TL;DR
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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 across three heart failure types, more than in the study’s international cohort. The findings point to a substantial inflammatory burden, but do not show that lowering inflammation improves heart failure outcomes; two trials of the IL-6 inhibitor ziltivekimab were stopped early for futility.
A U.S. analysis of the POSEIDON registry found that about half of participants with heart failure had elevated high-sensitivity C-reactive protein (hsCRP), a marker of inflammation, prompting fresh discussion of how to address inflammation when dedicated treatments remain unproven. The results were presented by Marat Fudim of Duke University at the Heart Failure Society of America annual conference; they describe how common the marker was, not whether treating it improves outcomes.
Among U.S. participants, hsCRP of 2 milligrams per liter or higher was recorded 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 comparable proportions across the full registry of participants with heart failure in 18 countries were 38.8%, 38.1% and 38.2%, respectively.
The U.S. heart failure groups included 315 people with HFpEF, 94 with HFmrEF and 392 with HFrEF. Across all three groups, elevated hsCRP was associated with higher levels of interleukin-6 (IL-6) and NT-proBNP. The analysis also noted higher insulin and diuretic use among people with high hsCRP, but it did not establish that those treatments or other characteristics caused the inflammation.
Fudim said inflammation remained a concern despite use of guideline-directed heart failure therapy. He identified obesity, diabetes and chronic kidney disease as important contributors, while describing hsCRP as a practical way to identify patients with residual inflammatory risk. Because this was a cross-sectional analysis, it measured inflammation at a point in time rather than testing a treatment or establishing cause and effect.
A High Inflammatory Burden, Few Targeted Options
The results highlight a gap between the prevalence of an elevated inflammation marker and the availability of proven treatments aimed specifically at inflammation in heart failure. The U.S. percentages were higher than the corresponding overall registry figures, but the analysis does not explain why, and differences between the groups cannot by themselves establish that U.S. patients have worse outcomes.
For clinicians, hsCRP may help flag residual risk and support conversations about health factors that can be addressed. Fudim pointed to lifestyle, exercise, weight management and attention to chronic kidney disease risk. These remarks are not evidence that lowering hsCRP through any particular approach will prevent heart failure events. The central clinical question remains whether interventions that reduce inflammation can also improve outcomes safely.
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Registry Findings Meet Trial Setbacks
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 report described a subanalysis of the U.S. heart failure participants, separating results by ejection-fraction group. Its observational design makes it useful for describing the burden of elevated hsCRP, but not for showing that inflammation caused heart failure or that a specific treatment would help.
The treatment outlook was clouded by the September announcement from Novo Nordisk that two placebo-controlled trials of the IL-6 inhibitor ziltivekimab, HERMES and ATHENA, had stopped early for futility. The trials were designed to assess clinical and other outcomes in heart failure patients with high hsCRP. The source report also noted that ziltivekimab had not reduced major adverse cardiovascular events in the ZEUS trial among people with atherosclerotic cardiovascular disease, chronic kidney disease and inflammation. These results concern particular trials and therapies; they do not establish that every possible anti-inflammatory strategy will fail.
““We are very inflamed as a nation of HF patients.””
— Marat Fudim, MD, MHS, Duke University Medical Center
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What the Analysis Cannot Establish
The registry analysis does not show whether elevated hsCRP predicts outcomes in these particular U.S. participants, whether lowering the marker changes those outcomes, or why the U.S. proportions exceeded the overall registry figures. It also cannot determine whether comorbidities caused the elevated readings. The report did not provide randomized evidence that lifestyle changes or any drug specifically reduce heart failure events by lowering inflammation.
It remains unclear whether therapies acting on multiple inflammatory pathways can benefit heart failure patients, which patients might respond, and how to balance potential benefit against effects on immune function. The early stops of HERMES and ATHENA narrow the evidence available for ziltivekimab in this setting, but do not settle the question for other treatments or approaches.
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Further Trials Must Show Patient Benefit
The immediate next step is to interpret the POSEIDON findings as a description of inflammatory burden, not as proof of a treatment effect. Future studies would need to test whether an intervention improves meaningful heart failure outcomes, identify which patients may benefit, and measure possible harms. The source report did not name a new trial or provide a timetable for further results.
For now, Fudim described using hsCRP to inform risk discussions and motivate attention to lifestyle and underlying health risks. Whether broader anti-inflammatory therapies can translate that signal into better outcomes remains an open research question.
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Key Questions
What did the POSEIDON analysis find?
It found hsCRP of 2 mg/L or higher in 50.8% of U.S. participants with HFpEF, 44.7% with HFmrEF and 50.3% with HFrEF. These are registry findings, not estimates of how many people across the entire U.S. population have elevated inflammation.
Does elevated hsCRP prove that inflammation causes heart failure?
No. The analysis describes an association and the prevalence of elevated hsCRP. Its cross-sectional design cannot establish that inflammation caused heart failure or determine whether changing hsCRP would improve health outcomes.
Is there a proven inflammation-targeting drug for heart failure?
The report says there is no dedicated treatment established for this purpose. Two trials of the IL-6 inhibitor ziltivekimab in heart failure patients with high hsCRP were stopped early for futility; the findings do not rule out every other possible approach.
What factors did the presenter identify as contributors to inflammation?
Fudim identified obesity, diabetes and chronic kidney disease as key drivers. He also discussed lifestyle, exercise and weight management, but the registry analysis did not test whether those measures reduce heart failure events.
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