๐Ÿซ€ High Cholesterol (Dyslipidaemia)

RCGP SCA Algorithm โ€” UK Primary Care

NICE NG238NICE CG181QRISK310-min consult
๐Ÿซ€
High Cholesterol โ€” New Result or Review Covers primary & secondary prevention, FH, statin initiation, and cardiovascular risk stratification
Progress 0 / 9
The full reasoning pathway โ€” spot familial hypercholesterolaemia, exclude secondary causes, treat by cardiovascular risk (QRISK3 for primary prevention only), check response to target, add lifestyle, and safety-net.StartDecisionInvestigateActionReferStop / Admit
Presentation ยท NG238Raised cholesterol โ€” to QRISK or not to QRISK?
A non-fasting lipid profile (total, HDL, non-HDL, triglycerides) is sufficient. First ask: is this person high-risk by definition (CVD, CKD, T1DM, age โ‰ฅ85) โ€” in whom you do not calculate risk โ€” or do they need a QRISK3?
Step 1 ยท Safety โ€” spot FH firstFamilial hypercholesterolaemia?
Suspect if total cholesterol >7.5, personal CHD <60y, or first-degree relative with CHD <60y; tendon xanthomata. Search records for cholesterol >9 (โ‰ฅ30y) / >7.5 (<30y). Do not use QRISK in FH.
YES โ€” ?FH
FH pathwayRefer for genetic testing + cascade
Refer if Simon Broome criteria met or Dutch Lipid score >5 (either may be used) for genetic testing, management & cascade testing of relatives. Suspect homozygous FH (refer directly, don't use the criteria) if LDL >13 (โ‰ฅ16y) / >11 (<16y).
NO
InvestigateExclude secondary + risk-assess
TFTs, HbA1c, LFT, U&E/ACR, alcohol. Then decide: high-risk by definition vs QRISK3.
Step 7 ยท choose the statin by group
Secondary prevention (CVD)
Atorvastatin 80 mg
No risk calculation โ€” high-risk by definition. Start at diagnosis; ยฑ ezetimibe to reach target.
CKD or T1DM
Atorvastatin 20 mg
CKD (eGFR <60 or ACR โ‰ฅ3): 20 mg for primary & secondary prevention; increase if eGFR โ‰ฅ30 & target not met (agree with renal if eGFR <30). T1DM: offer if >40y, diabetes >10y, other risk/nephropathy.
Primary prevention (everyone else 25โ€“84)
QRISK3 โ‰ฅ10% โ†’ atorvastatin 20 mg
QRISK <10%: don't rule out โ€” statin if patient chooses or risk underestimated (HIV, recently stopped smoking, dyslipidaemia drugs). HIV + โ‰ฅ40y: offer a statin (BHIVA). โ‰ฅ85y: consider 20 mg (no calculation).
Step 7 ยท check response at 2โ€“3 months
Action ยท TargetRecheck non-HDL at 2โ€“3 months โ€” target differs by track
Primary prevention: aim >40% reduction in non-HDL-C. Secondary prevention: LDL โ‰ค2.0 or non-HDL โ‰ค2.6 mmol/L. If not met: optimise adherence/dose, up-titrate (to atorvastatin 80 mg), add ezetimibe (can add even if target met) ยฑ inclisiran / PCSK9 inhibitor / bempedoic acid per NICE TA.
ReferLipid clinic
Lipid clinic familial hypercholesterolaemia, statin intolerance needing PCSK9 therapy, or very high levels.
Step 8 ยท lifestyle & CV risk reduction
Step 8 ยท Lifestyle & CV risk reductionFoundation for everyone (offered to all, not instead of statins)
Mediterranean-style diet (reduce saturated fat, increase oily fish, fruit/veg, fibre) ยท โ‰ฅ150 min/wk activity ยท weight loss ยท stop smoking ยท alcohol within limits. Optimise the whole CV risk โ€” BP, diabetes, and review drugs that raise lipids. Lifestyle alone for QRISK <10% who decline a statin, with reassessment.
Step 9 ยท monitoring & safety-net
Step 9 ยท Monitoring & safety-netBloods, adherence & when to return
Check LFTs before, at 3 and 12 months (stop only if transaminases >3ร— ULN); recheck non-HDL at 2โ€“3 months and titrate to target; review adherence. Statin myalgia: check CK if severe/widespread muscle pain โ€” stop and seek advice if CK markedly raised or features of rhabdomyolysis. Reassess QRISK and lipids periodically in those not on treatment.
โš ๏ธ QRISK has limits: never use it in FH, established CVD, type 1 diabetes or CKD โ€” these patients are already high-risk and warrant treatment on that basis.
1
Safety

Red Flags โ€” When Hypercholesterolaemia Is Part of Urgent Disease

Most high cholesterol is incidental โ€” but do not miss these critical associated presentations.

