Journal of cardiovascular development and diseaseApr 27, 2026

Obesity and Heart Failure: An Introduction

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Apr 28, 2026

Abstract

Obesity affects nearly one-third of the global population and is a major independent risk factor for heart failure, particularly heart failure with preserved ejection fraction.

Excess fat, especially visceral and epicardial adipose tissue, contributes to chronic inflammation and heart problems.
Increased body mass index is associated with a higher risk of developing heart failure.
Obesity-related heart failure with preserved ejection fraction is marked by specific heart changes, including left ventricular hypertrophy and impaired relaxation.
Traditional heart failure treatments focus on managing blood flow and hormone levels but may not fully address obesity-related factors.
Sodium-glucose cotransporter 2 inhibitors may lower hospitalizations for heart failure, while certain weight-loss medications show potential benefits for heart health in obese patients.
Recognizing obesity-related heart failure as a separate condition supports a treatment approach that combines weight loss with standard heart failure medications.

Simplified

Obesity is a chronic, highly prevalent disease affecting nearly one-third of the global population and represents a major independent risk factor for heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF). Excess adiposity-especially visceral and epicardial adipose tissue (EAT)-acts as an active endocrine and immune organ, promoting chronic low-grade inflammation, oxidative stress, endothelial dysfunction, and adverse myocardial remodeling. Expanded EAT exerts both paracrine inflammatory effects and mechanical constraint on the myocardium, contributing to diastolic dysfunction, microvascular impairment, atrial arrhythmogenesis, and elevated filling pressures despite preserved systolic function. Evidence demonstrates a dose-response relationship between increasing body mass index and incident HF. Clinically, obesity-related HFpEF is characterized by concentric left ventricular hypertrophy, impaired relaxation, increased plasma volume, reduced exercise tolerance, and relatively low natriuretic peptide levels, complicating diagnosis. HF management includes traditional treatment with diuretics, renin-angiotensin system inhibitors, β-blockers, mineralocorticoid receptor antagonists, and angiotensin receptor-neprilysin inhibitors. These agents widely remain foundational as they primarily target hemodynamic and neurohormonal pathways in HF. In contrast, sodium-glucose cotransporter 2 inhibitors consistently reduce HF hospitalizations across the ejection fraction spectrum, while glucagon-like peptide-1 receptor agonists and dual incretin therapies (e.g., tirzepatide) promote substantial weight loss, improve symptoms, and demonstrate promising anti-remodeling effects in obesity-related HFpEF. Recognizing obesity-driven HF as a distinct cardiometabolic entity supports an integrated therapeutic strategy combining structured weight reduction with guideline-directed HF polypharmacotherapy to address both hemodynamic burden and upstream adiposity-related mechanisms.

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The authors declare no conflicts of interest.

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Obesity and Heart Failure: An Introduction

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