In recent years, the possibility that disorders of cardiac metabolism play a role in the mechanisms that lead to ventricular dilatation and dysfunction in heart failure has attracted much attention. Electron transport chain is constituted by a series of multimeric protein complexes, located in the inner mitochondrial membranes, whose genes are distributed over both nuclear and mitochondrial DNA. Its normal function is essential to provide the energy for cardiac function. Many studies have described abnormalities in mitochondrial DNA genes encoding for electron transport chain (ETC) in dilated cardiomyopathies. In some cases, heart failure is one more or less relevant symptom among other multisystem manifestations characteristic of mitochondrial encephalomyopathies, being heart failure imputable to a primary mitochondrial disease. In the case of idiopathic dilated cardiomyopathies (IDC), many mitochondrial abnormalities have also been described using hystological, biochemical or molecular studies. The importance of such findings is under debate. The great variability in the mitochondrial abnormalities described has prompted the proposal that mitochondrial dysfunction could be a secondary phenomenon in IDC, and not a primary one. Among other possible explanations for such findings, the presence of an increased oxidative damage due to a free radical excess has been postulated. In this setting, the dysfunction of ETC could be a consequence, but also a cause of the presence of an increased free radical damage. Independently of its origin, ETC dysfunction may contribute to the persistence and worsening of heart failure. If this hypothesis, still to be proven, was certain, the modulation of cardiac metabolism could be an interesting approach to treat IDC. The precise mechanisms that lead to ventricular dilatation and dysfunction in heart failure are still nowadays poorly understood. Circumstances such as cytotoxic insults, viral infections, immune abnormalities, contractile protein defects, ischemic factors and familial conditions have been thoroughly investigated [1]. It is possible that several mechanisms combine to produce the clinical syndrome of heart failure. In recent years the possibility that disorders of energy metabolism, either isolated or in combination with the other aforementioned factors, may play a role in the development of heart failure in susceptible patients has attracted much attention. The present paper reviews the current knowledge on mitochondrial function in the failing myocardium. We restrain our discussion to heart failure where an impaired inotropic state leads to a weakened systolic contraction (i.e. the so-called systolic heart failure). Idiopathic dilated cardiomyopathy (IDC) is the prototype of the conditions under discussion. Other circumstances where a defect in myocardial contraction is due to a chronic excessive work load (i.e., hypertension, valvular or congenital heart diseases), and states in which the principal abnormality involves impaired relaxation of the ventricle (i.e. diastolic heart failure), as well as mitochondrial defects outside the electron transport chain (i.e., defects in Krebs cycle or beta-oxidation of fatty acids) are only approached circumstantially.