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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 point to a substantial inflammatory burden, but they do not show that lowering hsCRP improves outcomes; recent trials of the IL-6 inhibitor ziltivekimab were stopped early for futility.
A U.S. analysis of the POSEIDON registry found elevated high-sensitivity C-reactive protein (hsCRP) in about half of participants with heart failure, pointing to a substantial inflammatory burden even as dedicated anti-inflammatory treatments remain unproven. The findings were presented by Duke University cardiologist Marat Fudim at the Heart Failure Society of America annual conference in Phoenix.
Among U.S. participants, hsCRP of at least 2 mg/L was detected in 50.8% of those 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 corresponding proportions across the full registry, which covered 18 countries, were 38.8%, 38.1%, and 38.2%.
The U.S. heart failure groups included 315 people with HFpEF, 94 with HFmrEF, and 392 with HFrEF. POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease (ASCVD), heart failure, or both during routine care from 2023 to 2025. The reported analysis was cross-sectional, so it describes the prevalence of elevated hsCRP rather than showing that inflammation caused particular outcomes.
Fudim said elevated hsCRP was associated with higher levels of interleukin-6 (IL-6) and NT-proBNP across all three heart failure groups. He also noted that high-inflammation groups appeared to have more insulin and diuretic use. The analysis does not establish why those differences occurred, or whether any particular treatment would reduce risk.
A High Burden Without a Proven Target
The results identify a sizable group of U.S. heart failure patients with a marker associated with systemic inflammation. Fudim described obesity, diabetes, and chronic kidney disease as key contributors to inflammatory burden in heart failure. The finding matters because inflammation may persist alongside standard heart failure care, creating interest in ways to identify and address residual risk.
However, a high hsCRP result is not evidence that an anti-inflammatory drug will help. The registry analysis measured a biomarker; it did not test treatment or show that reducing hsCRP lowers hospitalizations or deaths. The gap between widespread inflammation and uncertain treatment benefit is central to the clinical challenge.
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Why Targeted Trials Disappointed
Fudim said residual inflammatory risk was present despite use of guideline-directed medical therapy. He called hsCRP a practical way to identify patients with persistent inflammation and said he uses the measure to inform risk discussions. He also pointed to lifestyle measures, exercise, weight management, and attention to conditions such as kidney disease as part of care, rather than presenting them as a proven substitute for an anti-inflammatory drug.
Drug development has produced setbacks. In September 2026, Novo Nordisk announced that two placebo-controlled trials of the IL-6 inhibitor ziltivekimab—HERMES and ATHENA—had been stopped early for futility. They were designed to assess clinical and other endpoints in heart failure patients with high hsCRP. Before those decisions, ziltivekimab had also failed to reduce major adverse cardiovascular events in the ZEUS trial among people with ASCVD, chronic kidney disease, and inflammation.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, MD, MHS, Duke University Medical Center
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What the Registry Cannot Show
The cross-sectional analysis cannot determine whether elevated hsCRP predicts future outcomes in these participants, whether inflammation is a cause or consequence of illness, or whether lowering the marker would improve health. Although Fudim said prior cohorts have linked inflammatory burden with mortality, this particular analysis reported prevalence and biomarker associations, not mortality results.
It is also unclear why the U.S. proportions were higher than the overall POSEIDON figures. The reported data do not establish that the difference reflects national characteristics, differences in participants, or other factors. No dedicated heart failure treatment targeting inflammation has been shown here to improve outcomes, and the early termination of HERMES and ATHENA leaves their planned questions unanswered.
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Further Evidence and Clinical Caution
The registry findings add a measure of inflammatory burden for researchers to investigate, but they do not change the evidence from the stopped trials or establish a new treatment. Future studies would need to show whether selecting patients by hsCRP and targeting inflammation can improve meaningful clinical outcomes, while also evaluating potential harms from interfering with immune pathways.
For now, Fudim described hsCRP as a tool for risk assessment and patient discussion, not a treatment in itself. The source report does not specify a next milestone or provide a timeline for further trial results. Whether broader anti-inflammatory strategies can succeed where single-pathway approaches have disappointed remains open.
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Key Questions
What did the POSEIDON analysis find?
It found hsCRP of at least 2 mg/L in 50.8% of U.S. participants with HFpEF, 44.7% with HFmrEF, and 50.3% with HFrEF. These are prevalence figures from a cross-sectional analysis, not treatment outcomes.
Does elevated hsCRP mean a patient should take an anti-inflammatory drug?
No treatment recommendation follows from this registry analysis. It measured hsCRP and related biomarkers but did not test whether an anti-inflammatory medicine improves heart failure outcomes. Treatment decisions should be discussed with a qualified clinician.
What happened to the ziltivekimab heart failure trials?
Novo Nordisk announced in September 2026 that the HERMES and ATHENA trials were stopped early for futility. The trials had been designed to assess ziltivekimab in heart failure patients with high hsCRP.
Why are researchers interested in hsCRP?
Fudim described hsCRP as a practical marker for identifying persistent inflammatory risk. In the analysis, elevated hsCRP was associated with higher IL-6 and NT-proBNP across the heart failure groups, but those associations do not prove cause and effect.
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