Empagliflozin to prevent worsening of left ventricular volumes and systolic function after myocardial infarction
Abstract
Background Heart failure following an acute myocardial infarction (MI) is associated with significant morbidity and mortality, making its prevention a key therapeutic goal. Progressive adverse ventricular remodelling, characterised by ventricular dilation and declining systolic function, is a key precursor to the development of heart failure after MI. Early reperfusion therapy and medications that reduce mortality and heart failure post-MI, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and beta-blockers, also prevent adverse remodelling. The mineralocorticoid receptor antagonist (MRA) eplerenone improved outcomes post-MI but showed a significant anti-remodelling effect only after adjusting for baseline covariates. Sacubitril/valsartan did not reduce the risk of developing heart failure or cardiovascular mortality in high-risk post-MI patients and had minimal impact on remodelling. Sodium-glucose co-transporter 2 (SGLT2) inhibitors lower the risk of heart failure progression and mortality in patients with chronic heart failure across all ranges of left ventricular ejection fraction (LVEF). One of their key mechanisms of benefit in heart failure with reduced ejection fraction (HFrEF) is a positive effect on ventricular remodelling. Empagliflozin did not significantly reduce the primary outcome of heart failure hospitalisation or all-cause mortality in high-risk post-MI patients, but did lower the incidence of first and total…
How strong is the evidence?
Evidence Hub reads this as a randomized trial. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design. Reported size: 104 participants or records.
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