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Lipid Testing6 min read

What Is Lp(a)? Levels, Risk, and Treatment

Lipoprotein(a) is set mostly by your genes, doesn't show up on a standard cholesterol test, and is high in roughly 1 in 5 people. Here's what your number means and what to do with it.

Lp(a)
April 12, 2025
Updated October 2026Medically reviewed by Kaustubh Dabhadkar, MD, MPH, FACC

Lp(a), short for lipoprotein(a), is an inherited cholesterol-carrying particle that raises the risk of heart attack, stroke, and aortic valve narrowing. Your level is mostly set by your genes, a standard cholesterol test doesn't measure it, and roughly 1 in 5 people have a high one. One blood test tells you where you stand.

What is Lp(a)?

Lp(a) looks a lot like an LDL particle, with an extra protein, apolipoprotein(a), attached. It's pronounced "L-P-little-a."

That extra protein makes Lp(a) particles more prone to building plaque and to promoting blood clots.

Your genes mostly determine your Lp(a) level. Unlike LDL cholesterol (LDL-C), diet and exercise don't change it much. You're born with your level, and it stays fairly stable through life.

Key Takeaway

Lp(a) is genetically determined and does not change with lifestyle. One test is enough, and the result stays useful for life.

Why does Lp(a) matter?

High Lp(a) raises your risk of heart disease, stroke, and aortic valve disease on top of your other risk factors. That's what "independent risk factor" means: even with a well-controlled LDL-C, a high Lp(a) still adds risk.

Elevated Lp(a) is common. About 1 in 5 people have a level of 50 mg/dL (about 125 nmol/L) or higher, and most of them haven't been tested, because Lp(a) isn't included in standard lipid panels. It has to be ordered by name.

Source

Kronenberg F et al. “Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement.” European Heart Journal (2022).

View paper

Particle for particle, Lp(a) is also more harmful than LDL. A 2024 genetic analysis estimated it is about 6 times as likely to cause coronary disease per particle.

Source

Björnson E, Adiels M, Taskinen MR, et al. “Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis.” Journal of the American College of Cardiology (2024).

View paper

What is a normal Lp(a) level?

Under 75 nmol/L (about 30 mg/dL) is considered lower risk, and 125 nmol/L (about 50 mg/dL) or higher is high risk, according to the National Lipid Association. Labs report Lp(a) in either nmol/L or mg/dL, and the units don't convert cleanly because Lp(a) particle size varies from person to person, so compare your result to the cutoff in the same unit.

Lp(a) risk levels (National Lipid Association, 2024)

Lower risk
Under 75 nmol/LUnder 30 mg/dL
Intermediate risk
75 to 125 nmol/L30 to 50 mg/dL
High risk
125 nmol/L or higher50 mg/dL or higher

Source

Koschinsky ML, Bajaj A, Boffa MB, et al. “A focused update to the 2019 NLA scientific statement on use of lipoprotein(a) in clinical practice.” Journal of Clinical Lipidology (2024).

View paper

The higher the level, the greater the risk.

Can Lp(a) be treated?

No FDA-approved medicine targets Lp(a) yet. For now, you lower your other risks harder, and PCSK9 inhibitors lower Lp(a) modestly along the way.

What helps now

  • Lower LDL-C and ApoB further. A high Lp(a) gives you more reason to push LDL-C and ApoB lower to offset the extra risk. Our guide on how to lower ApoB covers the options.
  • PCSK9 inhibitors lower Lp(a) by roughly 20 to 30% as a side benefit, on top of their main job of lowering LDL (in pooled evolocumab studies, Lp(a) fell by about 20 to 38%). The class now includes Repatha, Praluent, the once-monthly Lerochol, and the daily pill Lipfendra. See our PCSK9 inhibitor prescription page for who qualifies.
  • Statins still help. They don't lower Lp(a), and in a pooled analysis of six trials they raised it slightly, but they lower LDL and ApoB, which lowers total risk.

Source

Toth PP, Jones SR, Monsalvo ML, Elliott-Davey M, López JAG, Banach M. “Effect of Evolocumab on Non-High-Density Lipoprotein Cholesterol, Apolipoprotein B, and Lipoprotein(a): A Pooled Analysis of Phase 2 and Phase 3 Studies.” Journal of the American Heart Association (2020).

View paper

Knowing your Lp(a) tells you how aggressively to treat your other risk factors, which makes the test valuable.

What is coming

Several drugs built to lower Lp(a) directly are in large outcome trials. They cut Lp(a) dramatically in earlier studies. The outcome trials will show whether that prevents heart attacks and strokes.

Lepodisiran (Eli Lilly) is an siRNA, a medicine that tells the liver to make less of the protein Lp(a) is built from. In the phase 2 ALPACA trial, a single high dose lowered Lp(a) by about 94% over six months. A phase 3 outcomes trial is under way.

