Empagliflozin Improves Left Ventricular Diastolic Dysfunction in a Genetic Model of Type 2 Diabetes

Empagliflozin Improves Left Ventricular Diastolic Dysfunction in a Genetic Model of Type 2 Diabetes Cardiovasc Drugs Ther (2017) 31:233–246 DOI 10.1007/s10557-017-6734-1 ORIGINAL ARTICLE Empagliflozin Improves Left Ventricular Diastolic Dysfunction in a Genetic Model of Type 2 Diabetes 1,2 1 1 1,3 Nadjib Hammoudi & Dongtak Jeong & Rajvir Singh & Ahmed Farhat & 2 4 1 1,3,5 Michel Komajda & Eric Mayoux & Roger Hajjar & Djamel Lebeche Published online: 22 June 2017 Springer Science+Business Media New York 2017 Abstract significantly lowered HbA1c and slightly reduced body Purpose Cardiovascular (CV) diseases in type 2 diabetes weight compared to vehicle treatment with no obvious chang- (T2DM) represent an enormous burden with high mortality es in insulin levels. Empagliflozin also improved LV maxi- and morbidity. Sodium-glucose cotransporter 2 (SGLT2) in- mum pressure and in vivo indices of diastolic function. While hibitors have recently emerged as a new antidiabetic class that systolic function was grossly not affected in both groups at improves glucose control, as well as body weight and blood steady state, response to dobutamine stimulation was signifi- pressure with no increased risk of hypoglycemia. The first CV cantly improved in the empagliflozin-treated group, suggest- outcome study terminated with empagliflozin, a specific ing amelioration of contractile reserve. This was paralleled by SGLT2 inhibitor, has shown http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cardiovascular Drugs and Therapy Springer Journals

Empagliflozin Improves Left Ventricular Diastolic Dysfunction in a Genetic Model of Type 2 Diabetes

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Medicine & Public Health; Cardiology
ISSN
0920-3206
eISSN
1573-7241
D.O.I.
10.1007/s10557-017-6734-1
Publisher site
See Article on Publisher Site

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