Why is Lp(a) different?
Lipoprotein(a), or Lp(a), resembles an LDL particle but also carries apolipoprotein(a). The concentration is largely determined by genetics and usually remains relatively stable through adulthood.
How does it relate to risk?
Genetic and epidemiologic evidence supports elevated Lp(a) as a causal risk factor for atherosclerotic cardiovascular disease and calcific aortic valve stenosis. Risk rises across the concentration range; there is no perfect biological line between “normal” and “abnormal.”
Who should be tested?
The 2026 ACC/AHA dyslipidemia guideline recommends that Lp(a) be measured at least once in adulthood. The result is especially relevant with premature cardiovascular disease, a strong family history, familial hypercholesterolemia, or risk that appears greater than standard factors explain.
What is considered high?
The 2026 U.S. guideline identifies 125 nmol/L or 50 mg/dL and above as elevated. The result should still be interpreted as part of overall risk rather than as an isolated diagnosis.
Are mg/dL and nmol/L interchangeable?
No—not precisely. The units measure different properties, and a fixed conversion can be inaccurate because apolipoprotein(a) particle size varies. Use the unit reported by the laboratory.
What happens if the level is elevated?
Do not self-treat. The practical response is to refine risk and address modifiable factors—such as LDL-C, blood pressure, smoking, diabetes, nutrition, and physical activity—through an individualized prevention plan. Clinical trials of therapies that specifically lower Lp(a) are evolving, so treatment claims should be tied to current outcome evidence and regulatory approval.