Jaclyn Carberry, Mark C. Petrie, Matthew M.Y. Lee, Bethany Stanley, Katriona J.M. Brooksbank, Ross T. Campbell, Richard Good, Pardeep S. Jhund, Peter Kellman, Ninian N. Lang, M. Mitchell Lindsay, Kenneth Mangion, Roy S. Gardner, Patrick B. Mark, Barbara Meyer, Joanne O'Donnell, Vanessa Orchard, Aadil Shaukat, Stuart Watkins, Alex McConnachie, John J.V. McMurray, Paul Welsh, Naveed Sattar, Colin Berry, Kieran F. Docherty
{"title":"Empagliflozin to prevent worsening of left ventricular volumes and systolic function after myocardial infarction (EMPRESS‐MI)","authors":"Jaclyn Carberry, Mark C. Petrie, Matthew M.Y. Lee, Bethany Stanley, Katriona J.M. Brooksbank, Ross T. Campbell, Richard Good, Pardeep S. Jhund, Peter Kellman, Ninian N. Lang, M. Mitchell Lindsay, Kenneth Mangion, Roy S. Gardner, Patrick B. Mark, Barbara Meyer, Joanne O'Donnell, Vanessa Orchard, Aadil Shaukat, Stuart Watkins, Alex McConnachie, John J.V. McMurray, Paul Welsh, Naveed Sattar, Colin Berry, Kieran F. Docherty","doi":"10.1002/ejhf.3560","DOIUrl":null,"url":null,"abstract":"AimsPatients with a reduced left ventricular ejection fraction (LVEF) following an acute myocardial infarction (MI) are considered to be at risk of progressive adverse cardiac remodelling which 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 resultsWe performed a randomized, double‐blind, placebo‐controlled, multicentre trial using cardiovascular magnetic resonance imaging (MRI), in 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 MRI. Patients were randomized to empagliflozin 10 mg once a day or matching placebo. The primary outcome was the change in left ventricular end‐systolic volume indexed to body surface area (LVESVI) from baseline to 24 weeks. Secondary outcomes included measures of left ventricular and atrial volumes, left ventricular mass, LVEF, and high‐sensitivity troponin I (hs‐TnI) and N‐terminal prohormone of B‐type natriuretic peptide (NT‐proBNP) concentrations. From October 2022 to January 2024, 105 eligible patients were randomized. The mean age was 63 ± 11 years and 90 (87%) were male. The mean LVEF was 34.8 ± 6.0%. In the placebo group, LVESVI decreased by 7.8 ± 16.3 ml/m<jats:sup>2</jats:sup>, left ventricular end‐diastolic volume index (LVEDVI) did not change (−0.3 ± 18.7 ml/m<jats:sup>2</jats:sup>) and LVEF increased by 8.5 ± 7.4% at 24 weeks from baseline. Empagliflozin did not affect the change in LVESVI from baseline to 24 weeks (between‐group difference = 0.3 ml/m<jats:sup>2</jats:sup>, 95% confidence interval −5.2 to 5.8; <jats:italic>p</jats:italic> = 0.92). Compared with placebo, empagliflozin also had no effect on LVEDVI, LVEF, left atrial volume index, left ventricular mass index, NT‐proBNP, or hs‐TnI, but did increase haematocrit and reduced uric acid and weight.ConclusionsIn patients with left ventricular systolic dysfunction after an acute MI receiving contemporary standard of care, treatment with empagliflozin had no effect on cardiac volumes or LVEF compared with placebo. Progressive adverse cardiac remodelling did not occur in the majority of patients.","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"75 1","pages":""},"PeriodicalIF":16.9000,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Heart Failure","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/ejhf.3560","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
AimsPatients with a reduced left ventricular ejection fraction (LVEF) following an acute myocardial infarction (MI) are considered to be at risk of progressive adverse cardiac remodelling which 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 resultsWe performed a randomized, double‐blind, placebo‐controlled, multicentre trial using cardiovascular magnetic resonance imaging (MRI), in 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 MRI. Patients were randomized to empagliflozin 10 mg once a day or matching placebo. The primary outcome was the change in left ventricular end‐systolic volume indexed to body surface area (LVESVI) from baseline to 24 weeks. Secondary outcomes included measures of left ventricular and atrial volumes, left ventricular mass, LVEF, and high‐sensitivity troponin I (hs‐TnI) and N‐terminal prohormone of B‐type natriuretic peptide (NT‐proBNP) concentrations. From October 2022 to January 2024, 105 eligible patients were randomized. The mean age was 63 ± 11 years and 90 (87%) were male. The mean LVEF was 34.8 ± 6.0%. In the placebo group, LVESVI decreased by 7.8 ± 16.3 ml/m2, left ventricular end‐diastolic volume index (LVEDVI) did not change (−0.3 ± 18.7 ml/m2) and LVEF increased by 8.5 ± 7.4% at 24 weeks from baseline. Empagliflozin did not affect the change in LVESVI from baseline to 24 weeks (between‐group difference = 0.3 ml/m2, 95% confidence interval −5.2 to 5.8; p = 0.92). Compared with placebo, empagliflozin also had no effect on LVEDVI, LVEF, left atrial volume index, left ventricular mass index, NT‐proBNP, or hs‐TnI, but did increase haematocrit and reduced uric acid and weight.ConclusionsIn patients with left ventricular systolic dysfunction after an acute MI receiving contemporary standard of care, treatment with empagliflozin had no effect on cardiac volumes or LVEF compared with placebo. Progressive adverse cardiac remodelling did not occur in the majority of patients.
期刊介绍:
European Journal of Heart Failure is an international journal dedicated to advancing knowledge in the field of heart failure management. The journal publishes reviews and editorials aimed at improving understanding, prevention, investigation, and treatment of heart failure. It covers various disciplines such as molecular and cellular biology, pathology, physiology, electrophysiology, pharmacology, clinical sciences, social sciences, and population sciences. The journal welcomes submissions of manuscripts on basic, clinical, and population sciences, as well as original contributions on nursing, care of the elderly, primary care, health economics, and other related specialist fields. It is published monthly and has a readership that includes cardiologists, emergency room physicians, intensivists, internists, general physicians, cardiac nurses, diabetologists, epidemiologists, basic scientists focusing on cardiovascular research, and those working in rehabilitation. The journal is abstracted and indexed in various databases such as Academic Search, Embase, MEDLINE/PubMed, and Science Citation Index.