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Immunometabolic Organ Crosstalk in Heart Failure with Preserved Ejection Fraction: The Role of Dietary Patterns in Obesity-Related Inflammation

28 May 2026

Kalisz M, Litwiniuk A, Sławkowska N, Stępień D, Bik W.

Summary

What the study found

This research identifies heart failure with preserved ejection fraction (HFpEF) as a systemic inflammatory disease driven by communication between the heart, liver, spleen, and fat tissue. The study concludes that dietary interventions can modulate these inflammatory signals and that personalized nutrition is essential because different types of heart failure require distinct metabolic strategies.

Key findings

Heart failure is a systemic disorder involving complex "crosstalk" between the heart and other metabolic organs like the liver and spleen.
Chronic, low-grade metabolic inflammation originating in dysfunctional fat tissue is a primary driver of heart stiffness and blood vessel dysfunction.
The accumulation of ectopic lipids in non-fat tissues worsens organ damage and promotes the development of myocardial fibrosis.
Effective treatment requires precision nutrition that targets specific biomarkers and the unique metabolic profile of the individual, such as obesity-related versus aging-related phenotypes.

Practical takeaways

To support long-term heart health, individuals should prioritize dietary patterns that reduce systemic inflammation and prevent fat accumulation around internal organs. Integrating personalized nutritional shifts alongside standard medical care can improve cardiac elasticity and overall longevity by addressing the underlying metabolic causes of heart dysfunction.

Limitations

The study is a review of existing literature rather than a new clinical trial, so specific dietary protocols still require more direct human testing. Furthermore, the precise biomarkers needed to guide personalized nutrition are not yet universally accessible in standard clinical practice.

Abstract

Heart failure with preserved ejection fraction (HFpEF) is a major healthcare problem affecting approximately 1-2% of the adult population in highly developed countries. It is a heterogeneous condition with cardiometabolic disorders such as obesity, insulin resistance, diabetes mellitus, and hypertension. Pathophysiologically, HFpEF is currently recognized as a systemic disease characterized not only by impaired left ventricular relaxation and increased ventricular stiffness but also by chronic inflammation, endothelial dysfunction, myocardial fibrosis, and multi-organ involvement. This study aims to investigate the role of metabolic organ crosstalk and nutritional modulation in different HFpEF phenotypes. This review analyzes the current literature to investigate the interactions between the heart, adipose tissue, liver, and spleen in the pathophysiology of HFpEF. Chronic low-grade inflammation and adipose tissue dysfunction play central roles in the progression of HFpEF by activating the immune system, favoring ectopic lipid accumulation, and exacerbating fibrosis. The identification of specific HFpEF phenotypes (e.g., obesity-related versus aging-related) requires the application of distinct nutritional strategies that target metabolic inflammation and organ crosstalk, which may improve both myocardial and systemic function. HFpEF is a complex systemic disorder that requires phenotype-specific therapeutic approaches. Precision nutrition based on specific biomarkers, together with comprehensive cardiovascular management, may enhance therapeutic efficacy and complement pharmacological treatment in patients with HFpEF.

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