Lipoprotein(a): the genetic risk factor hiding in plain sight

Lp(a) (pronounced "L‑P‑little‑a") is one of the most important cholesterol-related risk factors that most people have never had measured.

It's largely genetic, doesn't respond much to lifestyle, and can meaningfully raise lifetime risk for heart attack, stroke, and aortic valve disease.

TL;DR

• Lp(a) is genetic and usually stable for life.
• A one-time test is recommended for many people (especially with family history or early disease).
• If Lp(a) is high, the plan is usually: treat everything else more aggressively (LDL/ApoB, BP, weight, glucose, smoking).
• New Lp(a)-lowering therapies are in late-stage trials, but you can reduce risk today.

What exactly is Lp(a)?

Lp(a) is an LDL-like particle with an extra protein attached (apo(a)). That extra protein can make Lp(a):

• more likely to promote atherosclerosis, and
• potentially more "pro-thrombotic" (clot-promoting), though the biology is complex.

The key clinical point: high Lp(a) is an independent risk enhancer.

Who should test Lp(a)?

In practice, I think of Lp(a) as a "once-in-a-lifetime" test for many adults—especially if you have:

• Family history of early heart attack or stroke
• Personal history of early ASCVD
• High LDL or suspected familial hypercholesterolemia
• Aortic stenosis or family history of it
• "Unexplained" plaque despite "normal" routine cholesterol

Many societies support broader or universal testing at least once—because it changes how aggressive we should be with prevention.

How do I interpret the number?

Labs report Lp(a) in mg/dL or nmol/L (not directly interchangeable in a simple way). Interpretation is best done using the unit your lab reports.

As a general framework:

• Higher Lp(a) = higher lifetime risk
• Risk also depends on other factors: LDL/ApoB burden, BP, diabetes, smoking, CAC score, etc.

This is where a prevention visit can be very helpful: we translate a number into a plan.

If Lp(a) is high, what can you do right now?

This is the part I want patients to hear clearly:

High Lp(a) is not a diagnosis. It's a risk signal—and risk is modifiable.

Because lifestyle doesn't reliably lower Lp(a) itself, we reduce risk by:

1. Lowering LDL-C / ApoB more aggressively
2. Optimizing blood pressure
3. Optimizing metabolic health (weight trajectory, A1c/glucose, fatty liver)
4. Avoiding tobacco and limiting exposures that raise inflammation risk
5. Considering CAC scoring in the right patient to refine intensity

Therapy decisions are individualized, but the prevention philosophy is consistent: reduce the total atherogenic "load" over time.

Do statins lower Lp(a)?

Statins are still foundational for ASCVD risk reduction when indicated, but they do not meaningfully lower Lp(a) (and in some people Lp(a) may rise slightly). The outcome benefit of statins is still strong because they reduce LDL/ApoB and plaque risk overall.

What about aspirin?

This is nuanced. Aspirin is not for everyone in primary prevention. But in select higher-risk patients (for example, high Lp(a) plus evidence of plaque), clinicians sometimes discuss aspirin after weighing bleeding risk. This should be a personalized decision.

Practical next steps

• If you've never checked Lp(a), ask your clinician for a one-time test.
• If it's elevated, ask: "What is my ApoB goal?" and "Should we consider CAC to refine my risk?"
• Make sure the basics are locked in: BP, sleep, movement, nutrition quality, weight trend, glucose, and smoking status.

References (patient-friendly)

• 2018 AHA/ACC Multisociety Cholesterol Guideline (Circulation, 2019)
• 2022 ACC Expert Consensus Decision Pathway on nonstatin therapies (JACC, 2022)
• European Atherosclerosis Society consensus statements on Lp(a) (various updates)

Educational content only; not medical advice.