The role of inflammatory mediators in chronic heart failure: cytokines, nitric oxide, and endothelin-1

Int J Cardiol. 2000 Jan 15;72(2):175-86. doi: 10.1016/s0167-5273(99)00186-2.


There is now considerable evidence to suggest that neurohormonal and immune mechanisms may play a central role in the pathogenesis of chronic heart failure (CHF), which is likely to have important implications for the management of this condition. It has been proposed that CHF is a state of immune activation with inflammatory cytokines contributing to both the central and the peripheral manifestations of this syndrome. The immune system is the body's natural defence mechanism against infection and other stresses, which has several different components that interact with each other in a complex manner. The main components which are thought to be relevant to the pathogenesis of CHF are: cytokines, adhesion molecules, autoantibodies, nitric oxide, and endothelin-1, and this review will concentrate on these factors. This article will also discuss the potential role of anti-cytokine therapies in the treatment of CHF.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Autoantibodies / physiology
  • Cardiac Output, Low / drug therapy
  • Cardiac Output, Low / immunology*
  • Cardiac Output, Low / physiopathology
  • Cell Adhesion Molecules / physiology
  • Chronic Disease
  • Cytokines / physiology*
  • Endothelin-1 / physiology*
  • Humans
  • Inflammation Mediators
  • Nitric Oxide / physiology*
  • Oxidative Stress / physiology
  • Tumor Necrosis Factor-alpha / physiology


  • Autoantibodies
  • Cell Adhesion Molecules
  • Cytokines
  • Endothelin-1
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide