title: New therapeutics for chronic heart failure.
abstract: Traditionally, clinicians have viewed heart failure either as a problem of excessive salt and water retention caused by abnormalities of renal blood flow, or as a hemodynamic problem associated with a reduced cardiac output and excessive peripheral vasoconstriction. Recently, clinicians have begun to adopt a neurohormonal model in which heart failure progresses because of the toxic effects of endogenous biological systems that become activated in heart failure. We review the rationale for existing heart failure therapies and discuss the reasoning behind the development of some emerging therapies.
authors.affiliation: Winters Center for Heart Failure Research, Department of Medicine, Baylor College of Medicine, 6565 Fannin Street, Houston, Texas 77030, USA.
authors.forename: Douglas L
authors.initials: DL
authors.lastname: Mann
authors.forename: Anita
authors.initials: A
authors.lastname: Deswal
authors.forename: Biykem
authors.initials: B
authors.lastname: Bozkurt
authors.forename: Guillermo
authors.initials: G
authors.lastname: Torre-Amione
mesh_terms: D000818:Animals; D002317:Cardiovascular Agents / Q000009:adverse effects / Q000627:therapeutic use*; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000097:blood; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology; D006801:Humans; D018377:Neurotransmitter Agents / Q000037:antagonists & inhibitors / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000209:etiology; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D002317:Cardiovascular Agents; D016207:Cytokines; D018377:Neurotransmitter Agents