title: Hormonal consequences and prognosis of chronic heart failure.
abstract: OBJECTIVE
  Chronic heart failure (CHF) is a major public health problem. The failure to provide peripheral tissues with sufficient amounts of oxygen is accompanied by maladaptive responses that include pathophysiological pathways that may lead to an anabolic-catabolic imbalance with the development of cardiac cachexia. This review aims to highlight players of the catabolic-anabolic imbalance, regulators or appetite, and other mediators that are involved in the progression of CHF to cachexia.
  
  
  RESULTS
  Clinical research has buttressed the view that deficiencies or resistance to growth hormone and testosterone plays an important role in the pathophysiology of CHF. The role of appetite regulation in the development of cardiac cachexia is also subject of recent studies. The resistance of CHF patients to the effects of appetite-stimulating peptide ghrelin may be one of the contributing factors. These circumstances drive muscle, bone, and fat wasting. Plasma levels of the adipokines leptin and adiponectin may have a role in the detection of such wasting processes.
  
  
  CONCLUSIONS
  Hormonal signaling pathways play an essential role in the development of cardiac cachexia. Recent findings enhance our understanding of the complex interplay between these regulators and may serve as a hub for the development of therapeutic interventions to prevent or potentially even to treat cardiac cachexia.
authors.affiliation: Department of Cardiology, Charite Medical School, Campus Virchow-Klinikum, Berlin, Germany.
authors.forename: Philipp
authors.initials: P
authors.lastname: Attanasio
authors.forename: Stefan D
authors.initials: SD
authors.lastname: Anker
authors.forename: Wolfram
authors.initials: W
authors.lastname: Doehner
authors.forename: Stephan
authors.initials: S
authors.lastname: von Haehling
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D001066:Appetite; D002100:Cachexia / Q000209:etiology / Q000378:metabolism; D002908:Chronic Disease; D054439:Ghrelin / Q000378:metabolism; D006333:Heart Failure / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism; D019382:Human Growth Hormone / Q000378:metabolism; D006801:Humans; D020738:Leptin / Q000378:metabolism; D036361:Peptide Hormones / Q000378:metabolism*; D011379:Prognosis; D015398:Signal Transduction; D013739:Testosterone / Q000378:metabolism
chemical_list: D052242:Adiponectin; D054439:Ghrelin; D020738:Leptin; D036361:Peptide Hormones; D019382:Human Growth Hormone; D013739:Testosterone