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

Why does CV inflammation matter?

Cardiovascular (CV) inflammation quietly drives disease progression, leading to significantly worse patient outcomes.^8,16

HEALTH RISKS

In patients with heart failure, CV inflammation is associated with a more than two-fold increased risk of CV death and heart failure hospitalisation, compared to those without CV inflammation.^10†

In patients with prior myocardial infarction (MI), those with CV inflammation, compared to those without, carry a 44% increased risk of CV death.^9*

Even when traditional risk factors are controlled, CV inflammation continues to drive worse outcomes^8,16

Regardless of low-density lipoprotein cholesterol (LDL-C) levels, there is a ~2.7x increased risk of CV death for patients with CV inflammation, compared to those without, in individuals with or at high risk of atherosclerotic cardiovascular disease (ASCVD).^7‡

CV inflammation is an independent risk factor

CV inflammation is an independent risk factor, meaning its actions alone can drive development and progression of cardiovascular disease (CVD).¹¹

Among individuals with known cardiovascular disease both treated and untreated with statins, hsCRP is at least as powerful a predictor of events as that of LDL cholesterol

Inflammation and Cardiovascular Disease: 2025 American College of Cardiology (ACC) 2025 Scientific Statement ¹¹

Addressing this inflammatory risk is one of the most critical frontiers in modern cardiology.¹¹

At a glance

CV inflammation is an independent risk factor across CVDs^7,11
Elevated CV inflammation leads to worse outcomes for patients^8,16
This risk is present in patients even when traditional risk factors are Managed⁷

What is CV inflammation?

How widespread is CV inflammation?

How is CV inflammation measured using hsCRP?

Footnotes 
*A healthcare-based study of 17,464 patients with a median hsCRP level of 2.2 (interquartile range, 1.0-6.0 mg/L) and a median of 2.2 (interquartile range, 0.8-4.9 mg/L) years since their MI. Adjusted for age, sex, time since MI, haemoglobin, eGFR, undertaken procedures, and ongoing medications. Compared with hsCRP <2 mg/L, patients with hsCRP ≥2 mg/L had a higher risk of MACE (n=3,900, adjusted HR 1.28, 95% CI, 1.18–1.38), all-cause death (n=4,138, 1.42, 1.31–1.53), and CV death (n=2,343, 1.44, 1.29–1.60).⁹
†A post hoc biomarker substudy of the TOPCAT study including 232 patients with heart failure with preserved ejection fraction (HFpEF). Compared with hsCRP <2 mg/L, patients with hsCRP ≥2 mg/L had a higher risk of cardiovascular death or heart failure hospitalisation (adjusted HR 2.36, 95% CI, 1.27–4.38; p=0.006). Adjusted for age, sex, body mass index, comorbidities, heart failure severity, and relevant clinical characteristics.¹⁰
‡A collaborative analysis of 31,245 statin-treated patients who had or were at high risk of atherosclerotic disease from across the PROMINENT12 (n=9,988), REDUCE-IT13 (n=8,179), and STRENGTH14 (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).⁷

Abbreviations
ACC=American College of Cardiology; AHA=American Heart Association; ASCVD=atherosclerotic cardiovascular disease; CHD= coronary heart disease; CI=confidence interval; CKD=chronic kidney disease; CV=cardiovascular; CVDs=cardiovascular diseases; eGFR=estmi ated glomerular filtration rate; HF=heart failure; HR=hazard ratio; hsCRP=high-sensitivity C-reactive protein; IL-6=interleukin-6;LDL=low-density lipoprotein; LVEF=left ventricular ejection fraction; MACE=major adverse cardiovascular events; MI=myocardial infarction; sHR=subdistribution hazard ratio; SMuRF=standard modifiable risk factor.

1. Feng Yet al. Front Cardiovasc Med 2022; 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. SuJ et al. Front Pharmacol 2021; 12:745061. 5. Knopp T et al. EurHeart J Open 2024; 4(4):oeae046. 6. Kurt B et al. CurrHeart Fail Rep2025; 22:35. 7. Ridker P et al. Lancet 2023; 401(10384):1293–1301. 8. Mazhar F et al. EurHeart J 2024; 45(44): 4719–4730. 9. Carrero J et al. J Am HeartAssoc 2019; 8:e012638. 10. Ferreira J et al. Int J Cardiol 2024; 395:132–139. 11. Mensah Get al. 2025;S0735-1097(25)07555-2. 12. Pradhan A et al. NEngJ Med 2022;387(21):1923–1934. 13. Bhatt D et al. N Engl J Med 2019;380(1):11–12. 14. Nicholls S et al. JAMA 2020;324(22):2268–2280. 15. Markousis-Mavrogenis G et al. Eur Heart J 2019; 21: 965–973. 16. Ridker P. JACC 2018;72(25):3320-3331. 17. Lam C et al. Eur Heart J 2026. https://doi.org/10.1093/ejhf/xuag155 18. 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