hs-CRP (C-Reactive Protein)

What is High-Sensitivity C-Reactive Protein (hs-CRP)?

High-sensitivity C-reactive protein, commonly called hs-CRP, is a protein produced by your liver in response to inflammation anywhere in your body. We use hs-CRP as a “smoke detector” for inflammation—when inflammation is present, your liver releases more CRP into your bloodstream, and the hs-CRP test can detect even very small increases in this protein.[1] CRP has been known to doctors for decades as a marker of acute inflammation from infections, injuries, or inflammatory diseases. However, the standard CRP test wasn’t sensitive enough to detect the low-grade, chronic inflammation that smolders silently in your blood vessels and contributes to heart disease. The “high-sensitivity” version of the test was developed specifically to measure these much lower levels of CRP that are relevant to cardiovascular risk.[2] When your hs-CRP level is elevated, it indicates that your body is in a state of chronic, low-grade inflammation. This type of inflammation is now recognized as a central driver of atherosclerosis—the buildup of fatty plaques in your arteries that leads to heart attacks and strokes.[3][4]

The Role of Inflammation in Heart Disease

For many years, doctors thought of heart disease just as a “plumbing problem”—cholesterol building up in arteries like grease clogging a pipe. While cholesterol certainly plays a critical role, we now understand that inflammation is equally important in the development and progression of atherosclerosis.[3][5] When LDL cholesterol particles get trapped in your artery walls, they undergo chemical changes (oxidation) that trigger your immune system to respond. Your body sends white blood cells called monocytes to the area, where they transform into macrophages—immune cells that try to “clean up” the oxidized cholesterol by engulfing it. However, these macrophages become overloaded with cholesterol and transform into “foam cells,” which accumulate and form the core of atherosclerotic plaques.[3][5][6] When this happens, your body sets off an inflammatory response. The immune cells in the artery release chemical messengers (called cytokines) that act like alarm signals in your body. Two of the most important are IL-1β and IL-6. IL-6 travels to your liver and tells it to make C-reactive protein (CRP), which is why a high-sensitivity CRP blood test can give you a sense of how much inflammation is going on inside your arteries [6][8] The inflammation doesn’t just help plaques grow—it also makes them unstable and prone to rupture. When a plaque ruptures, it triggers a blood clot that can suddenly block blood flow, causing a heart attack or stroke. This is why inflammation is so dangerous: it’s involved in both the slow buildup of plaques over decades and the sudden events that cause heart attacks.[3][8]

How is hs-CRP Measured?

The hs-CRP test is a simple blood test that can be done at any time—you do not need to fast before the test. Your hs-CRP level remains relatively stable throughout the day and is not affected by recent meals.[9] It’s important to understand the difference between a “regular” CRP test and an hs-CRP test. The regular CRP test is designed to detect the large increases in CRP that occur with acute infections the hs-CRP test is specifically calibrated to accurately measure the much lower levels that are relevant for cardiovascular risk assessment.[2][1] One important consideration: hs-CRP can be temporarily elevated by acute infections, injuries, or other inflammatory conditions. If your hs-CRP comes back very high (above 10 mg/L), it may reflect a recent cold, flu, or other acute illness rather than your baseline cardiovascular risk. In this case, the test should be repeated in when you’re feeling well, and the lower value should be used for risk assessment.[1][9]

Understanding Your hs-CRP Numbers

Interpreting hs-CRP results is straightforward. The relationship between hs-CRP and cardiovascular risk is continuous and linear—meaning that higher levels correspond to progressively higher risk across the entire range of values.[1] We use the following categories for cardiovascular risk assessment:[1][9]

• Less than 1 mg/L: Lower cardiovascular risk—this reflects a low inflammatory state and is the desirable range
• 1 to 3 mg/L: Moderate cardiovascular risk—indicates average inflammatory burden
• Greater than 3 mg/L: Higher cardiovascular risk—indicates elevated inflammation that warrants attention
• Greater than 10 mg/L: May reflect an acute infection or inflammatory condition Approximately 30-50% of adults have hs-CRP levels of 2 mg/L or higher, making elevated inflammation a very common finding.[9] How do we know hs-CRP relates to heart disease? Recent large studies confirm the clinical importance of these thresholds. In a study of nearly 450,000 people without known heart disease, those with hs-CRP levels above 3 mg/L had a 34% higher risk of major cardiovascular events, a 61% higher risk of cardiovascular death, and a 54% higher risk of death from any cause compared to those with hs-CRP below 1 mg/L.[10]

How Does hs-CRP Compare to Other Risk Factors?

