Chronic β1-AR activation causes a number of detrimental effects, ultimately resulting in changes in the ECM and cell loss from necrosis and apoptosis,25 which in turn leads to cardiac dilatation and failure.157 However, the intracellular pathways responsible for these final acts are unclear.25 What is clear is that β1-AR antagonists improve clinical outcomes in patients with systolic heart failure and improve cardiac function and myocardial remodelling.158. This evidence concerns the gene ADRB1 and systolic heart failure.