Ativação imune-inflamatória na insuficiência cardíaca

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 discouraging: there is enough evidence suggesting that this problem will worsen in the future, since prevalence and mortality rates only increase year after year, in direct contrast to what has been observed for several other cardiovascular disorders 2,3 . All these considerations, that were formulated for a disease whose pathophysiological mechanisms have been recurrently reviewed and reformulated in the past years, only show how challenging it is to bring out the multifaceted character and the multisystemic progression inherent to HF 1,4

Evaluation of the Inflammatory Response to Two Different Intensities of Exercise in Individuals with Heart Failure

“…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].…”

“…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].…”

“…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].…”

“…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.…”

Efeito anti-inflamatório do treinamento físico na insuficiência cardíaca: papel do TNF-α e da IL-10

“…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.…”