ESC Heart Failure (Aug 2024)

Empagliflozin to prevent progressive adverse remodelling after myocardial infarction (EMPRESS‐MI): rationale and design

  • Jaclyn Carberry,
  • Mark C. Petrie,
  • Matthew M.Y. Lee,
  • Katriona Brooksbank,
  • Ross T. Campbell,
  • Richard Good,
  • Pardeep S. Jhund,
  • Peter Kellman,
  • Ninian N. Lang,
  • Kenneth Mangion,
  • Patrick B. Mark,
  • Alex McConnachie,
  • John J.V. McMurray,
  • Barbara Meyer,
  • Vanessa Orchard,
  • Aadil Shaukat,
  • Stuart Watkins,
  • Paul Welsh,
  • Naveed Sattar,
  • Colin Berry,
  • Kieran F. Docherty

DOI
https://doi.org/10.1002/ehf2.14830
Journal volume & issue
Vol. 11, no. 4
pp. 2001 – 2012

Abstract

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Abstract Aims Patients with a reduced left ventricular ejection fraction (LVEF) following an acute myocardial infarction (MI) are at risk of progressive adverse cardiac remodelling that can lead to the development of heart failure and death. The early addition of a sodium‐glucose cotransporter 2 (SGLT2) inhibitor to standard treatment may delay or prevent progressive adverse remodelling in these patients. Methods and results EMpagliflozin to PREvent worSening of left ventricular volumes and Systolic function after Myocardial Infarction (EMPRESS‐MI) is a randomized, double‐blind, placebo‐controlled, multi‐centre trial designed to assess the effect of empagliflozin on cardiac remodelling evaluated using cardiovascular magnetic resonance (CMR) in 100 patients with left ventricular systolic dysfunction following MI. Eligible patients were those ≥12 h and ≤14 days following acute MI, with an LVEF <45% by CMR. Patients were randomized to empagliflozin 10 mg once a day or matching placebo. The primary outcome will be change in left ventricular end‐systolic volume indexed to body surface area over 24 weeks from randomization. Secondary endpoints include measures of left ventricular and atrial volumes, left ventricular mass, LVEF, and circulating cardiac biomarkers. Conclusions EMPRESS‐MI will assess the effect of the SGLT2 inhibitor empagliflozin on cardiac remodelling in patients with left ventricular systolic dysfunction after an acute MI.

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