---
title: Elevated lipoprotein(a)
description: What lipoprotein(a) is, why a high level is inherited and raises the risk of heart attack and aortic stenosis, who should have it measured and when, and which treatment approaches clinical guidelines describe.
type: disease
aliases:
  - Lp(a)
  - lipoprotein(a)
  - lipoprotein little a
  - high lipoprotein(a)
  - raised Lp(a)
  - hyperlipoproteinaemia(a)
sources:
  - tier: guideline
    org: minzdrav-rf
    title: Нарушения липидного обмена
    year: 2023
    doi: 10.15829/1560-4071-2023-5471
    url: https://cr.minzdrav.gov.ru/view-cr/752_1
  - tier: guideline
    org: esc
    title: '2019 Рекомендации ESC/EAS по лечению дислипидемий: модификация липидов для снижения сердечно-сосудистого риска'
    year: 2020
    doi: 10.15829/1560-4071-2020-3826
    url: https://doi.org/10.15829/1560-4071-2020-3826
  - tier: guideline
    org: esc
    title: '2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias (abridged Russian translation: Ateroskleroz, 2025, vol. 21, no. 4)'
    year: 2025
    doi: 10.52727/2078-256X-2025-21-4-465-477
    url: https://doi.org/10.52727/2078-256X-2025-21-4-465-477
  - tier: reference
    org: msd-manuals
    title: Dyslipidemia (MSD Manual Professional Version)
    year: 2026
    url: https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/lipid-disorders/dyslipidemia
  - tier: reference
    org: msd-manuals
    title: Overview of Lipid Metabolism (MSD Manual Professional Version)
    year: 2026
    url: https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/lipid-disorders/overview-of-lipid-metabolism
  - tier: reference
    org: msd-manuals
    title: Dyslipidemia (MSD Manual Consumer Version)
    year: 2026
    url: https://www.msdmanuals.com/home/hormonal-and-metabolic-disorders/cholesterol-disorders/dyslipidemia
sources_checked: 2026-10-14
review: null
---

Lipoprotein(a), or Lp(a), is a particle that carries cholesterol in the blood. It resembles a low-density lipoprotein (LDL, "bad" cholesterol) particle, but has an extra protein attached to it: apolipoprotein(a), or apo(a).<Cite n={[5, 6]} /> The Lp(a) level is determined by genes more than the level of any other lipoprotein, and a high level is inherited.<Cite n={[3, 6]} /> Elevated Lp(a) is common.<Cite n={3} /> It is linked to a higher risk of heart and blood vessel disease, above all [heart attack](../myocardial-infarction/) and [aortic stenosis](../aortic-stenosis/).<Cite n={3} />

The routine cholesterol test, assessment of overall risk and treatment of high cholesterol are covered in the article on [dyslipidaemia](../dyslipidemia/), and inherited high LDL cholesterol in the article on [familial hypercholesterolaemia](../familial-hypercholesterolemia/). This article is only about Lp(a).

<Diagram name="lipoprotein-a">
  <p slot="normal">
    The diagram shows an artery cut lengthwise. LDL particles and Lp(a) particles travel along it
    with the blood; an Lp(a) particle resembles LDL but has an extra protein attached to it,
    apo(a).<Cite n={[5, 6]} /> Here there are only a few Lp(a) particles in the blood.
  </p>
  <p slot="disease">
    With elevated Lp(a) there are more of these particles in the blood. They are small and, like LDL
    particles, can enter the artery wall and be retained there; this raises the risk of
    atherosclerosis, and a plaque may start to grow in the wall.<Cite n={2} />
  </p>
</Diagram>

## Why it happens

<Patient>

The Lp(a) level is set almost entirely by the genes inherited from one's parents, so a high level runs in families.<Cite n={[3, 6]} /> It also depends on ancestry: on average, people of different ethnic backgrounds have different Lp(a) levels.<Cite n={[3, 4]} />

Lp(a) particles are small. Like LDL particles, they can pass into the inner layer of the artery wall and be retained there, and this raises the risk of atherosclerosis.<Cite n={2} /> One part of the apo(a) protein resembles plasminogen, a substance involved in dissolving blood clots. This is thought to be why Lp(a) hinders the breakdown of clots and promotes their formation.<Cite n={5} /> Lp(a) also appears to promote inflammation.<Cite n={[2, 5]} />

Lp(a) levels can be higher in chronic kidney disease, especially in people on dialysis.<Cite n={[1, 5]} />

