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Review
. 2024 Jul;12(7):1157-1165.
doi: 10.1016/j.jchf.2024.04.025. Epub 2024 Jun 12.

Where Are We With Treatment and Prevention of Heart Failure in Patients Post-Myocardial Infarction?

Jaclyn Carberry  1 , Guillaume Marquis-Gravel  2 , Eileen O'Meara  2 , Kieran F Docherty  3
Affiliations
Free article
Review

Where Are We With Treatment and Prevention of Heart Failure in Patients Post-Myocardial Infarction?

Jaclyn Carberry et al. JACC Heart Fail. 2024 Jul.
Free article

Abstract

As a result of the widespread use of reperfusion therapies and secondary prevention over the last 30 years, there has been a dramatic reduction in the risk of mortality and development of heart failure (HF) following acute myocardial infarction (MI). Despite this, the development of chronic HF remains a common occurrence in the days, months, and years following MI. Neurohormonal inhibition remains the mainstay of pharmacologic prevention of HF following MI, with recent trials showing an additive benefit of a neprilysin inhibitor or a sodium glucose co-transporter 2 inhibitor in reducing the risk of development of HF but no significant effect on mortality. Novel imaging tools may help refine risk stratification in high-risk patients and allow greater targeting of preventative therapies in patients most likely to benefit. Research is ongoing into novel therapies aiming to minimize the degree of myocardial damage and prevention of progressive adverse remodeling following MI.

Keywords: coronary artery disease; heart failure; myocardial infarction.

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Conflict of interest statement

Funding Support and Author Disclosures Dr Carberry’s employer, the University of Glasgow, has received research funding from Boehringer Ingelheim. Dr Marquis-Gravel’s institution has received research funding for his participation in EMPACT-MI (Empagliflozin in Patients Post Myocardial Infarction) or Advisory Boards or has received speaker fees from Novartis, JAMP Pharma, Servier, KYE, Pharmascience, Boston Scientific, Bayer, KYE, and HLS Therapeutics and has received research funding from Bayer. Dr Docherty’s employer, the University of Glasgow, has been remunerated by AstraZeneca for his work on clinical trials, and he has received speaker fees from AstraZeneca, Boehringer Ingelheim, Pharmacosmos, and Radcliffe Cardiology; has served on Advisory Boards for Us2.ai and Bayer AG; has served on a Clinical Endpoint Committee for Bayer AG; and has received research grant support (paid to his institution) from AstraZeneca, Roche, Novartis, and Boehringer Ingelheim. Dr O’Meara has reported that she has no relationships relevant to the contents of this paper to disclose.

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