Lipid-regulating Drugs including Statins

Authored by , Reviewed by Dr Hayley Willacy | Last edited | Meets Patient’s editorial guidelines

Added to Saved items
This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Statins and other Lipid-lowering Medicines article more useful, or one of our other health articles.

Read COVID-19 guidance from NICE

Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

Lipid-regulating drugs are used to treat dyslipidaemias, primarily raised cholesterol. Hypercholesterolaemia is a major cause of atherosclerosis and contributes to the high levels of mortality and morbidity in the UK due to cardiovascular disease (CVD). It is important as one of the three main modifiable risk factors for CVD (the others being smoking and hypertension).

Patients often ask what a 'normal' or 'healthy' serum cholesterol should be. Unfortunately, there is no clear dividing line between what constitutes a safe level and what constitutes an unsafe level; rather, a continuous spectrum from low to higher risk, along which an individual's cholesterol should be interpreted in context with their other cardiovascular risk factors.[1, 2] Statin therapy reduces individuals' relative risk of cardiovascular events by approximately 30% after around four years of treatment.[3] Determining the absolute risk reduction, and therefore estimating the magnitude of benefit of treatment, requires calculating the baseline cardiovascular risk for that individual. In short, people with a high baseline cardiovascular risk are more likely to benefit from lipid-lowering therapy, whereas those with a low risk are less likely to see any benefits.

See the separate Hyperlipidaemia article.

See the separate Prevention of Cardiovascular Disease and Cardiovascular Risk Assessment articles.

(Or 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors)

The statins (atorvastatin, fluvastatin, pravastatin, rosuvastatin, and simvastatin) competitively inhibit HMG-CoA reductase. Statins are more effective than other lipid-regulating drugs at lowering LDL-cholesterol concentration but are less effective than fibrates in reducing triglyceride concentration.[4]

Mode of action and indications

  • Competitive inhibitors of the rate-limiting step of hepatic cholesterol synthesis. With a reduced cholesterol pool in the liver, LDL receptor expression is upregulated and increased LDL uptake from plasma takes place, lowering plasma LDL-C. This protects against the development of atheroma and there is a firm evidence base for their use in both primary and secondary prevention of CVD. The relative risk reduction in primary and secondary prevention is about the same. Since the absolute risk is by definition higher in secondary prevention, the benefit of statins is greater in this scenario than in primary prevention.[5]
  • Statins are also thought to have non-cholesterol-related effects such as restoring/improving endothelial function, and anti-inflammatory properties. These are implicated in benefits seen when use of high-intensity statins is initiated early following an acute myocardial infarction, after percutaneous coronary angiography and in acute coronary syndrome.[6]
  • Statins have a role to play in the regression of atheroma. They reduce the lipid content of plaques and stabilise them through the formation of fibrous caps and microcalcification.[7]
  • Statins may also reduce the risk of developing atrial fibrillation.[8]

Who should be on a statin?

National Institute for Health and Care Excellence (NICE) guidelines suggest that statins should be offered:[9]

  • To all adults with:
  • For primary prevention:
    • All those aged up to 84 years who have a 10-year risk of CVD of 10% or more as measured by the QRISK3 risk assessment tool, if lifestyle measures to reduce CVD risk have been ineffective. The ESC guidelines of 2019 recommend that statins are recommended for primary prevention, according to the level of risk, for older people aged 75 or less, and may be considered for over-75s if at high risk or above.[5]
    • All those aged 85 years and over by virtue of age alone, unless comorbidities, patient preference or contra-indications make this inappropriate.
    • All adults with type 1 diabetes, particularly those who:
      • Are aged over 40 years; or
      • Have had diabetes for more than 10 years; or
      • Have established nephropathy; or
      • Have other cardiovascular risk factors.
    • All adults with chronic kidney disease (CKD).[10]
    • In the past there has been much debate as to the long-term benefits versus risk of statins in primary prevention. A Cochrane review has confirmed a reduction in all-cause mortality, vascular events and revascularisations.[11] A more recent Irish review concluded that the evidence for the effectiveness of statins in primary prevention was mixed,.[12] and a 2022 meta-analysis of primary and secondary prevention randomised controlled trials highlighted that although statins offer reasonable relative risk reduction, the absolute risk reduction is modest.[13] During discussions with patients, the degree of risk reduction should be discussed, along with the possibility of harms and side-effects, to allow for informed decision-making. Patient decision aids, such as the one produced by NICE, may be helpful.[14]

NICE recommends using a 'systematic strategy to identify people who are likely to be at high risk' of developing CVD, and reviewing this risk on an ongoing basis for people over the age of 40 - thereby essentially advocating population screening for CVD risk.[15]

Lipid dysfunction is an early feature of type 2 diabetes but further research is required to elucidate the risk:benefit ratio of individuals with low CVD risk;[16] NICE currently recommends that statins are only offered for primary prevention to people with type 2 diabetes if their 10-year cardiovascular risk is 10% or greater.


