---
title: High cholesterol (dyslipidaemia)
description: What dyslipidaemia is, why high cholesterol is dangerous for the arteries, how it is detected and what treatment approaches the clinical guidelines describe.
type: disease
aliases:
  - dyslipidaemia
  - dyslipidemia
  - hypercholesterolaemia
  - high cholesterol
  - hyperlipidaemia
  - familial hypercholesterolaemia
  - FH
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: nice
    title: 'Cardiovascular disease: risk assessment and reduction, including lipid modification (NG238)'
    year: 2023
    url: https://www.nice.org.uk/guidance/ng238
  - tier: reference
    org: msd-manuals
    title: Dyslipidemia (Hyperlipidemia)
    year: 2025
    url: https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/lipid-disorders/dyslipidemia
sources_checked: 2026-10-12
review: null
---

Dyslipidaemia is a condition in which the levels of lipids (fats) and lipoproteins in the blood are outside the normal range.<Cite n={1} /> It can mean high cholesterol, high triglycerides or both, or a low level of high-density lipoprotein (HDL) cholesterol.<Cite n={4} /> Dyslipidaemia contributes to atherosclerosis, a disease of the arteries that leads to heart attacks and strokes.<Cite n={[1, 4]} /> In the Russian ESSE-RF study, raised total cholesterol (5.0 mmol/L or higher) was found in more than half of the people examined: 58.4% on average.<Cite n={1} />

<Diagram name="dyslipidemia">
  <p slot="normal">Cholesterol and other fats are carried in the blood inside particles called lipoproteins, including low-density lipoproteins (LDL).<Cite n={2} /> The fewer of these particles there are in the blood, the fewer are deposited in the artery wall.<Cite n={2} /></p>
  <p slot="disease">When there are many LDL particles in the blood, they enter the artery wall and are retained there. Lipids build up in the wall and an atherosclerotic plaque starts to form; over time it grows.<Cite n={2} /></p>
</Diagram>

## Why it happens

<Patient>

LDL particles, which carry cholesterol, can enter the inner layer of the artery wall and stay there.<Cite n={[1, 2]} /> Little by little, fats build up in the wall and an atherosclerotic plaque grows.<Cite n={2} /> The higher the LDL cholesterol level and the longer it stays high, the more advanced the atherosclerosis.<Cite n={2} />

Most often, high cholesterol results from a combination of small inherited influences and lifestyle: smoking, an unhealthy diet and lack of physical activity.<Cite n={1} /> Lipid levels can also be raised by other conditions, such as diabetes, an underactive thyroid, kidney disease and liver disease, as well as by drinking too much alcohol and by some medicines.<Cite n={[1, 3, 4]} />

There is also an inherited disease called familial hypercholesterolaemia. In it, LDL cholesterol is persistently high and atherosclerosis develops early.<Cite n={1} /> Its milder form affects about 1 in 250 people.<Cite n={1} />

</Patient>

<Student>

Dyslipidaemias can be secondary (acquired) or inherited (primary); in the great majority of cases they are primary polygenic dyslipidaemias, resulting from a combination of weak genetic influences and environmental factors: smoking, poor diet and a sedentary lifestyle.<Cite n={1} /> The main causes of secondary dyslipidaemia are diabetes mellitus, hypothyroidism and chronic kidney disease.<Cite n={1} /> NICE recommends excluding possible common secondary causes of dyslipidaemia (such as excess alcohol intake, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome) before referring for specialist review.<Cite n={3} />

Familial hypercholesterolaemia (FH) is an autosomal dominant disease caused by mutations in the LDLR, APOB and PCSK9 genes, with persistently raised LDL cholesterol (LDL-C) and early atherosclerosis; there is a milder heterozygous form and a more severe homozygous form.<Cite n={1} /> The prevalence of the heterozygous form is 1/250 and of the homozygous form 1/300,000.<Cite n={1} />

ApoB-containing lipoproteins smaller than 70 nm in diameter can cross the endothelial barrier, especially in the presence of endothelial dysfunction, and be trapped by extracellular structures such as proteoglycans.<Cite n={2} /> Lipoproteins retained in the arterial wall trigger a process that results in lipid deposition and the formation of an atheroma.<Cite n={2} /> The size of the plaque is determined by the concentration of circulating LDL and other apoB-containing lipoproteins and by the total duration of exposure to them.<Cite n={2} /> LDL-C is causally associated with the risk of atherosclerotic cardiovascular disease (CVD), and lowering LDL-C reduces this risk in proportion to the absolute reduction in LDL-C.<Cite n={2} />

</Student>

## Symptoms

<Patient>

High cholesterol on its own usually causes no symptoms: many people with high lipid levels have no complaints at all.<Cite n={[1, 4]} /> Symptoms appear as atherosclerosis progresses.<Cite n={1} /> Atherosclerosis of the heart arteries shows itself as angina and heart attack; of the brain arteries, as poor blood supply to the brain, which can go as far as a stroke; and of the leg arteries, as intermittent claudication (leg pain when walking).<Cite n={1} />

High cholesterol can cause visible signs: flat yellow patches on the eyelids (xanthelasma), lumps on the tendons (xanthomas) and lipid deposits in the cornea around the iris (corneal arcus); corneal arcus is a meaningful sign if it is found in someone under 45.<Cite n={[1, 4]} /> High triglycerides can cause acute pancreatitis, an inflammation of the pancreas.<Cite n={4} />

