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 ejection-fraction groups. The findings point to a high measured inflammatory burden, but they do not establish that inflammation caused worse outcomes or identify an effective targeted treatment.
A U.S. analysis of the POSEIDON registry found that about half of participants with heart failure had elevated high-sensitivity C-reactive protein, or hsCRP, a marker of inflammation. Presented by Duke University cardiologist Marat Fudim at the Heart Failure Society of America annual conference, the results highlight a common risk marker but do not show that a specific anti-inflammatory treatment improves heart failure outcomes.
Among U.S. participants, hsCRP at or above 2 mg/L was found 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). In the full POSEIDON heart failure population across 18 countries, the corresponding proportions were lower: 38.8%, 38.1%, and 38.2%.
The analysis included 801 U.S. participants: 315 with HFpEF, 94 with HFmrEF, and 392 with HFrEF. POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease and/or heart failure during routine care between 2023 and 2025. The U.S. figures are a subanalysis, not a randomized treatment comparison.
Fudim said elevated hsCRP was associated with higher levels of interleukin-6 (IL-6) and NT-proBNP across the heart failure groups. He also reported that inflammatory risk remained among patients receiving guideline-directed medical therapy. The analysis identified obesity, diabetes, and chronic kidney disease as important contributors discussed by the presenter; the registry findings do not establish that these conditions alone explain the U.S.-global difference.
Inflammation Without a Proven Targeted Drug
The findings matter because they suggest that a large share of U.S. patients in this registry had an elevated inflammation marker despite standard heart failure care. Measuring hsCRP may help clinicians identify patients with residual inflammatory risk, but a marker is not itself a treatment recommendation and this analysis does not show that lowering hsCRP would improve survival or prevent hospitalization.
The treatment question remains open. Novo Nordisk announced in September that it had stopped the HERMES and ATHENA trials of the IL-6 inhibitor ziltivekimab early for futility. The trials were designed to assess clinical and other outcomes in heart failure patients with high hsCRP. Ziltivekimab had also failed to reduce major adverse cardiovascular events in the ZEUS trial among people with atherosclerotic cardiovascular disease, chronic kidney disease, and inflammation. These results add to uncertainty about blocking a single inflammatory pathway, but they do not rule out every possible approach.
Fudim said lifestyle measures, exercise, weight loss, and attention to conditions such as kidney disease can be part of care. He also raised the possibility that treatments affecting multiple pathways, including GLP-1 drugs, could be relevant to inflammation. That was a proposed direction, not evidence from POSEIDON that these drugs treat heart failure inflammation.
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What POSEIDON Measured
POSEIDON is a prospective observational registry of adults with atherosclerotic cardiovascular disease and/or heart failure receiving routine care in 18 countries. The report discussed at the conference was a cross-sectional analysis: it compared hsCRP levels across groups at a point in the registry data, rather than assigning a treatment and tracking its effects.
High-sensitivity C-reactive protein is a blood marker used to assess inflammation. In this analysis, 2 mg/L or higher was the threshold for elevated hsCRP. The higher percentages in the U.S. heart failure groups are comparisons with the corresponding groups in the overall international registry; the data provided do not identify why the rates differ or show that the U.S. result applies to all American patients with heart failure.
““We are very inflamed as a nation of HF patients.””
— Marat Fudim, MD, MHS, Duke University Medical Center
What the Registry Cannot Show
The analysis does not establish why elevated hsCRP was more common in the U.S. subgroup, whether it predicts outcomes in these specific participants, or whether reducing the marker would improve health. Because the report is observational and cross-sectional, it cannot show that inflammation caused heart failure progression or that any treatment changed risk.
The source material does not provide a detailed account of participant characteristics, statistical uncertainty around the percentages, or a direct explanation for differences between countries. It also does not report final outcome data from HERMES or ATHENA after their early stoppage. The available information does not identify a proven anti-inflammatory drug for heart failure.
Trial Results and Treatment Research
The immediate next development is further reporting on the stopped HERMES and ATHENA trials, including what their available data show and how the futility decisions were made. Researchers and clinicians will also need evidence from treatment studies, rather than prevalence measurements alone, to determine whether targeting inflammation can improve outcomes in heart failure.
For now, Fudim described hsCRP as a practical tool to help discuss risk and motivate attention to lifestyle and related conditions. The registry report does not set out a new treatment guideline. Any care decisions, including the use of weight-loss or other medicines, should be made with a qualified clinician based on an individual patient’s circumstances.
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. The analysis compared registry participants and did not test a treatment.
Does elevated hsCRP mean inflammation caused a patient’s heart failure?
No. hsCRP is a marker of inflammation, and the registry analysis does not establish the cause of an individual patient’s heart failure or show that inflammation caused their condition.
Is there a proven anti-inflammatory drug for heart failure?
The report described no dedicated treatment established for the inflammatory risk pattern under discussion. The IL-6 inhibitor trials HERMES and ATHENA were stopped early for futility, according to Novo Nordisk’s September announcement.
What can patients do about inflammation?
Fudim discussed exercise, lifestyle measures, weight loss, and addressing conditions such as chronic kidney disease as areas of care. The registry did not test these approaches; patients should discuss treatment choices with a qualified clinician.
Source: rss
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