AGT and hydrops fetalis: The infarction-induced cardiac hypertrophy is triggered mainly by the local or systemic neuroendocrine hormones such as angiotensin II (Ang II), endothelin 1 (ET-1) or catecholamine, which activates the membrane-bound receptors and stimulates multiple downstream signaling pathways such as mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and calcineurin, ultimately affects transcriptional regulatory factors for the cardiac hypertrophy genes.1,2,16,17 That’s why neurohormonal blockade has been an effective pharmacological therapy for the regression of cardiac hypertrophy and HF.