The elevated plasma norepinephrine concentrations closely correlate to the poor prognosis in heart failure. Inhibition of myocardial norepinephrine effects on the heart by beta-blocker treatment are reported to improve left ventricular ejection fraction and to a lesser extent exercise tolerance. The mechanisms are a restoration of beta-adrenergic signal transduction, an increase of contractile reserve and a protection from toxic catecholamine effects. Bradycardic effects improve energetic situation of the failing heart and directly reduce neuroendocrine activation (plasma norepinephrine concentrations, renin activity). Randomized studies have shown a good clinical effectiveness with carvedilol, metoprolol, bucindolol, and bisoprolol in combination with cardiac glycosides, diuretics and ACE inhibitors. Improvement of survival has been shown for carvedilol and bisoprolol and possibly for metoprolol in dilated cardiomyopathy. In ischemic cardiomyopathy, carvedilol appears to be effective to improve prognosis. Therapy has to be started at very low concentrations of the beta-blocker and the patients must be followed up closely. The beta-blocker therapy is evidenced on pathophysiological research findings and could prove to be useful as additional component of the standard therapy of heart failure when the issue of improvement of survival is solved by future studies.