TL;DR
Get health and wellness essentials delivered free with Prime
- Fast, free delivery on millions of items
- Prime Video, Amazon Music and more included
- Member-only deals all year
A POSEIDON registry analysis presented at the Heart Failure Society of America conference found high-sensitivity C-reactive protein (hsCRP) at or above 2 mg/L in about half of U.S. participants with heart failure, across three ejection-fraction groups. The findings identify a substantial burden of inflammation, but do not show that lowering hsCRP improves outcomes; recent trials of the IL-6 inhibitor ziltivekimab were stopped early for futility.
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, while no dedicated inflammation-targeting treatment has been established for the condition. The findings were presented by Duke University cardiologist Marat Fudim at the Heart Failure Society of America annual conference; they describe how common the marker was, not whether treating it would improve patients’ health.
Among U.S. participants, hsCRP of 2 mg/L or higher 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 overall POSEIDON heart failure groups across 18 countries, the corresponding proportions were 38.8%, 38.1%, and 38.2%. These figures compare the reported U.S. and global registry groups; the analysis does not establish why their rates differed.
POSEIDON prospectively enrolled 18,904 adults with atherosclerotic cardiovascular disease, heart failure, or both during routine care from 2023 to 2025. The U.S. heart failure analysis included 315 people with HFpEF, 94 with HFmrEF, and 392 with HFrEF. The report describes a cross-sectional subanalysis, so it measures inflammation at a point in the registry rather than testing a treatment or proving cause and effect.
Fudim said elevated hsCRP was associated with higher levels of interleukin-6 (IL-6) and NT-proBNP across all three heart failure groups. He also said inflammation remained present despite guideline-directed medical therapy. In the high-hsCRP groups, insulin and diuretic use appeared more common, but the presentation did not identify these medicines as causes of inflammation.
Inflammation Without a Proven Targeted Therapy
The results point to a sizeable group of U.S. heart failure patients with elevated inflammation markers, including people receiving usual guideline-directed treatment. That may help clinicians and researchers identify residual inflammatory risk, but a marker’s prevalence does not show that reducing it will prevent hospitalization, cardiovascular events, or death.
Fudim described obesity, diabetes, and chronic kidney disease as key factors that can contribute to inflammation in these patients. He said lifestyle measures, exercise, weight-loss therapy, and attention to risk factors such as kidney disease are part of his approach, and that he uses hsCRP to inform risk discussions. These comments describe his clinical perspective; the registry analysis did not test the effectiveness of those approaches.
The treatment question remains unsettled. Fudim said there is no dedicated heart failure treatment for inflammation, and recent trial setbacks underscore the gap between an observed inflammatory burden and evidence that targeting a specific pathway helps patients.
As an affiliate, we earn on qualifying purchases.
Registry Findings and Trial Setbacks
POSEIDON is described as the largest global registry focused on inflammation in people with atherosclerotic cardiovascular disease or heart failure. The analysis reported at the conference compared the U.S. heart failure subset with the registry’s international heart failure groups. Because participants were recruited in routine care and the analysis was cross-sectional, it provides a snapshot of hsCRP levels rather than a randomized comparison of treatments.
The report also noted a recent setback in drug development. In September, Novo Nordisk announced that two placebo-controlled trials of ziltivekimab, an IL-6 inhibitor, had been stopped early for futility. HERMES and ATHENA were designed to assess clinical and other endpoints in heart failure patients with high hsCRP. Before those stoppages, 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.
Session discussant Amanda Vest of Cleveland Clinic said studies targeting individual inflammatory pathways in heart failure have often produced neutral or negative results. Fudim suggested that approaches acting across multiple pathways, including GLP-1 drugs, may merit consideration, while cautioning against excessive interference with immune function. These were expert views, not findings from a treatment comparison in POSEIDON.
“We are very inflamed as a nation of HF patients.”
— Marat Fudim, MD, MHS, Duke University Medical Center
heart failure inflammation supplement
As an affiliate, we earn on qualifying purchases.
As an affiliate, we earn on qualifying purchases.
What the Registry Cannot Establish
The analysis does not show whether high hsCRP itself worsens heart failure, whether lowering the marker changes outcomes, or why the U.S. proportions were higher than the overall international figures. It also does not establish whether the differences between HFpEF, HFmrEF, and HFrEF are meaningful beyond the observed percentages.
The U.S. subgroups were modest in size, particularly the 94-person HFmrEF group, and the report is a registry subanalysis rather than a controlled clinical trial. It does not provide evidence that a specific anti-inflammatory medicine, GLP-1 drug, lifestyle intervention, or biomarker-guided strategy improves heart failure outcomes. The long-term implications of the hsCRP findings and the next direction for drug development remain unclear.
anti-inflammatory omega-3 capsules
As an affiliate, we earn on qualifying purchases.
As an affiliate, we earn on qualifying purchases.
Further Evidence Needed on Treatment
The reported results establish a snapshot of hsCRP prevalence in the U.S. registry groups; the conference report does not specify a follow-up analysis or a new trial arising from them. The immediate next step for the treatment question is further clinical evidence showing whether an intervention can improve meaningful outcomes in heart failure patients with elevated inflammation, rather than only changing a biomarker.
HERMES and ATHENA, the ziltivekimab trials, were stopped early for futility, and no replacement treatment or new trial plan is identified in the report. Researchers and clinicians will need to weigh future trial results against the concern, raised by Fudim, that suppressing immune pathways too broadly could carry risks. Until such evidence is available, the findings support recognizing the prevalence of elevated hsCRP, not assuming that a particular anti-inflammatory therapy is effective.
As an affiliate, we earn on qualifying purchases.
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 prove that inflammation causes heart failure?
No. The report describes an association between elevated hsCRP and other markers, including IL-6 and NT-proBNP. Its cross-sectional design cannot establish that inflammation caused heart failure or determine cause and effect.
Is there a dedicated anti-inflammatory treatment for heart failure?
Fudim said there is no dedicated treatment established for heart failure inflammation. The report also describes ziltivekimab trials that were stopped early for futility; it does not identify a proven replacement therapy.
Why did the U.S. rates differ from the global figures?
The analysis reported higher proportions in the U.S. groups than in the corresponding global groups, but did not establish the reason. Fudim cited factors such as obesity, diabetes, and chronic kidney disease as inflammation drivers, not as a proven explanation for the regional difference.
Source: rss
Cold & flu season Picks
humidifiers
As an affiliate, we earn on qualifying purchases.
