Stimulation of the cAMP-dependent signalling pathway by β-adrenergic catecholamines is an important physiological mechanism to increase contractile force in the heart. In addition to this, long-term β-adrenergic stimulation by elevated catecholamines also influences the expressional control of functionally relevant cardiac regulatory proteins in human heart failure. The regulation of transcription by the cAMP-response element (CRE) is an important mechanism for a cAMP-mediated control of gene expression involved e.g. in spermiogenesis and memory/learning processes. This article discusses recent data leading to the hypothesis that this mechanism also contributes to altered gene regulation in heart failure.