Myeloperoxidase (MPO) blood test: what it measures and what a result can mean

Myeloperoxidase is a haem-containing enzyme made by white blood cells. A 2008 review of MPO as a cardiac biomarker describes it as stored in the azurophilic granules of polymorphonuclear neutrophils and macrophages, and released into the fluid around cells when an inflammatory process is under way. In everyday terms, it is part of the toolkit the immune system uses to kill bacteria.

The same review explains that MPO helps convert chloride and hydrogen peroxide into hypochlorite, a bleach-like chemical. That is useful against germs but potentially harmful to the body's own tissues. The American College of Cardiology, summarising a study in its journal, described MPO in just those terms: a protein secreted by white blood cells that signals inflammation and releases a bleach-like substance that can damage the cardiovascular system.

Because of this chemistry, MPO attracted interest from heart researchers. The enzyme has been implicated in the oxidation of the fats carried in low-density lipoprotein (LDL) cholesterol, and the review notes that high-density lipoprotein (HDL) also appears to be a target of MPO-driven oxidation, which may turn a protective particle into a dysfunctional one. MPO also uses up nitric oxide, a natural chemical that helps blood vessels relax.

Coronary artery disease develops when fatty deposits build up in the artery walls. The NHS describes this process as atherosclerosis. Not every plaque is equally dangerous: a plaque that becomes unstable and ruptures can trigger a blood clot and a heart attack. Researchers have long wanted a blood marker that points to plaque instability, rather than simply the amount of narrowing.

MPO was proposed as one such marker because it is abundant in ruptured plaque and can be measured in blood. The 2008 review reports that circulating neutrophils in people with heart attack or unstable angina had a lower MPO content, implying high MPO release into the circulation, compared with people with stable or variant angina. The authors read this as MPO being a marker of instability, not just of oxidative stress.

A second feature drew attention: MPO did not simply track troponin. Troponin is a protein released by damaged heart muscle and is the standard blood test for heart muscle injury; the NHS says that blood tests, alongside an ECG, are used to find out whether you are having a heart attack. The review points out that MPO rose in some people whose troponin was still negative, which is why it was explored as an early or complementary signal in the emergency department.

The best-known population study used UK data. The EPIC-Norfolk project followed healthy adults in Norfolk and compared stored baseline blood from 1,138 people who later developed coronary artery disease with matched people who stayed well. The American College of Cardiology summary reports that people in the highest fourth of MPO were 1.49 times as likely to develop coronary artery disease or have a heart attack as those in the lowest fourth, falling to 1.36 times once blood pressure, cholesterol, body mass index, smoking and diabetes were taken into account.

The review adds an important caveat: the association was weaker than that of traditional risk factors and C-reactive protein, although MPO was largely independent of them. In other words, it added a little extra information rather than replacing anything.

In people with acute coronary syndrome, the review describes the CAPTURE trial, in which an MPO cut-off of 350 micrograms per litre was associated with an adjusted hazard ratio of 2.25 for death or heart attack at six months. A smaller emergency-department study found rising risk across MPO quarters even when troponin was negative. The review also notes that MPO returned to baseline within a week.

• The studies used different assays, units and cut-offs (micrograms per litre, picomoles per litre, nanograms per millilitre), so there is no single agreed normal range.

• Most data come from selected groups, often people already admitted with chest pain or having angiography.

• The review itself concludes that the available data are relatively few and that a standardisation effort is needed.

• The ACC release ends by stating that more study is needed before MPO becomes part of routine screening.

The review is explicit that increased MPO is not likely to be specific for cardiac disease, because activation of neutrophils and macrophages can occur in any infectious, inflammatory or infiltrative process. A person with a chest infection or a flare of an inflammatory condition may therefore have a high value that says nothing about their arteries.

There is also the question of what a result would change. Knowing that MPO is high does not tell anyone which artery is narrowed, and the usual steps for lowering cardiovascular risk are the same whatever the number: not smoking, keeping blood pressure and cholesterol in check, being active and managing diabetes. The NHS lists these as the main ways to reduce risk of heart attack and coronary heart disease.

One study cited in the review found that atorvastatin lowered serum MPO and CRP in people with acute coronary syndrome, which suggests that statin treatment may influence the level. That is an observation from a single trial, not a reason to use MPO to guide treatment.

When doctors in the NHS assess possible coronary heart disease, the NHS says they may do a risk assessment that includes medical and family history, lifestyle and a blood test, followed if needed by an ECG, echocardiogram, chest X-ray or coronary angiogram. For a suspected heart attack, the NHS says you will need tests including an ECG and blood tests. Neither page names MPO.

The blood tests that are usually in play are cholesterol measurements and, when a heart attack is suspected, troponin. Our related pages explain those. MPO is generally better thought of as a research marker or an optional extra offered by some private laboratories than as part of the NHS pathway. If a private test report shows an MPO value, ask the clinician who ordered it what decision it is meant to inform.

It is also worth being careful with names. Other tests have similar names or share the letters MPO, and an unrelated result should not be confused with this enzyme level. Check the exact test name on the report.

No blood marker should delay emergency care. The NHS says to call 999 if you have chest pain that feels tight or like squeezing, chest pain that spreads to the arms, neck or jaw, severe difficulty breathing, pale, blue or grey lips or skin, or someone has passed out and is not responding normally. It advises not to drive yourself to A&E.

The NHS also advises calling NHS 111 if you are suddenly more short of breath than usual, or have chest pain with nausea, or chest pain with a racing, slow, skipping or fluttering heartbeat. For concerns about your long-term heart risk, such as a strong family history, a GP can arrange an assessment.