels and decrease of SOD activity. The most pronounced changes in the levels of above-mentioned markers were recorded in patients with reduced LVEF. According to the correlation analysis a direct relationship between the levels of markers of the OS and clinical manifestations of the disease was found.Conclusion.Changes in levels of MDA, SOD and AOPPs in patients with CHF were detected already in the early stages of the disease compared with the control group. In patients with higher FC CHF and preserved, moderately reduced and reduced LVEF, a statistically significant increase in the levels of MDA and AOPPs and a decrease of SOD activity were observed. The most pronounced changes in the levels of the markers were indicated in patients with reduced LVEF.

scholarly journals JAK2V617F-Mediated Endothelial Dysfunction Promotes Congestive Heart Failure in a Murine Model of Myeloproliferative Neoplasm

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 7-7
Author(s):  
Melissa Castiglione ◽  
Christopher Mazzeo ◽  
Ya-Ping Jiang ◽  
Juei-Suei Chen ◽  
Wei Yin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Murine Model ◽  
Cardiac Dysfunction ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Jak2v617f Mutation ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Vascular Endothelial Function ◽  
Hematopoietic Stem

Introduction Cardiovascular complications are the leading cause of morbidity and mortality in patients with myeloproliferative neoplasms (MPNs). The acquired kinase mutation JAK2V617F plays a central role in these disorders. Many studies have established that a significant number of vascular endothelial cells (ECs) in MPN patients carry the mutation.In this study, we tested the hypothesis that the JAK2V617F mutation alters vascular endothelial function to promote cardiovascular complications in patients with MPNs. Methods JAK2V617F Flip-Flop (FF1) mice and Tie2-Cre mice were crossed to generate the Tie2FF1 mice, in which human JAK2V617F is expressed specifically in hematopoietic cells and vascular ECs, so as to model the human diseases in which both the hematopoietic stem cells and ECs harbor the mutation. All mice were fed a standard chow diet. Results As we previously reported, Tie2FF1 mice develop a myeloproliferative phenotype with leukocytosis, thrombocytosis, significant splenomegaly, and greatly increased numbers of hematopoietic stem cells by 8 wk of age. We observed an increased incidence of sudden death during performance of minor procedures (e.g. submandibular bleeding) in Tie2FF1 mice, especially after 20 wk of age. Transthoracic echocardiography revealed significant decreases in left ventricular ejection fraction and fractional shortening, and increases in left ventricular end-diastolic volume and end-systolic volume in 20-22 wk old Tie2FF1 mice compared to age-matched Tie2-Cre controls, indicative of cardiac dysfunction. Pathological evaluation revealed increased heart size and heart weight, and evidence of pulmonary congestion in Tie2FF1 mice compared to controls, consistent with the diagnosis of congestive heart failure. No atherosclerotic lesions or myocardium infarctions were observed in Tie2FF1 mice. (Figure 1) No significant cardiac dysfunction was observed in Tie2FF1 mice at 10-12 wk of age, suggesting that the heart failure is apparently not present from birth. Next,we generated a chimeric murine model with JAK2V617F-mutant blood cells and wild-type vascular ECs by transplanting Tie2FF1 marrow cells into wild-type recipients. The transplantation of wild-type marrow cells into wild-type recipients served as a control. Recipients of Tie2FF1 marrow developed myeloproliferation and there was no difference in blood cell counts between these mice and the primary Tie2FF1 mice. However, serial echocardiography evaluation did not reveal any evidence of cardiac dysfunction in recipients of Tie2FF1 marrow. In addition, Ly-6Chighmonocytes, which are important participant at various stages of cardiovascular disease development, were significantly increased in primary Tie2FF1 micecompared to Tie2-Cre controls, but not in wild-type recipients of Tie2FF1 marrow. These observations suggest that JAK2V617F-mutant blood cells alone are not sufficient to generate the spontaneous heart failure phenotype we have observed in Tie2FF1 mice; JAK2V617F-mutant ECs are required, as cardiac dysfunction and inflammatory monocytes are only generated when the ECs bear the JAK2V617F mutation. (Figure 2) To begin to understand the roles of JAK2V617F-mutant ECs in the development of cardiovascular dysfunction in Tie2FF1 mice, we found that the expression levels of Kruppel-like factors 2 (KLF2) and 4 (KLF4), two important regulators of vascular homeostasis that contribute to an anti-adhesive, anti-thrombotic, and anti-inflammatory endothelial phenotype, as well as thrombomodulin and eNOS, two downstream targets of KLF2/4 signaling, were significantly down-regulated in JAK2V617F-mutant ECs compared to wild-type ECs. In addition, cell surface adhesion molecules PECAM and E-selection were significantly up-regulated in JAK2V617F-mutant ECs compared to wild-type ECs. Both PECAM and E-selectin were further up-regulated in flow sheared (60dyn/cm2) JAK2V617F-mutant ECs compared to un-sheared ECs, while their levels did not change in wild-type ECs. These results indicate that JAK2V617F-mutant ECs display a pro-adhesive phenotype that can contribute to the cardiovascular dysfunction we observed in Tie2FF1 mice. (Figure 3) Conclusions In summary, our findings indicate that the JAK2V617F mutation can alter vascular endothelial function to promote cardiovascular complications in a murine model of MPN. Disclosures No relevant conflicts of interest to declare.

