Heart failure, still nowadays an important cause of morbidity and mortality in many countries, is a complex of symptoms related to inadequate peripheric perfusion and often to the retention of fluid, that results from an impaired left ventricular pump function. Treatment of heart failure has seen considerable changes in the last years. Short term goals of therapy are directed towards the relieve of symptoms that can be commonly managed by the use of vasodilators, diuretics, digoxin, in order to obtain an improvement in myocardial functional capacity and quality of life of patients. Nevertheless, it is important to recognize that improvement of symptoms is not necessarily correlated with correction of left ventricular dysfunction and, most important, with improvement of survival. In late 1980s both experimental and clinical observations carried out in an attempt to explain the progression of the disease and its poor long-term survival, led the physicians to think about heart failure as a neurohormonal disorder. This new conceptual model has first led to the widespread introduction of angiotensin converting inhibitors in clinical practice; then, the evidence that sympathetic activation might play an important role in the progression of heart failure, led the investigators to propose that beta-blocking agents might be useful in the management of heart failure. Accumulating clinical evidence indicates that beta blocker therapy, particularly with third generation beta-blocking agents, not only improves left ventricular function but also may reduce and reverse pathological remodeling in the heart. Ongoing large scale clinical trials may confirm the mounting evidence, from numerous clinical studies, that these agents may prolong survival in patients with heart failure.