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A U.S. analysis from the POSEIDON registry found high-sensitivity C-reactive protein (hsCRP) levels of at least 2 mg/L in about half of participants with heart failure, more than in the registry’s overall international heart failure groups. The findings point to substantial inflammatory burden, but speakers at the Heart Failure Society of America meeting said there is no dedicated treatment established for heart failure inflammation, and recent drug-trial results have been disappointing.
A subanalysis of the POSEIDON registry found that about half of U.S. participants with heart failure had elevated hsCRP, a marker of inflammation, highlighting a treatment gap as recent trials of targeted anti-inflammatory drugs have faltered. The findings were presented by Duke University’s Marat Fudim at the Heart Failure Society of America annual conference in Phoenix.
Among U.S. participants, hsCRP of at least 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 registry’s participants across 18 countries, the corresponding proportions were 38.8%, 38.1%, and 38.2%.
POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease, heart failure, or both during routine care from 2023 through 2025. The U.S. heart failure analysis included 315 people with HFpEF, 94 with HFmrEF, and 392 with HFrEF. It was a cross-sectional analysis, so it describes the prevalence of elevated hsCRP rather than showing that inflammation caused particular outcomes.
Fudim said the analysis found residual inflammatory risk despite guideline-directed heart failure treatment. Elevated hsCRP was associated with higher IL-6 and NT-proBNP across all three heart failure groups. Participants with high hsCRP also appeared to have higher insulin and diuretic use, though the presentation did not establish those factors as causes of inflammation.
Inflammation Outpaces Available Treatments
The results underline a clinical problem: inflammation is common in the U.S. heart failure participants studied, but identifying it does not by itself provide a proven inflammation-targeting treatment. Fudim described hsCRP as a practical way to identify residual risk and said he uses the measurement to inform risk discussions with patients.
He pointed to lifestyle measures, exercise, weight-loss therapy, and management of conditions such as chronic kidney disease as ways to address risk factors. Those comments do not establish that these approaches will reduce heart failure events by lowering hsCRP in this registry population. The study also does not test whether acting on the biomarker changes outcomes.
The difference between the U.S. and overall registry proportions may help focus future research, but the figures are descriptive. The analysis does not explain why the U.S. rates were higher, or show that the result applies to every U.S. heart failure population.
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Recent Trials Complicate Targeted Therapy
The presentation comes amid setbacks for drugs aimed at specific inflammatory pathways. In September, Novo Nordisk announced that two placebo-controlled trials of the IL-6 inhibitor ziltivekimab in heart failure patients with high hsCRP—HERMES and ATHENA—had been stopped early for futility. The trials were designed to assess both clinical outcomes and other measures.
Before those decisions, ziltivekimab had also failed to reduce major adverse cardiovascular events in the ZEUS trial, which studied people with atherosclerotic cardiovascular disease, chronic kidney disease, and inflammation. These results do not settle whether other anti-inflammatory approaches could help people with heart failure, but they add to a history of neutral or negative trials targeting particular inflammatory pathways.
At the conference, discussant Amanda Vest of Cleveland Clinic described the field as difficult to interpret: observational evidence links inflammation with risk, while intervention trials have been disappointing. Fudim suggested that approaches affecting multiple pathways, including GLP-1 drugs, may merit attention, while cautioning against excessive interference with the immune system. That was a research perspective, not evidence from the POSEIDON analysis that such drugs treat heart failure inflammation.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, Duke University Medical Center
What the Registry Cannot Establish
The analysis does not show that elevated hsCRP causes worse heart failure outcomes, nor does it test whether lowering hsCRP improves survival or symptoms. Its cross-sectional design captures measurements at a point in time, and the reported U.S. groups were relatively small, particularly the 94-person HFmrEF cohort.
It is also unclear why the proportion with elevated hsCRP was higher in the U.S. participants than in the registry overall. Fudim cited obesity, diabetes, and chronic kidney disease as key drivers of inflammation, but the analysis did not establish that these conditions account for the difference. The presentation also offered no evidence that any particular treatment reduces heart failure risk by targeting inflammation.
Further Trials Must Test Strategies
The POSEIDON findings provide a prevalence snapshot; they do not set out a treatment plan or a next clinical milestone. The next evidence needed is from studies that test whether an intervention aimed at inflammation improves meaningful outcomes for heart failure patients, while tracking potential harms from immune suppression.
For now, Fudim described hsCRP as a tool for risk assessment and discussion, alongside attention to lifestyle and associated conditions. The status of future inflammation-targeting trials and whether broader approaches will prove beneficial remain open questions.
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 reported prevalence; it did not test treatment effects.
What is hsCRP?
High-sensitivity C-reactive protein is a blood marker used to measure inflammation. In this report, a level of 2 mg/L or higher counted as elevated.
Does the study show that inflammation causes heart failure?
No. The registry analysis describes how often elevated hsCRP appeared among participants with heart failure. It does not establish that inflammation caused heart failure or worsened outcomes.
Is there a dedicated anti-inflammatory treatment for heart failure?
Fudim said there is no dedicated treatment established for heart failure inflammation. Two ziltivekimab heart failure trials were stopped early for futility, and the registry analysis did not evaluate any therapy.
Why were U.S. rates higher than the overall registry rates?
The analysis did not determine the reason. Fudim cited obesity, diabetes, and chronic kidney disease as important inflammation-related conditions, but the reported results do not show that they explain the U.S.–international difference.
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