ADRB1 and hydrops fetalis: Chronic HF is accompanied by sympathetic overactivation, increased norepinephrine (NE) release from the heart and the kidneys into the plasma [4], depleted NE in the myocardium [5], increased production of reactive oxygen species (ROS) [6], and downregulated beta-1 adrenergic receptors (Adrb1), which all contribute to decreased contractility, fibrosis and further propagation of myocardial damage [7–9].