C-Reactive Protein, High Sensitivity (hs-CRP) Test
The high-sensitivity C-reactive protein (hs-CRP) test measures low concentrations of C-reactive protein in serum to assess chronic, low-grade systemic inflammation. It is used to refine cardiovascular risk stratification alongside lipid measures, with values below 1.0 mg/L indicating low risk and above 3.0 mg/L indicating high risk. Testing must be performed away from acute infection or injury.
1
Biomarkers
Blood (serum)
Sample
1–3 business days
Turnaround
No
Fasting
What is the hs-CRP test?
The hs-CRP Test measures C-reactive protein using a high-sensitivity assay capable of resolving the low concentrations associated with chronic, low-grade vascular inflammation. Because inflammation is integral to atherogenesis, hs-CRP provides an index of inflammatory burden that complements lipid measurements in cardiovascular risk assessment. Within the cardiovascular risk landscape, hs-CRP is the most extensively studied inflammatory marker and is positioned as an adjunct rather than a standalone test. It adds discriminatory value in patients at intermediate risk by conventional calculators, helping to reclassify risk and guide the intensity of preventive therapy. It is interpreted alongside lipid panels, ApoB, and Lp(a), and is distinct from standard CRP, which is used to assess acute or marked inflammation rather than subtle vascular risk. Two measurements at least two weeks apart, taken when the patient is metabolically stable and free of acute illness, are recommended to establish a reliable baseline.
What does the hs-CRP test measure?
C-reactive protein is an acute-phase pentraxin synthesised by hepatocytes in response to interleukin-6 and other pro-inflammatory cytokines. Plasma concentrations can rise more than a thousand-fold within 24–48 hours of an acute inflammatory stimulus, with a circulating half-life of approximately 19 hours. The high-sensitivity assay quantifies CRP at the low concentrations relevant to vascular inflammation, distinguishing values that conventional CRP assays cannot resolve. CRP participates in complement activation and opsonisation as part of innate immune defence.
hs-CRP is a marker of low-grade systemic inflammation used to refine cardiovascular risk stratification beyond conventional lipid assessment. Persistently elevated hs-CRP in otherwise stable patients is associated with increased atherosclerotic cardiovascular risk and can inform decisions on preventive intensity. It is distinct from standard CRP in analytical sensitivity, not in the molecule measured, and must be interpreted away from acute infection or injury to reflect baseline vascular inflammatory burden.
Why is the hs-CRP test ordered?
- Cardiovascular risk refinement in patients at intermediate risk by conventional calculators, where hs-CRP may reclassify risk and adjust preventive intensity
- Assessment of residual inflammatory risk in patients with controlled LDL cholesterol who remain at elevated cardiovascular risk
- Guiding statin and preventive therapy decisions where inflammatory burden is being weighed alongside lipid status
- Serial monitoring of vascular inflammatory burden in patients with established atherosclerotic disease under a prevention programme
- Evaluation of patients with a strong family history of premature coronary disease where conventional risk markers are inconclusive
- Comprehensive cardiometabolic and functional medicine panels assessing systemic inflammation alongside lipids, ApoB, and Lp(a)
- Investigation of unexplained low-grade systemic inflammation as part of a broader cardiovascular and metabolic workup, once acute causes are excluded
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
1–3 business days
Collection notes
Defer testing during acute infection, after recent trauma or surgery, or during a flare of inflammatory disease. Two measurements at least two weeks apart, taken when the patient is metabolically stable, are recommended to establish a baseline.
Specimen requirements
Minimum 0.5 mL serum. Separate serum from cells per LabCorp protocol. Specimen stable refrigerated; follow LabCorp transport guidelines.
What can affect hs-CRP results?
Any acute inflammatory stimulus raises CRP markedly, overwhelming the subtle vascular signal. Measurement during or shortly after infection does not reflect baseline cardiovascular risk and should be deferred.
Tissue damage triggers an acute-phase response that elevates CRP for days to weeks, confounding interpretation of baseline vascular inflammation.
Adipose tissue secretes interleukin-6, driving chronically higher hepatic CRP production. Elevated hs-CRP in obesity may reflect adiposity-related inflammation rather than vascular risk alone.
Oral oestrogens increase hepatic CRP synthesis independent of vascular inflammation, raising hs-CRP without a corresponding change in cardiovascular risk.
Statins lower hs-CRP independent of their lipid effect, and anti-inflammatory agents reduce CRP production. Treatment status should be documented when interpreting serial values.
Conditions such as rheumatoid arthritis or inflammatory bowel disease raise baseline CRP substantially, limiting the cardiovascular interpretability of hs-CRP in affected patients.
What do hs-CRP results mean?
Elevated
Values above 3.0 mg/L indicate higher cardiovascular risk when acute and chronic inflammatory causes are excluded. Markedly elevated values (>10 mg/L) usually reflect an acute-phase response from infection, injury, or active inflammatory disease rather than vascular risk, and the test should be repeated once the patient is stable.
Normal
Values of 1.0–3.0 mg/L represent average cardiovascular risk. Results are most meaningful as part of global risk assessment alongside lipids and clinical risk factors rather than in isolation.
Reduced
Values below 1.0 mg/L indicate low inflammatory cardiovascular risk. There is no clinically adverse low value for hs-CRP; lower results are favourable in the cardiovascular context.
Note: hs-CRP must be measured when the patient is free of acute illness; values above 10 mg/L should prompt deferral and repeat testing rather than cardiovascular interpretation. Two measurements at least two weeks apart establish a more reliable baseline. hs-CRP is non-specific and reflects total inflammatory burden, not a vascular-specific signal.
Frequently asked questions
hs-CRP and standard CRP measure the same protein but with different analytical sensitivity. The high-sensitivity assay resolves the low concentrations relevant to cardiovascular risk, whereas standard CRP is used to assess acute or marked inflammation.
How to access the hs-CRP test
The hs-CRP reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: June 2, 2026
Last reviewed: June 2, 2026
- Ridker PM, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. (2000)
- Ridker PM, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (JUPITER). N Engl J Med. (2008)
- Pearson TA, et al. Markers of inflammation and cardiovascular disease: AHA/CDC Scientific Statement. Circulation. (2003)
- Ridker PM, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease (CANTOS). N Engl J Med. (2017)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.
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