Current problems in cardiologyAug 12, 2026

Understanding and Treating Heart Failure with Preserved Pump Function Caused by Obesity

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Aug 13, 2026

Abstract

Sodium-glucose cotransporter 2 inhibitors are supported as the pharmacological foundation for obesity-driven heart failure with preserved ejection fraction (HFpEF).

Obesity and cardiometabolic dysfunction are increasingly recognized as significant drivers of HFpEF.
Key biological factors in this condition include visceral and epicardial fat, systemic inflammation, and impaired heart energy use.
Semaglutide has been shown to improve symptoms, physical limitations, exercise capacity, and body weight in trials targeting obesity-related HFpEF.
Tirzepatide may further enhance clinical status and decrease the risk of worsening heart failure events.
Finerenone may offer additional therapeutic options for heart failure with mildly reduced or preserved ejection fraction, though specific data for obesity are indirect.
Management of obesity-driven HFpEF should consider it as a cardiometabolic syndrome, integrating diagnosis, decongestion, and targeted therapies.

Simplified

Heart failure with preserved ejection fraction (HFpEF) is increasingly driven by obesity and cardiometabolic dysfunction. In this phenotype, the dominant biology extends beyond congestion alone and includes visceral and epicardial adiposity, systemic inflammation, impaired myocardial energetics, endothelial dysfunction, and exertional elevation in filling pressures. We performed a PRISMA-compliant systematic review with narrative evidence synthesis to evaluate pharmacological therapy in obesity-driven HFpEF. The available evidence supports sodium-glucose cotransporter 2 inhibitors as the pharmacological foundation because they provide the most mature outcome data across the preserved ejection fraction spectrum. Semaglutide improves symptoms, physical limitations, exercise capacity, and body weight in dedicated obesity-related HFpEF trials, whereas tirzepatide extends this signal by improving clinical status and reducing worsening heart failure events. Finerenone broadens the therapeutic platform in HF with mildly reduced or preserved ejection fraction, although obesity-specific data remain indirect. Conventional neurohormonal therapies retain a selective role, but they are not the principal biological match for this phenotype. Obesity-driven HFpEF should therefore be managed as a cardiometabolic syndrome with heart failure expression, using a phenotype-based sequence that links diagnosis, decongestion, SGLT2 inhibition, obesity-directed therapy, and selective adjunctive intensification.

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Understanding and Treating Heart Failure with Preserved Pump Function Caused by Obesity

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