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Empagliflozin in heart failure: beyond clinical endpoints

Session Poster Session 3

Speaker Susana Del Prado Diaz

Event : Heart Failure 2019

  • Topic : heart failure
  • Sub-topic : Chronic Heart Failure: Pharmacotherapy
  • Session type : Poster Session

Authors : M Abellas Sequeiros (Madrid,ES), S Del Prado (Madrid,ES), G Alonso Salinas (Madrid,ES), JM Vieitez Florez (Madrid,ES), A Lorente Ros (Madrid,ES), JL Moya Mur (Madrid,ES), A Garcia Martin (Madrid,ES), JJ Jimenez Nacher (Madrid,ES), C Fernandez-Golfin (Madrid,ES), JL Zamorano Gomez (Madrid,ES)

M Abellas Sequeiros1 , S Del Prado1 , G Alonso Salinas1 , JM Vieitez Florez1 , A Lorente Ros1 , JL Moya Mur1 , A Garcia Martin1 , JJ Jimenez Nacher1 , C Fernandez-Golfin1 , JL Zamorano Gomez1 , 1University Hospital Ramon y Cajal de Madrid - Madrid - Spain ,



Since publication of the EMPAREG trial demonstrated a beneficial prognostic impact, reducing death from cardiovascular causes and hospitalization for heart failure, the use of inhibitors of the sodium-glucose transport protein 2 has raised. Left ventricular ejection fraction (LVEF) and other echocardiographic parameters are independent prognostic factors in heart failure. Does empagliflozin improve ventricular remodeling? Does it improve diastolic function?


To answer these questions, a series of patients with heart failure who initiated empagliflozin between December 2016-June 2017 was prospectively assessed. Aetiology and baseline characteristics were collected. LVEF, ventricular volumes and diastolic function parameters were evaluated by transthoracic echocardiogram before and after 6-month treatment. Patients with reversible aetiologies, and those with modified treatment during follow-up were excluded. Patients without echocardiogram before and 6 months after therapy were also excluded. Wilcoxon test was conducted.


Twenty patients were included; mean age was 72 years old; 14 (70%) patients were men and 60% had ischaemic aetiology. Mean LVEF was 36,7% and median estimated glomerular filtration rate was 70 ml/min. Regarding to optimal medical treatment: 79% were on angiotensin-converting-enzyme inhibitor, 21% sacubitril-valsartan, 84% beta-blocker and 75% were receiving a mineralocorticoid-receptor antagonist. Empagliflozin was discontinued in 1 patient because of persistent genital candidiasis.

LVEF did not show significant changes 6 months after treatment (36,7±13,5 vs 39,9±12,6; p=0,16). However, lower left ventricular end systolic (111,6±62,2 vs 92,7±56,5; p=0,022) and left ventricular end diastolic volumes (170,5±72,5 vs 153,1±73,3; p=0,028) were described. The study of diastolic function showed no differences in E/e’( 15,5±4,6 vs 9,5±2,6; p=0,138), tricuspid regurgitation velocity (3,0±0,4 vs 3,0±0,3; p=0,462) nor left atrium volume (94,8±26,2 vs 76,3±33,1; p=0,059).


Empagliflozin significantly improves left ventricular end diastolic and end systolic volumes. In our small sample, its beneficial effect does not show an important difference in LVEF or diastolic function. Studies with larger number of patients included and longer follow-up periods are needed to characterise the influence of empagliflozin on heart structural remodeling.

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