[Mechanisms of inflammation in heart failure].

For a long time chronic heart failure was seen as a purely myocardial problem, which is characterized by symptoms in consequence of an impaired contractility. Later on it became apparent that chronic heart failure is at least in part characterized by activation of the neuroendocrine system, in particular the sympathetic nervous system and the renin-angiotensin-aldosterone system. This neuroendocrine system is an important system that is not only responsible for symptoms but probably very important for the development and progression of heart failure and therefore relevant to the prognosis of these patients. Apart from this neuroendocrine activation heart failure is characterized by an inflammatory component. The mechanisms of inflammation seem to play an important role in the process of left ventricular remodeling including structural and functional changes of the myocardium which are not only in part responsible for the development of symptoms but also for the progression of disease. It turns out that pathophysiological consequences of activated inflammation are deleterious in the long term, but may provide transient protective effects in the acute stage of ischemia. Regarding clinical trials it can be assumed that general inhibition of the inflammation process by inhibition of tumor necrosis factor-(TNF-)alpha does not necessarily exert favorable effects.