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Despite improvements in the invasive and pharmacological management of myocardial infarction (MI), patients remain at risk of adverse cardiovascular outcomes in the months and years following MI. For those with myocardial damage and residual left ventricular systolic dysfunction (LVSD), there is a high risk of developing heart failure with reduced ejection fraction (HFrEF). Much of the progress in the pharmacological management of patients at high risk of HFrEF has been achieved through the use of beta-blockers and the inhibition of the renin–angiotensin aldosterone system (RAAS) with ACE inhibitors (or angiotensin receptor blockers (ARBs)). Meta-analysis of randomised controlled trials of ACE inhibitors in MI has demonstrated that the greatest benefit in reducing mortality results from early administration of ACE inhibitors in the first few days post-MI, and this benefit is observed in all patients, irrespective of the presence or not of HF.1
In addition to RAAS blockade with ACE inhibitors or ARBs, in large randomised trials, mineralocorticoid receptor antagonists (MRAs) have been shown to reduce morbidity and mortality in a spectrum of patients from those with LVSD and HF as a complication of MI to those with established, symptomatic HFrEF irrespective of an ischaemic aetiology.2 3 The Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) demonstrated the efficacy of eplerenone compared with placebo when administered 3–14 days post-MI in reducing mortality in patients with LVSD and HF or diabetes.2 A post hoc analysis of the EPHESUS cohort reported that this benefit was greater in those administered eplerenone in the early phase (3–7) days post-MI compared with those receiving eplerenone at a later time point.4 This finding, along with the benefits of early ACE inhibition (in the first 24 hours), has led investigators to explore the potential role of MRA administration in the early, acute (<3 days) phase following MI.
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Footnotes
Contributors Both authors drafted the manuscript and revised it.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests PSJ has received consulting fees from Novartis and Vifor Pharma, advisory board and speaker’s fees from Novartis and grant funding from Boheringer Ingelheim.
Patient consent Not required.
Provenance and peer review Commissioned; internally peer reviewed.