Metabolic support for the heart: complementary therapy for heart failure?
The failing heart has an increased metabolic demand and at the same time suffers from impaired energy efficiency, which is a detrimental combination. Therefore, therapies targeting the energy-deprived failing heart and rewiring cardiac metabolism are of great potential, but are lacking in daily clinical practice. Metabolic impairment in heart failure patients has been well characterized for patients with reduced ejection fraction, and is coming of age in patients with 'preserved' ejection fraction. Targeting cardiomyocyte metabolism in heart failure could complement current heart failure treatments that do improve cardiovascular haemodynamics, but not the energetic status of the heart. In this review, we discuss the hallmarks of normal cardiac metabolism, typical metabolic disturbances in heart failure, and past and present therapeutic targets that impact on cardiac metabolism.
Centre for Molecular and Vascular Biology, Department of Cardiovascular Research, University of Leuven, Belgium.|Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands.|Cardiovascular Research Centre, Cardiology Service, OLV Hospital Aalst, Aalst, Belgium.
Ward A
WA
Heggermont
Centre for Molecular and Vascular Biology, Department of Cardiovascular Research, University of Leuven, Belgium.|Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands.
Anna-Pia
AP
Papageorgiou
Centre for Molecular and Vascular Biology, Department of Cardiovascular Research, University of Leuven, Belgium.|Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands.
Stephane
S
Heymans
Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands.
Marc
M
van Bilsen
D000102:Acetyl-CoA C-Acyltransferase / Q000037:antagonists & inhibitors; D002317:Cardiovascular Agents / Q000627:therapeutic use; D002331:Carnitine / Q000031:analogs & derivatives / Q000627:therapeutic use; D002334:Carnitine O-Palmitoyltransferase / Q000037:antagonists & inhibitors; D003999:Dichloroacetic Acid / Q000627:therapeutic use; D004734:Energy Metabolism; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D004852:Epoxy Compounds / Q000627:therapeutic use; D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism*; D010084:Oxidation-Reduction; D010480:Perhexiline / Q000627:therapeutic use; D000069458:Ranolazine / Q000627:therapeutic use; D013318:Stroke Volume; D014292:Trimetazidine / Q000627:therapeutic use
D002317:Cardiovascular Agents; D004791:Enzyme Inhibitors; D004852:Epoxy Compounds; D005227:Fatty Acids; C003223:propionylcarnitine; D003999:Dichloroacetic Acid; D000069458:Ranolazine; D000102:Acetyl-CoA C-Acyltransferase; D002334:Carnitine O-Palmitoyltransferase; D005947:Glucose; D010480:Perhexiline; C054207:etomoxir; D014292:Trimetazidine; D002331:Carnitine
Cardiac metabolism; Energy starvation; Foetal switch; Heart failure; Metabolic therapy