What is Lipoprotein(a)?
You’ll often see Lipoprotein(a) referred to as Lp(a), pronounced “L-P-little-A.”
It is an important genetic factor that increases the risk for both heart disease and stroke. Much like low-density lipoprotein (LDL) cholesterol, Lp(a) carries cholesterol in the blood.
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 does it mean to have high Lp(a)?
The first thing to know is that Lp(a) levels are genetically determined. You inherited your Lp(a) levels, and they are completely unrelated to diet and lifestyle choices.
You can find out your Lp(a) levels with a simple blood test.
If your Lp(a) level is greater than 125 nmol/L (50 mg/dL), you have high Lp(a).
Note: Unlike the measurement of LDL, the measurement of Lp(a) is not yet completely standardized, so there is more than one way to report Lp(a) levels. When you review your Lp(a) test results with your healthcare provider, 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).
If you have high Lp(a), this is an independent risk factor for cardiovascular disease. High levels of Lp(a) collect in your arteries, gradually narrowing them and limiting blood supply to the heart, brain, kidney, and legs.
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 remains stable thereafter — except during acute illness and menopause, which can both cause Lp(a) to increase. Lp(a) levels are completely 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 individuals than in white, Hispanic, or East Asian individuals.
More research and improved testing methods are needed to better understand the influence of race and ethnicity on Lp(a).