By augmenting the active natriuretic peptides, neprilysin inhibition increases generation of myocardial cyclic guanosine 3′5′ mono phosphate, which improves myocardial relaxation and reduces hypertrophy.[14, 15] However, the development of omapatrilat was discontinued because of an increased risk of angiooedema which caused by accumulation of bradykinin secondary to both neprilysin and ACE inhibition.[16] Furthermore, few systematic studies demonstrating whether cardiac function is improved after sacubitril-valsartan therapy in patients with HF have been reported. Here, MME is linked to hydrops fetalis.