Key result
Empagliflozin fails to improve LVESVI over placebo in post-MI LV systolic dysfunction.
Why the study?
Does empagliflozin 10 mg once daily prevent worsening of left ventricular volumes and systolic function in patients with left ventricular systolic dysfunction following acute myocardial infarction?
RCT (n=105)
double-blind
randomized
Yes
Does empagliflozin 10 mg once daily prevent worsening of left ventricular volumes and systolic function in patients with left ventricular systolic dysfunction following acute myocardial infarction?
In patients with left ventricular systolic dysfunction following an acute myocardial infarction, the addition of empagliflozin to standard care did not improve cardiac volumes or systolic function at 24 weeks.
Answers are grounded in this paper and cite their sources.
No remodeling or LVEF benefit with empagliflozin post-MI on standard care; challenges prior low-certainty evidence and redirects trials to clinical outcomes.
Aims 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. Methods and results 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/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. Conclusions 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.
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Carberry et al. (2024) conducted an RCT in left ventricular systolic dysfunction following acute myocardial infarction (n=105). Empagliflozin vs. placebo was evaluated on change in left ventricular end-systolic volume indexed to body surface area (LVESVI) from baseline to 24 weeks (MD 0.3, 95% CI -5.2 to 5.8, p=0.92).
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