A 68-year-old woman with heart failure with reduced ejection fraction (HFrEF; left ventricular ejection fraction 35%), hypertension, hyperlipidemia, and stable chronic kidney disease (CKD) is seen in the clinic 2 weeks after admission for acute decompensated heart failure (HF), for which she required several days of intravenous diuresis. She was discharged on her previous medications: metoprolol succinate 100 mg BID, sacubitril/valsartan 49/51 mg BID, spironolactone 12.5 mg daily, and furosemide 40 mg daily. During her hospitalization, dapagliflozin 10 mg daily was added to her regimen. Prior to discharge, her electrolyte levels were within reference ranges, creatinine (Cr) level was 1.47 mg/dL (glomerular filtration rate [GFR] 49 mL/min/1.73 m2), and N-terminal pro–B-type natriuretic peptide (NT-proBNP) level was 1,253 g/dL.
She states that she is feeling well today, is taking all her medications, and has no other reports. Her heart rate is 72 bpm and blood pressure is 118/75 mm Hg.
On examination, she appears euvolemic, with no jugular venous distention. Her repeat laboratory studies show Cr level 2.03 mg/dL, GFR 44 mL/min/1.73 m2, potassium level 4.5 mmol/L, and NT-proBNP level 937 g/dL.
The correct answer is: Fiction
This patient with HFrEF has an indication for all four pillars of guideline-directed medical therapy (beta-blocker, angiotensin receptor–neprilysin inhibitor, mineralocorticoid-receptor antagonist, and SGLT2i) according to the most recent HF guidelines.1 During the hospitalization, the inpatient team appropriately initiated the SGLT2i dapagliflozin, which is suitable for this patient with stable CKD and HFrEF, even in the absence of diabetes mellitus (the EMPEROR-Reduced [Empagliflozin Outcome Trial in Patients with Chronic Heart Failure with Reduced Ejection Fraction] had a GFR of ≥20 mL/min/1.73 m2 and the DAPA-CKD [Dapagliflozin And Prevention of Adverse outcomes in Chronic Kidney Disease]2,3).
Now, the patient has minimal symptoms and does not appear congested based on physical examination and NT-proBNP level. Despite the rise in Cr level and relatively stable GFR, it would not be recommended to discontinue dapagliflozin at present. The Cr level rise may relate to overdiuresis, particularly with the addition of sacubitril/valsartan and dapagliflozin, both of which have natriuretic and diuretic effects. However, it is also important to remember that SGLT2i cause reduction in GFR due to increased afferent arteriolar tone. This reduction of intraglomerular pressure may partially explain the nephroprotective effects of the drug. The strategy in this case is to assess for the presence of dehydration/overdiuresis and to consider a reduced loop diuretic dose, but not to over-react and discontinue the SGLT2i without considering all the options.4
Educational grant support provided by: Boehringer Ingelheim Pharmaceuticals Inc. (BIPI) and Lilly USA, LLC (Lilly).
To visit the course page for the Heart Failure & SGLT2is: The New Pillar in Care grant, click here!
References
- Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol 2022;79:e263-e421.
- Packer M, Anker SD, Butler J, et al.; EMPEROR-Reduced Trial Investigators. Cardiovascular and renal outcomes with empagliflozin in heart failure. N Engl J Med 2020;383:1413-24.
- Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al.; DAPA-CKD Trial Committees and Investigators. Dapagliflozin in patients with chronic kidney disease. N Engl J Med 2020;383:1436-46.
- Vardeny O, Vaduganathian M. Practical guide to prescribing sodium-glucose cotransporter 2 inhibitors for cardiologists. JACC Heart Fail 2019;7:169-72.
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