AGT and hydrops fetalis: Chronic SNS hyperactivation determines the maladaptive remodelling of the myocardium and the deterioration of HF through various mechanisms: (i) increase in heart rate and higher myocardial oxygen consumption through β1-receptors; (ii) diffuse vasoconstriction leading to an increase in afterload and preload with higher myocardial oxygen consumption through α1-receptors; (iii) renin release stimulating the production of angiotensin II and aldosterone with subsequent salt and fluid retention.