Lp(a) is made of an LDL-like particle attached to an apolipoprotein called apolipoprotein(a). Like bad cholesterol (LDL), Lp(a) appears to increase the risk of cholesterol buildup in the arteries.

The apolipoprotein(a) part of Lp(a) might increase the chance of clotting, but an important effect of high Lp(a) has to do with inflammation.

Lp(a) carries something called oxidized phospholipids. Those trigger inflammation and calcification of the aortic valve making it stiff. This leads to aortic stenosis.

Because Lp(a) isn’t measured with a standard cholesterol profile, many people don’t even know they have elevated levels.

Elevated Lp(a) is extremely common. It occurs in 1 in 5 people around the world.

It’s tricky because it can be measured in two different ways. If your Lp(a) is measured in mg/dl, a normal level is less than 30 and high is greater than 50. If your Lp(a) is measured in nmol/L, a normal level is less than 75 and high is greater than 100 by some, 125 by others.

No, diet and exercise don’t change Lp(a) levels.

Your Lp(a) is determined by your genetics. You inherit one “allele” (half of a full gene) for Lp(a) from each of your parents. If you have high Lp(a), it’s likely that at least one of your parents has a high Lp(a).

It’s also important to know that if you have elevated Lp(a), each time you have a child you have a 50/50 chance of passing it to them.

Many experts believe everyone should have their Lp(a) measured a least once in their lifetime.

Anyone with a family history of cardiovascular disease or a diagnosis of familial hypercholesterolemia (FH) should have their Lp(a) measured.

While high Lp(a) occurs in about 20% of the general population, people with FH have a 30-50% chance of having both elevated LDL and Lp(a). Added together, this results in a very high risk of early cardiovascular disease.

Yes, Lp(a) can rise dramatically with sudden illnesses like COVID-19 or during a heart attack.

It’s always been believed that Lp(a) levels remain relatively stable through a person’s life, but recent studies show there is a bit more variability than we previously thought. You shouldn’t be surprised if your Lp(a) levels fluctuate as much as 20% up or down.

Studies comparing people with the highest Lp(a) levels to those with the lowest levels found those with highest levels were at a 3-to-4-fold higher risk of a heart attack. They’re also at a 3-fold higher risk of aortic valve disease and almost twice the risk of stroke.

Currently, the only FDA-approved therapy to lower Lp(a) is lipoprotein apheresis. It’s a dialysis-like procedure where a machine physically removes both Lp(a) and LDL cholesterol from the blood stream on a weekly or bi-weekly basis. This 3-hour process involves removing blood from one arm, passing it through a special column to extract the LDL and Lp(a), and returning the blood to the other arm. For apheresis to be approved, a person must have an Lp(a) greater than 60 mg/dl, have FH, and known vascular disease.

Three other potential treatments are being studied in clinical trials. Should the two medications prove to be safe, effective, and reduce vascular risk, they may be available within 4-5 years.

Even without medication, you can work to reduce all other risk factors. If you are overweight, try to get to a healthier weight. If you smoke, please quit. There are not easy changes to make, but the sooner you do it – the better. If you have other medical complications, like high blood pressure or diabetes, take all prescribed medications.

Anyone who has an elevated Lp(a) should work on lowering their LDL cholesterol as much as possible. People with no history of vascular disease should aim for less than 100 mg/dl. People with vascular disease strive for levels less than 70 mg/dl (and even lower is better).

It’s difficult to give a precise percentage. In any given person, risk reduction depends on the age at which cholesterol-lowering medications were started and factors like diabetes, cigarette smoking, high blood pressure, and high Lp(a).

We can say that studies performed in people with very high, high, and modestly elevated cholesterol found that for every 40 points in reduction, cardiac risk is reduced by 20%.

There’s no one answer, but there are several reasons why this may happen.

The first reason is puberty. As young men go through puberty, their HDL (good cholesterol) tends to fall. This doesn’t happen to young women. This is an additional risk factor for early heart disease.

Women also appear to be protected from symptomatic heart disease until menopause. This is likely thanks to estrogen. This doesn’t mean they are not building up plaque in their arteries, though.

Women have smaller arteries than men, and it doesn’t take long for them to become blocked after menopause, so early treatment is important for women, too.

In the past, men typically smoked more than women. Smoking is poison for everyone, but for people with high Lp(a), smoking is doubly poisonous. It can lower HDL and oxidize LDL, which is more dangerous than non-oxidized LDL. So in the past, smoking put men with and without high Lp(a) at risk for earlier heart disease than their non-smoking female relatives.