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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 across three heart failure types. The findings show a substantial burden of inflammation, but they do not establish that an anti-inflammatory treatment will improve outcomes; recent targeted-drug trials have been stopped for futility or failed to reduce cardiovascular events.
A U.S. analysis from 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 Marat Fudim of Duke University at the Heart Failure Society of America annual conference, the findings highlight how common inflammatory risk was in this group, while recent drug-trial setbacks leave open how best to reduce it.
Elevated hsCRP was defined as at least 2 mg/L. In the U.S. heart failure subset, the marker was elevated in 50.8% of participants with preserved ejection fraction (HFpEF), 44.7% with mildly reduced ejection fraction (HFmrEF), and 50.3% with reduced ejection fraction (HFrEF). These are proportions within the study groups, not estimates of all U.S. patients with heart failure.
The corresponding figures across the wider POSEIDON heart failure groups in 18 countries were lower: 38.8% for HFpEF, 38.1% for HFmrEF and 38.2% for HFrEF. Fudim described the U.S. participants as having a higher inflammatory burden than the overall registry population. Elevated hsCRP was also associated with higher levels of interleukin-6 (IL-6) and NT-proBNP across the three heart failure types.
POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease (ASCVD), heart failure, or both during routine care between 2023 and 2025. The U.S. heart failure analysis included 315 people with HFpEF, 94 with HFmrEF and 392 with HFrEF. Fudim said residual inflammatory risk was present despite guideline-directed heart failure treatment. The analysis was cross-sectional, so it describes prevalence and associations rather than proving what caused inflammation or whether lowering hsCRP would change outcomes.
Why Inflammation Is Hard to Treat
The findings matter because inflammation was common across all three heart failure categories, including among people receiving standard guideline-directed treatment. A blood marker such as hsCRP may help clinicians identify patients with persistent inflammatory risk, but a high result is not itself proof that a particular anti-inflammatory drug will help that patient.
The treatment evidence described at the meeting remains unsettled. Novo Nordisk announced in September that it had stopped the HERMES and ATHENA trials of the IL-6 inhibitor ziltivekimab for futility. Those placebo-controlled trials involved heart failure patients with high hsCRP. Before that, the drug had not reduced major adverse cardiovascular events in the ZEUS trial among people with ASCVD, chronic kidney disease and inflammation. The registry findings therefore document a potential treatment need, not a validated therapy.
Fudim pointed to lifestyle measures, exercise, weight loss and addressing conditions such as chronic kidney disease as ways to approach risk factors. He also discussed GLP-1 drugs as agents that can affect multiple inflammatory pathways, but the report did not establish them as a proven treatment for heart-failure inflammation. Any treatment choice remains a clinical decision based on a patient’s circumstances and available evidence.
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How the POSEIDON Analysis Fits
POSEIDON is described as a large global registry studying inflammation in people with ASCVD or heart failure. The analysis presented at the conference focused on U.S. participants with heart failure and compared their hsCRP results with those in the registry’s international heart failure groups. The U.S. subset was divided by ejection fraction, a measure used to classify heart failure.
The report notes that obesity, diabetes and chronic kidney disease are important drivers of inflammation in heart failure, according to Fudim. It also says people with elevated hsCRP appeared to have higher insulin and diuretic use across heart failure types. Those observations do not show that these factors caused a particular participant’s elevated hsCRP. The analysis reports a snapshot of routine-care participants, rather than a treatment trial or a population-wide survey.
At the conference, discussant Amanda Vest of Cleveland Clinic placed the results against a history of neutral or negative trials targeting specific inflammatory pathways in heart failure. Her question captured the gap at the center of the report: high inflammatory burden has been observed, but interventions aimed at reducing it have not yet provided a clear answer.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, MD, MHS, Duke University Medical Center
What the Data Cannot Establish
The analysis does not establish that elevated hsCRP caused worse heart failure outcomes, or that lowering the marker would reduce hospitalizations or deaths. It reports the proportion above a threshold and associations with other blood markers; it does not test an intervention. The U.S. groups were also relatively small, particularly the 94 participants with HFmrEF, and the results may not represent all U.S. heart failure patients.
It remains unclear which, if any, anti-inflammatory strategy can improve clinical outcomes in heart failure, and whether broad approaches would be effective and safe. The conference report also does not provide detailed trial results for HERMES and ATHENA beyond the announcement that they were stopped early for futility. No dedicated treatment was identified in the source material as established for this inflammatory risk.
What Researchers Will Watch
Further results from POSEIDON and other research may clarify how hsCRP relates to outcomes across heart failure types and whether the U.S.-international difference holds in other populations. For treatment, the next evidence needed is from studies showing that an intervention improves meaningful patient outcomes, not simply that it changes an inflammation marker. The early stops of HERMES and ATHENA leave no reported positive result from those trials to guide practice.
For now, Fudim described hsCRP as a practical way to identify residual risk and inform conversations about lifestyle and associated conditions. The registry report does not establish a new standard of care. Decisions about testing or treatment should be made with a qualified health professional, using each patient’s clinical history and current evidence.
Key Questions
What did the POSEIDON analysis find?
Elevated hsCRP, defined as at least 2 mg/L, was found in 50.8% of U.S. participants with HFpEF, 44.7% with HFmrEF and 50.3% with HFrEF in the analysis presented at the conference.
Does elevated hsCRP mean a patient needs an anti-inflammatory drug?
No. The registry analysis measured inflammation and related markers; it did not test whether treatment based on hsCRP improves outcomes. The report says there is no dedicated heart-failure treatment established for this inflammatory risk.
Why were ziltivekimab trials stopped?
Novo Nordisk announced in September that the HERMES and ATHENA trials were stopped early for futility. The source report does not give detailed results from those trials. A prior study, ZEUS, did not find that ziltivekimab reduced major adverse cardiovascular events in people with ASCVD, chronic kidney disease and inflammation.
Can these findings be applied to all people with heart failure?
Not directly. The analysis covered a U.S. subset of a routine-care registry, with 315 HFpEF participants, 94 HFmrEF participants and 392 HFrEF participants. It is not a population-wide survey, and the results do not establish what an individual patient’s hsCRP means.
Source: rss
