Why Lowering Inflammation Markers May Not Prevent Heart

Medically reviewed | Published: | Evidence level: 1A
Novo Nordisk’s inflammation-targeting drug reportedly missed its goal in a heart disease study, illustrating the gap between improving a laboratory marker and preventing cardiovascular events. Previous trials confirm that inflammation contributes to atherosclerosis, but benefits depend on the pathway targeted, patient population, treatment safety and clinical endpoint.
📅 Published:
Reviewed by iMedic Medical Editorial Team
📄 Cardiovascular Health

Quick Facts

CANTOS Enrollment
10,061 patients
RESCUE Stage
Phase 2 trial
Key Biomarker
High-sensitivity CRP

Why Can an Inflammation Drug Lower Biomarkers but Not Prevent Heart Attacks?

Quick answer: A drug can affect an inflammatory pathway without changing enough of the biological processes that ultimately cause heart attacks or strokes.

Atherosclerosis is not simply cholesterol accumulating inside arteries. Immune cells, inflammatory proteins, blood clotting and changes in the vessel wall all contribute to plaque growth and rupture. High-sensitivity C-reactive protein, or hsCRP, can identify increased inflammatory activity, but it is primarily a risk marker rather than proof that a particular drug will prevent cardiovascular events.

Ziltivekimab is a monoclonal antibody designed to inhibit interleukin-6 signaling. In the randomized phase 2 RESCUE trial, it produced substantial reductions in hsCRP and several other inflammatory and clotting-related biomarkers among people with chronic kidney disease and elevated inflammation. However, biomarker improvement must be followed by adequately powered trials measuring outcomes such as myocardial infarction, stroke and cardiovascular death. According to STAT’s report, the newer heart disease study missed its objective; complete peer-reviewed results will be needed to understand why.

What Has Earlier Research Shown About Treating Cardiovascular Inflammation?

Quick answer: Earlier trials show that selected anti-inflammatory therapies can reduce cardiovascular events, although benefits and risks vary considerably between treatments.

The CANTOS trial provided important evidence that inflammation can be therapeutically targeted in atherosclerosis. It enrolled 10,061 people with a previous myocardial infarction and persistently elevated hsCRP. Canakinumab, an antibody targeting interleukin-1 beta, reduced recurrent cardiovascular events at one tested dose without lowering cholesterol, supporting a causal role for inflammation.

CANTOS also identified an increased risk of fatal infection, demonstrating why suppressing inflammation requires careful safety assessment. Trials of low-dose colchicine have provided additional evidence of cardiovascular benefit in selected patients with coronary disease. These findings do not mean that every anti-inflammatory medicine will work: different drugs affect different immune pathways, and excessive immune suppression may outweigh a modest cardiovascular benefit.

How Should Patients Interpret a Negative Cardiovascular Drug Trial?

Quick answer: A negative trial means the tested strategy did not demonstrate its intended benefit under the study conditions, not that inflammation is irrelevant to heart disease.

Clinical trials can fail because a drug does not sufficiently change disease biology, because patients were treated too early or too late, or because adverse effects offset potential benefits. Investigators must also determine whether participants had the specific inflammatory profile most likely to respond and whether background treatments left enough residual risk for an additional therapy to show value.

Patients should not stop statins, blood-pressure medicines, antiplatelet therapy or other prescribed treatments because of this result. Controlling LDL cholesterol, blood pressure, diabetes and tobacco exposure remains central to cardiovascular prevention. Anti-inflammatory treatment is an evolving addition to those measures, not a substitute for therapies with established clinical benefits.

Frequently Asked Questions

Not necessarily. CRP can rise because of infection, injury and many chronic conditions. Cardiovascular decisions require clinical context, and most anti-inflammatory drugs are not routinely prescribed solely because hsCRP is elevated.

No. Nonsteroidal anti-inflammatory drugs such as ibuprofen are not cardiovascular-prevention treatments and can increase cardiovascular, kidney or bleeding risks in some people.

No. CANTOS and colchicine trials support inflammation as a contributor to cardiovascular disease. The reported result instead suggests that success depends on selecting an effective target, an appropriate patient population and a tolerable treatment.

References

  1. STAT. Novo Nordisk inflammation-targeting drug misses mark in heart disease study. August 2026.
  2. Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. New England Journal of Medicine. 2017;377:1119-1131.
  3. Ridker PM, Devalaraja M, Baeres FMM, et al. IL-6 inhibition with ziltivekimab in patients at high atherosclerotic risk (RESCUE): a double-blind, randomised, placebo-controlled, phase 2 trial. The Lancet. 2021;397:2060-2069.
  4. Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in Patients with Chronic Coronary Disease. New England Journal of Medicine. 2020;383:1838-1847.