CV inflammation, driven by IL-6, is the common thread across multiple CVDs^1-5,7

Regardless of LDL-C levels, ~2.7x increased risk of CV death for patients with or high risk of ASCVD and CV inflammation, compared to those without^16*

~2 in 5 patients with ASCVD+CKD, or heart failure have CV inflammation despite SoC^24,25†

Patients with ≥2 mg/L have increased CV risk as per AHA/ACC and ESC/EAS guidelines^9,10

What is CV inflammation?

Cardiovascular (CV) inflammation is an inflammatory process that occurs within the blood vessels and heart tissue, primarily driven by the cytokine interleukin-6 (IL-6).^1-7

Through its actions, CV inflammation drives disease development and progression across multiple cardiovascular diseases (CVDs), leading to worse outcomes for patients.^11,12

The actions of CV inflammation extend beyond individual disease categories, opening new opportunities in clinical care.^1-5,7

ATHEROSCLEROTIC CARDIOVASCULAR DISEASE (ASCVD)

CV inflammation increases blood vessel permeability, allowing immune cells and cholesterol into the artery walls which can accelerate plaque buildup. CV inflammation then increases risk of plaque rupture, potentially causing a heart attack.^13-15

HEART ATTACK (MYOCARDIAL INFACTION)

In patients with CV inflammation, heart attacks may cause more tissue damage and have worse associated outcomes. Following a heart attack patients with continually high CV inflammation face increased risk of recurrent events.^1,4,11

INCREASED RISK OF CV EVENTS

In heart failure, CV inflammation accelerates damage to the heart by promoting the influx of immune cells and collagen, promoting ventricular stiffening, tissue scarring (fibrosis) and remodeling, with elevated levels directly linked to increased mortality.^1,4,7

CV inflammation can be identified when the biomarker high-sensitivity C-reactive protein (hsCRP) is measured to be ≥2 mg/L.^12,16

At a glance

CV inflammation is driven by the cytokine IL-6¹¹
CV inflammation is a key driver of multiple cardiovascular diseases¹¹
CV inflammation is detected when hsCRP ≥2 mg/L^16,17

What are the risks of CV inflammation?

How widespread is CV inflammation?

How is CV inflammation measured using hsCRP?

Footnotes
^*A collaborative analysis of 31,245 statin-treated patients who had or were at high risk of atherosclerotic disease from across the PROMINENT²¹ (n=9,988), REDUCE-IT²² (n=8,179), and STRENGTH²³ (n=13,078) trials found that residual inflammatory risk was significantly associated with CV death (highest hsCRP quartile [>4.2–>4.8 mg/L] versus lowest [<1.1–<1.2 mg/L], adjusted HR 2.68, 95% CI 2.22–3.23; p<0.0001).¹⁶

^†As measured by hsCRP >2 mg/L inpatients with ASCVD+CKD, or heart failure. The POSEIDON study was a global real-world evidence prevalence study which included 18,904 patients from 18 countries. It included patients with ASCVD with and without comorbid CKD, and patients with heart failure.^24,25

Abbreviations
ACC=American College of Cardiology; AHA=American Heart Association; ASCVD=atherosclerotic cardiovascular disease; CI=confidence interval; CV=cardiovascular; CKD=chronic kidney disease; CVD=cardiovascular disease; HR=hazard ratio; hsCRP=high-sensitivity C-reactive protein; IL-6=interleukin-6; LDL-C= low-density lipoprotein cholesterol; MACE=major adverse cardiovascular events; SoC=standard of care.

1. Feng Yet al. Front Cardiovasc Med2022; 9:818890. 2. Mehta N et al.Curr Atheroscler Rep 2024; 27(1):12. 3. Katkenov N et al. J Cardiovasc Dev Dis 2024; 11(7):206.  4. Su J etal. Front Pharmacol 2021; 12:745061. 5. Knopp T et al. EurHeart J Open 2024; 4(4):oeae046. 6. Pergola Pet al. Clin J Am Soc Nephrol. 2026.doi:10.2215/CJN.0000001054. 7. Kurt B et al. CurrHeart Fail Rep2025; 22:35. 8. Ridker P et al. Lancet 2023; 401(10384):1293–1301. 9. Mach F et al. Eur Heart J 2025;46(42):4359–4378. 10. Blumenthal R et al. JACC 2026;87(19):2624–2757. 11. Preda A et al. Eur J Clin Invest. 2026;56:e70161. 12. Mensah G et al.J Am Coll Cardiol2025;87:1381–1404. 13. Alfaddagh A et al. AmJ Prev Cardiol 2020; 4:100130. 14. Henein M et al. Int J MolSci 2022; 23(21):12906. 15. Libby P.Am J Clin Nutr 2006; 83(2):456S–460S. 16. Ridker P et al. Lancet 2023; 401(10384):1293–1301. 17. Ridker P. J Am Coll Cardiol 2018; 72:3320–3333. 18. Mazhar F et al. Eur Heart J. 2024; 45(44):4719–4730. 19. Ridker P, etal. Eur Heart J. 2022; 43(46):4832–4844. 20. Mazhar F et al. EurHeart J Open 2026; oeag023. 21. Pradhan A etal. NEngJ Med 2022;387(21):1923–1934. 22. Bhatt D et al. N Engl J Med 2019;380(1):11–12. 23. Nicholls S et al. JAMA 2020;324(22):2268–2280. 24. Lam C et al. Eur Heart J 2026. https://doi.org/10.1093/ejhf/xuag155 25. Navar A et al. Atherosclerosis 2026.

CV inflammation, driven by IL-6, is the common thread across multiple CVDs1-5,7

Regardless of LDL-C levels, ~2.7x increased risk of CV death for patients with or high risk of ASCVD and CV inflammation, compared to those without16*

~2 in 5 patients with ASCVD+CKD, or heart failure have CV inflammation despite SoC24,25†

Patients with ≥2 mg/L have increased CV risk as per AHA/ACC and ESC/EAS guidelines9,10