Lipoprotein(a), often written as Lp(a) and pronounced “L-P-little-a,” is a cholesterol-carrying particle in your blood that raises the risk of heart attack, stroke, and aortic valve disease. Unlike most cholesterol numbers, your Lp(a) level is almost entirely genetic. Over 90% of the variation in Lp(a) levels comes from a single gene you inherit from your parents, and roughly one in four people worldwide has levels high enough to increase cardiovascular risk.
How Lp(a) Differs From Regular LDL Cholesterol
Lp(a) is structurally very similar to LDL, the particle commonly called “bad cholesterol.” Both carry cholesterol through the bloodstream, and both contain the same core protein (called apoB-100). The key difference is that Lp(a) has a second protein attached to it, called apolipoprotein(a), which is linked to apoB-100 by a chemical bond. That extra protein makes Lp(a) uniquely dangerous in two ways: it promotes plaque buildup in arteries like LDL does, but it also interferes with your body’s ability to dissolve blood clots.
This clot-related risk exists because the extra protein on Lp(a) is remarkably similar to plasminogen, one of the body’s natural clot-dissolving molecules. Its amino acid sequence overlaps with plasminogen by 94%. But a single amino acid swap at a critical site means the protein can’t actually break down clots. Instead, it competes with real plasminogen for binding sites, essentially blocking the clot-dissolving system while also deactivating another natural clot-prevention mechanism. The result is a particle that builds up plaque and makes clots harder to clear.
Why Your Lp(a) Level Is Almost Entirely Inherited
Most cardiovascular risk factors respond to lifestyle changes. Lp(a) is a notable exception. Your level is set by the LPA gene, which accounts for more than 90% of the variation between people. Diet, exercise, age, and sex have minimal impact. Most people carry two different-sized versions of the Lp(a) protein, one inherited from each parent, and the size of these proteins is a major driver of how much Lp(a) circulates in your blood. Smaller protein sizes tend to correspond with higher blood levels.
This genetic determination means your Lp(a) level is relatively stable throughout your life. A single measurement is generally enough to know where you stand, which is why several major medical organizations now recommend measuring Lp(a) at least once in every adult’s lifetime. The European Society of Cardiology, the European Atherosclerosis Society, and the Canadian Cardiovascular Society all endorse this approach, with Canada recommending it as part of routine initial lipid screening.
What Counts as a High Level
Lp(a) is reported in two different units, and the distinction matters. The preferred unit is nanomoles per liter (nmol/L), which directly measures the number of Lp(a) particles. Older tests report milligrams per deciliter (mg/dL), which measures total particle mass. Because each person’s Lp(a) particles can be different sizes depending on their genetics, there is no reliable conversion between the two units. If your result is in mg/dL, it should not be mathematically converted to nmol/L.
The widely accepted threshold for elevated cardiovascular risk is 50 mg/dL or 125 nmol/L, used by both the American College of Cardiology and American Heart Association. The European Atherosclerosis Society breaks it down further: below 30 mg/dL (or 75 nmol/L) is considered normal, 30 to 50 mg/dL is intermediate, and above 50 mg/dL is abnormal. In studies of people with established heart disease, about 28% had levels at or above 50 mg/dL.
Heart Disease and Aortic Valve Damage
Lp(a) contributes to cardiovascular disease through several overlapping mechanisms. It promotes inflammation in artery walls, encourages the growth of smooth muscle cells that thicken plaque, and impairs the body’s clot-dissolving system. These effects compound over a lifetime, which is why elevated Lp(a) is considered a causal, independent risk factor for heart attacks and strokes, not just a marker that correlates with them.
Beyond artery disease, Lp(a) plays a distinct role in aortic valve stenosis, a condition where the heart’s aortic valve stiffens and narrows. Lp(a) carries oxidized fats into the valve tissue, triggering a cascade of inflammation that eventually causes calcium deposits to form on the valve. Lab studies show that valve cells exposed to Lp(a) develop significantly more calcium buildup compared to unexposed cells. This process stiffens the valve over time, restricting blood flow from the heart. High Lp(a) is now recognized as a genetic risk factor that can accelerate this progression.
Current Treatment Options
No widely available medication is specifically designed to lower Lp(a), which makes it one of the more frustrating cardiovascular risk factors to manage. The treatments that do exist offer only modest reductions. PCSK9 inhibitors, a class of injectable cholesterol-lowering drugs, reduce Lp(a) by about 20% to 30% in addition to their primary effect on LDL cholesterol. A blood-filtering procedure called lipoprotein apheresis can remove over 60% of Lp(a) per session, but levels rebound between treatments, and the long-term average reduction is closer to 30%. Apheresis also requires regular visits to a treatment center, typically every one to two weeks.
Standard cholesterol medications like statins do not meaningfully lower Lp(a). Some evidence suggests statins may slightly increase Lp(a) levels, though they remain important for managing overall cardiovascular risk in people with elevated Lp(a).
New Therapies in Development
Several drugs in clinical trials take a fundamentally different approach by targeting the liver’s production of Lp(a) at the genetic level. These therapies work by silencing or blocking the gene’s instructions before the Lp(a) protein is ever made, and early results show reductions far beyond what current treatments achieve.
Pelacarsen is an antisense therapy (a drug that intercepts genetic instructions in the cell) currently in phase 3 trials, with results expected in mid-2025. Olpasiran, which uses a different silencing technology, is also in a phase 3 trial evaluating whether reducing Lp(a) by this method actually prevents heart attacks and strokes. A third drug, lepodisiran, has a phase 3 trial in recruitment. If any of these trials succeed, they would represent the first medications specifically approved to lower Lp(a), and a significant shift in how elevated levels are managed.
What To Do if Your Lp(a) Is Elevated
Because you can’t lower Lp(a) through diet or exercise, the practical strategy for people with high levels centers on aggressively managing every other cardiovascular risk factor you can control. That means keeping LDL cholesterol, blood pressure, and blood sugar well within target ranges, maintaining a healthy weight, staying physically active, and not smoking. The logic is straightforward: if Lp(a) adds a fixed amount of risk you can’t remove, reducing every modifiable risk factor becomes even more important.
Knowing your Lp(a) level also changes how your overall cardiovascular risk is calculated. Standard risk calculators don’t account for Lp(a), so an elevated level can tip someone from “borderline” into a category where more aggressive prevention makes sense. For people with both high Lp(a) and a family history of early heart disease, this information can be especially useful in guiding treatment decisions around cholesterol-lowering therapy.