Inflammatory mediators in chronic heart failure: an overview

Abstract

hronic heart failure (CHF) represents a major public health burden, and its prognosis is comparable to that of different malignant diseases. Our understanding of CHF has developed from the rather simplistic model of mere pump failure to that of a multisystem disorder which affects not only the cardiovascular system but also the musculoskeletal, renal, neuroendocrine, and immune systems. Thus, the pathophysiology of CHF is exceedingly complex. Therapies to block excessive neuroendocrine activation have become a cornerstone of treatment. CHF progresses because of activation of neurohormones and pro-inflammatory cytokines following an initial cardiac injury or a mutation of the genetic programme. 1 Virtually any heart disease can ultimately lead to heart failure, although the initial event leading to the development of this syndrome is in many cases unknown. However, CHF is always the result of some underlying process and the diagnosis cannot stand alone.