Should I Test My Lp(a)
Last updated on January 26, 2025
Overview
This article provides a comprehensive explanation of Lipoprotein(a), or Lp(a), a unique blood particle that combines LDL cholesterol with a special protein. It explores Lp(a)’s role in the body, including its evolutionary purpose in wound healing and tissue repair, while explaining how elevated levels can increase cardiovascular disease risk through both plaque formation and blood clotting mechanisms. The article addresses key clinical aspects, including the lack of FDA-approved treatments specifically for Lp(a), the potential for statins to raise Lp(a) levels, and the complexities of managing cardiovascular risk when different biomarkers move in opposite directions. It concludes with practical information about Lp(a) testing, including how to request the test, associated costs, availability through major laboratories, and the importance of comprehensive cardiovascular risk assessment through additional blood markers.
What is Lp(a)?
Lipoprotein(a), or Lp(a), is a unique particle in the blood that combines a low-density lipoprotein (LDL) with a protein called apolipoprotein(a). It’s largely determined by genetics and has been identified as an independent risk factor for cardiovascular disease, particularly heart attacks and strokes. Unlike other cholesterol markers, Lp(a) levels are relatively resistant to lifestyle changes and most conventional cholesterol-lowering medications, making it an important but often overlooked biomarker in cardiovascular risk assessment.
What’s the relationship between lipoproteins and cholesterol?
Lipoproteins and cholesterol have a key “transport” relationship. Since cholesterol can’t travel through blood on its own (because it’s fat-soluble and blood is water-based), lipoproteins act as specialized carriers that package and transport cholesterol throughout the body.
Think of lipoproteins as boats (made of proteins and phospholipids) that carry cargo (cholesterol, triglycerides, and other fat-soluble substances) through the bloodstream. Different types of lipoproteins have different roles:
• LDL (low-density lipoprotein) delivers cholesterol to tissues
• HDL (high-density lipoprotein) removes excess cholesterol from tissues and returns it to the liver
• VLDL (very low-density lipoprotein) mainly transports triglycerides
• IDL (intermediate-density lipoprotein) is formed as VLDL loses triglycerides
• Chylomicrons transport dietary fats from the intestines
• Lp(a) (lipoprotein(a)) transports cholesterol like LDL but with an added protein that helps with blood clotting and tissue repair, making it a unique particle that combines cholesterol transport with wound healing functions
So when we talk about “good” or “bad” cholesterol, we’re really talking about the different lipoprotein carriers and their roles in cholesterol transport and metabolism.
Is Lp(a) a type of cholesterol?
Not exactly. While Lp(a) contains cholesterol as part of its structure (since it includes an LDL particle), it’s more accurate to describe it as a specialized lipoprotein complex. Think of it like a package where the LDL cholesterol particle is wrapped with an extra protein (apolipoprotein(a)) that gives it unique properties. This is why Lp(a) behaves differently from regular cholesterol in the body and why it’s considered a distinct risk factor for heart disease.
How does Lp(a) contribute to heart disease?
Lp(a) contributes to heart disease through two main mechanisms. First, like LDL cholesterol, it can penetrate artery walls and contribute to the buildup of plaque (atherosclerosis). Second, and uniquely, its apolipoprotein(a) component interferes with the body’s natural clot-breakdown process and promotes inflammation in blood vessel walls. This dual action of promoting both plaque formation and blood clotting makes Lp(a) particularly dangerous for cardiovascular health, as it can both narrow arteries over time and increase the risk of sudden blockages that lead to heart attacks and strokes.
Is Lp(a) bad?
Lp(a) isn’t inherently “bad”—it likely served important biological functions during human evolution. However, elevated levels (generally considered to be above 50 mg/dL or 125 nmol/L) are associated with increased risk of cardiovascular disease, particularly heart attacks and strokes. The risk appears to be dose-dependent, meaning higher levels correspond to higher risk. Whether Lp(a) is problematic for an individual depends on its concentration and other cardiovascular risk factors, which is why it’s important to discuss personal Lp(a) levels with a healthcare provider.
Why does the body produce Lp(a)?
The exact evolutionary purpose of Lp(a) isn’t fully understood, but research suggests it may have played a beneficial role in wound healing and tissue repair by promoting blood clotting and delivering cholesterol for cell membrane repair. Some scientists theorize it might have helped our ancestors survive injuries and infections. However, in modern times, these same properties (particularly its ability to promote clotting and accumulate in artery walls) can contribute to cardiovascular disease, especially given our longer lifespans and different environmental conditions than our ancestors faced.
What medications lower Lp(a)?
