hs-CRP
Blood test · no fasting needed
Also known as: High-sensitivity C-reactive protein, hsCRP
- Low relative risk Below 1 mg/L
- Average relative risk 1 to 3 mg/L
- High relative risk Above 3 mg/L
Above 10 mg/L, the test is repeated in about two weeks and a source of infection or other inflammation is looked for (AHA/CDC scientific statement, 2003).
A level of 2 mg/L or higher on more than one test counts as a factor that raises heart risk (ACC/AHA dyslipidemia guideline, 2026).
Units and reference ranges differ between labs.
Cutoffs: AHA/CDC scientific statement, 2003
hs-CRP measures C-reactive protein, a protein the liver makes when there is inflammation anywhere in the body. The high-sensitivity test reads the low levels found in healthy people, where CRP carries information about future heart attack and stroke. It needs no fasting.
What it tells you
- CRP rises steeply with infection, injury and inflammatory disease. The high-sensitivity test is built to measure the much smaller differences between healthy people.
- The three risk groups come from splitting adults into thirds. People in the top third have about twice the relative risk of heart disease of people in the bottom third.
- The groups are meant for the average of two tests, taken about two weeks apart while you are well.
- Higher CRP goes with more heart attacks and strokes. But genetic studies show CRP itself does not cause heart disease. It is a marker of risk, not a target.
- The 2003 statement suggests testing mainly for people at intermediate heart risk, at the physician's discretion. It advises against screening every adult.
What can throw it off
- A cold, infection, injury or flare of an inflammatory illness raises it, often above 10 mg/L. Testing waits until it has settled.
- Ongoing inflammation, such as gum disease, bronchitis or rheumatoid arthritis, raises it.
- Extra body weight, diabetes, high blood pressure, smoking, low HDL and high triglycerides raise it. Weight loss lowers it.
- Regular exercise and moderate alcohol go with lower levels.
- Statins and some other cholesterol medicines lower it. Estrogen or progestogen hormones raise it. Incretin drugs, such as tirzepatide, lower it in trials.
- Fasting and time of day make no difference.
- It varies from test to test about as much as cholesterol does, which is why two results are averaged.
- A standard CRP test cannot read the low range. The heart-risk groups need the high-sensitivity test, reported in mg/L.
Evidence
Predicting heart disease and stroke
Across 54 studies of over 160,000 people, a threefold higher CRP went with about 1.4 times the risk of heart disease. That was after other risk factors were counted. It predicted deaths from other causes about as well. Genetic studies in about 194,000 people found that lifelong higher CRP did not raise heart risk.
Adding to a heart-risk score
In 52 studies of about 247,000 people, adding CRP to a standard risk score improved prediction only slightly. Screening 400 to 500 people at intermediate risk would prevent about one extra heart event over 10 years.
Choosing who gets a statin
A trial enrolled 17,802 people with LDL cholesterol below 130 mg/dL and hs-CRP of 2 mg/L or more. A statin cut heart attacks, strokes and related events by about 44%. The trial had no low-CRP group. It shows statins work in these people, not that CRP is the best way to choose them.
Limits
- It is not specific to the heart. Any infection, injury or inflammatory illness raises it.
- It is a marker, not a cause. Lowering CRP is not a goal in itself.
- It adds only a little to a standard heart-risk estimate. It matters most when a treatment decision is close.
- One reading is not enough. The risk groups assume the average of two tests, two weeks apart, in a well person.
- Much of its signal reflects body weight and metabolic health.
- No guideline sets a treatment target for it. The 2003 statement advises against repeat testing to track treatment.
References
- Pearson TA, et al. Circulation. 2003;107:499-511 (AHA/CDC scientific statement on markers of inflammation).
- Emerging Risk Factors Collaboration. Lancet. 2010;375:132-140.
- Emerging Risk Factors Collaboration. N Engl J Med. 2012;367:1310-1320.
- C Reactive Protein Coronary Heart Disease Genetics Collaboration. BMJ. 2011;342:d548.
- Ridker PM, et al. N Engl J Med. 2008;359:2195-2207.
This page is for education only. It is not medical advice. Decisions about any treatment belong with a physician who knows your history.