What Is Lp(a), and When Should We Check It?
Published : July 10, 2025 on Medscape– Scientific Summary:
1. What is Lp(a)?
– Lipoprotein(a) [Lp(a)] is an LDL-like lipoprotein particle with an added apolipoprotein(a) tail, making it more atherogenic,
proinflammatory, and prothrombotic.
– (Measuring LDL, ApoB, lipoprotein(a), and triglycerides provides a comprehensive assessment of a patient’s atherogenic lipid profile and is usually sufficient to evaluate cardiovascular risk related to dyslipidaemia. While LDL is the primary driver of atherosclerosis,ApoB, on the other hand represents the total number of atherogenic particles; LDL, VLDL, IDL, and Lp(a). Each of these particles contains one molecule of ApoB, making ApoB a reliable indicator of the total atherogenic particle burden. Triglycerides reflect the burden of triglyceride-rich lipoproteins such as VLDL and remnants, which are particularly relevant in metabolic syndrome and diabetes. Together, this panel offers a practical and advanced lipid evaluation to guide cardiovascular prevention)
– Lipoprotein(a) is a genetically determined, independent risk factor for both:
* Atherosclerotic cardiovascular disease (ASCVD)
* Calcific aortic valve stenosis
2. Why is Lp(a) important?
– Lp(a) levels are not significantly modified by diet, exercise, or statin therapy.
– It contributes to plaque progression and rupture even when LDL-C is low.
– It is found in atherosclerotic plaques and accelerates cardiovascular events like MI and stroke.
3. How common is elevated Lp(a)?
– Roughly 1 in 5 people worldwide have high Lp(a) levels that raise ASCVD risk.
4. Inheritance pattern:
– Lp(a) is inherited in an autosomal dominant manner.
– A child of a parent with elevated Lp(a) has a 50% chance of having elevated levels as well.
5. Risk thresholds for Lp(a) (nmol/L):
• 32–90: Mild risk
• 90–200: Moderate risk
• 200–400: High risk
• >400: Very high risk
➤ In most cases, One-time lifetime measurement to assess inherited risk.
6. Who should be tested? (Targeted screening recommended):
– Individuals with personal or family history of premature ASCVD (<60 years)
– Those with familial hypercholesterolemia (FH) or other inherited dyslipidaemias
– First-degree relatives of someone with Lp(a) > 200 nmol/L
– Patients with calcific aortic valve stenosis
– Individuals with borderline 10-year CV risk (10–15%), to help reclassify risk and guide statin initiation
– Anyone with an unexplained atherosclerotic event despite low traditional risk factors
7. What is the clinical utility?
– Identifying elevated Lp(a) can:
* Explain “cryptogenic” cardiac events
* Justify earlier or more aggressive statin use
* Trigger family (cascade) screening
8. Current management for elevated Lp(a):
– No currently approved Lp(a)-lowering medications
– Apheresis (LDL filtration) is available but costly and invasive—reserved for very high-risk cases
– Novel therapies (e.g. antisense oligonucleotides) are in late-stage development
– Meanwhile, treat all modifiable risk factors intensively:
* High-intensity statin for Lp(a) > 90 nmol/L
* Target: LDL-C < 70 mg/dL (≈ 1.8 mmol/L)
or non-HDL-C < 100 mg/dL (≈ 2.5 mmol/L)
* Address BP, smoking, glucose, weight, and lifestyle
9. Specialist referral :
– Refer patients with Lp(a) > 200 nmol/L to lipid clinics
– Offer cascade screening to first-degree relatives of those with elevated Lp(a) or early CVD
10. Clinical call to action:
– Lp(a) screening is underutilised, despite being a powerful predictor of CV risk.
– GPs should be proactive in identifying at-risk individuals using Lp(a) testing.
– Even a single test can significantly alter prevention strategies and help reduce future events.