</Patient>

<Student>

Clinical manifestations are caused by the progression of atherosclerosis driven by dyslipidaemia.<Cite n={1} /> Physical examination looks for corneal arcus in people under 45, xanthelasma and xanthomas.<Cite n={1} /> High LDL-C levels can cause tendinous xanthomas at the Achilles, elbow and knee tendons and over the metacarpophalangeal joints.<Cite n={4} />

Very high triglyceride (TG) levels can cause paraesthesia, dyspnoea and confusion, and high TG levels can cause acute pancreatitis.<Cite n={4} />

</Student>

The danger of atherosclerosis is that a plaque can rupture: a blood clot forms on it and blocks the vessel. Depending on where this happens, the result is unstable angina, myocardial infarction or ischaemic stroke.<Cite n={1} /> The signs of a heart attack, and when to call your local emergency number (112 in the EU, 911 in the US and Canada, 999 in the UK) straight away, are described in the article on [coronary heart disease](../../disease/coronary-heart-disease/).

## How it is diagnosed

<Patient>

Dyslipidaemia is detected with a blood test called a lipid profile, which measures total cholesterol, LDL and HDL cholesterol, and triglycerides.<Cite n={[1, 3, 4]} /> Everyone over 40 is advised to have this test to assess their risk of heart and blood vessel disease.<Cite n={1} /> For this check you usually do not need to fast; if triglycerides are high, the blood sample is taken after fasting.<Cite n={1} /> At least once in their life, every adult is advised to have one more measurement: lipoprotein(a).<Cite n={1} />

Based on the results, the doctor assesses the overall risk of heart and blood vessel disease.<Cite n={1} /> People who already have heart or blood vessel disease, familial hypercholesterolaemia, diabetes, stage 3–5 chronic kidney disease or LDL cholesterol above 4.9 mmol/L are placed straight away in the high or very high risk group.<Cite n={1} />

</Patient>

<Student>

Screening with a lipid profile is recommended for everyone over 40 to stratify cardiovascular risk using SCORE2; LDL-C is the main measure for risk assessment.<Cite n={1} /> The lipid profile is measured in venous blood, with calculation of LDL-C and non-HDL-C.<Cite n={1} /> For screening, fasting is not required, but in hypertriglyceridaemia blood should be taken fasting.<Cite n={1} /> Lp(a) should be measured at least once in a lifetime in every adult; an Lp(a) level > 50 mg/dL is associated with increased cardiovascular risk.<Cite n={1} />

Patients with established CVD, FH, diabetes mellitus, stage 3–5 chronic kidney disease (CKD), very high risk on SCORE2 or LDL-C > 4.9 mmol/L are classed as high or very high risk.<Cite n={1} />

</Student>

## How it is treated

<Patient>

The doctor chooses treatment according to the overall risk of heart and blood vessel disease: the higher the risk, the lower the target LDL cholesterol level.<Cite n={1} /> Treatment rests on lifestyle: a diet with vegetables, fruit, wholegrain foods, nuts and fish, and limited sweets, sugary drinks and red meat; stopping smoking; regular physical activity; and losing excess weight.<Cite n={[1, 3]} />

The main medicines are statins: they lower LDL cholesterol and, with it, illness and death from heart and blood vessel disease.<Cite n={[1, 4]} /> If a statin is not enough or is not suitable, the doctor may add other medicines or prescribe them instead, including injections.<Cite n={1} /> Treatment is usually long-term, in practice lifelong.<Cite n={1} /> Which medicines are needed and at what dose is decided by the doctor together with the patient.

</Patient>

<Student>

LDL-C targets in the Russian Ministry of Health guideline: at very high risk < 1.4 mmol/L and a reduction of at least 50% from baseline; at high risk < 1.8 mmol/L and a reduction of at least 50%; at moderate risk < 2.6 mmol/L; at low risk < 3.0 mmol/L.<Cite n={1} /> For patients with established atherosclerotic CVD who have had a recurrent vascular event within 2 years despite the maximum tolerated statin dose, an LDL-C target < 1.0 mmol/L is recommended.<Cite n={1} /> The UK NICE guideline sets a different target for secondary prevention: LDL-C ≤ 2.0 mmol/L or non-HDL-C ≤ 2.6 mmol/L.<Cite n={3} />

A healthy lifestyle is recommended at every level of risk, and lipid-lowering drugs are added depending on risk and LDL-C level; in patients with CVD, statins are prescribed regardless of cholesterol level.<Cite n={1} /> Statin therapy at the doses needed to reach the LDL-C target is recommended for all patients with dyslipidaemia.<Cite n={1} /> If the target is not reached on maximum tolerated statin doses, combination therapy should be considered, including a statin with ezetimibe, which inhibits intestinal cholesterol absorption, preferably in a single tablet or capsule.<Cite n={1} /> In very-high-risk patients who do not reach the target on a statin plus ezetimibe, adding alirocumab, evolocumab (monoclonal antibodies against PCSK9) or inclisiran is recommended for secondary prevention; these drugs are given by subcutaneous injection.<Cite n={1} /> For patients who cannot tolerate any dose of statin, ezetimibe is recommended.<Cite n={1} /> NICE describes bempedoic acid with ezetimibe as an option if statins are contraindicated or not tolerated, and ezetimibe alone does not control LDL cholesterol well enough.<Cite n={3} />

To lower TG, fibrates and omega-3 polyunsaturated fatty acids are used, among other options.<Cite n={[1, 4]} /> If the LDL-C target is not reached after 6 months of combination lipid-lowering therapy at maximum tolerated doses, extracorporeal removal of atherogenic lipoproteins is used: plasmapheresis or plasmasorption.<Cite n={1} />

</Student>

<Quiz />