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 annual conference found hsCRP levels of at least 2 mg/L in roughly 45% to 51% of U.S. participants across three heart failure types. The findings point to a substantial inflammation burden, but they do not show that treating inflammation improves heart failure outcomes; two ziltivekimab trials were stopped early for futility.
A U.S. subanalysis of the POSEIDON registry found elevated high-sensitivity C-reactive protein (hsCRP) in about half of participants with heart failure, highlighting a common marker of inflammation as researchers continue to face setbacks developing targeted treatments. The results, presented by Marat Fudim of Duke University at the Heart Failure Society of America annual conference, describe how often the marker was elevated; they do not establish that reducing it will improve patients’ outcomes.
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). Across the full POSEIDON study, which included participants in 18 countries, the corresponding shares were lower: 38.8%, 38.1% and 38.2%, respectively. These figures describe the study groups, not all U.S. patients with heart failure.
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 analysis was cross-sectional, so it reports the prevalence of elevated hsCRP rather than whether inflammation caused later health outcomes. Elevated hsCRP was associated with higher interleukin-6 (IL-6) and NT-proBNP across all three heart failure groups.
Fudim said inflammation risk persisted despite use of guideline-directed heart failure medicines. He identified obesity, diabetes and chronic kidney disease as important contributors, and said people with higher hsCRP also appeared to have greater insulin and diuretic use. Those observations do not show that any one condition or treatment caused the elevated marker.
Inflammation Is Common, Treatment Is Unsettled
The results point to a sizeable group of heart failure patients with elevated hsCRP, a blood marker that can help identify inflammation. Fudim described it as a practical way to identify residual inflammatory risk and inform discussions with patients. The difference between U.S. and global registry percentages also gives clinicians and researchers a reason to examine how patient characteristics and care patterns vary across populations.
But prevalence is not proof that a treatment aimed at inflammation will help. That gap matters because the report describes a high burden of a measurable risk marker alongside limited evidence for a dedicated anti-inflammatory medicine for heart failure. Any future treatment would also need to balance potential benefits against the risks of interfering with immune activity, a concern Fudim raised during the discussion.
As an affiliate, we earn on qualifying purchases.
Recent Trials Temper Treatment Hopes
At the conference, Fudim said that lifestyle measures, exercise, weight-loss treatment and attention to conditions such as chronic kidney disease can form part of efforts to address patients’ risk factors. He presented hsCRP as a tool to help inform that care, not as a treatment target with proven heart failure benefits. The registry findings alone cannot determine which interventions lower inflammation or whether lowering hsCRP changes outcomes.
The treatment outlook has been clouded by setbacks for ziltivekimab, an IL-6 inhibitor. Novo Nordisk announced in September that its placebo-controlled HERMES and ATHENA trials in heart failure patients with high hsCRP had been stopped early for futility. Before that, 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. These results concern specific trials and do not settle whether other approaches to inflammation could work.
Session discussant Amanda Vest of Cleveland Clinic noted a history of neutral or negative studies testing drugs aimed at particular inflammatory pathways in heart failure. Fudim suggested broader approaches that affect multiple pathways, mentioning GLP-1 drugs as an example. That was a view about possible research direction, not evidence from the POSEIDON analysis that such medicines treat heart failure inflammation.
““We are very inflamed as a nation of HF patients.””
— Marat Fudim, Duke University Medical Center
heart failure inflammation monitoring device
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 elevated hsCRP predicts individual patients’ outcomes, whether inflammation itself drives those outcomes, or whether lowering the marker would reduce heart failure events or deaths. It is a cross-sectional subanalysis, and the U.S. groups—particularly the HFmrEF group of 94 people—are subsets of a larger registry rather than a census of U.S. patients.
The reasons for the higher percentages in the U.S. subgroup are also unclear. Fudim pointed to obesity, diabetes and chronic kidney disease as key drivers, but the reported data do not prove those factors explain the difference. It remains unsettled whether medicines acting on several inflammatory pathways can improve heart failure outcomes, and how to weigh any benefit against effects on the immune system.
anti-inflammatory supplements for heart health
As an affiliate, we earn on qualifying purchases.
As an affiliate, we earn on qualifying purchases.
Further Trials Must Show Benefit
The immediate next step for researchers is to determine whether the registry pattern holds in other populations and whether hsCRP can help identify people who benefit from a particular intervention. The POSEIDON findings themselves do not announce a new treatment or a planned clinical trial. The early stops of HERMES and ATHENA leave their planned assessments of heart failure outcomes incomplete.
Future studies would need to test treatments against clinical outcomes, not rely only on a change in inflammation markers. Until such evidence is available, Fudim’s suggestions about lifestyle, risk-factor management and broader pathway approaches remain clinical perspectives rather than proof that a specific anti-inflammatory strategy improves heart failure.
As an affiliate, we earn on qualifying purchases.
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 measured prevalence; it did not test a treatment.
Does elevated hsCRP mean inflammation caused a patient’s heart failure?
No. The registry analysis shows that the marker was elevated in many participants, but it does not establish the cause of their heart failure or show that hsCRP itself caused worse outcomes.
Is there a proven anti-inflammatory drug for heart failure in this report?
No dedicated anti-inflammatory treatment was established by the findings. The report also notes that two ziltivekimab heart failure trials were stopped early for futility; that result does not determine whether every other treatment approach will fail.
Why did researchers stop the ziltivekimab trials?
Novo Nordisk announced in September that the HERMES and ATHENA trials were stopped early for futility. The supplied report does not give further details on the trials’ full results or explain which endpoints drove that decision.
Source: rss
Halloween Picks
halloween
As an affiliate, we earn on qualifying purchases.
