The Failing Heart

Heart failure is a highly lethal condition which carries a shorter life expectancy than most common malignancies. Despite the large number of efforts dedicated to understand why the heart fails, only limited possibilities are available to improve survival. This because the problem is very complex and is dependent upon multiple changes in the anatomical and functional properties of the heart as well as of other organs, together with modifications in systemic and local hormonal and neuronal interactions. This review has been focused on some results obtained in pathologic hearts explanted from subjects with intractable heart failure or in hearts from animals with spontaneous or induced myocardial damage with different degrees of cardiac dysfunction and failure performed in the last few years in our laboratories. Hearts in failure have different alterations at the anatomical, histological and cellular level that may justify, at least in part, the functional impairment and the progressive evolution of the disease. Recent findings of apoptotic myocyte cell death and myocytic hyperplasia are exciting prospectives to be followed with the expectation that new strategies may be discovered to alter the unfavourable outcome of heart failure. However, the complexity of the problem seems to require a large number of efforts before the results obtained can be applied to human beings. Thus, basic researches must be stimulated to explore the mechanisms which allow the development of heart failure despite the persistence in the damaged myocardium of a large number of contractile cells.