Lipoprotein a (Lp(a), pronounced “Lp little a”) is a genetically determined lipoprotein that’s emerged as an independent cardiovascular risk factor. Unlike LDL and HDL cholesterol, Lp(a) levels are largely fixed by genetics and don’t respond meaningfully to diet, exercise, or most cholesterol medications. About 20% of people have elevated Lp(a) — a significant portion of unexplained cardiovascular risk. This guide covers what Lp(a) is, normal ranges, clinical implications, and emerging treatments.
What Lp(a) is
Lipoprotein(a) is an LDL-like particle with an additional protein called apolipoprotein(a) attached. The apo(a) component varies in size based on the LPA gene. Unlike LDL cholesterol, which can be modified through diet and statins, Lp(a) levels are determined primarily by genetics and remain relatively stable throughout life.
Elevated Lp(a) increases risk for:
- Atherosclerotic cardiovascular disease (heart attacks)
- Calcific aortic valve stenosis
- Stroke
Reference ranges
Lp(a) is measured in mass units (mg/dL) or molar units (nmol/L):
- Optimal: under 30 mg/dL or 75 nmol/L
- Borderline: 30-50 mg/dL or 75-125 nmol/L
- High: above 50 mg/dL or 125 nmol/L
- Very high: above 100 mg/dL or 250 nmol/L
About 20% of the population has elevated Lp(a).
Why Lp(a) testing matters
Lp(a) is an independent risk factor — it adds risk beyond what’s captured by LDL, HDL, and other standard markers. A patient with normal LDL but high Lp(a) still has elevated cardiovascular risk that won’t be addressed by standard statin therapy alone.
The American Heart Association and other organizations now recommend at least one Lp(a) measurement in adulthood, particularly for patients with:
- Family history of premature cardiovascular disease
- Personal history of cardiovascular disease at younger ages
- Family history of elevated Lp(a)
- Cardiovascular events without conventional risk factors
Treatment of elevated Lp(a)
Currently no FDA-approved Lp(a)-lowering medications exist. Standard cholesterol medications (statins, ezetimibe) don’t significantly reduce Lp(a). Limited options:
- PCSK9 inhibitors: Reduce Lp(a) modestly (~25-30%)
- Niacin: Reduces Lp(a) modestly but cardiovascular benefit unclear
- Apheresis: Available for very high-risk patients
- Aggressive LDL lowering: Doesn’t lower Lp(a) but reduces overall risk
Several novel Lp(a)-targeted therapies are in late-stage clinical trials, including pelacarsen (antisense oligonucleotide), olpasiran (siRNA), lepodisiran, and others. These may achieve dramatic Lp(a) reductions, though cardiovascular outcomes data is pending.
Should everyone get Lp(a) tested?
Recent guidelines support universal once-in-lifetime Lp(a) testing in adulthood, particularly for cardiovascular risk assessment. The information is genetically determined and doesn’t change significantly, so a single test provides lifetime risk information.
Clinical impact depends on what you’d do with the result. Currently, elevated Lp(a) primarily intensifies attention to other modifiable risk factors (LDL, blood pressure, smoking) rather than enabling specific Lp(a)-targeted treatment. Once Lp(a)-lowering drugs are approved, screening becomes more actionable.
Frequently Asked Questions
Do I need to fast for Lp(a) testing?
Generally no. Lp(a) doesn’t fluctuate significantly with eating.
How often should I check Lp(a)?
Once in adulthood is typically sufficient. Levels are genetically determined and stable.
Can lifestyle change Lp(a)?
Minimally. Diet, exercise, and weight loss don’t significantly affect Lp(a).
What does high Lp(a) mean for my risk?
Increased cardiovascular and aortic stenosis risk independent of LDL. Most clinicians address by intensifying control of modifiable risk factors.
Will Lp(a)-lowering drugs become available?
Multiple agents are in late-stage clinical trials. FDA approvals expected in coming years if outcomes data confirms benefit.
The bottom line on the Lp(a) test
Lipoprotein(a) is an independent genetic cardiovascular risk factor that affects about 20% of people. Testing once in adulthood is increasingly recommended. Treatment is currently limited but novel Lp(a)-lowering therapies are in late-stage development. Elevated Lp(a) intensifies attention to other modifiable risk factors. Discuss with your healthcare provider in the context of overall cardiovascular risk assessment.