Myeloperoxidase Test · Blood

If your standard cholesterol panel, blood sugar, and even your high-sensitivity troponin all come back normal, you might assume your heart is in the clear. But research shows that a specific enzyme from your white blood cells can be quietly driving damage inside your arteries, years before a heart attack or stroke ever shows up on a conventional test. That enzyme is MPO (myeloperoxidase), and measuring it gives you a window into a kind of vascular risk that routine bloodwork simply does not capture.

MPO is a protein stored inside neutrophils, the most common type of white blood cell. When these cells activate in response to infection or inflammation, they release MPO into your blood. The enzyme uses hydrogen peroxide and chloride to produce a bleach-like oxidant called hypochlorous acid, which is extremely effective at killing bacteria. The problem is that when MPO release becomes chronic, the same chemistry damages your own tissues, particularly the lining of your blood vessels. Measuring plasma MPO tells you how much of this oxidative, inflammatory process is happening right now.

Heart Disease and Heart Attack Risk

The largest body of evidence for MPO centers on cardiovascular disease. In a landmark study of 604 people who came to the emergency department with chest pain, a single plasma MPO measurement at arrival predicted the risk of heart attack within 30 days, even in people whose troponin (the standard heart-damage marker) was completely normal. Those in the highest quarter of MPO levels had roughly four times the risk of a major cardiac event compared to the lowest quarter.

In a population-based study of apparently healthy individuals from the EPIC-Norfolk cohort (1,138 who later developed coronary artery disease and 2,237 matched controls), people in the top quarter of MPO levels had about 36% higher odds of developing coronary artery disease over eight years, even after adjusting for traditional risk factors. This association held even among people with low LDL cholesterol, high HDL cholesterol, or low CRP (C-reactive protein, a common inflammation marker).

For people already diagnosed with stable coronary artery disease, MPO continues to predict trouble ahead. In a study of 1,895 patients undergoing elective coronary angiography, those with MPO above 322 pmol/L (roughly the top 15%) had about 71% higher risk of death, heart attack, or stroke over three years, even after adjusting for traditional risk factors, kidney function, BNP (B-type natriuretic peptide, a marker of heart strain), and CRP.

Heart Failure

MPO also predicts who will develop heart failure in the first place. In 3,733 apparently healthy older adults from the Cardiovascular Health Study followed for about seven years, those with MPO above 432 pmol/L (top quarter) had roughly 34% higher risk of developing heart failure, independent of heart attack, blood pressure, smoking, diabetes, and cholesterol. The relationship was actually stronger in people without traditional cardiovascular risk factors, suggesting MPO captures a dimension of risk that standard screening misses.

In people who already have heart failure, higher MPO independently predicts one-year mortality and adds prognostic information beyond BNP, the standard heart failure biomarker. In 667 people presenting with shortness of breath to the emergency department, those with MPO above 99 pmol/L who also had high BNP were about 2.8 times more likely to die within a year compared to those with both markers low.

Kidney Disease

In the CRIC study (Chronic Renal Insufficiency Cohort), which followed 3,872 people with existing chronic kidney disease (CKD), each standard-deviation increase in MPO was associated with a 10% higher risk of CKD progression (defined as reaching dialysis, transplant, or losing half of kidney function). The link was strongest in people who still had relatively preserved kidney function (eGFR above 45), suggesting MPO may be especially useful as an early signal of accelerating kidney damage.

All-Cause Mortality

Perhaps the most striking finding comes from a study of 3,658 ambulatory adults followed for an average of 6.5 years. People with high MPO (540 pmol/L or above) had about four times the risk of dying from any cause compared to those with low MPO (below 470 pmol/L), after adjusting for age, sex, and cardiovascular risk factors. Non-cardiovascular death drove much of this risk, suggesting MPO reflects systemic inflammatory damage that extends well beyond the heart.

Sources: Tang et al. 2010 (stable CAD); Tang et al. 2009 (CHS heart failure); Penn et al. 2023 (all-cause mortality).

What this means for you: if your MPO is elevated, your white blood cells are actively producing oxidants that damage your arteries, promote plaque instability, and reduce the availability of nitric oxide (the molecule that keeps blood vessels relaxed). This is happening whether or not your cholesterol, blood sugar, or troponin look normal.