One of the most important findings from decades of research is that hs-CRP provides prognostic information about cardiovascular risk that is comparable to—and independent of—traditional risk factors like blood pressure and cholesterol.[1][9]

Residual Inflammatory Risk: A Critical Concept

One of the most important advances in cardiovascular medicine is the recognition that even after optimizing traditional risk factors like LDL cholesterol, many patients remain at elevated risk due to persistent inflammation—a concept called “residual inflammatory risk.”[12][13] A landmark collaborative analysis of over 31,000 patients who were already taking statins found that residual inflammatory risk (measured by hs-CRP) was a stronger predictor of future cardiovascular events, cardiovascular death, and all-cause death than residual cholesterol risk (measured by LDL cholesterol).[12] Specifically, among patients on statin therapy:[12]

• Those with hs-CRP ≥2 mg/L had approximately double the risk of cardiovascular death and all-cause death compared to those with hs-CRP 2 mg/L, regardless of their LDL cholesterol level
• The relationship between hs-CRP and cardiovascular events was much stronger than the relationship between LDL cholesterol and events
• More than half of patients on contemporary statin therapy still had hs-CRP levels of 2 mg/L or higher These findings have profound implications: for patients already taking statins, addressing residual inflammatory risk may be as important as—or even more important than—further lowering LDL cholesterol.[12]

Frequently asked questions

Why is hs-CRP Testing Important?

Testing your hs-CRP provides several important benefits for cardiovascular risk assessment and management: 1. It identifies hidden cardiovascular risk. Many people with elevated hs-CRP have no other obvious risk factors. In fact, elevated hs-CRP predicts heart disease even in people without any traditional modifiable risk factors—a group sometimes called “SMuRF-less but inflamed.” Without measuring hs-CRP, this risk would go undetected.[9] 2. It helps guide treatment decisions. The 2025 American College of Cardiology recommends universal screening of hs-CRP in both primary and secondary prevention because “clinicians will not treat what they do not measure.” Knowing your hs-CRP level helps your doctor decide whether to initiate or intensify preventive therapies.[9] 3. It identifies candidates for anti-inflammatory therapy. For patients with established heart disease and persistently elevated hs-CRP despite statin therapy, specific anti-inflammatory treatments like low-dose colchicine may provide additional cardiovascular protection.[9][18] 4. It can be used to monitor treatment response. Unlike genetic risk factors that don’t change, hs-CRP responds to both lifestyle modifications and medications. Tracking your hs-CRP over time can help assess whether your prevention strategies are working.[9][19] 5. It’s stable and reliable. When measured in stable outpatients (not during acute illness), hs-CRP has long-term stability comparable to LDL cholesterol and blood pressure, making it a reliable biomarker for risk assessment.[10][9]

How Can You Lower Your hs-CRP?

hs-CRP is very responsive to lifestyle changes, unlike some other risk markers, which makes it something you can actively improve. Eating an anti-inflammatory diet, exercising regularly, losing weight if needed, and quitting smoking are the most effective ways to bring hs-CRP down. When lifestyle isn’t enough, medications—especially statins—can also meaningfully lower hs-CRP and reduce cardiovascular risk.