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

scholarly journals Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 931
Author(s):  
Anureet K. Shah ◽  
Sukhwinder K. Bhullar ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Critical Role ◽  
Pressure Overload ◽  
Hypertrophied Heart ◽  
Vasoactive Hormones

Although heart failure due to a wide variety of pathological stimuli including myocardial infarction, pressure overload and volume overload is associated with cardiac hypertrophy, the exact reasons for the transition of cardiac hypertrophy to heart failure are not well defined. Since circulating levels of several vasoactive hormones including catecholamines, angiotensin II, and endothelins are elevated under pathological conditions, it has been suggested that these vasoactive hormones may be involved in the development of both cardiac hypertrophy and heart failure. At initial stages of pathological stimuli, these hormones induce an increase in ventricular wall tension by acting through their respective receptor-mediated signal transduction systems and result in the development of cardiac hypertrophy. Some oxyradicals formed at initial stages are also involved in the redox-dependent activation of the hypertrophic process but these are rapidly removed by increased content of antioxidants in hypertrophied heart. In fact, cardiac hypertrophy is considered to be an adaptive process as it exhibits either normal or augmented cardiac function for maintaining cardiovascular homeostasis. However, exposure of a hypertrophied heart to elevated levels of circulating hormones due to pathological stimuli over a prolonged period results in cardiac dysfunction and development of heart failure involving a complex set of mechanisms. It has been demonstrated that different cardiovascular abnormalities such as functional hypoxia, metabolic derangements, uncoupling of mitochondrial electron transport, and inflammation produce oxidative stress in the hypertrophied failing hearts. In addition, oxidation of catecholamines by monoamine oxidase as well as NADPH oxidase activation by angiotensin II and endothelin promote the generation of oxidative stress during the prolonged period by these pathological stimuli. It is noteworthy that oxidative stress is known to activate metallomatrix proteases and degrade the extracellular matrix proteins for the induction of cardiac remodeling and heart dysfunction. Furthermore, oxidative stress has been shown to induce subcellular remodeling and Ca2+-handling abnormalities as well as loss of cardiomyocytes due to the development of apoptosis, necrosis, and fibrosis. These observations support the view that a low amount of oxyradical formation for a brief period may activate redox-sensitive mechanisms, which are associated with the development of cardiac hypertrophy. On the other hand, high levels of oxyradicals over a prolonged period may induce oxidative stress and cause Ca2+-handling defects as well as protease activation and thus play a critical role in the development of adverse cardiac remodeling and cardiac dysfunction as well as progression of heart failure.

Very early detection of low dose anti-cancer therapy-related cardiotoxicity in lymphoma patients

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y.W Liu ◽  
H.Y Chang ◽  
C.H Lee ◽  
W.C Tsai ◽  
P.Y Liu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cancer Therapy ◽  
Cardiac Dysfunction ◽  
Systolic Dysfunction ◽  
Multivariable Analysis ◽  
Cardiopulmonary Exercise Test ◽  
Left Ventricular ◽  
Funding Source ◽  
Anti Cancer ◽  
All Cause Mortality

Abstract Background and purpose Left ventricular (LV) global peak systolic longitudinal strain (GLS) by speckle-tracking echocardiography is a sensitive modality for the detection of subclinical LV systolic dysfunction and a powerful prognostic predictor. However, the clinical implication of LV GLS in lymphoma patients receiving anti-cancer therapy remains unknown. Methods We prospectively enrolled 74 patients (57.9±17.0 years old, 57% male) with lymphoma who underwent echocardiography prior to chemotherapy, post 3rd and 6th cycle and 1 year after chemotherapy. Cancer therapy-related cardiac dysfunction (CTRCD) is defined as the reduction of absolute GLS value from baseline of ≥15%. All the eligible patients underwent a cardiopulmonary exercise test (CPET) upon completion of 3 cycles of anti-cancer therapy. The primary outcome was defined as a composite of all-cause mortality and heart failure events. Results Among 36 (49%) patients with CTRCD, LV GLS was significantly decreased after the 3rd cycle of chemotherapy (20.1±2.6% vs. 17.5±2.3%, p&lt;0.001). In the multivariable analysis, male sex and anemia (hemoglobin &lt;11 g/dL) were found to be independent risk factors of CTRCD. Objectively, patients with CTRCD had lower minute oxygen consumption/kg (VO2/kg) and lower VO2/kg value at anaerobic threshold in the CPET. The incidence of the primary composite outcome was higher in the CTRCD group than in the non-CTRCD group (hazard ratio 3.21; 95% CI, 1.04–9.97; p=0.03). Conclusion LV GLS is capable of detecting early cardiac dysfunction in lymphoma patients receiving anti-cancer therapy. Patients with CTRCD not only had a reduced exercise capacity but also a higher risk of all-cause mortality and heart failure events. Change of LVEF and GLS after cancer Tx Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): The Ministry of Science and Technology (MOST), Taiwan

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