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A POSEIDON registry analysis presented at the Heart Failure Society of America annual conference found elevated hsCRP in about half of U.S. participants with each major heart failure ejection-fraction type. The findings point to common residual inflammation, but they do not show that treating it improves outcomes; recent 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, or hsCRP, a marker of inflammation. Presented by Duke University cardiologist Marat Fudim at the Heart Failure Society of America annual conference, the findings show that inflammation is common across heart failure types, but do not establish that lowering hsCRP improves patients’ health.
Among U.S. participants, hsCRP of at least 2 mg/L 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 analysis included 315 people with HFpEF, 94 with HFmrEF and 392 with HFrEF.
The U.S. percentages were higher than those reported across all 18 countries in POSEIDON: 38.8% for HFpEF, 38.1% for HFmrEF and 38.2% for HFrEF. The registry prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease and/or heart failure during routine care from 2023 to 2025. This report was a cross-sectional subanalysis, not a trial testing treatment.
Fudim said elevated hsCRP was associated with higher levels of interleukin-6 (IL-6) and NT-proBNP across the three heart failure groups. He also said residual inflammatory risk remained despite guideline-directed heart failure therapy. Participants with higher hsCRP appeared to have more insulin and diuretic use, though the analysis did not establish why those differences occurred.
Inflammation Persists Despite Heart Failure Care
The results suggest that inflammatory risk is common among U.S. patients receiving routine heart failure care, across different levels of pumping function. Fudim identified obesity, diabetes and chronic kidney disease as important contributors to inflammation in this population. Those conditions often coexist with heart failure, making the findings relevant to care beyond any single drug target.
However, a high hsCRP result is a risk signal, not proof of a treatable cause. The registry analysis cannot show that inflammation caused worse outcomes or that lowering the marker would prevent hospitalizations or deaths. Its value is in documenting how often elevated inflammation appears and in helping frame questions for future treatment studies.
Fudim described hsCRP as a practical biomarker that can help him discuss risk with patients. He cited lifestyle measures, exercise, weight loss therapy and management of conditions such as kidney disease as approaches to address risk factors. These comments are not evidence that a particular intervention reduced heart failure events in this registry.
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Why Anti-Inflammatory Trials Matter
The report comes amid uncertainty about whether specific anti-inflammatory drugs can improve heart failure outcomes. In September, Novo Nordisk said two placebo-controlled trials of ziltivekimab, an IL-6 inhibitor, had been stopped early for futility. The HERMES and ATHENA studies were designed to examine a range of clinical and other endpoints in heart failure patients with high hsCRP. The supplied report does not provide detailed trial results or specify which endpoints drove the futility decisions.
Before those stops, ziltivekimab had also failed to reduce major adverse cardiovascular events in the ZEUS trial, which enrolled people with atherosclerotic cardiovascular disease, chronic kidney disease and inflammation. Heart Failure Society of America session discussant Amanda Vest of Cleveland Clinic described a history of neutral or negative studies targeting specific inflammatory pathways in heart failure.
Fudim suggested that therapies affecting multiple pathways, including GLP-1 drugs, may warrant consideration, while cautioning against excessive interference with immune function. These were his views on possible directions for research, not findings from the POSEIDON analysis or proof that broad anti-inflammatory treatment improves heart failure outcomes.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, MD, MHS, Duke University Medical Center
Risk Marker, Not Treatment Proof
The analysis does not explain why the U.S. participants had higher elevated-hsCRP percentages than the overall international registry, or whether differences in participant characteristics, health care or other factors account for the gap. It also does not report whether elevated hsCRP predicted outcomes within these specific U.S. groups. While the report notes that other cohorts have linked inflammation to mortality, the POSEIDON subanalysis itself was not designed to test that relationship.
It remains unclear whether reducing inflammation through a particular drug strategy would improve heart failure outcomes, which patients might benefit, and how to balance possible benefits against effects on immune function. The early stops of HERMES and ATHENA add to the uncertainty, but the supplied account does not include their full data or explain the specific trial findings behind the futility decisions.
More Trial Results Needed
The next key evidence will come from fuller reporting of the HERMES and ATHENA trial results, including the endpoints assessed and the reasons the studies were stopped. Researchers will also need clinical trials to test whether interventions aimed at one or several inflammatory pathways improve outcomes, rather than only changing hsCRP or other biomarkers.
For now, Fudim said he uses hsCRP to inform discussions about risk and to motivate attention to lifestyle and related conditions. The registry findings support further study of inflammation in heart failure; they do not establish a new standard treatment or show that patients should change prescribed care based on hsCRP alone.
Key Questions
What did the POSEIDON analysis find?
It found hsCRP of at least 2 mg/L in about half of U.S. participants across HFpEF, HFmrEF and HFrEF groups. The analysis described prevalence; it did not test a treatment.
Does elevated hsCRP mean inflammation caused a patient’s heart failure?
No. The registry analysis shows that elevated hsCRP was common, but it cannot establish the cause of an individual patient’s heart failure or prove that inflammation drove their condition.
Is there a proven anti-inflammatory drug for heart failure?
This report says there is no dedicated treatment established for heart failure inflammation. Trials of the IL-6 inhibitor ziltivekimab were stopped early for futility, and further evidence is needed.
What did the report say patients can do now?
Fudim pointed to lifestyle measures, exercise, weight loss therapy and management of conditions such as chronic kidney disease as ways to address risk factors. The analysis did not test these approaches; patients should discuss medical decisions with their qualified health care professional.
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