Get to Know Lp(a)
What is Lp(a), and what makes it so dangerous?
In previous posts we have discussed the ways lipids are transported in the bloodstream. To summarize, they are carried in small bubble-like particles called lipoproteins (shown in the picture below) which we said function like submarines, shielding their cargo, made of cholesterol and triglyceride, from the water-like
blood stream around them. A well known example of a lipoprotein is LDL, an acronym standing for "low density lipoprotein", named for the way it floats in water compared to other lipoprotein particles. LDL has been clearly shown to trigger the process that leads to heart disease and stroke, and rightfully has attracted a lot of attention from physicians, patients, and drug companies. We will spend a lot of time discussing LDL in future posts.
So what does all this have to do with Lp(a)? Well, a lot actually! Research has helped us understand more about Lp(a) (most commonly referred to as "L-P-little a") and it is now recognized as a key player in heart disease just like LDL. Lp(a) is an LDL-like particle that has acquired super powers. But instead of using its powers for good, Lp(a) uses its powers for evil- namely accelerating people down the path toward heart attacks and strokes. To understand why this is, we must first take a moment to review what this particle looks like. As you can see in the image below (as seen on the FH foundation website) Lp(a) is an LDL particle with one modification- it has a protein stuck on to it called "apolipoprotein a", also called apo(a).
Apo(a) has several things about it that make it particularly wicked. First, due to its structure, the particles hang out in the bloodstream longer than LDL, and are more likely to get stuck in the wall of an artery, Additionally, apo(a) sticks off the side of the LDL particle and acts like the line on a fishing trawler. As it floats around the blood stream it collects junk in the form of oxidized debris. These oxidized molecules (the opposite of the anti-oxidants we like to have in our diet) cause a lot of inflammation and damage the artery wall- this accelerates the process of atherosclerosis and ultimately
leads to premature heart disease. Finally, the structure of apo(a) makes it more likely for clotting to occur- this clotting is what ultimately causes a heart attack.
It is important to realize that high Lp(a) is extremely common, in fact levels are elevated in 20% of the population!! So what can we do to fight back? The first step is to have your Lp(a) level measured- especially if you have a family history of heart attack or stroke. Lp(a) is sneaky because unless you look for it you'll never know it's there. It will show up as LDL on a basic blood panel. Levels are genetically determined, meaning there isn't a lot someone can do (or not do) to impact their Lp(a) levels. But this doesn't mean that nothing can be done to help.
High levels of Lp(a) are significantly correlated with increased risk. Levels above 50 mg/dL or 125 nmol/L are considered elevated. It is important to realize that Lp(a) levels can be measured 2 different ways, so be sure to recognize which way your lab is reporting the value. As of right now there are no medications which have been FDA approved to lower Lp(a) levels, though some are in development. Commonly used medications such as statins do not lower Lp(a), but some other medications on the market may help,
In summary: be sure to check your Lp(a), and if your levels are high you should be evaluated by your local lipidologist to help you manage your risk. Knowing those three letters could save your life!