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Chronic heart failure and systemic inflammatory response
[Abstract] Objective To study the systemic inflammatory response with chronic heart failure. Methods of CHF circulating levels of inflammatory mediators, inflammation of the sources, mechanisms of inflammation, inflammation of the results, summarized in the anti-inflammatory role of therapy in CHF .
[Keywords:] chronic heart failure systemic inflammation Chronic heart failure (chronic heart failure, CHF) in patients with circulation of inflammatory cytokines was significantly higher in the confirmed existence of the systemic inflammatory response in vivo. In addition to cardiac cells, white blood cells, platelets, tissue macrophages, endothelial cells and other tissues cells contributing to this inflammatory response, which not only cause myocardial damage, resulting in the occurrence and development of CHF, and organ dysfunction caused by other organizations, leading to cachexia, anemia, endothelial barriers outside the heart of change in terms of CHF.
A, CHF level of circulating inflammatory mediators CHF has been confirmed that circulating inflammatory cytokines, such as tumor necrosis factor alone (tumor necrosis factor @, TNF-@), interleukin-1p (interleukin, IL-1 @), interleukin (IL-6) and chemical factors such as monocyte chemotactic peptide -1 (monocyte chemoattractant peptide, MCP-1), interleukin 8 (IL-8), macrophage inflammatory protein -1 @ (macrophage inflammatory protein, MIP-1 @) and other higher in the development and progression of CHF play an important role, and anti-inflammatory cytokines such as interleukin 10 (IL-10) there is no corresponding increase, resulting in a net effect of inflammation. interleukin-10 can inhibit IL- 1β and IL-6 gene expression, regulation of immune function in CHF play an important role. circulating inflammatory cytokines and chemical factors and heart function NYHA classification and left ventricular ejection fr
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