High lipoprotein(a), often written as Lp(a), means your blood contains elevated levels of a cholesterol-carrying particle that independently raises your risk of heart disease and stroke. Levels above 50 mg/dL (or 125 nmol/L) are considered high, and roughly one in five people fall into that range. Unlike most cholesterol numbers, your Lp(a) level is almost entirely determined by your genes, which means diet and exercise won’t budge it.
How Lp(a) Differs From Regular Cholesterol
A standard cholesterol panel measures LDL (“bad” cholesterol), HDL (“good” cholesterol), and triglycerides. Lp(a) is a separate particle that doesn’t show up on that basic panel. It looks like an LDL particle, with the same cholesterol-rich core, but it has an extra protein called apolipoprotein(a) attached to it. That extra protein is what makes Lp(a) uniquely dangerous: it promotes inflammation, carries a significant proportion of oxidized fats in the blood, and contributes to plaque buildup in arteries through mechanisms that LDL alone does not.
The cardiovascular risk from Lp(a) and LDL are independent and additive. Even if you get your LDL cholesterol very low through medication, elevated Lp(a) continues to raise your risk. A large meta-analysis found that high Lp(a) increases cardiovascular danger across all levels of achieved LDL cholesterol, including people in the lowest quartile. This is why knowing your Lp(a) number matters separately from knowing your standard cholesterol results.
What the Numbers Mean
Lp(a) can be reported in two different units depending on the lab. The CDC defines high Lp(a) as greater than 50 mg/dL or 125 nmol/L. Levels can range enormously across the population, from less than 0.1 mg/dL to over 300 mg/dL. There is no “borderline” category the way there is for LDL cholesterol. You’re either below the threshold or above it, and the higher you go, the greater the risk.
People with Lp(a) at or above 75 mg/dL face an 88% higher risk of atherosclerotic cardiovascular disease compared to those with low levels. The stroke risk is especially pronounced: those at 75 mg/dL or above have more than double the risk of a first stroke. Each 25 mg/dL increase in Lp(a) is associated with a 23% higher risk of cardiovascular events overall and a 33% higher risk of stroke specifically.
Why Your Genes Control Your Level
Lp(a) levels are determined almost entirely by the LPA gene you inherited from your parents. You get one copy from each parent, and over 80% of people express two different versions of the apolipoprotein(a) protein, one from each copy. The trait is codominant, meaning both copies contribute to your blood level.
The key genetic variable is the number of repeating structural units (called kringle repeats) in the LPA gene. People with fewer repeats produce a smaller, more efficiently secreted protein, which results in higher Lp(a) levels. Those with small versions of the protein have median Lp(a) concentrations four to five times higher than those who carry only large versions. Specific genetic variants can individually raise levels by 30 to 45 mg/dL, and one common variant alone explains about 25% of the variation in Lp(a) across people of European descent.
Because your Lp(a) level is genetically fixed, it stays relatively stable throughout your life. This is why the 2026 ACC/AHA guidelines recommend that every adult have Lp(a) measured at least once in a lifetime. One test is usually enough to know where you stand.
Beyond Heart Attacks: Aortic Valve Disease
High Lp(a) doesn’t just affect arteries. It’s a causal risk factor for calcific aortic valve stenosis, a condition where the heart’s aortic valve gradually stiffens and narrows due to calcium deposits. Genetic studies have confirmed that Lp(a) directly drives both the calcification process and the progression to clinically significant valve disease. This link is especially important because aortic stenosis develops slowly and often isn’t caught until symptoms like breathlessness or chest pain appear.
Why Standard Treatments Fall Short
Statins, the most widely prescribed cholesterol medications, lower LDL cholesterol effectively but do not lower Lp(a). In fact, statins can increase Lp(a) levels in a subset of patients, specifically those who carry a smaller form of the apolipoprotein(a) protein. In one study, these patients saw their Lp(a) rise from a median of about 66 mg/dL to 97 mg/dL while on statin therapy.
Dietary changes and physical exercise also have no effect on Lp(a) levels. They remain valuable for overall cardiovascular health and should still be a priority, but they won’t move this particular number. PCSK9 inhibitors, a newer class of injectable cholesterol drugs, do lower both LDL and Lp(a), and their cardiovascular benefits appear to be greater in people who have elevated Lp(a).
New Drugs Targeting Lp(a) Directly
For the first time, drugs designed specifically to lower Lp(a) are in advanced clinical testing. These work by blocking the liver’s ability to produce the apolipoprotein(a) protein in the first place, preventing Lp(a) particles from being assembled.
Olpasiran, given as an injection every 12 weeks, reduced Lp(a) by more than 95% in a phase 2 trial. Even after patients stopped receiving the drug, levels remained about 40% to 50% lower than baseline nearly a year after their last dose. Pelacarsen, another injectable drug using a different mechanism, has reduced Lp(a) by up to 80% and is currently in a large phase 3 trial designed to determine whether lowering Lp(a) actually prevents heart attacks and strokes.
These drugs are not yet available outside of clinical trials. Their results so far demonstrate that dramatic Lp(a) reduction is biologically possible, but the critical question of whether that translates into fewer cardiovascular events is still being answered.
What to Do if Your Lp(a) Is High
If you’ve been told your Lp(a) is elevated, the most practical step right now is aggressive management of every other cardiovascular risk factor you can control. That means keeping LDL cholesterol as low as possible, maintaining a healthy blood pressure, staying physically active, and not smoking. Because Lp(a) risk stacks on top of LDL risk, reducing LDL becomes even more important when Lp(a) is high.
It’s also worth knowing that high Lp(a) is hereditary. If your level is elevated, your parents, siblings, and children have a meaningful chance of carrying the same genetic trait. A single blood test for each of them can clarify their risk.