title: Neurohormonal activation in heart failure with reduced ejection fraction.
abstract: Heart failure with reduced ejection fraction (HFrEF) develops when cardiac output falls as a result of cardiac injury. The most well-recognized of the compensatory homeostatic responses to a fall in cardiac output are activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). In the short term, these 'neurohormonal' systems induce a number of changes in the heart, kidneys, and vasculature that are designed to maintain cardiovascular homeostasis. However, with chronic activation, these responses result in haemodynamic stress and exert deleterious effects on the heart and the circulation. Neurohormonal activation is now known to be one of the most important mechanisms underlying the progression of heart failure, and therapeutic antagonism of neurohormonal systems has become the cornerstone of contemporary pharmacotherapy for heart failure. In this Review, we discuss the effects of neurohormonal activation in HFrEF and highlight the mechanisms by which these systems contribute to disease progression.
authors.affiliation: Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
authors.forename: Justin
authors.initials: J
authors.lastname: Hartupee
authors.affiliation: Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
authors.forename: Douglas L
authors.initials: DL
authors.lastname: Mann
mesh_terms: D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use; D018450:Disease Progression; D006333:Heart Failure / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D018377:Neurotransmitter Agents / Q000037:antagonists & inhibitors; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D002316:Cardiotonic Agents; D018377:Neurotransmitter Agents