</Patient>

<Student>

Lp(a) is an LDL-like particle containing apo(a), characterised by cysteine-rich regions called kringles; one of them is homologous with plasminogen and is thought to competitively inhibit fibrinolysis and thus predispose to thrombus formation.<Cite n={5} /> The particle is less than 70 nm in diameter, can cross the endothelial barrier and, like LDL, be retained in the arterial wall; its pro-atherogenic effect is also attributed to procoagulant and pro-inflammatory actions.<Cite n={2} />

Lp(a) concentration is determined by genetics (> 90%) to a greater extent than that of any other lipoprotein, and varies with ethnicity; at least one person in five has an elevated level.<Cite n={3} /> According to the 2025 ESC/EAS update, epidemiological and genetic studies strongly support a likely causal and continuous direct association between high plasma Lp(a) and the risk of cardiovascular disease (CVD) and aortic stenosis; MSD also cites Mendelian randomisation analyses, genome-wide association studies and large meta-analyses in support of a causal relationship.<Cite n={[3, 5]} /> The 2019 ESC/EAS guidelines suggest that extremely elevated Lp(a) may represent an inherited dyslipidaemia twice as prevalent as familial hypercholesterolaemia.<Cite n={2} />

</Student>

## Symptoms

<Patient>

Elevated Lp(a) on its own usually causes no symptoms, like other abnormal blood lipid levels: many people with them have no complaints at all.<Cite n={1} /> Symptoms appear when its consequences develop: atherosclerosis and its complications.<Cite n={1} />

High Lp(a) is most strongly linked to [heart attack](../myocardial-infarction/) and [aortic stenosis](../aortic-stenosis/), a narrowing of the aortic valve; less strongly to [peripheral artery disease](../peripheral-artery-disease/) in the legs and [heart failure](../heart-failure/); and least to ischaemic stroke.<Cite n={3} /> Genetic studies have also shown a link with aortic stenosis: a high Lp(a) level that persists over a long time is associated with narrowing and calcification of the aortic valve.<Cite n={2} /> This is about increased risk: high Lp(a) does not mean that a particular person will necessarily develop one of these diseases.

</Patient>

<Student>

According to studies from the UK, Denmark and the USA summarised in the 2025 ESC/EAS update, the highest risk with high Lp(a) is associated with myocardial infarction and aortic stenosis, a lower risk with peripheral artery disease and heart failure, and the lowest with ischaemic stroke.<Cite n={3} /> Mendelian randomisation studies show that long-standing elevated LDL cholesterol (LDL-C) and Lp(a) levels are associated with aortic valve stenosis and calcification.<Cite n={2} />

</Student>

## How it is diagnosed

<Patient>

Elevated Lp(a) is found with a blood test.<Cite n={[1, 3]} /> Every adult is advised to have Lp(a) measured at least once in their lifetime, at the first blood lipid test (lipid profile) or at the next one.<Cite n={[1, 3]} /> It usually needs to be measured only once.<Cite n={6} />

The test is especially important if close relatives developed heart and blood vessel disease early, if it started early in the person themselves with no other obvious cause, in familial hypercholesterolaemia, and when the person's risk is close to the threshold at which the doctor decides to start treatment.<Cite n={[1, 3]} /> Lp(a) may rise after menopause, so it makes sense to repeat the test, especially if the earlier result was borderline.<Cite n={3} /> During an acute illness it is better to postpone the test: inflammation raises the Lp(a) level.<Cite n={4} />

The doctor assesses Lp(a) together with other risk factors. If it is not taken into account, the risk of heart and blood vessel disease may be considerably underestimated, and high Lp(a) can move a person into a higher risk category.<Cite n={3} />

</Patient>

<Student>

According to the 2025 ESC/EAS update (recommendation table 4, class IIa, level B), in all adults an Lp(a) level above 50 mg/dL should be considered a CVD risk-enhancing factor, with higher levels associated with a greater increase in risk.<Cite n={3} /> Risk increases slightly at levels from 30 to 50 mg/dL and becomes clinically significant above 50 mg/dL; this threshold is regarded as a risk modifier for potential reclassification, particularly in people at moderate risk or close to treatment decision thresholds.<Cite n={3} />

