INS and hydrops fetalis: This association is supported by multiple pathophysiological mechanisms commonly observed in HF, as the increase in catecholamine levels, which inhibit pancreatic insulin secretion and stimulates hepatic glycogenolysis and gluconeogenesis, and the shift of myocardial metabolic substrate (from fatty acids to glucose) as a result of the low oxygenation state characteristic of HF, which causes a cardiac accumulation of toxic lipids that inhibit insulin signaling [9, 10, 11].