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Should We Be Testing for Lp(a)?

No doubt those with elevated Lp(a) have a higher risk of ASCVD, but the question is whether testing for Lp(a) is beneficial if we don’t have effective therapies for lowering it.

Lipoprotein (a)

It isn’t the best nomenclature, but this word refers to a low-density lipoprotein that has the ability to create atherosclerotic plaque.

Blood levels of Lp(a) are affected by several factors, including the LPA gene that encodes this molecule. Dietary habits, age, or sex don’t seem to affect Lp(a) values.

It’s important to check for Lp(a) in the same lab for monitoring levels, but it may not be the best way to work with this lab value. Most experts will check this once or twice in the patient’s lifetime because it indicates overall risk and not ongoing risk based on which direction it trends.

Lp(a) is made up of a liporptein plus apoB and Apo(a). The Apo(a) portion can independently elevate the risk of clotting, so perhaps this lipoprotein has some inflammatory competence or clotting ability.

Read more about Lp(a) from Dr. Paul Thomson.

Lp(a) & Disease Association

We know from observational studies that those who walk around with higher Lp(a) levels tend to have a higher risk of ASCVD, coronary heart disease (CHD), cerebrovascular disease (CVD), and aortic stenosis.

This molecule is also an acute phase reactant, so those with inflammation will have higher values. Meaning that it shouldn’t be checked during times of inflammation.

A UK study of half a million individuals revealed an increased association with ASCVD for levels above 20 nmol/L, translating to a 10% higher risk for each 50 nmol/L increment above this value.

Lowering Lp(a)

Unlike someone’s LDL values, we don’t have good tools to lower a patient’s Lp(a). At least, that’s the current widespread consensus. Some experts believe treatments (medications) in the pipeline will lower the serum level of Lp(a) by as much as 80%.

The next question is whether lowering this biomarker level would change someone’s health outcome.

With HDL and homocysteine levels, we have seen that changing the value of these in the blood through directly targeted medications doesn’t have an actual cardiovascular disease outcome.

So, we’ll see if medications that lower Lp(a) will change a person’s ASCVD. Some of the upcoming clinical research should reveal that.

How To Treat Elevated Lp(a)

Some countries, such as the UK, regularly test their patients for Lp(a). However, all countries are still waiting for final results to determine which Lp(a) lowering treatments will lower the risk of atherosclerotic heart disease.

It’s important to recognize that statin therapy can sometimes elevate Lp(a). Again, this is the tough part of understanding the complicated interplay between the key players in heart disease.

Fortunately, despite the rise in Lp(a) caused by statins, those at risk will still benefit from statin’s independent anti-inflammatory and LDL lower effects.

1. PCSK9 Inhibitor

Though PCSK9 inhibitors seem to lower Lp(a) values, it’s unclear whether they can lower the risk of heart attacks in those with high Lp(a) values.

2. Lipoprotein Apheresis

Similar to dialysis, though not as severe, this can be used weekly to lower Lp(a) values by 70% or more.

3. Antisense Therapies

Some antisense oligonucleotide treatments are being researched to lower patients’ Lp(a) levels.

4. Inclisiran

Leqvio is a medication for those with elevated ASCVD disease risk who may not be candidates for standard treatment alone.

This molecule works in the synthesis pathway of the PCSK9 protein.

Serum Lp(a) Values

Serum values above 165 nmol/L seem to be associated with the highest risk, such as coronary heart disease death, heart attack, or needing immediate vascular intervention.

Some believe values above 125 nmol/L equate to elevated risk; other experts set that bar at 50 nmol/L. The patient’s clinical history obviously matters a lot.

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