References

1. A Test in Context: High-Sensitivity C-Reactive Protein. Ridker PM. Journal of the American College of Cardiology. 2016;67(6):712-723. doi:10.1016/j.jacc.2015.11.037.
2. CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: Report From the Laboratory Science Discussion Group. Myers GL, Rifai N, Tracy RP, et al. Circulation. 2004;110(25):e545-9. doi:10.1161/01.CIR.0000148980.87579.5E.
3. The Role of Inflammation in Cardiovascular Disease. Henein MY, Vancheri S, Longo G, Vancheri F. International Journal of Molecular Sciences. 2022;23(21):12906. doi:10.3390/ijms232112906.
4. Hegemony of Inflammation in Atherosclerosis and Coronary Artery Disease. Attiq A, Afzal S, Ahmad W, Kandeel M. European Journal of Pharmacology. 2024;966:176338. doi:10.1016/j.ejphar.2024.176338.
5. Targeting the Immune System in Atherosclerosis: JACC State-of-the-Art Review. Zhao TX, Mallat Z. Journal of the American College of Cardiology. 2019;73(13):1691-1706. doi:10.1016/j.jacc.2018.12.083.
6. NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis. Grebe A, Hoss F, Latz E. Circulation Research. 2018;122(12):1722-1740. doi:10.1161/CIRCRESAHA.118.311362.
7. Inflammation, Atherosclerosis, and Coronary Artery Disease. Hansson GK. The New England Journal of Medicine. 2005;352(16):1685-95. doi:10.1056/NEJMra043430.
8. Targeting Inflammation After Acute Myocardial Infarction. Imbesi A, Greco A, Spagnolo M, et al. Journal of the American College of Cardiology. 2025;86(15):1146-1169. doi:10.1016/j.jacc.2025.07.064.
9. Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement: A Report of the American College of Cardiology. Mensah GA, Arnold N, Prabhu SD, Ridker PM, Welty FK. Journal of the American College of Cardiology. 2025;:S0735-1097(25)07555-2. doi:10.1016/j.jacc.2025.08.047.
10. C-Reactive Protein and Cardiovascular Risk in the General Population. Kurt B, Reugels M, Schneider KM, et al. European Heart Journal. 2025;:ehaf937. doi:10.1093/eurheartj/ehaf937.
11. Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events. Ridker PM, Rifai N, Rose L, Buring JE, Cook NR. The New England Journal of Medicine. 2002;347(20):1557-65. doi:10.1056/NEJMoa021993.
12. Inflammation and Cholesterol as Predictors of Cardiovascular Events Among Patients Receiving Statin Therapy: A Collaborative Analysis of Three Randomised Trials. Ridker PM, Bhatt DL, Pradhan AD, et al. Lancet (London, England). 2023;401(10384):1293-1301. doi:10.1016/S0140-6736(23)00215-5.
13. Clinician’s Guide to Reducing Inflammation to Reduce Atherothrombotic Risk: JACC Review Topic of the Week. Ridker PM. Journal of the American College of Cardiology. 2018;72(25):3320-3331. doi:10.1016/j.jacc.2018.06.082.
14. Inflammation, Cholesterol, Lipoprotein(a), and 30-Year Cardiovascular Outcomes in Women. Ridker PM, Moorthy MV, Cook NR, et al. The New England Journal of Medicine. 2024;391(22):2087-2097. doi:10.1056/NEJMoa2405182.
15. Association Between C Reactive Protein and Coronary Heart Disease: Mendelian Randomisation Analysis Based on Individual Participant Data. Wensley F, Gao P, Burgess S, et al. BMJ (Clinical Research Ed.). 2011;342:d548. doi:10.1136/bmj.d548.
16. Genetics: Implications for Prevention and Management of Coronary Artery Disease. Assimes TL, Roberts R. Journal of the American College of Cardiology. 2016;68(25):2797-2818. doi:10.1016/j.jacc.2016.10.039.
17. Relationship of C-Reactive Protein Reduction to Cardiovascular Event Reduction Following Treatment With Canakinumab: A Secondary Analysis From the CANTOS Randomised Controlled Trial. Ridker PM, MacFadyen JG, Everett BM, et al. Lancet (London, England). 2018;391(10118):319-328. doi:10.1016/S0140-6736(17)32814-3.
18. State of the Art: Evaluation and Medical Management of Nonobstructive Coronary Artery Disease in Patients With Chest Pain: A Scientific Statement From the American Heart Association. Slipczuk L, Blankstein R, Bucciarelli-Ducci C, et al. Circulation. 2025;152(23):e443-e466. doi:10.1161/CIR.0000000000001394.
19. The Relation Between Healthy Lifestyle Changes and Decrease in Systemic Inflammation in Patients With Stable Cardiovascular Disease. van ‘t Klooster CC, van der Graaf Y, Ridker PM, et al. Atherosclerosis. 2020;301:37-43. doi:10.1016/j.atherosclerosis.2020.03.022.