title: [Metabolic therapy for heart failure].
abstract: Heart failure may promote metabolic changes such as insulin resistance, in part through neurohumoral activation, and determining an increased utilization of non-carbohydrate substrates for energy production. In fact, fasting blood ketone bodies as well as fat oxidation have been shown to be increased in patients with heart failure. The result is depletion of myocardial ATP, phosphocreatine and creatine kinase with decreased efficiency of mechanical work. A direct approach to manipulate cardiac energy metabolism consists in modifying substrate utilization by the failing heart. To date, the most effective metabolic treatments include several pharmacological agents that directly inhibit fatty acid oxidation. The results of current research are supporting the concept that shifting the energy substrate preference away from fatty acid metabolism and toward glucose metabolism could be an effective adjunctive treatment in patients with heart failure. Trimetazidine is the most studied drug in this context. Several small studies have evidenced the usefulness of such additional therapeutic tools for heart failure. More specifically, recent meta-analyses and a multicenter retrospective study have shown that additional use of trimetazidine in patients with heart failure, along with symptoms and cardiac function improvement, also provides a significant protective effect on all-cause mortality, cardiovascular events and hospitalization due to cardiac causes. Nevertheless, the exact role of metabolic therapy in heart failure is yet to be established, and a large multicenter randomized trial is necessary.
authors: Ferdinando
authors: F
authors: Loiacono
authors: Luca
authors: L
authors: Alberti
authors: Ludovica
authors: L
authors: Lauretta
authors: Patrizia
authors: P
authors: Puccetti
authors: Carmen
authors: C
authors: Silipigni
authors: Alberto
authors: A
authors: Margonato
authors: Gabriele
authors: G
authors: Fragasso
mesh_terms: D050260:Carbohydrate Metabolism / Q000187:drug effects; D019317:Evidence-Based Medicine; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance; D009206:Myocardium / Q000378:metabolism; D016896:Treatment Outcome; D014292:Trimetazidine / Q000494:pharmacology / Q000627:therapeutic use*; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D005227:Fatty Acids; D014665:Vasodilator Agents; D005947:Glucose; D014292:Trimetazidine