Statins are usually well tolerated. Side-effects may including fatigue, headache, nausea, indigestion or change in bowel habit. Important but rarer side-effects include:

Muscle effects[5, 17]

  • The most important adverse effect of these drugs is myalgia characterised by muscle and tendon pain, stiffness, muscle weakness and cramping. This affects 10-15% of patients taking statins in observational trials. However, these symptoms are common in the general population, especially with increasing age, and recent research suggests that, in many cases, these may not be directly attributable to statins. In randomised controlled trials, in which patients are blind to whether they are taking statin or placebo, there is little or no increase in muscle symptoms between statin and placebo groups.[18] This has also been investigated at the individual patient level: the StatinWISE trial investigated the effect of statins on muscle symptoms in people who had stopped, or were considering stopping, statins due to muscle symptoms. Participants were given atorvastatin, then placebo, in sequence and were blind to which they were taking; there was no difference in self-reported muscle symptoms when taking atorvastatin, compared to placebo.[19]
  • Statin-induced myopathy includes a spectrum from asymptomatic increase in serum creatine kinase (CK) to myalgia, myositis and, most seriously, rhabdomyolysis. Rhabdomyolysis is rare (0.1-0.3 per 10,000 treatment years) but potentially life-threatening.
  • Mean duration of treatment prior to onset of symptoms is six months. Muscle symptoms that develop in a patient who has been on statins over several years are unlikely to be due to the drugs.
    Risk of myopathy is increased with:
    • Underlying muscle disorders.
    • Multisystem diseases (eg, diabetes).
    • Renal or liver impairment.
    • Untreated hypothyroidism.
    • Vigorous exercise.
    • Intercurrent illness.
    • Major surgery or trauma.
    • Alcohol abuse.
    • Age over 70 years.
    • Co-prescription with other lipid-lowering drugs.
    • Past history of myopathy with any lipid-lowering drug.
    • Co-prescription of drugs that inhibit cytochrome P450 CYP3AE (eg, fibrates, nicotinic acid, calcium-channel blockers, ciclosporin, amiodarone, macrolide antibiotics, azole antifungals, protease inhibitors, warfarin).
    • Diet - intake of grapefruit (simvastatin, atorvastatin and lovastatin) or cranberry juice (fluvastatin).
  • Genetic factors, such as polymorphisms in cytochrome P450 isoenzymes, that increase the risk of statin-induced myopathy are increasingly being identified and may become more important in the future.[20]

This is rare and dose-dependent and usually reversible. Statins should not be withheld in patients with high cardiovascular risk who have raised transaminases of no clinical relevance or who have stable hepatic disease - decisions should be made on an individual basis.

Statin-induced diabetes
Observational studies and meta-analyses have revealed a recognised link between statin use and new-onset diabetes. This risk is relatively small, with new-onset diabetes attributable to statins occurring in approximately 1 in 200 people treated with statins for five years.[21] The mechanism is thought to involve insulin resistance and insulin secretion. Current evidence suggests that this risk is far outweighed by the beneficial effects that statins exert on hyperlipidaemia.[22]

Current NICE guidance does not recommend an absolute lipid target value, but does recommend targeting a 40% reduction in non-HDL cholesterol, or greater, after three months of treatment with statins.[9]

Initial treatment for primary prevention should be with atorvastatin 20 mg. If a 40% or greater reduction in non-HDL cholesterol is not achieved, medication, diet and lifestyle adherence should be explored with the patient. If these have been adequately addressed, the atorvastatin dose can be increased.

Initial treatment for secondary prevention should be atorvastatin 80 mg, unless there are potential drug interactions, a high risk of adverse effects, or the patient prefers otherwise, in which case a lower starting dose can be used.