How MPO Drives Vascular Damage

MPO does not just mark inflammation; it participates in the damage. The enzyme chemically modifies LDL cholesterol into a form that macrophages (immune cells in artery walls) aggressively absorb, accelerating plaque growth. It also oxidizes HDL cholesterol, stripping it of its protective ability to remove cholesterol from artery walls. On top of that, MPO consumes nitric oxide, the signaling molecule that keeps arteries flexible and open. The result is stiffer vessels, higher blood pressure, and plaques that are more likely to crack open and trigger a clot.

Reference Ranges

MPO does not yet have a single universally standardized cutpoint. Different assays report results in different units (pmol/L, ng/mL, or µg/L), and values vary by lab method and sample handling. The ranges below are drawn from the largest clinical studies using pmol/L and reflect where risk begins to climb. They are orientation for tracking your trend, not rigid diagnostic thresholds.

Compare your results within the same lab over time for the most meaningful trend. A study of stable coronary artery disease patients used a threshold of 322 pmol/L to define elevated risk in that specific population, while the EPIC-Norfolk study of healthy individuals found the top quartile began at 728 pmol/L. Context matters: a value of 400 pmol/L may mean different things in a healthy 40-year-old versus someone with existing heart disease.

When Results Can Be Misleading

MPO is extremely sensitive to anything that activates your neutrophils, which means several common situations can produce a temporarily inflated reading that does not reflect your baseline vascular risk.

• Recent exercise: Strenuous exercise causes the release of MPO from neutrophils and can raise plasma MPO by 30% to 85% or more within minutes, returning toward baseline within hours. Even moderate prolonged exercise (4 hours at 45% of maximal capacity) can increase MPO by about 85%. Avoid vigorous exercise for at least 24 hours before testing.
• Acute illness or cardiovascular event: Heart attack, stroke, sepsis, or any significant acute inflammation can spike MPO dramatically. Testing during or shortly after an illness does not reflect your chronic baseline.
• Smoking: Active smoking raises MPO. If you smoke, your result reflects both chronic vascular risk and the direct effect of smoke on neutrophil activation.
• Assay and sample handling: MPO values depend heavily on the specific test method, whether the lab uses plasma or serum, and how quickly the sample was processed. Always compare results from the same lab using the same assay.

Tracking Your Trend

A single MPO measurement is a snapshot of your neutrophil activation at one moment. Because MPO can fluctuate by roughly 30% from day to day due to normal biological variation, any single reading near a risk threshold should be confirmed with at least one repeat test, drawn on a different day in a stable clinical state (no recent illness, no exercise in the prior 24 hours).

The real power of MPO comes from tracking it over time. In the largest longitudinal study, each 100 pmol/L decrease in MPO during follow-up was associated with about a 5% reduction in the risk of death. That means the direction your MPO is moving may matter as much as any single value. If you are making lifestyle changes, starting a statin, or managing inflammation, repeating MPO every 3 to 6 months lets you see whether the number is actually responding.

A practical cadence: get a baseline when you are healthy and have not exercised hard that day. If MPO is elevated, retest in 2 to 4 weeks to confirm. Then retest every 3 to 6 months as you work on reducing it, and at least annually once it is in a stable range.

What to Do with an Elevated Result

An elevated MPO is not a diagnosis. It is a signal that your immune system is producing oxidative damage at a rate that puts your blood vessels, kidneys, and heart at higher risk. The next steps depend on what else is going on.

• Confirm the result: Retest in a stable state to rule out a transient spike from exercise, acute illness, or sample handling.
• Check companion markers: Order hs-CRP (high-sensitivity C-reactive protein) to assess broader systemic inflammation, ApoB (apolipoprotein B) to measure atherogenic particle burden, Lp(a) (lipoprotein(a)) to rule out inherited lipid risk, and a lipid panel to evaluate LDL and HDL. If MPO is high but CRP is normal, you may have localized neutrophil-driven oxidative stress that CRP alone would miss.
• Assess cardiovascular risk broadly: Consider a coronary calcium score or advanced lipid testing if you have not already. MPO adds information beyond what standard risk calculators capture.
• Address modifiable factors: Smoking cessation, blood pressure control, blood sugar management, and statin therapy all target pathways that feed into chronic neutrophil activation.
• Consider specialist input: If MPO is persistently elevated alongside other inflammatory markers, or if you already have coronary artery disease or heart failure, a cardiologist or lipidologist can integrate this data into a treatment plan.