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A POSEIDON registry analysis presented at the Heart Failure Society of America meeting found elevated hsCRP in about half of U.S. participants with heart failure, across three ejection-fraction groups. The findings show a high measured inflammatory burden, but they do not establish that inflammation caused worse outcomes or identify a proven inflammation-targeting treatment.
A U.S. analysis of the POSEIDON heart failure registry found that about half of participants had elevated high-sensitivity C-reactive protein (hsCRP), a marker of inflammation, despite treatment with guideline-directed heart failure medicines. The results, presented by Duke University cardiologist Marat Fudim at the Heart Failure Society of America annual conference, point to a substantial measured inflammatory burden; they do not show that a specific anti-inflammatory drug can reduce it or improve patient outcomes.
Among U.S. participants, hsCRP of at least 2 milligrams per liter was recorded in 50.8% of people with heart failure with preserved ejection fraction (HFpEF), 44.7% with mildly reduced ejection fraction (HFmrEF), and 50.3% with reduced ejection fraction (HFrEF). The analysis included 315 HFpEF, 94 HFmrEF and 392 HFrEF participants.
Those proportions exceeded the corresponding figures across all 18 countries in POSEIDON: 38.8% for HFpEF, 38.1% for HFmrEF and 38.2% for HFrEF. Elevated hsCRP was also associated with higher interleukin-6 (IL-6) and NT-proBNP levels across the three heart failure groups. The study was a cross-sectional analysis, so it describes biomarker levels at a point in time rather than showing cause and effect.
Fudim said residual inflammatory risk remained among patients receiving guideline-directed therapy and described hsCRP as a practical way to identify that risk. He pointed to obesity, diabetes and chronic kidney disease as important factors associated with inflammation in heart failure. The report also noted higher insulin and diuretic use among participants with elevated hsCRP, but did not establish that either medication caused the higher levels.
High Biomarker Levels, Few Targeted Options
The findings highlight a gap between the frequency of elevated inflammation markers and the availability of treatments proven to target inflammation in heart failure. A biomarker may help clinicians describe risk, but this analysis does not show that lowering hsCRP itself would improve symptoms, prevent hospitalization or extend life.
The treatment question is particularly relevant because two trials of the IL-6 inhibitor ziltivekimab, HERMES and ATHENA, were stopped early for futility, according to Novo Nordisk’s September announcement cited in the report. The source also says the drug had not reduced major adverse cardiovascular events in the ZEUS trial among people with atherosclerotic cardiovascular disease, chronic kidney disease and inflammation. These results complicate hopes for a single pathway approach, but do not settle whether other strategies could help people with heart failure.
Fudim discussed lifestyle measures, exercise, weight-loss therapy and management of associated conditions as ways to address risk factors. These comments are not evidence that any one measure treats the inflammatory signal identified in this registry analysis. Any treatment decisions remain a matter for patients and their clinicians.
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What the POSEIDON Analysis Measured
POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease, heart failure or both, during routine care in 18 countries from 2023 to 2025. The conference report focused on a U.S. heart failure subset and compared the prevalence of elevated hsCRP across ejection-fraction categories with the overall international figures.
Because this was a cross-sectional subanalysis, the reported percentages describe how many participants met the hsCRP threshold; they do not establish why their levels were elevated or whether the U.S. differences reflect particular patient characteristics, healthcare patterns or other factors. The report notes that comorbidities such as obesity, diabetes and chronic kidney disease may contribute to inflammation.
““We are very inflamed as a nation of HF patients.””
— Marat Fudim, MD, MHS, of Duke University Medical Center
What the Biomarker Cannot Establish
The analysis does not show whether elevated hsCRP directly contributes to heart failure progression, predicts outcomes in this U.S. subgroup, or changes with any particular intervention. It also does not explain why the U.S. prevalence was higher than the overall POSEIDON figures. The reported relationship with IL-6 and NT-proBNP is an association, not proof that one marker caused another.
It remains unclear whether drugs that target one inflammatory pathway, broader therapies that affect several pathways, or other approaches can improve meaningful outcomes for heart failure patients. The source provides no trial results demonstrating that GLP-1 medicines treat heart failure-related inflammation, and Fudim’s comments about them were an example of a broader biological approach, not a treatment recommendation.
Trials Will Test Treatment Strategies
The immediate next step is further research to determine whether people identified by elevated hsCRP benefit from any intervention and which outcomes, if any, change. The reported analysis itself is observational and does not test a treatment. HERMES and ATHENA, the cited trials of ziltivekimab in heart failure patients with high hsCRP, were stopped early for futility; the source does not report a new trial or a replacement therapy.
For now, the conference findings support using hsCRP as a marker of inflammatory burden in research and clinical risk assessment, as Fudim described, rather than as proof that a specific anti-inflammatory treatment works. Whether a broader multi-pathway strategy can safely improve heart failure outcomes remains an open research question.
Key Questions
What did the U.S. POSEIDON analysis find?
It found hsCRP of at least 2 mg/L in 50.8% of the HFpEF group, 44.7% of the HFmrEF group and 50.3% of the HFrEF group in the U.S. subset.
Does elevated hsCRP prove that inflammation caused heart failure?
No. The analysis measured biomarker levels and their associations. It does not establish that inflammation caused heart failure or that lowering hsCRP would improve outcomes.
Is there a proven anti-inflammatory drug for heart failure?
The report says there is no dedicated, established treatment targeting inflammation in heart failure. Two ziltivekimab trials, HERMES and ATHENA, were stopped early for futility, according to the source.
What factors were linked to inflammation in the report?
Fudim identified obesity, diabetes and chronic kidney disease as key factors associated with inflammation. The analysis also found higher IL-6 and NT-proBNP levels among participants with elevated hsCRP, but these associations do not establish causation.
Source: rss
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