Atrial natriuretic peptide (ANP) is a circulating hormone released from the atria in response to wall stretch and volume overload in the setting of heart failure. When atrial fibrillation (AF) becomes long-standing persistent, ANP secretion in response to volume overload is impaired due to degenerative changes of the atria. Here, we report a case of heart failure with preserved ejection fraction and impaired ANP secretion due to long-standing AF. N-terminal pro-brain natriuretic peptide (NT-proBNP) level was elevated (269 pg/mL), whereas the increase in ANP level was marginal (46.1 pg/mL), suggesting impaired ANP secretion due to long-standing AF. Valsartan (80 mg/day) was replaced with sacubitril/valsartan (100 mg/day) without changing other medications. Administration of sacubitril/valsartan was effective in improving the patient's symptoms, such as dyspnea and edema, and reducing NT-proBNP level by increasing endogenous ANP level from 46.1 pg/mL to 117 pg/mL in the first four weeks. This case highlights the possibility of impaired ANP secretion in response to volume overload as a predictor of the diuretic effect of sacubitril/valsartan in heart failure. This may lead to individualized treatment for each patient with heart failure based on natriuretic peptide profiles.