High-intensity statins are defined as those which reduce LDL cholesterol by at least 40%. A prospective cohort study of over 165,000 primary care patients has shown that 51% do not reduce their LDL by at least 40% even after two years of statin therapy. Patients prescribed low-intensity statins were less likely to reach target than those prescribed high-intensity statins. When adjusted for age and baseline LDL, patients who did not reach target were 22% more likely to have a CVD event over 6.2 years of follow-up.[23]

The current high-intensity statin regimes are:

  • Atorvastatin: 20-80 mg.
  • Rosuvastatin: 10-40 mg.
  • Simvastatin: 80 mg.

Other medical societies have suggested progressively lower targets of LDL-C in recent years - eg, the European Society of Cardiology recommends an LDL-C <70 mg/dL in patients for secondary prevention in patients with known coronary artery disease. One study reported that whilst patients achieved this target initially, this was attenuated over time, possibly due to issues of compliance with intensive regimes by patients and physicians.[24]

Initiating and monitoring treatment

Choosing a statin[9]
Before starting lipid modification therapy for primary prevention of CVD, a blood test for full lipid profile should be taken (total cholesterol, HDL cholesterol, non-HDL cholesterol and triglycerides).

  • NICE currently recommends atorvastatin 20 mg daily as the first-choice drug for primary prevention and atorvastatin 80 mg daily for secondary prevention.
  • Where this is not tolerated, suggested alternatives are:
    • Dose reduction of statin.
    • Switching to an alternative statin preparation.


  • Check lipids, LFTs, HbA1c, renal function, and TSH prior to starting treatment (if not already done). Fasting samples for lipids are not required.
  • If LFTs are abnormal, perform further testing to establish the cause (eg, non-alcoholic fatty liver disease). Liver enzymes that are up to three times the upper limit of normal do not preclude statin initiation.
  • Exclude any secondary causes of hypercholesterolaemia (eg, excess alcohol, hypothyroidism) or, if present, ensure maximally treated before commencing specific lipid-lowering therapy.
  • There is no need to measure CK prior to initiating statin therapy unless the patient is complaining of generalised muscle pains. If the CK is >5 times upper limit of normal, re-test after seven days. If the level remains >5 times the upper limit of normal, do not prescribe a statin. If CK is raised but <5 times the upper limit of normal, prescribe a statin, but in the lower-dose range.
  • Measure CK if a patient reports muscle pain, tenderness, or weakness whilst taking statins. .
  • Do not routinely monitor CK unless clinically indicated:
    Where CK is:[25]
    • Normal: this is myalgia. Continue a statin where symptoms are tolerable and not progressive. If intolerable, offer the patient the options of stopping the statin and re-starting when symptoms improve, reducing the dose, or changing to a lower-intensity statin.
    • Raised but <10 x upper limit of normal (ULN): this is myositis. NICE recommends stopping statin therapy if the CK is five times the upper limit of normal or greater. If below this level, statins can be continued if symptoms are tolerable or stopped and consider alternatives if not. Where muscular symptoms or raised CK continue to persist despite statin cessation, refer for electromyography and/or muscle biopsy.
    • >10 x ULN: this is rhabdomyolysis. Statin therapy should be discontinued. Be suspicious clinically of this situation, where the patient has brown urine. Check renal function and urine myoglobin. An alternative lipid-lowering drug should be considered and re-exposure to statins only after a careful risk:benefit analysis.
  • If the CK level is less than 10 x the upper limit then a low dose of the same or different statin can be tried. If myalgia returns then ezetimibe monotherapy can be tried. Ezetimibe can also be combined with a low-dose statin to help achieve target cholesterol levels.[26]
  • Repeat LFTs after three months of treatment, at a year, and if there are any signs or symptoms of hepatotoxicity. Do not repeat again unless clinically indicated:
    • A rise in aspartate transaminase (AST) and alanine aminotransferase (ALT) <3 x ULN - relatively common, reported in 1-2% of patients and usually occurs in the first three months. Do not routinely stop statin treatment at this level.
    • A rise in transaminases >3 x ULN - stop the statin temporarily before rechallenging or reduce the dose with closer monitoring.

