Patients suffering from chronic heart failure (CHF) caused or promoted by autoantibodies against cardiac beta1-adrenergic receptors (beta1AR) could benefit from specific therapies aimed at tolerance induction, removal or neutralisation of beta1AR autoantibodies, provided the patients can be selected for these therapies by reliable detection and quantitation of beta1AR autoantibodies in their circulation and by a valid assessment of the autoantibodies's putative cardio-pathogenic potential. Here, we discuss the current state of knowledge regarding the effects of CHF-associated (auto)antibodies on beta1AR function and beta1AR-mediated signal tranduction and discuss the presumed role of these effects in the development and progression of CHF. Identification of disease-relevant functional autoantibody effects and their specific assessment in medical diagnostic will be a prerequesite for the implementation of novel specific therapies not only for CHF caused or promoted by beta1AR autoantibodies but alos for most other diseases involving autoantibodies that target G-protein coupled receptors.