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. Here, EDN1 is linked to hydrops fetalis.