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Summary

Heart failure (HF) is a public health problem that has affected 2.5% of the population over the last 20 years. Despite the developments in therapy over recent decades, the mortality rate and number of admissions remain high. Ischemic heart disease is still the primary etiological factor. Heart failure involves inflammatory activation with increased plasma levels of tumor necrosis factor a (TNF-a), interleukin 1b (IL-1b), IL-2, IL-6, IL-8, soluble IL-6 receptor, cluster of differentiation 14 (CD14) and endothelin 1A and 1B. This inflammatory activation is described by the cytokine hypothesis. The magnitude of the increase in cytokines is related to the severity of the condition, and ischemic HF exhibits higher plasma cytokine levels. The cytokine hypothesis provoked a search for potential therapeutic targets. Attempts to antagonize TNF-a, endothelin A and matrix metalloproteinase, however, were ineffective or harmful. Despite the failure of extensive clinical trials, smaller-scale studies have shown promising results with nonspecific anti-inflammatory drugs such as thalidomide, pentoxifylline and methotrexate.



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