Even though persistent inflammation and extracellular matrix remodeling are recognized as central in the pathogenesis of HF [7,8], the current therapy offered to HF patients is aimed at the heart workload (e.g., beta blockers) and neurohormonal axis (e.g., Angiotensin-converting enzyme inhibitors (ACEi), both with hypotension and bradycardia as their main limiting factors [9]. Here, ACE is linked to hydrops fetalis.