Source

Nissen SE, Ni W, Shen X, et al. “Lepodisiran: A Long-Duration Small Interfering RNA Targeting Lipoprotein(a).” New England Journal of Medicine (2025).

View paper

Muvalaplin (Eli Lilly) is a daily pill that blocks Lp(a) particles from forming. In the phase 2 KRAKEN trial, it lowered Lp(a) by up to about 70 to 86% at 12 weeks compared with placebo, depending on the lab method used. A phase 3 outcomes trial began in 2025.

Source

Nicholls SJ et al. “Oral Muvalaplin for Lowering of Lipoprotein(a): A Randomized Clinical Trial.” JAMA (2025).

View paper

Results have been mixed so far. In September 2026, Novartis announced that pelacarsen, the first Lp(a)-lowering drug to finish a large outcomes trial (Lp(a)HORIZON), lowered Lp(a) but did not meet its main goal of reducing cardiovascular events. Results for the siRNA drugs are still pending. Our guide to emerging Lp(a) therapies tracks where each one stands.

Should you get tested?

Yes, at least once as an adult. The 2026 ACC/AHA multisociety guideline on dyslipidemia recommends measuring Lp(a) at least once in every adult, in line with the European Atherosclerosis Society (2022) and the National Lipid Association (2024). Since the result rarely changes, one test gives lasting information.

Source

Blumenthal RS, Morris PB, Gaudino M, et al. “2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.” Journal of the American College of Cardiology (2026).

View paper

Testing is especially worthwhile if you have:

  • A family history of early heart disease (before age 55 in men, 65 in women)
  • A personal history of cardiovascular events despite well-controlled cholesterol
  • A family member with known elevated Lp(a)
  • Other cardiovascular risk factors where a more complete picture would help guide treatment

Lp(a) is a simple blood test available through Quest, Labcorp, and most large lab networks. Our guide on how to get an ApoB or Lp(a) test covers what to ask for and what it costs. Because Lp(a) is inherited, it also runs in families; our genetic testing page covers the optional add-on for inherited cholesterol conditions.

Summary

Lp(a) is a common, inherited risk factor, and one test tells you whether you have it. Knowing your level shapes what you and your care team do about your overall cardiovascular risk.

If your Lp(a) is high, treating ApoB and LDL-C more aggressively helps offset the extra risk, and drugs aimed at Lp(a) itself are working through outcome trials.

At Preval Health, we include Lp(a) testing in every initial assessment because it changes risk assessment and treatment decisions.

Medical review

Medically reviewed by Kaustubh Dabhadkar, MD, MPH, FACC on October 2, 2026. Dr. Dabhadkar is a board-certified preventive cardiologist in Charlotte, North Carolina, and founder of Preval Health, where he writes the treatment protocols.

Common Questions

Should I take a statin if I have high Lp(a)?

Often, yes, depending on your overall risk. Statins don't lower Lp(a), and can raise it slightly, but they lower LDL and ApoB, which reduces your total risk. Guidelines count high Lp(a) as a risk enhancer that favors starting a statin when your risk is borderline or intermediate, so decide with your clinician.

Can you lower your Lp(a)?

Not meaningfully through diet or exercise, because Lp(a) is mostly set by your genes. PCSK9 inhibitors lower it by roughly 20 to 30% as a side benefit. Drugs designed to lower Lp(a) directly, such as lepodisiran, olpasiran, and muvalaplin, are still in outcome trials, and none is FDA-approved yet.

Do PCSK9 inhibitors lower Lp(a)?

Yes, modestly. In a pooled analysis of evolocumab (Repatha) studies, Lp(a) fell by about 20 to 38%. The drop comes as a side benefit: PCSK9 inhibitors are approved to lower LDL cholesterol, and none is approved specifically for high Lp(a).

Why isn't Lp(a) part of a standard cholesterol test?

A standard lipid panel measures total cholesterol, HDL, and triglycerides, and Lp(a) is a separate test that has to be ordered by name. For years there was no treatment aimed at it, so it wasn't routine. The 2026 ACC/AHA guideline now recommends measuring Lp(a) at least once in every adult.

Is Lp(a) genetic?

Yes. Your Lp(a) level is mostly inherited through the LPA gene and stays fairly stable through life. So one test is usually enough, and close relatives of someone with high Lp(a) are worth testing too.

Can you live a long life with high Lp(a)?

Yes, especially with early awareness and good control of every other risk factor. A high Lp(a) raises your risk, and your other numbers still shape the outcome. Knowing your level early gives you and your care team a reason to drive LDL-C and ApoB lower to offset it.

What does it mean if your Lp(a) is high?

It means you carry an inherited risk factor for heart attack, stroke, and aortic valve disease on top of your other risk factors. Those other factors still shape what happens, so they deserve more attention than they otherwise would.

Next step

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