Literature DB >> 34325888

Mechanistic Insights of Empagliflozin in Nondiabetic Patients With HFrEF: From the EMPA-TROPISM Study.

Juan Antonio Requena-Ibáñez1, Carlos G Santos-Gallego1, Anderly Rodriguez-Cordero1, Ariana P Vargas-Delgado1, Donna Mancini2, Samantha Sartori2, Farah Atallah-Lajam2, Chiara Giannarelli2, Frank Macaluso2, Anuradha Lala2, Javier Sanz2, Valentin Fuster2, Juan José Badimon3.   

Abstract

OBJECTIVES: The goal of this study was to evaluate the effect of empagliflozin, in addition to optimal medical treatment, on epicardial adipose tissue (EAT), interstitial myocardial fibrosis, and aortic stiffness in nondiabetic patients with heart failure with reduced ejection fraction (HFrEF).
BACKGROUND: Several randomized clinical trials have established the benefits of the inhibitors of the sodium-glucose cotransporter-2 receptor (SGLT2-i) in HFrEF, independent of their hypoglycemic effects. The mechanisms of the benefits of SGLT2-i in HFrEF have not been well defined.
METHODS: This study was a secondary analysis of patients enrolled in the EMPA-TROPISM [ATRU-4] (Are the cardiac benefits of Empagliflozin independent of its hypoglycemic activity?) clinical trial. It was a double-blind, placebo-controlled randomized clinical trial investigating the effect of empagliflozin in nondiabetic patients with HFrEF. Patients underwent cardiac magnetic resonance at baseline and after 6 months. Interstitial myocardial fibrosis was calculated by using T1 mapping (extracellular volume). Aortic stiffness was calculated by using pulsed wave velocity, and EAT was measured from the cine sequences.
RESULTS: Empagliflozin is associated with significant reductions in EAT volume (-5.14 mL; 95% CI: -8.36 to -1.92) compared with placebo (-0.75 mL; 95% CI: -3.57 to 2.06; P < 0.05); this finding was paralleled by reductions in subcutaneous adipose tissue area (-5.33 cm2 [95% CI: -12.61 to 1.95] vs 9.13 cm2 [95% CI: -2.72 to 20.99]; P < 0.05). Empagliflozin-treated patients reported a reduction in extracellular volume (-1.25% [±0.56 95% CI] vs 0.24% [±0.57 95% CI]; (P < 0.01)]; specifically, empagliflozin reduced both matrix volume (-7.24 mL [95% CI: -11.59 to -2.91] vs 0.70 mL [95% CI: -0.89 to 2.29]; P < 0.001) and cardiomyocyte volume (-11.08 mL [95% CI: -19.62 to -2.55] vs 0.80 mL [95% CI: -1.96 to 3.55]; P < 0.05). Pulsed wave velocity was also significantly reduced in the empagliflozin group (-0.58 cm/s [95% CI: -0.92 to -0.25] vs 0.60 cm/s [95% CI: 0.14 to 1.06]; P < 0.01). Using proteomics, empagliflozin was associated with a significant reduction in inflammatory biomarkers.
CONCLUSIONS: Empagliflozin significantly improved adiposity, interstitial myocardial fibrosis, aortic stiffness, and inflammatory markers in nondiabetic patients with HFrEF. These results shed new light on the mechanisms of action of the benefits of SGLT2-i. (Are the "Cardiac Benefits" of Empagliflozin Independent of Its Hypoglycemic Activity [ATRU-4] [EMPA-TROPISM]; NCT03485222).
Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  CMR; SGLT2-inhibitors; epicardial adipose tissue; heart failure; myocardial fibrosis

Year:  2021        PMID: 34325888     DOI: 10.1016/j.jchf.2021.04.014

Source DB:  PubMed          Journal:  JACC Heart Fail        ISSN: 2213-1779            Impact factor:   12.035


  24 in total

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8.  Effects of the sodium-glucose cotransporter 2 inhibitor empagliflozin on vascular function in patients with chronic heart failure.

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10.  Empagliflozin protects the heart against ischemia/reperfusion-induced sudden cardiac death.

Authors:  Zhaoyang Hu; Feng Ju; Lei Du; Geoffrey W Abbott
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