Carberry Jaclyn, Petrie Mark C, Lee Matthew M Y, Stanley Bethany, Brooksbank Katriona J M, Campbell Ross T, Good Richard, Jhund Pardeep S, Kellman Peter, Lang Ninian N, Lindsay M Mitchell, Mangion Kenneth, Gardner Roy S, Mark Patrick B, Meyer Barbara, O'Donnell Joanne, Orchard Vanessa, Shaukat Aadil, Watkins Stuart, McConnachie Alex, McMurray John J V, Welsh Paul, Sattar Naveed, Berry Colin, Docherty Kieran F
British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK.
Golden Jubilee National Hospital, Clydebank, UK.
Eur J Heart Fail. 2025 Mar;27(3):566-576. doi: 10.1002/ejhf.3560. Epub 2024 Dec 15.
Patients 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.
We 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, left ventricular end-diastolic volume index (LVEDVI) did not change (-0.3 ± 18.7 ml/m) 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, 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.
In 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.
急性心肌梗死（MI）后左心室射血分数（LVEF）降低的患者被认为有进行性不良心脏重塑的风险，这可能导致心力衰竭和死亡。在标准治疗中早期加用钠-葡萄糖协同转运蛋白2（SGLT2）抑制剂可能会延迟或预防这些患者的进行性不良重塑。
我们使用心血管磁共振成像（MRI）对MI后左心室收缩功能障碍的患者进行了一项随机、双盲、安慰剂对照、多中心试验。符合条件的患者为急性MI后≥12小时且≤14天，MRI显示LVEF<45%的患者。患者被随机分为每日一次服用10毫克恩格列净或匹配的安慰剂。主要结局是从基线到24周时，以体表面积指数化的左心室收缩末期容积（LVESVI）的变化。次要结局包括左心室和心房容积、左心室质量、LVEF以及高敏肌钙蛋白I（hs-TnI）和B型利钠肽前体N端（NT-proBNP）浓度的测量。从2022年10月到2024年1月，105名符合条件的患者被随机分组。平均年龄为63±11岁，90名（87%）为男性。平均LVEF为34.8±6.0%。在安慰剂组中，LVESVI在24周时较基线下降了7.8±16.3ml/m²，左心室舒张末期容积指数（LVEDVI）没有变化（-0.3±18.7ml/m²），LVEF较基线增加了8.5±7.4%。恩格列净对从基线到24周的LVESVI变化没有影响（组间差异=0.3ml/m²，95%置信区间-5.2至5.8；p=0.92）。与安慰剂相比，恩格列净对LVEDVI、LVEF、左心房容积指数、左心室质量指数、NT-proBNP或hs-TnI也没有影响，但确实增加了血细胞比容，降低了尿酸和体重。
在接受当代标准治疗的急性MI后左心室收缩功能障碍的患者中，与安慰剂相比，恩格列净治疗对心脏容积或LVEF没有影响。大多数患者没有发生进行性不良心脏重塑。
