The detrimental upregulation of the RAAS mediates the pathophysiology and progression in HF, leading to fluid retention, vasoconstriction of the peripheral arteries, hypertrophy, and remodeling of the cardiac tissue [7]. For this reason, angiotensin-converting-enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) have been recommended as the mainstays of management of the condition. This evidence concerns the gene ACE and hydrops fetalis.