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.
It isn’t the best nomenclature, but this word refers to a low-density lipoprotein containing a particular molecule called apolipoprotein(a) or Apo(a).
The blood levels of Lp(a) are affected by a few factors, one of which, of course, is the LPA gene that encodes this molecule. Dietary habits, age, or sex don’t seem to affect your 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 one or two times in the patient’s lifetime because it’s meant to be an indicator of overall risk.
Lp(a) is made up of a liporptein plus ApoB and Apo(a). The Apo(a) portion can independently elevate the risk for clotting.
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 also it shouldn’t be checked during times of inflammation.
From a UK study of half a million individuals we know that for levels above 20 nmol/L there was an increased association with ASCVD. Which translates to a 10% higher risk for each 50 nmol/L increment above this value.
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 there are treatments (medications) in the pipeline that will lower the serum level of Lp(a) but as much as 80%.
The next question is whether lowering Lp(a) levels 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). But all countries are still waiting for final results to figure out which Lp(a) lowering treatments will actually 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 different key players in heard 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.
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, and other experts set that bar at 50 nmol/L. The patient’s clinical history obviously matters a lot.