It is now generally accepted that chronically elevated stimulation of the cardiac ß-adrenergic system is toxic to the heart and that such stimulation may contribute to the pathogenesis of congestive heart failure of various causes. Administration of either ß-adrenergic agonists or phosphodiesterase inhibitors has been shown to decrease survival of patients with chronic heart failure, even though they produce immediate and long-term hemodynamic benefits. 1 Moreover, in human heart failure, as well as in several animal models, elevated circulating catecholamines lead, via various compensatory mechanisms, to decreased levels and functional activity of cardiac ß1-adrenergic receptors (ß1ARs) and thus to marked desensitization of the heart to inotropic ß-adrenergic stimulation. 2