Lipoprotein(a)

What is Lipoprotein(a)?

You’ll often see lipoprotein(a) referred to as Lp(a), pronounced “L-P-little-A.”

Lp(a) is a particle that carries cholesterol in the blood just like LDL cholesterol. High Lp(a) levels are associated with higher risk for heart disease and stroke related to buildup of plaque in the arteries, development of blood clots, and inflammation. Lp(a) levels are inherited and not associated with diet, exercise, or obesity.

Lp(a) looks like LDL cholesterol with some key differences. LDL has a single apolipoprotein B attached to its surface. Lp(a), however, has an apolipoprotein B attached to its surface, and that apolipoprotein B has an apolipoprotein(a) attached to it.

Lp(a) and artery clogging
The apolipoprotein(a) part of Lipoprotein(a) looks like something called plasminogen. Plasminogen is an important protein we all have in our blood that protects us from uncontrolled clotting. While apolipoprotein(a) looks like plasminogen, it doesn’t act like plasminogen. It may actually compete with plasminogen. When apolipoprotein(a) binds to a clot, it can’t break it up. This is why it’s believed that elevated Lp(a) favors clotting.

When plaque has formed and there’s a clot in an artery, that can spell trouble. If plaque ruptures and a blood clot forms on top of the ruptured plaque, it can completely block the flow of blood. In the case of a heart artery, this is how a heart attack happens.

Lp(a) and inflammation
Lp(a) also contains oxidized phospholipids (OxPL).

We all have OxPLs in our cell membranes, and they promote inflammation. This is a problem for many reasons including increasing the risk of plaque rupture.

When it comes to Lp(a), the OxPL portion plays a role in the start of atherosclerosis and aortic valve stenosis.

OxPL also appears to be “pro-osteogenic” in the aortic valve. This literally means “producing bone.” Essentially, the OxPLs deposits calcium in the valve. While you want calcium in your bones, you don’t want it in your aortic valve. A calcified valve is stiff, doesn’t open completely, and reduces blood flow.

What Lp(a) levels are considered high?

Unlike measuring LDL cholesterol, measuring Lp(a) is not completely standardized yet. This means there is more than one way to report Lp(a) levels.

When you review your Lp(a) test results with your healthcare team, you should take note of which method of measurement is used: mg/dL, mg/L, or nmol/L.

If your Lp(a) was measured in mg/L you can easily convert to mg/dL by dividing your Lp(a) value by ten (1000 mg/L ÷ 10 = 100 mg/dL).

Your Lp(a) is high if it’s greater than:

  • 125 nmol/L
        OR
  • 50 mg/dL

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What does it mean to have high Lp(a)?

The first thing to know is that your Lp(a) levels are for the most part genetically determined. You inherited your Lp(a) level from your parents, and your levels are unrelated to diet and lifestyle choices.

You can find out your Lp(a) levels with a simple blood test.

If you have high Lp(a), this is an independent causative risk factor for cardiovascular disease. High levels of Lp(a) can cause buildup of plaque in the arteries, development of blood clots, and inflammation.

If my Lp(a) level is high, what should I do?

If your Lp(a) is high, it is important to address and control all of your other heart-related risk factors. This might include cholesterol-lowering medications, including statins, and other medications that address heart-related risk.

You should also partner with your clinical care team to select approaches to control all your other heart-related risk factors.

How do genetics play a role in Lp(a)?

The amount of Lp(a) in your body is determined by the genes you received at birth from your parents.

Lp(a) reaches its adult level by around age 5 and generally remains relatively stable thereafter — except during acute illness, menopause, and when there are changes in kidney and thyroid function, which can all cause Lp(a) to increase. Lp(a) levels are unrelated to your lifestyle.

Do different ethnicities have different Lp(a) levels?

High Lp(a) occurs in all ethnicities, but it seems to be more common in Black and South Asian people than in White, Hispanic, or East Asian people.

More research and improved testing methods are needed to better understand the influence of race and ethnicity on Lp(a).