Reaching lipid targets[9, 27]

  • For people on a high-intensity statin, a full lipid profile should be measured after three months of treatment (both primary and secondary prevention) and the target should be a greater than 40% reduction in non-HDL cholesterol.
  • Do not forget concordance. Many patients stop taking statins altogether within a year or take them at less than the prescribed dose. Statins need to be taken in the long term (over years) to derive the fullest benefit. A Cochrane Review looking at improving concordance with lipid-lowering medication found that intensification of patient intervention improved compliance in the long- and short-term. Effective interventions included electronic reminders, pharmacist-led interventions, healthcare professional education of patients, improved patient information and education, telephone reminders and simplifying drug regimens.[28]

Patient advice[27]

Good patient information and education improve adherence. Important messages to get across include:

  • These drugs reduce cardiovascular risk. In the case of primary prevention, we are not treating established disease and an individual's perception of their risk will alter the likelihood of their taking the drug therapy as prescribed.
  • Offer clear information regarding an individual's absolute risk of CVD and about the absolute benefits and harms of an intervention over a 10-year period. Decision-making aids are available.[14]
  • These drugs need to be taken as ongoing medications. Stopping taking them will result in the loss of benefit.
  • Serious side-effects are unlikely but if muscle pain or weakness is experienced, this should be reported immediately to the doctor.
  • These drugs may have multiple interactions, both with prescribed medication, over-the-counter remedies (eg, St John's wort) and non-drugs (eg, grapefruit juice). Always seek advice.
  • Take statins at night when they have a slightly greater effect.

Statins in children[29]

NICE recommends considering the use of lipid-modifying drugs in children with familial hypercholesterolaemia by the age of 10 years. Consideration should be given to:

  • Age.
  • Age of onset of coronary heart disease within the family.
  • Presence of other cardiovascular risk factors, including their LDL‑C concentration.

Treatment should be initiated by a specialist.

Studies suggest that in the case of statin treatment, adverse effects are few.[30]

NICE recommends that ezetimibe be used as a treatment for adults with primary heterozygous-familial or non-familial hypercholesterolaemia in the following circumstances:

  • Where statins are contra-indicated or not tolerated.
  • In conjunction with a statin where serum TChol or LDL-C is not appropriately controlled by initial statin therapy (after appropriate dose titration or because dose titration is limited by intolerance) and when consideration is being given to changing the initial statin therapy to an alternative statin.

If ezetimbe monotherapy does not reduce LDL-C enough, bempedoic acid can be added.[31]

These are a new class of medicines which act on proprotein coinvertase subtilisin/kexin type 9 (PCSK9), an important regulator of cholesterol mechanism. There are currently two monoclonal antibodies available, alirocumab and evolocumab, which reduce PCSK9 activity, and a small interfering RNA (siRNA) drug, inclisiran, which inhibits the hepatic translation of PCSK9.

NICE has approved the use of alirocumab and evolocumab in the following situations only:[32, 33]

  • Secondary prevention of CVD in non-familial hypercholesterolaemia or dyslipidaemia, where, despite maximal lipid-lowering treatment, LDL-C concentration is persistently above 4.0 mmol/L (or above 3.5 mmol/L in people at very high CVD risk).
  • Primary or secondary prevention in heterozygous familial hypercholesterolaemia, where despite maximal lipid-lowering treatment, LDL-C concentration is persistently above 5.0 mmol/L in primary prevention, or above 3.5 mmol/L in secondary prevention.

NICE has approved inclisiran for secondary prevention of CVD only, and only where LDL-C concentrations are persistently 2.6 mmol/L or more, despite maximum-tolerated lipid-lowering therapy (ie maximum-tolerated statins, with or without other lipid-lowering therapies, or other lipid-lowering therapies where statins are not tolerated or are contra-indicated).[34]

NICE does not recommend routinely using a fibrate for primary or secondary prevention of CVD, or for people with CKD, type 1 diabetes or type 2 diabetes.[9]

The fibrates (bezafibrate, ciprofibrate, fenofibrate, and gemfibrozil) act mainly by decreasing serum triglycerides.

  • They are uncommonly used in primary CVD prevention and for most other dyslipidaemias, fibrates have been superseded by statins.[1]
  • They act in the liver to reduce cholesterol synthesis, reduce secretion of very low-density lipoproteins (VLDLs) and increase the removal of VLDLs from the blood, consequently lowering plasma TGs (by 30-50%) and, to a lesser extent, plasma cholesterol TChol and LDL reduction of 0-30%). They increase the plasma HDL (by 2-20%) by increasing apoA-I and apoA-II gene transcription.
  • Evidence of efficacy in treating cardiovascular risk and of safety is less substantial than for statins: trials showed significant lipid-lowering but this did not necessarily translate into significant clinical gains.

