title: The treatment of heart failure: the role of neurohumoral activation.
abstract: Neurohumoral activation refers to increased activity of the sympathetic nervous system, renin-angiotensin system, vasopressin and atrial natriuretic peptide. It is now known that neurohumoral activation contributes to the transition from ventricular dysfunction to clinical heart failure, and is an independent predictor of poor prognosis in heart failure. Although the treatment of heart failure has traditionally focused on drugs to improve ventricular function, there is increasing evidence that therapeutic modulation of neurohumoral activation is a key to successful treatment of heart failure. For example, there is mounting evidence that angiotensin converting enzyme inhibitors (the unquestioned cornerstone for treatment of heart failure), beta receptor blockers, digitalis, and endurance exercise training exert their benefit in heart failure in large part through neurohumoral modulation. This observation--discussed in this brief review--highlights the concept that compensatory neurohumoral activation to decreased cardiac function may itself contribute to the development of heart failure and its poor prognosis.
authors.affiliation: UCLA School of Medicine, Department of Medicine, Los Angeles, California 90095, USA.
authors.forename: H R
authors.initials: HR
authors.lastname: Middlekauff
authors.forename: A L
authors.initials: AL
authors.lastname: Mark
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D004077:Digoxin / Q000627:therapeutic use; D005081:Exercise Therapy; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology; D018377:Neurotransmitter Agents / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D018377:Neurotransmitter Agents; D004077:Digoxin