Currently, there are no FDA-approved medications specifically for lowering Lp(a). Traditional cholesterol-lowering drugs like statins have minimal to no effect on Lp(a) levels. PCSK9 inhibitors and niacin may modestly reduce Lp(a), but these effects are generally considered insufficient for high-risk patients. However, there are promising new drugs in development, particularly antisense oligonucleotides (like pelacarsen) and small interfering RNA therapies specifically designed to lower Lp(a), which are currently in clinical trials and showing significant potential for reducing Lp(a) levels.
Can statins raise Lp(a)?
Yes, statins can raise Lp(a) levels, an effect that has been documented across different types of statins (a class effect), though the magnitude varies significantly between individuals. While the increase is typically modest for most people, some may experience more substantial elevations. This effect has been observed in multiple clinical studies, including the JUPITER trial with rosuvastatin, though it’s often under-discussed in clinical practice since Lp(a) isn’t routinely measured. For patients with known elevated Lp(a) or significant cardiovascular risk factors, monitoring Lp(a) levels before and after starting statin therapy may be particularly important for understanding their complete cardiovascular risk profile.
If statins make my ApoB go down but my Lp(a) go up, how does my risk profile change?
A decrease in ApoB with an increase in Lp(a) creates a mixed risk picture that needs careful evaluation. While lower ApoB generally reduces cardiovascular risk, a significant Lp(a) increase adds risk through both plaque formation and blood clotting mechanisms. The net effect on your overall cardiovascular risk would depend on the magnitude of these changes, your starting levels, and your other risk factors. Since both particles contribute independently to heart disease risk, you’d want to discuss these opposing changes with your doctor to determine whether the treatment strategy needs adjustment.
How do I ask for an Lp(a) test?
You can ask your healthcare provider to add Lp(a) to your next blood work by saying something like “I’d like to know my Lp(a) level given my interest in cardiovascular health” or “Could we check my Lp(a) level?” Be aware that some insurance companies may not cover this test routinely, so you might want to ask about cost. The test is particularly relevant if you have a family history of early heart disease, high cholesterol, or if you’ve had cardiovascular events despite normal cholesterol levels. Since Lp(a) levels are genetically determined and relatively stable, you typically only need to test it once in your lifetime unless you’re monitoring changes due to medication.
What other tests should I consider getting when I get an Lp(a) test?
A comprehensive cardiovascular risk assessment alongside Lp(a) typically includes a complete lipid panel (total cholesterol, LDL, HDL, triglycerides), ApoB (which measures all atherogenic particles), high-sensitivity C-reactive protein (hsCRP, for inflammation), and fasting glucose or HbA1c (for diabetes risk). Some doctors may also include tests for homocysteine, vitamin D, and thyroid function, as these can affect cardiovascular health. This combination of tests provides a more complete picture of your cardiovascular risk profile than any single marker alone.
What’s it like to get an Lp(a) test?
Getting an Lp(a) test is just like any routine blood test. You’ll have blood drawn from a vein in your arm using a needle, which takes just a few minutes. You might feel a brief pinch when the needle goes in, and there might be slight bruising afterward. Most people don’t need to fast before an Lp(a) test since the level is genetically determined and doesn’t fluctuate much with food intake, but your doctor might want you to fast if they’re doing other blood tests at the same time. The blood sample is then sent to a lab for analysis, and you’ll typically get results within a few days.
Where are Lp(a) tests available, and how much do they cost?
Lp(a) tests are available through most major medical laboratories in the United States, including Quest Diagnostics and LabCorp. The test can be ordered by any licensed healthcare provider or purchased directly through LabCorp’s website without a prescription for around $50. Many hospital labs and specialized cardiac centers also offer this test. Availability and cost can vary by location and insurance coverage.
Conclusion
Understanding your Lp(a) level is becoming increasingly important in cardiovascular risk assessment, particularly given its genetic nature and resistance to traditional treatments. While elevated Lp(a) can’t currently be effectively lowered with FDA-approved medications, knowing your level can still significantly impact your healthcare decisions. If you have elevated Lp(a), your doctor might recommend more aggressive management of other cardiovascular risk factors, closer monitoring of your heart health, or consideration of emerging treatments in clinical trials. Additionally, since statins can potentially raise Lp(a) levels, knowing your baseline level before starting statin therapy can help inform treatment decisions and monitoring strategies. The good news is that Lp(a) testing is becoming more accessible and affordable, and promising new treatments are on the horizon. Whether you have a family history of heart disease, unexplained cardiovascular events, or simply want to better understand your heart disease risk, measuring your Lp(a) level can provide valuable information for making informed healthcare decisions.