Abstract:as from indirect costs related to the reduction in the quality of life and to productivity loss [1][2][3] . Two million Brazilians are currently estimated to live with HF, and up to one third of hospital admissions in the Brazilian public health system are estimated to result from this disease 2,3 ; moreover, among patients older than 60 years of age, HF is the major cause of hospital admissions and mortality in Brazil and in the rest of the Western world 1,3 . The epidemiological setting seems to be even more… Show more
“…The form chosen to analyze TNF-α was the measurement of s-TNFr1 because TNF-α has a short half-life and may be more unstable in the blood stream when compared with the soluble receptors [3]. The sTNFr1 mediates the most part of the actions of TNF-α, and it has already been demonstrated that this soluble receptor is a more reproducible marker and an indicator that reflects better the action of TNF-α, and thus, the inflammatory activity [3].…”
Section: Blood Analysismentioning
confidence: 99%
“…The sTNFr1 mediates the most part of the actions of TNF-α, and it has already been demonstrated that this soluble receptor is a more reproducible marker and an indicator that reflects better the action of TNF-α, and thus, the inflammatory activity [3].…”
Section: Blood Analysismentioning
confidence: 99%
“…Patients with heart failure (HF) have chronic inflammation activation characterized by an increase in the levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), both in the plasma and heart [1][2][3]. The major cardiac alterations owing to the deleterious action of TNF-α are hypertrophy, cell apoptosis, changes in the extracellular matrix with the worsening of ventricular function, endothelial dysfunction, and an increase in the adhesion cells [4].…”
Section: Introductionmentioning
confidence: 99%
“…In cardiac myocytes, the increase in TNF-α is one of the factors that stimulate the induction of IL-6 [3,6]. IL-6 is characterized as a multifunctional cytokine, which can act as a pro-and anti-inflammatory agent.…”
The aim of this study is to compare the response of interleukin-6 (IL-6) and soluble tumor necrosis factor alpha receptor 1 (s-TNFr1) to two submaximal intensities of exercise in individuals with heart failure (HF). Thirty-two HF individuals aged 45.53 ± 9.41 years, classes II and III of the New York Heart Association (NYHA) classification underwent two sessions of exercise at low and moderate intensities with blood analysis at baseline, exercise and after exercise. The differences were evaluated by Friedman test and factorial ANOVA. Alpha = 5% was considered. No difference in IL-6 was detected for low intensity. At moderate intensity, there was a significant increase after exercise. The s-TNFr1 increased in moderate-intensity exercise and went back to baseline levels after it. A session of moderate-intensity exercise is better than low-intensity exercise at promoting positive immediate inflammatory responses in individuals with HF class II and III of the NYHA.
“…The form chosen to analyze TNF-α was the measurement of s-TNFr1 because TNF-α has a short half-life and may be more unstable in the blood stream when compared with the soluble receptors [3]. The sTNFr1 mediates the most part of the actions of TNF-α, and it has already been demonstrated that this soluble receptor is a more reproducible marker and an indicator that reflects better the action of TNF-α, and thus, the inflammatory activity [3].…”
Section: Blood Analysismentioning
confidence: 99%
“…The sTNFr1 mediates the most part of the actions of TNF-α, and it has already been demonstrated that this soluble receptor is a more reproducible marker and an indicator that reflects better the action of TNF-α, and thus, the inflammatory activity [3].…”
Section: Blood Analysismentioning
confidence: 99%
“…Patients with heart failure (HF) have chronic inflammation activation characterized by an increase in the levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), both in the plasma and heart [1][2][3]. The major cardiac alterations owing to the deleterious action of TNF-α are hypertrophy, cell apoptosis, changes in the extracellular matrix with the worsening of ventricular function, endothelial dysfunction, and an increase in the adhesion cells [4].…”
Section: Introductionmentioning
confidence: 99%
“…In cardiac myocytes, the increase in TNF-α is one of the factors that stimulate the induction of IL-6 [3,6]. IL-6 is characterized as a multifunctional cytokine, which can act as a pro-and anti-inflammatory agent.…”
The aim of this study is to compare the response of interleukin-6 (IL-6) and soluble tumor necrosis factor alpha receptor 1 (s-TNFr1) to two submaximal intensities of exercise in individuals with heart failure (HF). Thirty-two HF individuals aged 45.53 ± 9.41 years, classes II and III of the New York Heart Association (NYHA) classification underwent two sessions of exercise at low and moderate intensities with blood analysis at baseline, exercise and after exercise. The differences were evaluated by Friedman test and factorial ANOVA. Alpha = 5% was considered. No difference in IL-6 was detected for low intensity. At moderate intensity, there was a significant increase after exercise. The s-TNFr1 increased in moderate-intensity exercise and went back to baseline levels after it. A session of moderate-intensity exercise is better than low-intensity exercise at promoting positive immediate inflammatory responses in individuals with HF class II and III of the NYHA.
“…Currently, the deteriorative changes involved in the progression of HF, which were previously interpreted as arising from changes in salt and water retention or changes in hemodynamic parameters, have been described as recurring processes that culminate in local and systemic inflammatory activation [5][6][7][8][9] , which can be evidenced by the increase in the gene expression and the production of proinflammatory cytokines, such as tumor necrosis factor α (TNF-α); interleukins 1β (IL-1β), 6 (IL-6) and 18 (IL-18 ); cardiotropin-1; CC and CXC chemokines, among other inflammatory markers, in plasma, muscle-skeletal and heart, as well as in peripheral lymphocytes of rats and HF patients. In addition to contributing to the pathophysiology and the progression of structural and functional changes in the heart muscle, these inflammatory mediators may directly lead to peripheral manifestations of the HF syndrome, especially in those changes related to a decrease in muscle mass and functional changes 10,11 , among others.…”
Over the past 50 years, the understanding of the deteriorative changes involved in the progression of heart failure (HF), initially described as resulting from changes in salt and fluid retention, or changes in hemodynamic parameters, have changed significantly. Recently, several studies conducted in HF patients showed altered plasma (or serum) levels of pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukins 1, 6, and 18, and cardiotropin-1, among other inflammatory markers. These changes were independent of HF etiology, suggesting a common pathogenic pathway. In response to these new findings, interventions to prevent and/or reduce these inflammatory changes have been proposed.The aerobic training-induced cardiovascular benefits of physical exercises performed at intensities ranging from mild to moderate have been previously reported. Moreover, it has been shown that moderate aerobic physical training seems to be able to modulate, in the presence of an abnormal chronic inflammatory condition, the overexpression of pro-inflammatory cytokines, soluble adhesion molecules, chemoattractant factors and oxidative stress. Altogether, these data indicate a possible anti-inflammatory effect induced by physical training.Therefore, this review aims to assess the role of physical training as an alternative non-pharmacological adjuvant to be administered in some pathological conditions in which TNF-α chronic changes are predominant, as in HF. The "antiinflammatory effect" induced by physical training seems to be primarily mediated by IL-10.
Background Previous studies suggested that inflammation was involved in chronic heart failure (CHF), but their sample sizes were small. Objective To summarise the clinical cytokine data systematically and emphasise the importance of proinflammatory cytokines in the pathogenesis of CHF, we conducted a meta-analysis of relevant literatures. Methods Articles about cytokines and CHF were searched in Pubmed, EMBASE, Cochrane Library, Chinese National Knowledge Infrastructure and Chinese Wanfang Database. The pooled effects were measured by weighted mean difference (MD) and 95% CI, which were calculated by RevMan 5.1 software.
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