title: [Heart energy metabolism and its role in the treatment of heart failure].
abstract: It is unknown why heart failure progresses even when patients are treated with the best therapy available. Evidences suggest that heart failure progression is due to loss of neurohumoral blockade in advanced stages of the disease and to alterations in myocardial metabolism induced, in part, by this neurohumoral activation. Alterations in cardiac energy metabolism, especially those related to substrate utilization and insulin resistance, reduce the efficiency of energy production, causing a heart energy reserve deficit. These events play a basic role in heart failure progression. Therefore, modulation of cardiac metabolism has arisen as a promissory therapy in the treatment of heart failure. This review describes myocardial energy metabolism, evaluates the role of impaired energy metabolism in heart failure progression and describes new therapies for heart failure involving metabolic intervention.
authors.affiliation: Departamento de Enfermedades Cardiovasculares, Pontificia Universidad Católica de Chile, Chile. pcastro@med.puc.cl
authors.forename: Pablo
authors.initials: P
authors.lastname: Castro
authors.forename: Luigi
authors.initials: L
authors.lastname: Gabrielli
authors.forename: Hugo
authors.initials: H
authors.lastname: Verdejo
authors.forename: Douglas
authors.initials: D
authors.lastname: Greig
authors.forename: Rosemarie
authors.initials: R
authors.lastname: Mellado
authors.forename: Roberto
authors.initials: R
authors.lastname: Concepción
authors.forename: Luis
authors.initials: L
authors.lastname: Sepúlveda
authors.forename: José Luis
authors.initials: JL
authors.lastname: Vukasovic
authors.forename: Lorena
authors.initials: L
authors.lastname: García
authors.forename: Marcela
authors.initials: M
authors.lastname: Pizarro
authors.forename: Deisy
authors.initials: D
authors.lastname: Pivet
authors.forename: Constanza
authors.initials: C
authors.lastname: Carrillo
authors.forename: Fabiola
authors.initials: F
authors.lastname: Tapia
authors.forename: Mario
authors.initials: M
authors.lastname: Navarro
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Troncoso
authors.forename: Fernando
authors.initials: F
authors.lastname: Baraona
authors.forename: Silvana
authors.initials: S
authors.lastname: Llevaneras
authors.forename: Claudia
authors.initials: C
authors.lastname: Hernández
authors.forename: Iván
authors.initials: I
authors.lastname: Godoy
authors.forename: Jorge E
authors.initials: JE
authors.lastname: Jalil
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Quintana
authors.forename: Pilar
authors.initials: P
authors.lastname: Orellana
authors.forename: Mario
authors.initials: M
authors.lastname: Chiong
authors.forename: Sergio
authors.initials: S
authors.lastname: Lavandero
mesh_terms: D018450:Disease Progression; D004734:Energy Metabolism / Q000502:physiology*; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D009206:Myocardium / Q000378:metabolism*