Diagram of Lipoprotein little a

Lipoprotein (a): Five things you should know

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You may have heard about Lipoprotein (a), Lp(a) or often referred to as “Lp little a." Lp(a) is an independent risk factor for cardiovascular disease.The level of Lp(a) found in a person’s blood is entirely genetically predetermined. This means that unlike other cardiac risk factors, Lp(a) can’t be modified by diet or exercise.  Your level of Lp(a) is the same at age 5 as at age 45. The only exception is that your level can increase at menopause and in certain disease states such as chronic kidney disease.

What is Lp(a)?

Lp(a) looks like LDL except it has an added protein attached called apolipoprotein (a).  Like LDL which is a cholesterol rich lipoprotein, Lp(a) can block up arteries (increase the plaque in the artery). The apolipoprotein (a) gives Lp(a) an additional quality, it behaves like a clotting factor. The combination of, increased plaque and increased clotting, can increase the risk of heart attacks and stroke.

Why is this important for a person with familial hypercholesterolemia (FH)?

It turns out that between a third and a half of people with FH also have an elevated Lp(a). This puts them at higher risk for even earlier heart disease or stroke than having FH alone.  As a result, your health care practitioner might want to work harder to get all of your other risk factors under perfect control. If your Lp(a) is elevated your family members should also be screened.

What level of Lp(a) is considered high?

There is agreement among a number of expert organizations including the National Lipid Association (NLA), American Heart Association (AHA) and the American College of Cardiology (ACC) that a level > 50 mg/dL or >125 nmol/L should be considered elevated. Notice that Lp(a) can be measured in mg/dL and nmol/L so it will be important to look at the units of measure in order to know if your level is elevated.

How do I lower Lp(a)?

Unfortunately, at this point in time there are not a lot of medicines known to lower Lp(a).  Both estrogen and niacin (a B vitamin) lower Lp(a) but have not been shown to protect people from developing heart disease.  A new class of medications called PCSK9 inhibitors that came on the market in 2015, have been shown to lower Lp(a) modestly but more work needs to be done before they can be recommended to reduce Lp(a). Lipoprotein apheresis, a dialysis like procedure that is performed in some people on a biweekly basis, can lower both LDL and Lp(a) is sometimes used to lower Lp(a).  Finally, there are a number of Lp(a) lowering medications in clinical trials now.  We will wait to see the outcomes of these trials in the next few years.

For now, if you have FH, you should ask your health care practitioner to test your Lp(a) level, if you are found to have an elevated level, your first-degree relatives should also be screened and you should work to reduce all your modifiable risk factors especially your LDL cholesterol. More information is also available on the FH Foundations’ website.

 

About the Author

Dr. Mary McGowan is the Chief Medical Officer at the FH Foundation and the Co-Director of the Lipid Clinic at Dartmouth Hitchcock Heart and Vascular Center.

 

References

Journal of Clinical Lipidology: Wilson DP, Jacobson TA, Jones PH, et al. Use of Lipoprotein (a) in clinical practice: A biomarker  whose time has come. A scientific statement from the National Lipid Association.  Journal of Clinical Lipidology. 2019;13:374-392.

Journal of Renal Care: Hopewell JC, Haynes R, Baiquent C. The role of lin (a) in chronic kidney disease. J Lipid Res. 2018;59(4):577-585.

National Heart, Lung and Blood Institute

 

2 Responses to “Lipoprotein (a): Five things you should know”

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  2. Chad Spackman

    The comments regarding lp(a) being genetically determined and immune to interventional means are somewhat incorrect. lp(a) is highly responsive to dietary intervention. The reason this is not known (or rather, publicized) is that effective interventions go against the status quo of what constitutes a “heart healthy” diet. lp(a) responds well to the intake of animal and dairy derived saturated fats. Saturated fats are potentially problematic unless consumed in the context of a low sugar/carbohydrate diet. Statins effectively lower LDL, but raise lp(a). This reverse correlation with standardized drug and dietary treatments normal prescribed to heart patients, present the cardiologist with a dilemma. Is lp(a) worse than elevated LDL? No one appears to know but there are strong arguments on both sides. Unfortunately the real dilemma falls to the patient who must do his or her own research and come up with a plan that suits.

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