Lipoprotein(a) [Lp(a)] Test
The lipoprotein(a) [Lp(a)] test measures a genetically determined, LDL-like particle that is an independent risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis. Because its level is largely inherited and stable through life, a single measurement usually suffices to establish lifelong risk.
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Biomarkers
Blood (serum)
Sample
2–4 business days
Turnaround
No — Lp(a) is not meaningfully affected by fasting
Fasting
What is the Lp(a) test?
The Lipoprotein(a) Test measures Lp(a), a genetically determined, LDL-like particle that is an independent risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis. Because its concentration is largely inherited and stable through life, it identifies a component of cardiovascular risk that the standard lipid panel does not capture and that diet and lifestyle do little to change. Within cardiovascular risk assessment, Lp(a) is increasingly recommended as a once-in-a-lifetime measurement to refine risk, particularly in people with premature atherosclerotic disease, a family history of it, a family history of elevated Lp(a), or recurrent events despite controlled LDL cholesterol. An elevated Lp(a) raises the estimated cardiovascular risk and prompts more intensive management of modifiable risk factors, since conventional therapies have limited effect on Lp(a) itself. It complements LDL-C, ApoB, and hs-CRP, and is best reported in nmol/L. Because it is genetically driven, an elevated result also carries implications for screening relatives.
What does the Lp(a) test measure?
Lipoprotein(a) is an LDL-like particle in which apolipoprotein(a) is covalently linked to apolipoprotein B-100. Its plasma concentration is largely genetically determined by the LPA gene, with the apo(a) isoform size inversely related to concentration, and levels remain relatively stable through life and are minimally affected by diet or lifestyle. Lp(a) is thought to be pro-atherogenic, pro-inflammatory, and pro-thrombotic, contributing to atherosclerosis and aortic valve disease. Because levels are inherited and stable, a single measurement is usually sufficient to establish lifelong risk.
Lp(a) is an independent, genetically determined risk factor for atherosclerotic cardiovascular disease and aortic stenosis, identifying inherited risk not captured by the standard lipid panel. It is used to refine risk assessment, particularly in those with a personal or family history of premature cardiovascular disease, and to inform the intensity of risk-factor management. Reporting in nmol/L (particle concentration) is preferred over mg/dL (mass) because the two are not directly interchangeable across the range of isoform sizes.
Why is the Lp(a) test ordered?
- Refinement of cardiovascular risk in individuals with a personal history of premature atherosclerotic cardiovascular disease
- Assessment of those with a family history of premature cardiovascular disease or of elevated Lp(a)
- Evaluation of recurrent cardiovascular events or progressive disease despite well-controlled LDL cholesterol
- Risk stratification in patients with familial hypercholesterolaemia or strong overall cardiovascular risk profiles
- Assessment of unexplained or borderline cardiovascular risk where an inherited contributor is suspected
- Evaluation of aortic valve stenosis risk where elevated Lp(a) is a recognised contributor
- Once-in-a-lifetime measurement as part of comprehensive cardiovascular risk assessment, given its stable, genetically determined level
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No — Lp(a) is not meaningfully affected by fasting
Collection method
Venipuncture at patient service centre
Turnaround
2–4 business days
Collection notes
Fasting is not required. Prefer an assay reporting in nmol/L (particle number) for accuracy across isoform sizes. Measure when the patient is clinically stable, as significant inflammation can transiently raise Lp(a). A single measurement usually suffices given the genetically stable level.
Specimen requirements
Minimum 0.5 mL serum. Separate serum from cells per Access Medical Laboratories protocol. Specimen stable refrigerated; follow Access Medical Laboratories transport guidelines.
What can affect Lp(a) results?
Lp(a) is largely set by the LPA gene and remains stable through life, so a single measurement usually suffices and repeat testing rarely changes the result, unlike modifiable lipids.
Apo(a) isoform-size variation affects mass-based (mg/dL) assays, which can over- or under-estimate Lp(a) depending on isoform. Particle-number assays reporting nmol/L are less affected and preferred for accuracy.
As an acute-phase reactant to a modest degree, Lp(a) can rise transiently during significant inflammation or illness, so measurement is best made when the patient is stable.
Chronic kidney disease, particularly nephrotic syndrome, can raise Lp(a) levels independent of the underlying genetic set point.
Lp(a) tends to be modestly higher after menopause, and oestrogen therapy can lower it slightly, though these effects are minor relative to the dominant genetic determinant.
Statins do not lower Lp(a) and may modestly raise it, so an Lp(a) result is interpreted as a fixed risk marker rather than a treatment-responsive target with conventional therapy.
What do Lp(a) results mean?
Elevated
An elevated Lp(a) marks increased, genetically determined risk of atherosclerotic cardiovascular disease and aortic stenosis. It prompts intensified management of modifiable risk factors, particularly LDL cholesterol, since Lp(a) itself responds little to standard therapy, and supports consideration of screening first-degree relatives.
Normal
An Lp(a) within the desirable range suggests this genetic risk factor is not elevated. Because the level is stable through life, a normal result usually does not need repeating, though overall cardiovascular risk still depends on the full risk-factor profile.
Reduced
A low Lp(a) is favourable and indicates this inherited contributor is not adding to cardiovascular risk. There is no recognised adverse effect of a low Lp(a).
Note: Lp(a) is largely genetic and stable, so it is generally a once-in-a-lifetime measurement and is interpreted as a fixed risk marker. nmol/L reporting is preferred because mass-based mg/dL assays are affected by isoform size and the two units are not directly convertible. Inflammation and renal disease can transiently raise it, and standard lipid-lowering therapy does little to change it, so management focuses on the broader risk profile and an elevated result has implications for relatives.
Frequently asked questions
It measures Lp(a), a genetically determined, LDL-like particle that is an independent risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis, identifying inherited risk not captured by the standard lipid panel.
How to access the Lp(a) test
The Lp(a) reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: June 2, 2026
Last reviewed: June 2, 2026
- Wilson DP, et al. Use of Lipoprotein(a) in clinical practice: a biomarker whose time has come. A scientific statement from the National Lipid Association. J Clin Lipidol. (2019)
- Kronenberg F, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: an EAS consensus statement. Eur Heart J. (2022)
- Nordestgaard BG, et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. (2010)
- Tsimikas S. A Test in Context: Lipoprotein(a). J Am Coll Cardiol. (2017)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.
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