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NewsInflammation is rampant in U.S. heart failure patients, with roughly half showing elevated hsCRP levels — well above global averages. Despite the clear burden, anti-inflammatory drug development has largely flopped, including two recently halted Novo Nordisk trials. Experts say a broader, multi-pathway approach may be the way forward.
About half of U.S. heart failure (HF) patients have elevated levels of high-sensitivity C-reactive protein (hsCRP), a key marker of cardiovascular inflammation, according to a new subanalysis of the POSEIDON registry — the largest global study of inflammation in patients with atherosclerotic cardiovascular disease or HF. That's significantly higher than the global average of roughly 38% across 18 countries, with obesity, diabetes, and chronic kidney disease identified as the main drivers.
The troubling part? Inflammation persisted even in patients receiving guideline-directed medical therapy, and the drug pipeline to address it has hit a wall. Novo Nordisk recently halted two trials of its IL-6 inhibitor ziltivekimab (HERMES and ATHENA) early for futility — following a prior failure in the ZEUS trial. Experts at the Heart Failure Society of America conference described the field as "a bit tricky to navigate."
By the Numbers:
Why it matters: With no dedicated anti-inflammatory therapy approved for HF, clinicians are left using hsCRP as a risk-stratification and patient motivation tool. Researchers are now eyeing broader approaches — like GLP-1 drugs that reduce inflammation across multiple pathways — as the next frontier.
