Cardiac energy metabolism is essential for maintenance of the mechanical function and any disturbances of energetics translate directly into cardiac dysfunction. In addition to well recognized effects of insufficient coronary perfusion and oxygen deficit, number of other issues has been recognized. Regulation of cardiac substrate preference has been found interesting not only for basic research but also because of therapeutic potential. Cardiac cells normally use fatty acids but it has been well documented that glucose is better substrate under conditions of oxygen deficit or in heart failure. This is a consequence of slightly higher P/O ratio for glucose and also because glycolytic ATP is preferentially used by systems supporting cell viability. It is also well established that mitochondrial structure and function is distorted in heart failure. It could be even primary cause of heart failure e.g. in mitochondrial enzymes defects or because of presence of antibodies against mitochondrial adenine nucleotide transporter. There is also evidence for partial mitochondrial uncoupling in heart failure. There is ongoing debate regarding sequence of events relating to cardiac energetics in heart dysfunction. Some studies relate it to inability to use energy by contractile apparatus considering all changes in energy metabolism as adaptation to lower energy demand. However, other evidence, in particular direct measurements of energy equilibrium using localized nuclear magnetic resonance spectroscopy in patients with heart failure indicates that energy imbalance directly precipitates deterioration of heart function. Studies on cardiac energetics could be crucial for development of therapy to regenerate failing hearts. It has been recently demonstrated that transient support of failing heart with mechanical ventricular assist devices facilitates cardiac regeneration and restoration of normal mechanical performance. Biochemical analysis indicated prominent changes in expression of enzymes and proteins involved in cardiac energy metabolism. Pharmacological modification of cardiac substrate preference that reduces fatty acids utilization is already established treatment in ischemic heart disease and heart failure. Studies on transcriptional regulation of these mechanisms are very promising from therapeutic point of view. In particular, agonists and antagonists of peroxisome proliferator activated receptors that profoundly affect cardiac energetics may find its application in the treatment of heart disease.

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1. Formation of 4-Pyridone-3-carboxamide-1-β-D-ribonucleoside triphosphate in the Erythrocytes, Endothelium and Cardiomyocytes and its Effect on ATP Concentration