# The prognostic impact of beta blockers in ischemic heart failure: time for a paradigm shift?

**Authors:** Domenico Simone Castiello, Pierangelo Calvelli, Andrea Anniballo, Letizia Rosa Romano, Alberto Polimeni, Antonio Curcio

PMC · DOI: 10.1007/s10741-026-10615-5 · Heart Failure Reviews · 2026-03-21

## TL;DR

This paper reviews the changing role of beta-blockers in ischemic heart failure, suggesting a more tailored approach is needed in the modern reperfusion era.

## Contribution

Proposes a tailored approach to beta-blocker use in ischemic HF based on patient-specific factors and modern treatment advances.

## Key findings

- Evidence for beta-blockers in ischemic HF is largely from the pre-reperfusion era.
- Modern reperfusion therapies have altered the impact of beta-blockers in heart failure.
- A one-size-fits-all approach to beta-blocker therapy is no longer justified.

## Abstract

Beta-blockers are traditionally considered a cornerstone of the pharmacological therapy in heart failure (HF) post-myocardial infarction (MI) and their use in this setting recognizes a pathophysiological rationale. However, most of evidence supporting their administration in ischemic HF is dated and was conceived before the introduction of modern reperfusion therapies (the so-called “pre-reperfusion era”). The introduction of cutting-edge techniques for revascularization and pharmacological strategies changed the history of MI, reducing mortality and allowing to many patients to overcome the acute event without residual ventricular dysfunction. In the “reperfusion era”, the impact of beta-blocker therapy is different than previously observed and evidence coming from new studies lead to question their role as inevitable drugs after acute events, principally in patients with preserved left ventricular ejection fraction. Consequently, the clinical need of prescribing beta-blockers across the full spectrum of ischemic HF patients has become a debated question. This review aims to retrace the history of beta-blockers in ischemic HF, focusing on recent and ongoing trials, that will offer new and update evidence to guide clinical practice in the next future. Since a “one-size-fits-all” approach cannot be justified, our aim is to propose a tailored approach to each patient’s profile, based on left ventricular ejection fraction, comorbidities, arrhythmic burden and quality of life. Furthermore, we propose an algorithm to guide the therapeutic decision of begin, withhold or withdrawn therapy with beta-blockers from the MI onset to the chronical phase of ischemic HF.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252), myocardial infarction (MONDO:0005068)

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}
- **Diseases:** coronary stenoses (MESH:D023921), arrhythmic (OMIM:212500), angina (MESH:D000787), ischemic (MESH:D002545), Acute Myocardial Infarction (MESH:D009203), atrial fibrillation (MESH:D001281), sudden cardiac death (MESH:D016757), sudden (MESH:D003639), fibrosis (MESH:D005355), migraine headache (MESH:D008881), coronary disease (MESH:D003327), ventricular ectopy (MESH:D050030), malignant (MESH:D009369), ventricular fibrillation (MESH:D014693), HFmrEF (MESH:D054143), respiratory disease (MESH:D012140), ischemic myocardium (MESH:D017682), HF (MESH:D006333), calcium (MESH:D002128), bradyarrhythmias (MESH:D001919), hypertension (MESH:D006973), hypertrophy (MESH:D006984), arrhythmia (MESH:D001145), muscle tremor (MESH:D014202), LV Dysfunction (MESH:D018487), left ventricular remodeling (MESH:D020257), ischemic disease (MESH:D017202), dyslipidemia (MESH:D050171), stroke (MESH:D020521), Acute coronary syndrome (MESH:D054058), glaucoma (MESH:D005901), cardiac death (MESH:D003643), no-reflow injury (MESH:D054318), Infarct (MESH:D007238), hypotension (MESH:D007022), systolic damage (MESH:D000092244), ischemic ventricular dysfunction (MESH:D018754), arteriosclerotic heart disease (MESH:D006331), post-MI (MESH:D006342), Congestive (MESH:D002311), arrhythmogenic (MESH:D019571), ACS (MESH:D000168), cardiogenic shock (MESH:D012770), Cardiac Insufficiency (MESH:D000309), cytotoxicity (MESH:D064420), Cardiac Events (MESH:D002318), NSTEMI (MESH:D000072658), cardiac arrest (MESH:D006323), ST-elevation MI (MESH:D000072657), CAD (MESH:D003324), frailty (MESH:D000073496), diabetes (MESH:D003920), mitochondrial injury (MESH:D028361), ischaemic (MESH:D018917), sudden deaths (MESH:D003645), myocardial injury (MESH:D009202), ischemia (MESH:D007511)
- **Chemicals:** aspirin (MESH:D001241), nebivolol (MESH:D000068577), alinidine (MESH:C022192), propranolol (MESH:D011433), Clopidogrel (MESH:D000077144), Carvedilol (MESH:D000077261), Sotalol (MESH:D013015), BHAT (-), calcium (MESH:D002118), catecholamine (MESH:D002395), Bisoprolol (MESH:D017298), atenolol (MESH:D001262), oxygen (MESH:D010100), Metoprolol (MESH:D008790), esmolol (MESH:C036604), lipid (MESH:D008055), Oxprenolol (MESH:D010096), timolol (MESH:D013999)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC13005812/full.md

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Source: https://tomesphere.com/paper/PMC13005812