# Mechanisms of Cardiac Inflammation in Heart Failure: Role of Dietary Patterns, Nutrients, and Therapeutic Strategies

## TL;DR

This review explores how diet and inflammation affect heart failure, highlighting the potential of anti-inflammatory diets and therapies to improve outcomes.

## Contribution

The paper integrates current evidence on dietary patterns and anti-inflammatory therapies as modifiable factors in heart failure progression.

## Key findings

- High-DII diets increase inflammation, while Mediterranean diets reduce pro-inflammatory biomarkers like CRP and IL-6.
- SGLT2 inhibitors and therapies like vagus nerve stimulation show anti-inflammatory effects by suppressing cytokines.
- Combining dietary patterns with pharmacological agents may synergistically improve endothelial function and reduce fibrosis.

## Abstract

Background: Systemic inflammation is a key driver of heart failure (HF) progression across all ejection fraction (EF) phenotypes, with diet emerging as a modifiable factor influencing cardiac metabolism and inflammatory signaling. This narrative review integrates current evidence on the inflammatory mechanisms underlying HF, their links with common comorbidities and emerging anti-inflammatory therapeutic strategies, with a particular focus on the role of nutrition in supporting healthy cardiac metabolism. Methods: We searched MEDLINE/PubMed, EMBASE, Web of Science, the Cochrane Library, Scopus and reference lists of relevant publications using terms related to systemic inflammation, dietary patterns and HF prioritizing high-impact studies on nutrition–inflammation–HF interactions published from 2000 onward. Results: Major HF comorbidities sustain chronic, low-grade inflammation through elevated cytokine activity. Dietary patterns—especially those with high Dietary Inflammatory Index (DII)—substantially shape inflammatory milieu. The Mediterranean diet appears to have a favorable inflammatory profile with reduction in circulating pro-inflammatory biomarkers, especially C-reactive protein (CRP) and interleukin-6 (IL-6). Established therapies for HF with reduced ejection fraction and vagus nerve stimulation elicit anti-inflammatory efficacy through cytokine suppression. Sodium glucose cotransporter-2 (SGLT2) inhibitors demonstrate positive metabolic effects and anti-inflammatory actions through decrease in IL-6 and tumor necrosis factor-α (TNF-α). Interleukin-1 blockade has produced heterogeneous clinical outcomes, while definitive findings examining the role of IL-6 inhibitors in inflammation suppression and possible benefit on cardiac outcomes are anticipated. Preliminary data show the potential synergistic effects of dietary patterns/nutrients and pharmacological agents combination on improvement of endothelial function and attenuation of the fibrotic process, although there is a need for further research in large-scale trials. Conclusions: Systemic inflammation demonstrates a key role in HF initiation and progression, and the effect of diet on inflammatory pathways is central. Dietary patterns targeting inflammation-related mechanisms (inflammasome, gut dysbiosis) can lead to attenuation of systemic inflammatory response and restoration of cardiac metabolic flexibility. A deeper mechanistic discernment of cardiac inflammatory cascades, together with identification of HF subpopulations with excessive inflammatory activity, may facilitate the design of targeted randomized controlled trials (RCTs) aiming for novel personalized, inflammation-targeted HF therapies with potential clinical benefit.