According to the Russian Ministry of Health guideline, Lp(a) should be measured at least once in a lifetime in every adult and in patients with a positive family history; an Lp(a) level above 50 mg/dL is associated with increased cardiovascular risk, and above 180 mg/dL the risk is equivalent to heterozygous familial hypercholesterolaemia; according to the 2019 ESC/EAS guidelines, such people may have a lifetime risk of atherosclerotic CVD equivalent to that of heterozygous familial hypercholesterolaemia.<Cite n={[1, 2]} /> The Russian guideline lists *hyperlipoproteinaemia(a)* among its examples of how to word a diagnosis.<Cite n={1} />

Assays report Lp(a) either in molar units (nmol/L) or in mass units (mg/dL); conversion between them depends on both particle size and concentration, and there is considerable variability between assays, partly related to the structure of apo(a) and the number of kringle IV repeats.<Cite n={[2, 3]} /> The 2025 ESC/EAS update prefers molar units but accepts mass units for clinical use.<Cite n={3} />

</Student>

## How it is treated

<Patient>

There are no medicines in routine use yet that specifically lower Lp(a).<Cite n={3} /> Nor has it been proven that lowering Lp(a) by itself reduces the risk of heart and blood vessel disease or aortic stenosis, and it is not known how much it would need to be lowered.<Cite n={3} /> Diet and most cholesterol-lowering medicines do not affect the Lp(a) level; statins do not lower it.<Cite n={[3, 6]} />

So with high Lp(a), the main goal is to lower overall risk: find other risk factors early and lower LDL cholesterol more intensively.<Cite n={[3, 4]} /> If the risk is high enough, the doctor may prescribe high-intensity statins.<Cite n={3} /> How LDL cholesterol is lowered and what you can do yourself is described in the article on [dyslipidaemia](../dyslipidemia/). Which medicines are needed and at what dose is decided by the doctor together with the patient.

For people with high Lp(a) and coronary heart disease (CHD), especially when cholesterol cannot be lowered enough with medicines, specialised hospital units may perform apheresis: removing LDL and Lp(a) from the blood with a special machine.<Cite n={[1, 4]} /> Medicines that specifically lower Lp(a) are now being studied in clinical trials.<Cite n={[3, 4]} />

</Patient>

<Student>

According to the 2025 ESC/EAS update, in the absence of specific Lp(a)-lowering therapy, early identification of risk factors and more intensive LDL-C lowering are reasonable, taking into account both absolute cardiovascular risk and the Lp(a) level; patients with high Lp(a) are recommended to take or continue high-intensity statins if their risk is high enough.<Cite n={3} /> An analysis of participants in seven randomised placebo-controlled trials showed that statins do not affect Lp(a) concentration.<Cite n={3} /> MSD: the usual approach in elevated Lp(a) is to lower LDL-C aggressively; few data exist to guide treatment of elevated Lp(a) or to establish treatment efficacy.<Cite n={4} />

Unlike statins, PCSK9-inhibiting monoclonal antibodies also lower Lp(a); the relative contribution of this effect to risk reduction needs to be assessed in appropriately designed clinical trials.<Cite n={[2, 4]} /> In randomised trials, therapies that moderately lowered Lp(a) did not show a reduction in CVD risk beyond what is explained by lowering apoB-containing lipoproteins; data on PCSK9 inhibitors suggest that lowering Lp(a) may matter.<Cite n={2} />

According to the Russian Ministry of Health guideline, plasmapheresis and plasma sorption are performed only in specialised hospital units; the indications include hyperlipoproteinaemia(a) in patients with CHD, especially combined with hypercholesterolaemia refractory to therapy.<Cite n={1} /> Agents that specifically lower Lp(a) — injectable RNA-based therapy (an antisense oligonucleotide or a small interfering RNA) targeting apo(a) production in hepatocytes, and an oral small-molecule inhibitor — are being studied in randomised clinical trials.<Cite n={[3, 4]} />

</Student>

## When to call an ambulance

Elevated Lp(a) on its own does not need emergency care; the danger lies in the complications of atherosclerosis it is linked to: heart attack and ischaemic stroke.<Cite n={[1, 3]} /> For chest pain or pressure, severe shortness of breath, fainting or signs of a stroke, call your local emergency number (112 in the EU, 911 in the US and Canada, 999 in the UK) at once: this is the site's general safety rule. The signs of a heart attack are described in the article on [myocardial infarction](../myocardial-infarction/), and the signs of a stroke in the article on [carotid artery stenosis](../carotid-artery-stenosis/).

<Quiz />