Fibrates should generally not be initiated in primary care, but may be considered by secondary care services.

Hypoalbuminaemia, gallbladder disease, nephrotic syndrome, and photosensitivity to fibrates.


As with statins, myotoxicity is the most important adverse effect of this class of drugs. Risk is increased by:

  • Concomitant treatment with statins (CK levels >10 x ULN occur in about 1 in 1,000 individuals on combination therapy).
  • Concomitant treatment with ciclosporin.
  • Renal insufficiency (check U&Es prior to commencing treatment).
  • Older age.
  • Female sex.


These include:

  • Myopathy and rhabdomyolyis - risk is increased if impaired renal function.
  • Gastrointestinal side-effects - more common.
  • Hypersensitivity reaction (urticaria, pruritus, photosensitive rash).

Icosapent ethyl is a purified preparation of the omega-3 fatty acid eicosapentaenoic acid. NICE has recommended it as an option for secondary prevention of CVD in people who: are at high risk of CVD, and are taking statins, and have raised fasting triglycerides (1.7 mmol/L or above), and have LDL-C levels between 1.04 mmol/L and 2.60 mmol/L.

Icosapent ethyl is also licensed for primary prevention in people who have diabetes and one other cardiovascular risk factor. NICE has not recommended it for primary prevention but it can be used as secondary prevention in people with diabetes and established cardiovascular disease.

Clinical trial evidence suggests that icosapent ethyl reduced the risk of cardiovascular events in people with raised fasting triglycerides (1.7 mmol/L or above) who are taking statins compared to placebo. The trial only included people with LDL-C levels above 1.04 mmol/L and below or equal to 2.60 mmol/L.

People must be taking a statin to have icosapent ethyl. People who cannot have statins are not covered by icosapent ethyl's marketing authorisation, so NICE has not made any recommendations in this area.

Other lipid-regulating drugs are unlikely to be initiated in primary care but may be used on occasion by secondary care lipid clinics. They include:

  • Colestyramine and colestipol.
  • Nicotinic acid and acipimox.
  • Omega-3 fish oils.

NB: NICE does not recommend using any of these medications for primary or secondary prevention of CVD, or for people with CKD, type 1 diabetes or type 2 diabetes.[9]

Are you protected against flu?

See if you are eligible for a free NHS flu jab today.

Check now

Further reading and references

  1. Report of the Joint British Societies for the Prevention of Cardiovascular Disease; JBS3, 2014

  2. QRISK®3-2018 risk calculator

  3. Brugts JJ, Yetgin T, Hoeks SE, et al; The benefits of statins in people without established cardiovascular disease but with cardiovascular risk factors: meta-analysis of randomised controlled trials BMJ. 2009 Jun 30338:b2376. doi: 10.1136/bmj.b2376.

  4. British National Formulary (BNF); NICE Evidence Services (UK access only)

  5. Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk; European Society of Cardiology/European Atherosclerosis Society (2019)

  6. Ibanez B, James S, Agewall S, et al; 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2017 Aug 26. doi: 10.1093/eurheartj/ehx393.

  7. Almeida SO, Budoff M; Effect of statins on atherosclerotic plaque. Trends Cardiovasc Med. 2019 Jan 7. pii: S1050-1738(18)30223-8. doi: 10.1016/j.tcm.2019.01.001.

  8. Oesterle A, Liao JK; The Pleiotropic Effects of Statins - From Coronary Artery Disease and Stroke to Atrial Fibrillation and Ventricular Tachyarrhythmia. Curr Vasc Pharmacol. 201917(3):222-232. doi: 10.2174/1570161116666180817155058.

  9. Lipid modification - cardiovascular risk assessment and the modification of blood lipids for the prevention of primary and secondary cardiovascular disease; NICE Clinical Guideline (July 2014 - updated September 2016)

  10. Chronic kidney disease in adults; NICE Quality Standard (July 2017)

  11. Taylor F, Huffman MD, Macedo AF, et al; Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2013 Jan 311:CD004816. doi: 10.1002/14651858.CD004816.pub5.

  12. Byrne P et al; Statins for the primary prevention of cardiovascular disease: an overview of systematic reviews BMJ Open 20199(4)

  13. Byrne P, Demasi M, Jones M, et al; Evaluating the Association Between Low-Density Lipoprotein Cholesterol Reduction and Relative and Absolute Effects of Statin Treatment: A Systematic Review and Meta-analysis. JAMA Intern Med. 2022 May 1182(5):474-481. doi: 10.1001/jamainternmed.2022.0134.

  14. Taking a statin to reduce the risk of coronary heart disease and stroke; NICE Patient Decision Aid, November 2014

  15. Cardiovascular disease: risk assessment and reduction, including lipid modification; NICE Guidance (July 2014 - last updated 2016)

  16. Koo BK; Statin for the primary prevention of cardiovascular disease in patients with diabetes mellitus. Diabetes Metab J. 2014 Feb38(1):32-4. doi: 10.4093/dmj.2014.38.1.32.

  17. Selva-O'Callaghan A, Alvarado-Cardenas M, Pinal-Fernandez I, et al; Statin-induced myalgia and myositis: an update on pathogenesis and clinical recommendations. Expert Rev Clin Immunol. 2018 Mar14(3):215-224. doi: 10.1080/1744666X.2018.1440206. Epub 2018 Feb 23.

  18. Collaboration for authored content; Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022 Sep 10400(10355):832-845. doi: 10.1016/S0140-6736(22)01545-8. Epub 2022 Aug 29.

  19. Herrett E, Williamson E, Brack K, et al; Statin treatment and muscle symptoms: series of randomised, placebo controlled n-of-1 trials. BMJ. 2021 Feb 24372:n135. doi: 10.1136/bmj.n135.

  20. Ramakumari N, Indumathi B, Katkam SK, et al; Impact of pharmacogenetics on statin-induced myopathy in South-Indian subjects. Indian Heart J. 2018 Dec70 Suppl 3:S120-S125. doi: 10.1016/j.ihj.2018.07.009. Epub 2018 Aug 10.

  21. Sattar N, Preiss D, Murray HM, et al; Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010 Feb 27375(9716):735-42. doi: 10.1016/S0140-6736(09)61965-6. Epub 2010 Feb 16.

  22. Carmena R, Betteridge DJ; Diabetogenic Action of Statins: Mechanisms. Curr Atheroscler Rep. 2019 Apr 3021(6):23. doi: 10.1007/s11883-019-0780-z.

  23. Weng SF et al; Sub-optimal cholesterol response to initiation of statins and future risk of cardiovascular disease, BMJ, 2019

  24. Dykun I, Wiefhoff D, Totzeck M, et al; Disconcordance between ESC prevention guidelines and observed lipid profiles in patients with known coronary artery disease. Int J Cardiol Heart Vasc. 2018 Dec 2822:73-77. doi: 10.1016/j.ijcha.2018.12.004. eCollection 2019 Mar.

  25. Sathasivam S, Lecky B; Statin induced myopathy. BMJ. 2008 Nov 6337:a2286. doi: 10.1136/bmj.a2286.

  26. Vavlukis M, Vavlukis A; Adding ezetimibe to statin therapy: latest evidence and clinical implications. Drugs Context. 2018 Jul 97:212534. doi: 10.7573/dic.212534. eCollection 2018.

  27. Lipid modification - CVD prevention; NICE CKS, August 2022 (UK access only).

  28. van Driel ML, Morledge MD, Ulep R, et al; Interventions to improve adherence to lipid-lowering medication. Cochrane Database Syst Rev. 2016 Dec 2112:CD004371. doi: 10.1002/14651858.CD004371.pub4.

  29. Familial hypercholesterolaemia: identification and management; NICE Clinical Guideline (2008, last updated October 2019)

  30. Alonso R, Cuevas A, Cafferata A; Diagnosis and Management of Statin Intolerance. J Atheroscler Thromb. 2019 Mar 126(3):207-215. doi: 10.5551/jat.RV17030. Epub 2019 Jan 19.

  31. Bempedoic acid with ezetimibe for treating primary hypercholesterolaemia or mixed dyslipidaemia. NICE Technology appraisal guidance, April 2021

  32. Evolocumab for treating primary hypercholesterolaemia and mixed dyslipidaemia; NICE Technology Appraisal Guidance, June 2016

  33. Alirocumab for treating primary hypercholesterolaemia and mixed dyslipidaemia; NICE Technology Appraisal Guidance, June 2016

  34. Inclisiran for treating primary hypercholesterolaemia or mixed dyslipidaemia; NICE Technology appraisal guidance, October 2021

  35. Icosapent ethyl with statin therapy for reducing the risk of cardiovascular events in people with raised triglycerides; NICE Technology appraisal guidance, July 2022