Corneal arcus <45 years + TC >7.5 mmol/L Or tendon xanthomata โ†’ Urgent Familial hypercholesterolaemia โ€” Simon Broome or Dutch Lipid criteria
Triglycerides >10 mmol/L Nausea, abdominal pain, vomiting โ†’ Same-day Acute pancreatitis risk โ€” urgent review, consider admission
Chest pain + high cholesterol Exertional chest pain, known CAD, acute onset โ†’ 999 Do not conflate lipid result with urgency โ€” treat chest pain as ACS until proven otherwise
Xanthelasma + young patient Eyelid xanthelasma in <50 year old, family history of early MI โ†’ Urgent Possible FH โ€” refer lipid clinic
Hypothyroidism as cause TSH elevated, new or uncontrolled โ€” secondary hyperlipidaemia. Do NOT start statin until thyroid treated
Nephrotic syndrome as cause Proteinuria +++, hypoalbuminaemia, peripheral oedema โ†’ Same-day Do not treat cholesterol in isolation

Familial hypercholesterolaemia affects 1 in 250 people in the UK (260,000 individuals) but only 7% are diagnosed. Untreated FH carries a 50% risk of CHD by age 50 in men, 30% in women. The key is cascade screening โ€” every FH patient identified has 50% chance of first-degree relative being affected. Hypertriglyceridaemia >10 mmol/L requires urgent management as acute pancreatitis risk is substantial. Secondary causes (hypothyroid, nephrotic, DM, alcohol) must be treated before statin initiation or the lipid picture will not resolve.

2
Diagnose

Calculate Cardiovascular Risk โ€” QRISK3 Score

Risk stratification using QRISK3 determines whether to treat, not cholesterol level alone.

QRISK3 calculator
Use qrisk.org or embedded in clinical systems. Requires: age, sex, ethnicity, smoking, SBP, total cholesterol:HDL ratio, BMI, family history, comorbidities (DM, CKD, AF, RA, SLE, SMI)
<10% 10-year CV risk
Low risk. Lifestyle advice. Statin NOT routinely offered. Recheck lipids + QRISK3 in 5 years or if risk factors change
10โ€“20% 10-year CV risk
Moderate risk. Offer statin after 3-month lifestyle trial. Discuss shared decision making. Atorvastatin 20 mg OD
>20% 10-year CV risk
High risk Offer statin promptly. Do not delay with lifestyle-only period. Atorvastatin 20 mg OD (primary prevention)
Established CVD (secondary)
Previous MI, stroke, TIA, PVD, stable angina โ€” offer high-intensity statin regardless of cholesterol: Atorvastatin 80 mg OD
Type 1 DM >40y or >10y duration
Offer statin regardless of QRISK3 โ€” treat as high-risk even without calculated score
CKD (eGFR <60)
Offer atorvastatin 20 mg โ€” SHARP trial evidence. Do not use simvastatin >10 mg with eGFR <45

QRISK3 replaced Framingham in UK guidelines because it includes additional risk factors (SMI, SLE, AF, deprivation, migraine) with better calibration in UK populations. NICE NG238 (2023) uses 10% threshold for statin offer โ€” this is a change from previous 10% primary prevention threshold. The key insight is that a patient with TC 8 mmol/L but QRISK3 of 5% needs lifestyle advice, not a statin, while a patient with TC 5 mmol/L but QRISK3 25% needs atorvastatin today.

3
Diagnose

Classify โ€” Primary vs Secondary, FH Screening

Primary hypercholesterolaemia
No identifiable secondary cause. Common polygenic (most cases). FH if TC >7.5 or LDL >4.9 + family history. Rule out secondary causes first
Secondary causes (treat first)
Hypothyroidism (check TSH), nephrotic syndrome (urine dipstick), DM (HbA1c), CKD (eGFR), alcohol excess, pregnancy, drugs (ciclosporin, amiodarone, retinoids)
FH โ€” Simon Broome criteria
Definite FH: TC >7.5 (adult) or LDL >4.9 + tendon xanthomata in patient or 1st/2nd degree relative. Possible FH: TC >7.5 + family history MI <60y or TC >7.5 in 1st degree relative
Mixed dyslipidaemia
Raised TG + raised LDL + low HDL โ€” often metabolic syndrome. Check: TG (fasting), HbA1c, waist circumference, BP. Statin primary treatment
Hypertriglyceridaemia
Fasting TG 2โ€“10 mmol/L: lifestyle + fibrate if severe. TG >10: urgent referral, pancreatitis risk. Secondary causes: DM, alcohol, hypothyroid
Low HDL in isolation
HDL <1.0 (men) or <1.2 (women) โ€” no specific drug treatment. Address lifestyle. Low HDL + high TG = high CV risk

Always exclude secondary causes before labelling someone as primary hypercholesterolaemia โ€” hypothyroidism is present in ~5% of new dyslipidaemia referrals and treating thyroid normalises lipids without statin. FH identification matters enormously: a 35-year-old with untreated FH has the same risk as a 55-year-old without it. Cascade screening should be offered to all first-degree relatives of FH patients โ€” 50% will be affected.

