Lp(a)

Blood test · no fasting needed

Also known as: Lipoprotein(a), Lipoprotein little a

Below the risk-enhancer level Below 125 nmol/L
Raises heart risk (about 1.4 times) 125 to 249 nmol/L
About 2 to 3 times the risk 250 to 429 nmol/L
About 4 times the risk, like inherited high cholesterol 430 nmol/L and above

Units and reference ranges differ between labs.

Cutoffs: 2026 ACC/AHA Guideline on the Management of Dyslipidemia

Lp(a) is a particle like LDL with an extra protein attached. Its level is set almost entirely by your genes and stays fairly steady through life. A high level raises the risk of heart disease, stroke and a narrowed aortic valve.

What it tells you

One gene explains more than 90% of the differences in Lp(a) between people. Adult levels are usually reached by about age 5.
US guidelines recommend measuring Lp(a) at least once in every adult, to help judge heart risk. When it is high, testing close family members is also recommended.
At 125 nmol/L or more, Lp(a) counts as a factor that raises heart risk, by about 1.4 times. At 250 nmol/L or more, the risk is about twice as high.
There is no Lp(a) treatment goal. A high level is a reason to lower LDL cholesterol harder and to manage other risks.
Results come in nmol/L, which counts particles, or mg/dL, which weighs them. The two can't be reliably converted, so always check the unit.

What can throw it off

Fasting and exercise make little or no difference. Diet changes move it only a little.
Kidney disease raises it. Liver disease lowers it, because Lp(a) is made in the liver.
An underactive thyroid and pregnancy raise it. An overactive thyroid lowers it.
Estrogen therapy after menopause lowers it slightly. Growth hormone therapy raises it.
Statins do not lower it and may raise it slightly. That is not a reason to stop a statin.
Niacin lowers it, but in a large trial that did not reduce heart events.
Levels drawn around a heart attack can differ from the usual level.
Some lab tests misread it in people with very large or very small Lp(a) particles. Guidelines ask labs to use tests that particle size does not affect.

Evidence

Predicting heart disease and stroke

Strong human evidenceCEBM Level 1a

In 36 studies of 126,634 people, higher Lp(a) predicted heart disease even after other risks were counted. In 460,506 UK adults, risk rose about 11% for each 50 nmol/L. Genetic studies support Lp(a) as a cause.

Predicting aortic valve narrowing

Strong human evidenceCEBM Level 1b

In 77,680 Danish adults, those in the top 5% of Lp(a) had about 2.9 times the risk of a narrowed aortic valve. That was against those in the bottom 22%. A gene variant that raises Lp(a) also predicted valve narrowing and valve replacement.

Guiding treatment

Some human evidenceCEBM Level 2b

No trial has tested treating people differently because of their Lp(a) result. In one large trial, a cholesterol drug cut heart events more when Lp(a) was above the middle value, but that was a later subgroup look. The first outcome trial of an Lp(a)-lowering drug missed its main goal in early results.

Limits

It is one risk factor, not a diagnosis. A high value raises the chance of disease but does not show disease is present.
No drug that lowers Lp(a) has yet been shown to prevent heart attacks or strokes. Care focuses on the risks that can be changed.
The risk steps come mostly from one UK population. In some groups, risk doubles at 200 nmol/L rather than 250.
Black adults tend to have higher levels than White adults, with similar risk for each step up.
A normal ApoB does not cancel a high Lp(a). Lp(a) particles are a small share of the ApoB count.

References

Reviewed by Shubham Gupta, MD — Founder & President · November 1, 2026

This page is for education only. It is not medical advice. Decisions about any treatment belong with a physician who knows your history.