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A POSEIDON registry analysis presented at the Heart Failure Society of America meeting found elevated hsCRP in roughly 45% to 51% of U.S. participants with heart failure, depending on ejection-fraction group. The findings identify a substantial burden of inflammation, but do not show that a specific anti-inflammatory treatment improves heart failure outcomes; recent 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) in about half of participants with heart failure, but the findings do not point to an established inflammation-targeting treatment. Presented by Duke University cardiologist Marat Fudim at the Heart Failure Society of America annual conference, the analysis highlights a common risk marker even as recent drug trials have failed to establish a dedicated therapy.
Among U.S. participants, hsCRP at or above 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 U.S. proportions were higher than those reported across the full 18-country POSEIDON heart failure groups: 38.8% for HFpEF, 38.1% for HFmrEF, and 38.2% for HFrEF.
The U.S. analysis included 801 people with heart failure: 315 with HFpEF, 94 with HFmrEF, and 392 with HFrEF. POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease and/or heart failure in routine care from 18 countries between 2023 and 2025. This presentation was a cross-sectional analysis, so it describes the prevalence of elevated hsCRP rather than proving that inflammation caused particular outcomes.
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 was present despite use of guideline-directed medical therapy. The report identified obesity, diabetes, and chronic kidney disease as important comorbidities linked to inflammation, while noting higher insulin and diuretic use among participants with elevated hsCRP.
Inflammation Without a Proven Drug
The results point to a sizeable group of people with heart failure who have an elevated inflammatory marker, including patients already receiving standard heart failure care. That may help clinicians identify a risk profile and discuss relevant health factors, but the registry analysis does not establish that lowering hsCRP will improve survival, symptoms, or hospitalisation rates.
The treatment gap is underscored by recent trial setbacks. In September, Novo Nordisk announced that it had stopped the HERMES and ATHENA trials of the IL-6 inhibitor ziltivekimab early for futility. The trials were designed to test clinical and other endpoints in heart failure patients with high hsCRP. Ziltivekimab had also failed to reduce major adverse cardiovascular events in the ZEUS trial involving people with atherosclerotic cardiovascular disease, chronic kidney disease, and inflammation.
For patients, the distinction matters: an elevated marker is not itself a diagnosis of a treatable inflammatory disorder, and these data do not support adding an anti-inflammatory drug for heart failure. Fudim described lifestyle measures, exercise, weight management, and addressing conditions such as chronic kidney disease as practical areas of focus, while the search for a proven drug approach continues.
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POSEIDON and Recent Trial Setbacks
POSEIDON is described in the report as the largest global registry of inflammation in people with atherosclerotic cardiovascular disease or heart failure. Its participants were recruited during routine care across 18 countries. The U.S. heart failure subset was divided by ejection fraction, allowing the analysis to compare the prevalence of elevated hsCRP across three clinical groups.
Fudim said comorbidities including obesity, diabetes, and chronic kidney disease are key drivers of inflammation in heart failure. He called hsCRP a practical biomarker that can help identify residual inflammatory risk and inform conversations with patients. However, the registry did not test whether using hsCRP to guide treatment changes outcomes.
Drug development has faced repeated difficulties, according to session discussant Amanda Vest of Cleveland Clinic. Fudim suggested that future approaches might target multiple inflammatory pathways rather than focus on IL-6 alone, citing GLP-1 drugs as an example of medicines that can affect inflammation through different mechanisms. Those remarks were a view on possible research directions, not evidence from this analysis that such drugs treat heart failure inflammation.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, MD, MHS, Duke University Medical Center
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What the Marker Cannot Show
The analysis does not establish why the U.S. participants had higher elevated-hsCRP proportions than the international groups, or whether the difference reflects population characteristics, care settings, or other factors. It also cannot show that elevated hsCRP itself caused worse outcomes: the reported comparison was cross-sectional, and no treatment was assigned on the basis of the marker.
The source does not provide outcome estimates for the U.S. heart failure groups or detailed results from the halted HERMES and ATHENA trials. It remains unclear whether other drugs, including medicines that affect several biological pathways, can reduce clinically important heart failure events by lowering inflammation. The potential benefits and risks of broader immune effects also require evidence from trials.
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Evidence Needed for Treatment Choices
The next step for the field is to determine whether inflammation markers can identify patients who benefit from a specific intervention, rather than simply describe risk. That requires clinical trials measuring patient outcomes and harms, not only changes in hsCRP or other laboratory values. The report did not identify a new trial milestone or a confirmed replacement treatment following the ziltivekimab setbacks.
For now, Fudim said he uses hsCRP as a way to discuss risk and motivate attention to exercise, weight loss, and associated conditions such as chronic kidney disease. These comments are not evidence that any one measure will reduce inflammation or improve heart failure outcomes for every patient. Treatment decisions remain a matter for patients and their qualified clinicians, based on individual circumstances and established care.
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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 prevalence and did not test a treatment.
Does elevated hsCRP mean someone has heart failure?
No. The analysis examined hsCRP among people already in heart failure groups. It does not establish hsCRP as a stand-alone diagnostic test for heart failure.
Is there a proven anti-inflammatory drug for heart failure?
The report says there is no dedicated, established treatment for heart failure inflammation. Two trials of the IL-6 inhibitor ziltivekimab were stopped early for futility, according to Novo Nordisk’s September announcement.
What factors were linked to inflammation in the report?
Fudim identified obesity, diabetes, and chronic kidney disease as key comorbidities associated with inflammatory risk. The analysis also reported higher insulin and diuretic use among participants with elevated hsCRP, but does not show those treatments caused the marker elevation.
What should patients do with this information?
The registry findings do not prescribe a treatment. Fudim described exercise, weight management, and attention to associated conditions as discussion points; patients should speak with a qualified clinician about decisions suited to their health and existing care.
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