Abstract 13395: Dapagliflozin Reduces Myocardial Sodium Content and Correlates With Reverse Cardiac Remodeling in Nondiabetic Patients With Heart Failure and Preserved Ejection Fraction (Dapa-Sodium)

Abstract

Introduction: Myocardial sodium overload is a major determinant of adverse cardiac remodeling in heart failure (HF). Sodium tissue content by 23Na magnetic resonance imaging (23Na-MRI) has been validated in human studies. SGLT-2 inhibition blocks sodium reabsorption in renal proximal tubular cells with remarkable cardiovascular outcomes in HF due to mechanisms not yet fully understood. Hypothesis: SGLT-2 inhibition will decrease myocardial sodium content and it will correlate with reverse remodeling in HFpEF. Aim: To determine whether Dapagliflozin leads to decreased myocardial sodium content and reverses pathological hypertrophy in HFpEF. Methods: Prospective, single-center, open-label study of sixty nondiabetic outpatients with HFpEF underwent baseline 23Na-MRI and initiated with dapagliflozin 10 mg once daily according to GDMT. Absolute changes in myocardium relative sodium signal intensity (rSSI) and left ventricular mass index (LVMi) were analyzed from baseline and at 3-month follow-up with 23Na-MRI. Results: All patients exhibited significantly high baseline myocardium rSSI [0.32 (0.28, 0.34)]; 66% above median [0.24 (0.20, 0.27), P = 0.004], decreasing -30% to [0.27 (0.22, 0.30), P<0.001] at 3 months with Dapagliflozin therapy. These changes were correlated with a significant reduction in LVMi of -13 g/m 2 [from 84 g/m 2 (72, 120) to 71 g/m 2 (63, 95), P<0.001]. Conclusions: Dapagliflozin reduces myocardial sodium content and reverses pathological hypertrophy in patients with HFpEF. These findings suggest that SGLT-2 inhibition acts directly on cardiomyocytes and explains the cardioprotective effects demonstrated though large randomized trials.