Lp(a) and the LPA Gene: The Cholesterol Number Most People Never Get

What Lp(a) is

Lipoprotein(a), usually written Lp(a), is a cholesterol-carrying particle in the blood. NHLBI describes it as structurally similar to LDL, the so-called bad cholesterol. Like LDL, it can deposit cholesterol in artery walls.

It also appears to do extra harm. NHLBI researchers note it may promote clotting, and one described it as having "all the same bad features as LDL" plus more. The 2024 NLA statement calls it an established, independent, causal risk factor for cardiovascular disease.

The AHA says high Lp(a) can raise the risk of heart disease and stroke, often without any symptoms. The only way to know your level is a blood test.

How common is high Lp(a)?

The NLA and AHA both put it at about 1 in 5 people. An NHLBI feature gives a range of 20% to 30% worldwide, depending on the cutoff used.

The AHA notes levels tend to be higher in people of African and South Asian descent. Levels may also rise during pregnancy and menopause, and with kidney, liver or thyroid disease.

The LPA gene and why it is hard to read

Lp(a) levels are largely controlled by a single gene, LPA, according to a 2022 review by Coassin and Kronenberg in Atherosclerosis. NIH researchers have called it likely the leading inherited risk factor for cardiovascular disease.

The key feature of LPA is a repeated stretch of DNA called kringle IV type 2, or KIV-2. People carry different numbers of copies, which produces more than 40 versions, or isoforms, of the apo(a) protein.

Fewer repeats generally mean higher levels. The review reports that people with the smallest isoforms have median Lp(a) concentrations up to five times higher than people with large ones.

Why your DNA test probably will not tell you

That repeated structure is a problem for genetic testing. The same review says several functional variants sit inside the KIV-2 repeat, where they are "not accessible to conventional sequencing and genotyping technologies."

In practice, the blood test is what guidelines use. A genetic report on LPA, if your test includes one, cannot replace a measured level. For background on how the two main consumer methods differ, see our explainer on whole genome sequencing vs genotyping.

Who should be tested

Recommendations have moved toward testing everyone once.

The NLA also says the 2026 ACC/AHA dyslipidemia guideline supports universal adult testing. The AHA defines early heart disease in a relative as before age 55 in men and 65 in women.

The AHA lists a diagnosis of familial hypercholesterolemia (FH), a separate inherited cause of high LDL, as one reason testing matters. Our guide to genetic testing for familial hypercholesterolemia covers that side.

How to get the test

1. Ask for it by name. Lp(a) is not part of a standard lipid panel. Ask your clinician to add a lipoprotein(a) test to your next blood draw.
2. Note the units. Labs report Lp(a) in nmol/L or mg/dL. Write down which one yours used so later comparisons make sense.
3. Keep the result. Experts quoted by NHLBI say a single test is enough for most people, because levels are largely genetic and fairly stable.
4. Share it with family. If your level is high, relatives have a reason to be tested too.

Reading your result

The NLA uses three bands. Treat them as risk tiers, not diagnoses.

The AHA adds that a level of 250 nmol/L (100 mg/dL) or more may roughly double heart disease and stroke risk. It also stresses that your personal risk depends on other factors, such as age and blood pressure.

If your Lp(a) is high

Because Lp(a) itself is hard to lower, guidelines focus on everything else. The NLA calls for earlier and more intensive management of other risk factors, including lifestyle changes.

• Lower LDL harder. The NLA supports lipid-lowering drugs in high-risk people, mainly to reduce LDL cholesterol.
• Control blood pressure and blood sugar. The AHA lists cholesterol, blood pressure and diabetes management as the core response.
• Keep the healthy habits. The AHA says lifestyle will not lower Lp(a), but diet, activity, weight, not smoking and 7 to 9 hours of sleep still cut overall risk.
• Test your relatives. The NLA recommends screening first-degree relatives: parents, siblings and children.

Apheresis for the highest-risk patients

For a narrow group, the FDA has approved lipoprotein apheresis, a blood-filtering procedure. According to the NLA, it applies to people with FH and documented coronary or peripheral artery disease whose Lp(a) is at least 60 mg/dL and LDL at least 100 mg/dL despite maximum tolerated therapy.

If you are bringing an Lp(a) result together with genetic findings to an appointment, our guide on bringing DNA results to your doctor can help you prepare.

Where treatment stands in 2026

As of October 30, 2026, no medicine is approved specifically to lower Lp(a). Some existing drugs have a partial effect. NHLBI notes that PCSK9 inhibitors, a class of LDL-lowering drugs, reduce Lp(a) by about 20% to 30%.

Targeted drugs are in development, and 2026 brought a setback. On September 4, 2026, Novartis announced that its Phase III Lp(a)HORIZON trial of pelacarsen, in 8,323 people with high Lp(a) and existing cardiovascular disease, did not meet its primary goal of reducing cardiovascular events.

The National Lipid Association noted that pelacarsen lowered Lp(a) but did not reduce major events, and that full results were not yet public. It said clinicians and patients "should continue to measure Lp(a)."

NHLBI noted in 2024 that other trials were testing ways to block Lp(a) production. Until outcome data show a benefit, the practical value of knowing your number is earlier, tighter control of the risks that already have proven treatments.