High Lp(a) Test Result?

Yes. Lipoprotein(a) is genetically determined and not reflected in standard cholesterol panels. Approximately 20% of people have elevated Lp(a) regardless of their lifestyle or other cholesterol numbers.

Since high Lp(a) can multiply cardiovascular risk up to 4 times, specific testing is the only way to identify this hidden risk factor.

Lp(a) testing requires a specific blood test that's not included in standard lipid panels. You'll need to request it specifically from your healthcare provider using the lab code for Lipoprotein(a).

Most insurance plans cover Lp(a) testing when medically indicated, and out-of-pocket costs are typically $30-75 if paying directly.

Lp(a) levels are measured in mg/dL or nmol/L. Generally:

• < 30 mg/dL (< 75 nmol/L): Low risk
• 30-49 mg/dL (75-124 nmol/L): Mildly elevated
• ≥ 50 mg/dL (≥ 125 nmol/L): High risk (2-4x increased cardiovascular risk)
• ≥ 180 mg/dL (≥ 430 nmol/L): Very high risk

Absolutely not. While elevated Lp(a) significantly increases cardiovascular risk, it means you need more proactive, targeted prevention strategies.

This includes aggressive management of other risk factors (LDL cholesterol, blood pressure) and adopting heart-protective lifestyle habits. Knowing your Lp(a) status empowers you to take precisely the right protective actions.

Lp(a) contributes to cardiovascular disease through multiple mechanisms:

• Accelerated plaque buildup: Promotes atherosclerosis more aggressively than LDL
• Increased inflammation: Triggers chronic inflammatory responses in artery walls
• Enhanced clotting: Interferes with natural clot-dissolving processes
• Valve damage: Contributes to aortic valve calcification and stenosis
• Risk multiplication: Amplifies damage from other risk factors

Lp(a) levels are primarily genetically determined and show minimal response to dietary changes or exercise. However, you can significantly reduce your overall cardiovascular risk by aggressively managing other modifiable factors.

Focus on optimizing LDL cholesterol, blood pressure, blood sugar, and inflammation markers. Emerging therapies specifically targeting Lp(a) reduction are in advanced clinical trials.

Today's care focuses on overall cardiovascular risk reduction and selected therapies that also influence Lp(a). Access/indications vary by region and patient profile.

• PCSK9 monoclonal antibodies (evolocumab, alirocumab): typical Lp(a) change ↓ ~25–30%
• Niacin: typical Lp(a) change ↓ ~35–40% (not routinely recommended in guidelines due to tolerability and neutral outcomes)
• CETP inhibitors (class; investigational, e.g., obicetrapib): typical Lp(a) change ↓ ~45%
• Inclisiran: typical Lp(a) change ↓ ~10–20%
• Statins: may show ~0% change or a small increase (up to ~20%); still cornerstone for LDL-C risk reduction

Lp(a)-specific agents are in Phase 3/late stages with cardiovascular outcomes readouts expected in the coming years.

Yes. Lp(a) levels are strongly inherited, and first-degree relatives (parents, siblings, children) have approximately a 50% chance of sharing similar risk levels.

While testing children isn't typically recommended (levels stabilize around age 5), adult family members should discuss Lp(a) testing with their healthcare providers, especially if there's a family history of early heart disease.

Lp(a) levels stabilize in early childhood and remain relatively constant throughout life. Knowing your status early allows for decades of targeted prevention.

Many cases of "unexpected" cardiovascular events in apparently healthy individuals can be traced to undetected high Lp(a). Early knowledge enables long-term, proactive risk management rather than reactive treatment.