A 41-year-old man, with a history ACC/AHA stage C heart failure with reduced ejection fraction secondary to idiopathic dilated cardiomyopathy, presented at the HF clinic for follow-up visits, status post hospitalization due to acute decompensated heart failure in March 2019. After the initiation of milrinone during the hospitalization, two attempts to wean off milrinone were made but failed due to malperfusion and symptomatic hypotension with significant drops of the cardiac index to 1.3 L/min/m2 and 1.76 L/min/m2 , respectively. As such the patient was discharged on inotropic support with milrinone 0.25 mcg/kg/min and guideline-directed medical treatment. Lisinopril was held right before discharge due to hypotension.The patient returned to the clinic one month after discharge for 2nd follow-up visit. The BP was 136/98 mmHg with a HR of 90 beats/min. He was generally well with a stable weight and had no major/new complaints. The NT-proBNP level was reduced significantly. Given the considerable improvement of his clinical status, sacubitril/ valsartan 24/26 mg twice daily was initiated. No hypotension was reported thereafter. Two weeks after the initiation of sacubitril/valsartan therapy, the NT-proBNP normalized and the patient was admitted to the cardiac observation unit as planned to discontinue milrinone, followed by same-day discharge. His mixed venous oxygen saturation 6-hour after discontinuation of milrinone was 64.1%. His BP was 122/87 mmHg before the admission and remained stable with systolic BP in the low 120s, and HR of 70s beats/min. During the exam, he was warm and well-perfused without clinical evidence of hypoperfusion. Thus, this patient was successfully weaned from milrinone after the initiation of sacubitril/valsartan. The trend in NT-proBNP levels during treatment is shown in the Figure. The latest echocardiogram in the 8th month after discharge showed that left ventricular internal diameter in diastole (LVIDd) decreased to 5.91 cm from 8.35 cm measured before discharge. Left atrial cavity size diminished from severely increased to mildly increased with a reduction of left atrial dimension from 5.5 cm to 4.3 cm. Mitral valve regurgitation improved from moderate to mild. Left ventricular systolic function remained severely reduced with estimated ejection fraction < 20%. To our knowledge, this is the first case of initiating sacubitril/valsartan in a patient with inotropedependent heart failure in the outpatient setting. This approach has the potential to expand the use of sacubitril/valsartan to facilitate the weaning off intravenous inotropic therapy in the outpatient setting.