A patient with type 2 diabetes and heart failure with reduced EF is started on empagliflozin. The cardiac benefit of SGLT2 inhibitors in heart failure is PRIMARILY attributed to:

• A Glycaemic control reducing myocardial glucose toxicity
• B Osmotic diuresis and natriuresis reducing cardiac preload, along with metabolic shift to ketone body utilisation ✓
• C Direct inhibition of the sodium-hydrogen exchanger (NHE1) in cardiomyocytes
• D Inhibition of angiotensin-converting enzyme reducing afterload

Explanation

SGLT2 inhibitors block renal glucose and sodium reabsorption in the proximal tubule, producing glucosuria, natriuresis, and mild osmotic diuresis. This reduces cardiac preload and afterload (volume unloading). Additionally, SGLT2 inhibitors shift myocardial fuel metabolism toward ketone bodies (which are more oxygen-efficient substrates), improving energy metabolism in the failing heart. While NHE inhibition has been proposed as a mechanism, osmotic/natriuretic unloading and metabolic effects are the primary accepted explanations.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.