Why the study?
Despite observational and experimental evidence linking inflammation to heart failure, clinical trials of anti-inflammatory therapies have produced inconsistent results.
Do anti-inflammatory therapies improve clinical outcomes and functional status in patients with heart failure?
Do anti-inflammatory therapies improve clinical outcomes and functional status in patients with heart failure?
Answers are grounded in this paper and cite their sources.
Anti-inflammatory therapies in heart failure require precise patient phenotyping and staging, as benefits appear limited to early disease stages or specific inflammatory profiles, while advanced stages may experience harm.
Heart failure (HF) is a leading cause of cardiovascular morbidity and mortality, with inflammation recognized as a key cause and byproduct. Despite observational studies linking elevated indices of inflammation with HF severity, as well as experimental models highlighting the centrality of inflammation to the pathogenesis of various types of HF, clinical trials of anti-inflammatory therapies in HF have produced inconsistent results. This variability may relate to the substrate included - differences in HF stage and/or clinical phenotype - as well as the mechanisms and target of therapeutics, whether aimed at preventing new-onset HF or treating established disease. This review evaluates clinical trials directly targeting inflammation in HF, with a focus on disease stage and symptomatology. Ultimately, by highlighting the importance of HF staging and the timing of therapeutics in prior inflammation-targeted interventions, we aim to inform more precise targets from a disease substrate perspective when designing trials of inflammation-modulating therapies in HF.
No takes yet. Share an insight, caveat, or question.
Nagasaka et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: