Cardiovascular risk reduction - quality prescribing guidance 2026-2029: consultation
Cardiovascular disease (CVD) is largely preventable, and many modifiable risk factors increase the likelihood of developing CVD. This guide highlights how to support people in modifying risk factors such as diet, healthy weight, alcohol, physical activity, stress and tobacco smoking.
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10. Hyperlipidaemia
10.1 Why is hyperlipidaemia important in CV risk reduction?
It is estimated that over half of adults in Scotland have an elevated cholesterol.[35]
Cholesterol is an essential component of cell membranes; it is packaged into lipoproteins for distribution through the bloodstream. High-density lipoprotein (HDL) helps remove excess cholesterol from the body and can have an anti-inflammatory effect.[36] Low-density lipoprotein (LDL) delivers cholesterol to cells around the body, but high levels of LDL can damage the walls of arteries. Elevated cholesterol is one of five classic risk factors that lead to early premature cardiovascular mortality across the globe.26 Evidence from clinical and genetic studies show that LDL causes atherosclerotic cardiovascular disease (ASCVD).[37]
This guide focuses on prevention of cardiovascular disease – individuals who have established atherosclerotic cardiovascular disease follow a different treatment pathway.
See:
Lipid pathway | Right Decisions
Long-term management and secondary prevention - National Clinical Guideline for Stroke
All patients with established atherosclerotic cardiovascular disease should be offered intensive statin therapy with atorvastatin 80mg/day following an informed discussion of risks and benefits between the individual and responsible clinician.
10.2 When to measure lipids
Measurement of lipids is required for the assessment of cardiovascular risk, alongside the determination of several other key risk factors.14 Current guidance recommends cardiovascular risk assessment in all adults over the age of 40 years, and all adults (irrespective of age) with a family history of early-onset atherosclerotic cardiovascular disease or suspected inherited hyperlipidaemia.17 For those not identified to be at high-risk, re-assessment should be considered every five years.17
10.3 How to measure lipids
- Non-fasting sampling of lipid parameters is recommended for general risk screening, since it has the same prognostic value as fasting samples.12
- Both total cholesterol and high-density lipoprotein (HDL) cholesterol measurements are required to estimate CVD risk [38]
- A full lipid profile (total, HDL, LDL cholesterol and triglycerides) is recommended before starting a statin, or where an inherited hyperlipidaemia is suspected37
Where LDL-C ≥5.0 (or non-HDL-C ≥6.0) mmol/L and there is a family history of either early-onset ASCVD or hyperlipidaemia – consider Familial Hypercholesterolaemia.
- Lipoprotein(a) is a cholesterol-carrying particle associated with increased risk of ASCVD and aortic stenosis. Levels are largely genetically-determined and invariant throughout adulthood. Measurement is not currently included within routine laboratory lipid panels. It is recommended that measurement only be requested by (or upon the advice of) a specialist lipid or CV risk clinic.
10.4 Lifestyle (and non-inherited) causes of hyperlipidaemia
Certain lifestyle (and other non-inherited) factors can cause or contribute to hyperlipidaemia. These should be considered and (where possible addressed) irrespective of whether it is decided to initiate cholesterol-lowering medication:14
Common:
- alcohol excess
- uncontrolled hypothyroidism
- diabetes
- obesity
- metabolic dysfunction-associated steatotic liver disease (MASLD) / fatty liver
Medication-related (not exhaustive):[39]
- corticosteroids (systemic)
- ciclosporin (systemic)
- oestrogen (oral contraceptives, not HRT)
- retinoids
- antipsychotics
- antiretrovirals
- antidepressants
Other:
- nephrotic syndrome
- cholestatic liver disease
- keto- or high-fat diets
- eating disorders
Hypertriglyceridaemia and low HDL cholesterol are often associated with insulin resistance (prediabetes, diabetes), overweight, obesity and MASLD. For appropriate patients, non-HDL cholesterol can be lowered effectively with a statin. But the raised triglycerides and low HDL-C tend to respond inadequately to statin therapy; these are most effectively addressed by tackling the underlying cause (usually through weight loss). Please see the chapters on lifestyle, obesity and diabetes for further information.
10.5 Current lipid-lowering therapies
10.5.1 Statins
In adults at increased CVD risk but without prior CVD events, statin therapy for primary prevention of CVD is associated with reduced risk of all-cause mortality and CVD events. Benefits of statin therapy appear to be present across diverse demographic and clinical populations.[40] The relative risk reduction with statin therapy is estimated to be about 22% per 1mmol/L reduction in LDL cholesterol (over approximately 5 years).[41] This means that for a given statin dose, the largest absolute reductions in risk will be achieved for patients with a combination of both high baseline ASCVD risk and high pre-treatment LDL cholesterol.
10.5.2 Ezetimibe and other lipid-lowering therapies
Statins should be used first-line. Failure to achieve sufficient cholesterol-lowering or problems with statin-associated symptoms should, in the first instance, be addressed by adjusting the statin dose or type. Ezetimibe can be offered where such attempts are unsuccessful and may be prescribed alongside the maximum-tolerated dose of a statin, or as a monotherapy (if an individual is unable to take a statin). [42]
Bempedoic acid has been accepted by the SMC for restricted use within NHS Scotland. It may be offered to individuals who are unable to take (or tolerate) a statin, and who are unable to achieve sufficient cholesterol-lowering with ezetimibe alone. Bempedoic acid must be prescribed alongside ezetimibe. Unless a statin is contraindicated, those reporting symptoms of statin intolerance should be offered alternative statin types or lower statin doses before non-statin lipid-lowering medication (such as bempedoic acid) is considered. Most formularies require bempedoic acid to be initiated by, or on the advice of a specialist.
Further lipid-lowering therapies, such as PCSK9 modulating drugs and icosapent-ethyl, are outside the scope of this guideline as they are restricted for use in individuals with existing atherosclerotic cardiovascular disease or with genetically-confirmed FH. Other lipid-lowering drugs such as fibrates and bile acid sequestrants should not be prescribed without specialist advice.
10.6 Patients who may benefit from lipid-lowering medication
The following pathway describes the approach to lipids for those without atherosclerotic cardiovascular disease:
Lipids for those without atherosclerotic cardiovascular disease pathway | Right Decisions
Primary prevention using a statin is recommended for any of the following groups:
- ASSIGN v2.0 score ≥10%
- CKD eGFR <60 or ACR >3mg/mmol (approx. equal to 30mg/g)
- Familial hypercholesterolaemia (FH)
- Type 1 diabetes who are over 40 years old, or disease duration >10 years, or nephropathy or other CVD risk factors.
Note: In some ethnic minorities, risk tools under- and overestimate CVD risk, because they have not been validated in these populations. For example, in people originating from the south Asian subcontinent it is safest to assume that the CVD risk is modestly higher than predicted from most scoring tools. More information on risk could be obtained in such individuals using alternative scores such as QRISK3.
10.7 Lipid-lowering for primary prevention
Offer atorvastatin 20mg daily, following a person-centred consultation.
Aim for a reduction of 40% or greater in non-HDL (or LDL) cholesterol, to be assessed by repeat lipids after 2-3 months.
Where the above is not achieved:
- Discuss treatment adherence and consider factors which may contribute to hyperlipidaemia.
- If at higher risk (based on comorbidities, risk score or clinical judgement) consider increasing the dose every two to three months up to a maximum dose of atorvastatin 80mg daily. (If eGFR <30mL/min/1.73m2, discuss dose increase with a renal specialist.)[43]
Where individuals experience unacceptable side-effects, consider a reduction in dose or an alternative statin. Consider factors which may predispose to side-effects.
- Note that different statins provide different degrees of cholesterol-lowering, see Table 10:
- Rosuvastatin 10mg provides a similar degree of cholesterol-lowering to atorvastatin 20mg, and may be used as an alternative
- Do not exceed a dose of rosuvastatin 20mg once-daily for individuals with the above risk-factors, or for those of Asian origin. [44]
- Low-doses of atorvastatin (10mg once-daily), or rosuvastatin (5mg once-daily) may provide a reasonable degree of cholesterol-lowering, while posing a lower risk of adverse effects. Both of these statins have longer half-lives and can be prescribed once every two days. [45]
- Consider the addition of ezetimibe to a statin, where the maximum-tolerated statin dose fails to achieve a 40% reduction in non-HDL (or LDL) cholesterol
For patients unable to take any statin:
- Ezetimibe may be used as a monotherapy. Cholesterol-lowering response should be assessed at 12 weeks.
- Bempedoic acid may be an option (but only in combination with Ezetimibe) for higher risk individuals who are unable to take any statin. [46] Most formularies require bempedoic acid to be initiated by, or on the advice of a specialist. Before initiating bempedoic acid with ezetimibe, consider whether all of the following apply:
- Unable to take a statin. If this is due to statin intolerance (rather than a contraindication), then consider whether a reasonable attempt has been made to find a tolerated statin – including low-dose or less than once-daily regimens. Statin intolerance is generally defined as an inability to tolerate at least three different statins.
- Higher risk individual. This depends on clinical judgement and would include those with particularly adverse CV risk factors (e.g. heavy smoker, strong family history of early-onset ASCVD) or significantly elevated risk score.
| Statin dose (mg/day) | 5 | 10 | 20 | 40 | 80 |
|---|---|---|---|---|---|
| Fluvastatin | - | - | 21% | 27% | 33% |
| Pravastatin | - | 20% | 24% | 29% | - |
| Simvastatin * max. dose 20mg alongside certain medications (e.g. amlodipine) ** avoid 80mg due to increased risk of muscular side-effects | - | 27% | 32% | 37%* | 42%** |
| Atorvastatin | - | 37% | 43% | 49% | 55% |
| Rosuvastatin | 38% | 43% | 48% | 53% | - |
| Atorvastatin and ezetimibe 10mg | - | 52% | 54% | 57% | 61% |
Non-statin therapies:
- Ezetimibe monotherapy lowers LDL cholesterol by 15 – 20%[48]
- Bempedoic acid combined with ezetimibe lowers LDL cholesterol by 39%[49]
10.8 Monitoring of lipid-lowering medication
It is recommended that the effects of lipid-lowering treatment should be evaluated, and that treatment intensification should be considered, taking into account likely benefit, comorbidities, frailty and individual preference.12
10.8.1 Adherence and lipid-lowering efficacy
The current evidence base suggests that sustained lowering of lipids translates into lower long-term risk of atherosclerotic cardiovascular disease. There is limited evidence to suggest that regular monitoring of lipids is a cost-effective means to achieve that goal.[50] Many individuals (for example those living with diabetes or CKD) may already receive an annual review of their lipids.
At present it is not possible to make a specific recommendation for regular lipid measurement in all primary prevention patients who are prescribed lipid-lowering therapy. An ongoing review of lipids may be considered for those with adverse risk factors, or where medication adherence is likely to be poor. Monitoring is not usually required more frequently than every 12 months. If lipids are well-controlled and stable then monitoring may be less frequent or discontinued altogether.
All individuals should be made aware that both lipid-lowering and reduction in risk depend upon taking their lipid-lowering medication regularly as prescribed. They should be encouraged to seek advice if they experience difficulties taking their medication regularly, or have doubts about whether to continue it.
10.8.2 Liver function tests (LFTs)
Statins are known to cause elevated liver function tests (LFTs) in a minority of individuals, typically characterised by mildly raised transaminases (ALT or AST). Higher levels, where transaminases rise to more than three times the upper limit of normal, have been estimated to occur at a rate of approximately 2%,[51] however statin-induced liver injury is very rare.[52] Outside of these instances, there is no evidence that elevated LFTs observed with statin treatment is associated with liver injury or disease.[53] Statins are generally safe for those with suspected or known MASLD in whom LFTs are often mildly deranged.[54]
Measure LFTs before starting a statin, and then again at 3 and 12 months (and not thereafter, unless clinically indicated).17,37 Repeat checks are recommended after each increase in statin dose (at 3 and 12 months). Note that individual health boards may have their own local guidance for such monitoring.
Approach to asymptomatic elevated liver function tests (LFTs):
- Prior to statin therapy
- Mildly elevated LFTs (ALT or AST up to three times upper limit of normal) - do not routinely exclude from statin treatment. Follow local guidance regarding any further investigation of LFTs. Re-check LFTs at 1, 3 and 12 months.
- Elevated LFTs (including ALT or AST above three times upper limit of normal) – do not initiate statin. Follow local guidance regarding any further investigation of LFTs. For those with persistently elevated LFTs at this level, consider seeking specialist advice regarding the initiation of a statin.
- Elevated LFTs (including ALT or AST above three times upper limit of normal) – discontinue statin. Re-check LFTs within one month. For those with persistently elevated LFTs at this level, consider seeking specialist advice. Otherwise continue to monitor until LFTs return to baseline. If LFTs remain mildly elevated, follow local guidance regarding the need for further investigation.
- Previous asymptomatic mild elevation of LFTs (including ALT or AST up to three times upper limit of normal) – consider re-trying a low-dose e.g. atorvastatin 10mg or rosuvastatin 5mg. Re-check LFTs at 1, 3 and 12 months. If repeated attempts to establish statin therapy fail consider ezetimibe and/or bempedoic acid.
- During statin therapy
- Mildly elevated LFTs (ALT or AST up to three times upper limit of normal) – continue statin. Re-check LFTs at one month, and if mildly elevated then repeat at six months.
- Elevated LFTs (including ALT or AST above three times upper limit of normal) – discontinue statin. Re-check LFTs within one month. For those with persistently elevated LFTs at this level, consider seeking specialist advice. Otherwise continue to monitor until LFTs return to baseline. If LFTs remain mildly elevated, follow local guidance regarding the need for further investigation.
- Previous asymptomatic mild elevation of LFTs (including ALT or AST up to three times upper limit of normal) – consider re-trying a low-dose e.g. atorvastatin 10mg or rosuvastatin 5mg. Re-check LFTs at 1, 3 and 12 months. If repeated attempts to establish statin therapy fail consider ezetimibe and/or bempedoic acid.
- History of previous statin discontinuation due to elevated LFTs
- Previous confirmed (or strongly suspected) statin-induced liver injury - do not re-challenge with a statin. Seek specialist advice.
- Previous asymptomatic mild elevation of LFTs (including ALT or AST up to three times upper limit of normal) – consider re-trying a low-dose e.g. atorvastatin 10mg or rosuvastatin 5mg. Re-check LFTs at 1, 3 and 12 months. If repeated attempts to establish statin therapy fail consider ezetimibe and/or bempedoic acid.
Monitoring of liver function tests (LFTs) – ezetimibe, bempedoic acid
Clinical trials have reported a higher rate of elevated LFTs (ALT or AST above three times upper limit of normal) for both ezetimibe and bempedoic acid when compared to placebo. However, it should be noted that rates were relatively low at 1.6% for bempedoic acid[55] and 0.5% for ezetimibe (and 1.3% where ezetimibe was prescribed alongside a statin).[56]
It is recommended that LFTs be measured at baseline and at three months when starting either ezetimibe or bempedoic acid.
10.9 Adverse effects
This section lists some of the adverse effects commonly associated with lipid-lowering therapies and outlines a suggested approach to statin intolerance. It does not provide an exhaustive list of potential adverse effects. For detailed, comprehensive and up-to-date advice please refer to the BNF or relevant SPC.
10.9.1 List of adverse effects associated with statin therapy
The most commonly reported adverse effects are myalgia (muscle pain), arthralgia (joint pain) and fatigue. Less commonly reported effects include gastrointestinal symptoms (nausea, diarrhoea) and a range of neurological symptoms (brain fog, vivid dreams, sleep disturbance, mood disturbance and sexual dysfunction).
10.9.2 Statin intolerance
Statin intolerance is broadly defined as the presence of symptoms, signs or laboratory abnormalities which lead to reduced adherence and/or discontinuation of the statin. It is a common phenomenon, and a large proportion of people discontinue statin therapy within the first few years of initiation.[57],[58]
While symptoms may be genuinely associated with statin therapy, in many cases symptoms stem from a variety of other causes, and there is evidence that negative media coverage of statin side-effects has driven large numbers of patients to discontinue statin therapy.[59]
Clinical trials have consistently found relatively low rates of statin-associated symptoms,[60] leading some to question whether the design of these trials accurately captured a range of factors inherent in “real-world” clinical practice. More recent studies, following patients within a general practice setting, have also found relatively low rates of statin-induced muscular adverse effects. Among patients reporting such side-effects, approximately 90% reported adverse effects irrespective of whether they were prescribed a placebo or a statin.[61]
10.9.3 Approach to statin intolerance (including muscular symptoms)44
- Explore individual concerns. Consider whether the nocebo effect, or statin reluctance may be factors. Consider whether discussion of the evidence for benefits and adverse effects may be helpful
- Nocebo-effect is the experience of symptoms, which are not associated with a particular treatment (and are equally likely with both placebo and active treatment). Symptoms are driven by the expectation that a treatment will cause harm
- Statin-reluctance describes an attitudinal state where an individual is opposed to taking a statin, often without any previous exposure to statin treatment
- In some cases it may be helpful to try alternate-day dosing of atorvastatin or rosuvastatin
- Consider whether the timing and distribution of symptoms appears consistent with a statin-mediated effect e.g. did symptom-onset follow initiation or an increase in dose? Is myalgia or joint pain on both sides of the body? (Symptoms that appear several years into an unchanged prescription or are unilateral are less likely to be associated with statin therapy.)
- Explore potential alternative causes, or pre-disposing factors for symptoms e.g. poorly-controlled hypothyroidism, a drug-drug interaction etc.
- For most individuals reporting muscular symptoms, creatine kinase (CK) measurement is unlikely to be helpful. Consider CK measurement if there are severe and/or persistent symptoms of muscular pain and/or weakness
- For sleep disturbance, change the timing of doses from evening to morning
- Adverse effects are more likely where maximum doses are prescribed
- Where symptoms are unacceptable, consider stopping statin therapy for a short period (typically several weeks) to establish if symptoms resolve:
- Discuss re-starting the statin at a reduced dose in the first instance, or if necessary switching to an alternative statin
- In some cases it may be helpful to try alternate-day dosing of atorvastatin or rosuvastatin
- For further information on statin intolerance, see the NHS England statin intolerance pathway which aims to support prescribers in managing individuals at high CVD risk who report potential intolerance to high intensity statin therapy
10.9.4 When to measure creatine kinase (CK)
Mild elevations in CK are common (irrespective of statin treatment) and the underlying cause is usually multifactorial. If mild-moderate muscular pain prompts either statin dose reduction or discontinuation, and symptoms subsequently resolve then CK measurement is unlikely to be helpful.
Where there is severe muscular pain, or symptoms of muscular weakness, lipid-lowering therapy should be stopped and measurement of CK may help guide further assessment. CK measurement may be helpful where muscular symptoms persist despite statin discontinuation. Where CK is elevated, ongoing monitoring may be indicated.
10.9.5 Elevated CK – interpretation and further assessment
Interpretation of elevated CK depends upon the estimated muscle mass of an individual. While a slightly raised CK in a young individual with significant muscle bulk is very unlikely to reflect myopathy, the same result for a frail individual with low muscle bulk may be clinically significant. Note that local laboratory reference ranges for CK will vary, and that black people have a slightly higher upper limit of normal for CK.
CK up to four times ULN (approx. 800 to 1,200 U/L) is unlikely to require specialist advice:
- Consider common causes (including recent strenuous exercise), and any pre-disposing factors for myopathy (including uncontrolled hypothyroidism)
- Discontinue statin where symptoms persist, or CK rises further. Re-check CK within two weeks, to ensure stable or falling levels
- For significant or progressive muscular weakness, consider referral for specialist assessment
CK more than four times ULN (approx. 800 to 1200 U/L), but below CK 7500 U/L:
- Have a low threshold for same-day hospital assessment in generally unwell or frail patients – who have an increased risk of rhabdomyolysis
- Otherwise, for most individuals:
- Consider common causes (including recent strenuous exercise), and any pre-disposing factors for myopathy
- Discontinue statin unless all of the following apply: clearly exercise-induced, normal U&Es, passing urine normally and asymptomatic
- Re-check CK within two to three days, and monitor until stable. Where persistently elevated at this level (despite statin discontinuation), consider referral for specialist assessment
CK more than 7500 U/L:
- Urgent review of patient. Consider same-day hospital assessment for possible rhabdomyolysis
10.9.6 Very rare muscular adverse effects
- Myasthenia gravis – very infrequent cases of new-onset (or exacerbation of existing diagnosis) within three months of statin initiation have been reported.
- Statin-induced autoimmune myopathy – consider where progressive muscular weakness and ongoing CK elevation despite statin discontinuation. Refer for urgent specialist assessment.
10.9.7 Liver function test (LFT) derangement
Statins (and ezetimibe, bempedoic acid) may cause asymptomatic and usually temporary elevations in liver function tests (including ALT, AST, ALP, GGT). Do not routinely exclude from treatment people who have liver transaminase levels (ALT, AST) that are raised but are less than three times the upper limit of normal.37
10.9.8 Type 2 diabetes (statins only)
Statins can cause a moderate (dose-dependent) increase in new diagnoses of diabetes. The majority of new diabetes diagnoses occurred in those with prediabetes, and this is consistent with the finding that statins cause a small upward shift in glycaemia.[62]
The benefits of statin therapy to reduce risk of CV events are considered to outweigh the increased risk of developing T2D. For those without existing cardiovascular disease but assessed to be at high CV risk, five years of statin treatment is estimated to prevent about 1 CV event per 20 patients but cause one new T2D diagnosis for every 100 to 200 patients.[63]
- Advise individuals that there is a modest increase in risk of diabetes, but that this risk is overwhelmingly outweighed by the reduced risk of cardiovascular disease
- Advise all individuals starting statins (but particularly those with prediabetes, or risk factors for T2D) that modest changes in diet and physical activity can mitigate any increased risk for T2D, and further reduce cardiovascular risk
10.9.9 Ezetimibe
The most commonly reported side-effects include gastrointestinal disorders (diarrhoea, gastrointestinal discomfort), muscular pain or weakness, and headache. Rhabdomyolysis has been reported very rarely with monotherapy. An increased rate of elevated transaminases was recorded for ezetimibe compared to placebo.56
10.9.10 Bempedoic acid[64]
The most commonly reported side-effects include gout, hyperuricaemia, pain in an extremity and anaemia. An increased rate of elevated transaminases was recorded for bempedoic acid compared to placebo.
The risk of gout is highest for those with previous hyperuricaemia or diagnosis of gout. Avoid prescribing bempedoic acid to those with a previous diagnosis of gout and discontinue in those with new-onset gout.
10.9.11 Cautions and contraindications
The following provides an overview of the principal cautions and contraindications to consider when prescribing lipid-lowering therapy. It is not intended to be exhaustive. For detailed, comprehensive and up-to-date advice please refer to the BNF or relevant SPC.
10.9.12 Liver disease
Do not prescribe lipid-lowering therapy (statins, bempedoic acid or ezetimibe) to people with active liver disease, or unexplained persistent elevations of transaminases that are three or more times the upper limit of normal.
10.9.13 Renal impairment
Caution should be exercised in the prescribing of all statins and bempedoic acid where eGFR <30ml/min/1.73m2.
10.9.14 Individuals with risk factors for muscular toxicity
Use caution when prescribing any statin, bempedoic acid or ezetimibe to people with risk factors for muscular toxicity (myopathy, rhabdomyolysis). Note that the likelihood increases with increasing dose, and combinations of these drugs. Risk factors include:
- frailty
- older age, particularly >80 years
- high alcohol intake
- uncontrolled hypothyroidism
- strenuous exercise
- renal or liver disease
- personal or family history of muscular disorders
- use of certain medications – see BNF for specific drug-drug interactions
Do not exceed a dose of rosuvastatin 20mg once-daily for individuals with the above risk-factors, or for those of Asian origin.43
10.9.15 History of haemorrhagic stroke
Prescribe statins with caution or seek specialist advice.
10.9.16 Gout
Avoid prescribing bempedoic acid to those with a history of gout and discontinue treatment for those with new-onset gout.
10.9.17 Pregnancy and lactation
Do not prescribe lipid-lowering therapy (statins, bempedoic acid or ezetimibe) to pregnant women, women trying for pregnancy or during breastfeeding, as this poses a risk of harm to the unborn child or breast-feeding infant.
Individuals of child-bearing potential should be advised to use effective contraception and to stop lipid-lowering therapy at least three months before attempting to conceive. Lipid-lowering therapy should not be restarted until breastfeeding has stopped.46, [65]
Where pregnancy occurs during lipid-lowering therapy, all lipid-lowering medication should be stopped immediately, and referral (within 14 days) to a consultant obstetrician should be offered.
10.10 Special patient populations
10.10.1 Frailty
The Polypharmacy Guidance 2026 reviewed the evidence for use of statins in frailty and made the following recommendations:
| No. | Our recommendations | Strength of recommendation |
|---|---|---|
| 1 | Prescribers and older people with frailty might want to discuss reducing or stopping a statin because the evidence does not indicate: Reduction in morbidity/mortality in primary prevention A change in the frequency of admission to long-term care, or reduced frequency of admission to hospital | Good practice point |
| 2 | Prescribers and older people with frailty may wish to discuss what effect taking a statin has on treatment burden, or quality of life. Within the polypharmacy manage medicines app, prescribers and patients may wish to use shared decision-making tools, such as NNT charts or Cates plots to help visualise potential magnitude of benefit of medication for this intervention. | Good practice point |
10.11 Groups not covered by this guidance – where to seek further information
10.11.1 Familial hypercholesterolaemia (FH)
Familial hypercholesterolaemia (FH) causes life-long raised LDL cholesterol, and increased risk of early-onset coronary heart disease (CHD). If non-HDL-C ≥6.0 or LDL-C ≥5.0, then:
1. Exclude non-inherited causes of hyperlipidaemia
2. Measure (or re-measure) LDL-C
3. Consider FH where LDL-C ≥5.0, and at least one of:
- CHD-onset in individual or 1st-degree relative aged <60 years
- CHD-onset in 2nd-degree relative <50 years
- LDL-C ≥5.0 in 1st / 2nd degree relative
Where FH is suspected, refer to a specialist local lipid or cardiovascular risk clinic. Formal diagnosis of FH is usually confirmed via genetic testing through a specialist lipid clinic. FH genetic testing for affected families is available throughout Scotland and is vital for the prevention of early-onset coronary heart disease within this patient group.
All FH patients should receive long-term regular follow-up care.62 Such care is usually provided by a specialist lipid clinic, but in some circumstances may be delivered by primary care with specialist lipid clinic oversight. If in doubt, please seek advice from your local lipid or cardiovascular risk clinic.
Refer to the NICE Familial hypercholesterolaemia: identification and management clinical guideline CG71 for further guidance.62
10.11.2 Individuals eligible for injectable cholesterol-lowering therapy
Alirocumab,[66] evolocumab[67] and inclisiran[68] are medications given by injection which block the action (or production) of a protein called PCSK9. PCSK9 raises blood LDL cholesterol. These medications act (primarily in the liver) to reduce the effect of PCSK9, and hence reduce levels of LDL cholesterol in the blood.
These medications are SMC approved for primary prevention in individuals with Familial Hypercholesterolaemia and for individuals who have had a previous cardiovascular event and have not met their lipid target on maximum tolerated therapy.
| No. | Recommendation | Strength |
|---|---|---|
| 1 | Non-fasting sampling of lipid parameters is recommended for general risk screening | Good Practice Point from CVD guideline development group |
| 2 | Measure both total blood cholesterol and high-density lipoprotein (HDL) cholesterol to achieve the best estimate of CVD risk | Evidence-based recommendation (NICE 238) |
| 3 | Primary prevention using a statin is recommended in individuals with:
|
Evidence-based recommendation (NICE 238) |
| 4 | Atorvastatin 20mg daily is the statin of choice in primary prevention | Strong recommendation Evidence-based recommendation (SIGN 149) |
| 5 | Consider ezetimibe
|
Evidence-based recommendation (NICE 238) |
| 6 | If treatment is initiated, its effect must be evaluated, and subsequent treatment intensification to reach ultimate risk factor goals must be considered in all patients, taking into account additional benefit, comorbidities, and frailty, all of which converge with patient preferences in a shared decision-making process | Good Practice Point from CVD guideline development group |
| 7 | The absolute benefit of lowering LDL-C depends on the absolute risk of ASCVD and the absolute reduction in LDL-C, so even a small absolute reduction in LDL-C may be beneficial in a high- or very-high-risk patient | Good Practice Point from CVD guideline development group |
Contact
Email: EPandT@gov.scot