High Lipoprotein(a) 101
What is Lp(a)?
Lipoprotein(a) – sometimes referred to as lipoprotein “little a” – is an important genetic risk for heart disease and stroke. For a long time, it wasn’t well understood, but that’s changing. Much like LDL particles, Lipoprotein(a) particles carry cholesterol in the blood. High Lp(a) levels are associated with higher risk for heart attacks, aortic stenosis, and stroke. Learn more about what Lipoprotein(a) is here.
1 in 5 people have high levels of Lp(a); greater than 50 mg/dL) putting them at higher risk. This elevation begins at birth – it’s associated with genetic factors inherited from your parents – and is not linked to behavior.
What is a “normal” Lp(a) level, and when should I be concerned?
First of all, it’s important to know that Lp(a) levels are inherited – they’re unrelated to diet, exercise, obesity, and lifestyle.
If your Lp(a) level is greater than 50 mg/dL (100 nmol/L), you have an increased risk of heart attack and stroke.
Note: Unlike the measurement of LDL, the measurement of Lp(a) is not yet 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 or nmol/L.
How is Lp(a) related to “bad cholesterol?”
Because Lp(a) is made up of LDL-C and apolipoprotein (a), your Lp(a) levels can contribute to your level of LDL-C (“bad cholesterol”).
Math break: There’s a lack of precision and standardization in measuring Lp(a). But if you’re curious about how much of your LDL-C is associated with Lp(a), this little trick can give you a rough idea. Divide your Lp(a) (in mg/dL) by 3. So, for example, if your Lp(a) is 90 mg/dL, it’s contributing roughly 30 mg/dL to your LDL-C level. We are working to try to change the way Lp(a) is measured, but this is not yet being done in the US. So for now, if your lab report is in mg/dL, use the math above.
Does a high Lp(a) level increase my risk of heart disease?
Yes, Lp(a) is an independent risk factor for cardiovascular disease. Elevated levels of Lp(a) collect in the arteries, gradually narrowing them and limiting blood supply to the heart, brain, kidneys and legs.
Like LDL, Lp(a) can clog your arteries with plaque. Apolipoprotein (a) seems to add increased risk to this lipoprotein. Apolipoprotein (a) seems to behave like a clotting factor. The combination of plaque and clotting can heighten your risk of heart attacks and stroke.
By a variety of mechanisms, Apolipoprotein (a) also seems to be able to promote calcification of the aortic valve leading to aortic stenosis.
How are Lp(a) levels inherited?
The amount of Lp(a) your body produces is determined by 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 (with declining estrogen levels), which can both cause Lp(a) to increase. As noted above, Lp(a) level is not associated with lifestyle factors.
Do Lp(a) levels vary by ethnicity?
High Lp(a) occurs in all ethnicities, but it seems to be more common in Black individuals than in Whites, Hispanic, or Asian individuals. More research and improved testing methods are needed to better understand the influence of race and ethnicity on Lp(a).
Lp(a) and children
Elevated Lp(a) is linked to childhood stroke. However, strokes in children are rare and have distinct causes. (In adults, a stroke is typically related to high blood pressure, elevated cholesterol, smoking, diabetes, and other long-standing cardiac issues.)
Depending on the underlying cause of a childhood stroke, current pediatric guidelines may suggest the use of blood thinners and antiplatelet medications. In some cases, apheresis is used to lower Lp(a) in childhood stroke patients. Any treatment decisions in these settings should be made by experienced clinicians.
Kronnenberg F., Uterman G. Lipoprotein(a): resurrected by genetics. Internal Medicine J, 2013, 273;6-30
Nordestgaard F., Chapman J, et al. Lipoprotein(a) as a cardiovascular risk factor current status. European Heart J. 2010;31,2844-2853
Mortensen M, MD, PHD, Afzal S, MD, PHD et al. Primary Prevention with Statins. ACC/AHA Risk-Based Approach Versus Trial-Based Approaches to Guide Statin Therapy.
Page reviewed by Dr. Mary McGowan