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A POSEIDON registry analysis presented at the Heart Failure Society of America annual conference found elevated hsCRP in roughly 45% to 51% of U.S. participants with heart failure, depending on ejection-fraction group. The observational finding identifies a common marker of inflammation, but it does not show that treating 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 elevated high-sensitivity C-reactive protein (hsCRP), a marker of inflammation, in about half of participants with heart failure. Presented by Duke University’s Marat Fudim at the Heart Failure Society of America annual conference, the findings point to a frequent risk marker, but they do not establish that lowering inflammation improves heart-failure outcomes; targeted treatment options remain uncertain after recent trial setbacks.
Among U.S. participants, hsCRP levels of 2 mg/L or higher were 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 corresponding proportions across the full registry, which included participants from 18 countries, were 38.8%, 38.1%, and 38.2%. The figures describe the prevalence of an elevated biomarker, not a treatment effect.
The analysis was a cross-sectional subanalysis of POSEIDON, a prospective registry that enrolled 18,904 adults with atherosclerotic cardiovascular disease, heart failure, or both during routine care from 2023 to 2025. The U.S. heart-failure groups included 315 HFpEF, 94 HFmrEF, and 392 HFrEF participants. Fudim reported that elevated hsCRP was associated with higher levels of interleukin-6 and NT-proBNP across the three heart-failure groups. He also said residual inflammatory risk was present despite use of guideline-directed medical therapy.
Fudim identified obesity, diabetes, and chronic kidney disease as important potential drivers of inflammation in these patients. He described hsCRP as a practical way to identify and discuss residual risk, while saying there is no dedicated heart-failure treatment for inflammation. The registry analysis does not establish which factors caused elevated hsCRP or whether acting on the result changes clinical outcomes.
A Common Marker, Few Targeted Options
The findings highlight a gap between the frequent detection of inflammation and the limited evidence for therapies designed to target it in heart failure. A biomarker can help clinicians identify risk and frame discussions, but an elevated result alone does not prove that a particular anti-inflammatory drug will reduce hospitalization or death.
The distinction matters because patients and clinicians may otherwise interpret a high hsCRP result as a direct treatment target. Fudim discussed lifestyle measures, exercise, weight loss therapy, and addressing risk factors such as chronic kidney disease. These were his recommendations for risk management, not outcomes tested by this registry analysis. The report offers no evidence that a specific intervention based on hsCRP improves heart-failure outcomes.
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Registry Findings Meet Trial Setbacks
The POSEIDON comparison comes amid continuing difficulty in developing drugs that target individual inflammatory pathways in heart failure. Fudim pointed to Novo Nordisk’s September announcement that two placebo-controlled studies of the IL-6 inhibitor ziltivekimab, HERMES and ATHENA, had been stopped early for futility. The trials were designed to assess hard and softer endpoints among heart-failure patients with high hsCRP.
Ziltivekimab had also failed to reduce major adverse cardiovascular events in the ZEUS trial, which involved people with atherosclerotic cardiovascular disease, chronic kidney disease, and inflammation. Those results do not show that every approach to inflammation will fail, but they have added to uncertainty about targeting a single inflammatory pathway. Fudim suggested broader approaches could merit consideration, while cautioning that suppressing or interfering with the immune system carries risks.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, MD, MHS, of Duke University Medical Center
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What the Biomarker Cannot Show
Because the analysis was cross-sectional, it shows how often elevated hsCRP appeared in the sampled groups, not whether inflammation caused heart failure progression or whether lowering hsCRP would improve outcomes. The reported percentages also come from the registry’s U.S. participants; the source does not establish that they represent every U.S. patient with heart failure.
The findings do not identify an effective anti-inflammatory drug, a treatment threshold, or which patients would benefit from a particular approach. The reasons for the higher U.S. proportions compared with the overall registry figures are not resolved by the reported analysis. It is also unclear whether broad, multi-pathway treatments can reduce cardiovascular risk without unwanted effects on immune function.
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Awaiting Better Treatment Evidence
The immediate next step is further evidence from clinical research that tests whether acting on inflammation changes outcomes that matter to patients, such as heart-failure events and survival. The source does not give a new trial timetable or identify a replacement therapy following the early stops of HERMES and ATHENA.
For now, Fudim said hsCRP can help inform risk discussions and motivate attention to lifestyle and coexisting conditions. Whether that use translates into better outcomes, and whether a therapy aimed at multiple inflammatory pathways can do so safely, remain open questions.
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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. The analysis measured biomarker prevalence; it did not test an anti-inflammatory treatment.
Does elevated hsCRP prove that inflammation is causing heart failure?
No. The registry analysis found an association between elevated hsCRP and other markers, including IL-6 and NT-proBNP, but it cannot establish that inflammation caused heart failure progression.
Is there a dedicated anti-inflammatory treatment for heart failure?
Fudim said there is no dedicated treatment. Two trials of the IL-6 inhibitor ziltivekimab in heart-failure patients with high hsCRP were stopped early for futility, according to the source report.
What can patients do with an elevated hsCRP result?
Fudim described hsCRP as a tool for risk discussions and mentioned lifestyle, exercise, weight management, and addressing conditions such as chronic kidney disease. The analysis did not test whether these measures, when guided by hsCRP, improve heart-failure outcomes. Patients should discuss individual care decisions with a qualified health professional.
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