4
Diagnose

Targeted Examination & Clinical Assessment

Blood pressure
Essential โ€” hypertension and hyperlipidaemia are multiplicative CV risk factors. Both arms, seated. Target <130/80 in high-risk patients
BMI & waist circumference
BMI >30 or waist >102 cm (M) / >88 cm (F) โ†’ metabolic syndrome. Calculate with TC:HDL ratio and TG
Eyes
Corneal arcus (<45y = significant), xanthelasma (eyelid plaques = possible FH). Fundoscopy if diabetic (hypertensive/diabetic retinopathy)
Hands & tendons
Tendon xanthomata: thick Achilles tendons, extensor tendons of hands โ†’ pathognomonic of FH. Tuberous xanthomata over knuckles = familial combined
Cardiovascular exam
Carotid bruits, peripheral pulses (ABI if suspected PAD), cardiac murmurs, ankle oedema (HF)
Thyroid
Goitre, slow relaxing reflexes, dry skin, bradycardia โ†’ clinical hypothyroidism. Always check TSH if clinically suggested
Abdominal exam
Hepatomegaly (fatty liver disease, alcohol), splenomegaly, xanthomas over abdomen (severe hypertriglyceridaemia)

Tendon xanthomata are pathognomonic of FH โ€” finding them in a patient with TC >7.5 gives definite FH by Simon Broome criteria without genetic testing. Achilles tendons are the most common site โ€” run finger along the tendon and feel for nodules or thickening. Corneal arcus is significant in patients under 45 but is a normal finding in elderly patients. A thorough BP measurement at this consultation is as important as the lipid result โ€” undertreated hypertension quadruples CV risk even on statins.

5
Diagnose

Investigations โ€” Lipid Profile Interpretation

Fasting lipid profile
Total cholesterol LDL-C HDL-C TG TC:HDL ratio โ€” non-fasting acceptable for initial screening; fasting preferred if TG elevated
TC:HDL ratio target
<4 is desirable. QRISK3 uses this ratio. More predictive than TC alone. HDL is protective โ€” low HDL is independently risky
Treatment targets
Primary prevention: aim for a >40% reduction in non-HDL-C at 2โ€“3 months (no absolute LDL target). Secondary prevention: LDL โ‰ค2.0 mmol/L or non-HDL โ‰ค2.6 mmol/L (NICE NG238 / QOF)
Baseline bloods (pre-statin)
ALT/AST (baseline liver function), CK (only if muscle symptoms or high-risk), TSH, HbA1c, eGFR
Genetic testing for FH
Refer to lipid clinic โ€” LDLR, APOB, PCSK9 gene mutations. Positive confirms FH and enables cascade screening of relatives via NHS CHOL programme
When NOT to investigate
Do NOT repeat lipids within 3 months of last result. Do NOT order CK routinely before statin โ€” only if muscle symptoms. Do NOT order lipids in acute illness (falsely low)
Repeat post-treatment
Recheck fasting lipids at 3 months after statin initiation. Check LFTs at 3 months then annually. No need for routine CK unless symptoms

NICE NG238 (2023) moved to LDL-C targets rather than just TC:HDL ratio โ€” align with ESC guidelines. LDL <2.0 mmol/L in secondary prevention is backed by multiple RCTs showing progressive risk reduction with lower LDL (Mendelian randomisation studies support "lower is better"). Statins cause ALT elevation in ~1โ€“3% of patients โ€” baseline LFTs allow interpretation of subsequent results. Routine pre-statin CK is not recommended by NICE โ€” it causes unnecessary statin avoidance due to asymptomatically elevated CK from exercise.

6
Refer

Referral Criteria โ€” Lipid Clinic & Specialist Input

Same-day
TG >10 mmol/L (pancreatitis risk), xanthomatous eruption (eruptive xanthomata from severe hypertriglyceridaemia)
Lipid clinic โ€” urgent
Definite or possible FH (Simon Broome criteria met). LDL >4.9 mmol/L in adult. Tendon xanthomata. Young patient (<40) with LDL >4.0. Paediatric FH
Lipid clinic โ€” routine
LDL not at target despite maximum tolerated statin. Statin intolerance (trial โ‰ฅ3 different statins). Consideration of PCSK9 inhibitor (evolocumab, alirocumab). Complex mixed dyslipidaemia
Cardiology
Secondary prevention patient not at LDL target on atorvastatin 80 mg. Consider PCSK9 inhibitor โ€” requires specialist initiation in NHS
Endocrinology
Secondary hyperlipidaemia from uncontrolled DM or thyroid disease not responding to primary care management
Primary care manage
Primary prevention with QRISK3 10โ€“20% โ€” lifestyle trial then statin. Secondary prevention on atorvastatin 80 mg achieving LDL target. Mild mixed dyslipidaemia with lifestyle modifications

PCSK9 inhibitors (evolocumab, alirocumab) reduce LDL by a further 50โ€“60% on top of maximum statin โ€” they are indicated when LDL remains >2.6 mmol/L despite maximum tolerated statin in secondary prevention or FH. They are only available via specialist initiation on NHS due to cost (~ยฃ4,500/year vs ยฃ20/year for statin). FH cascade screening through NHS CHOL programme is free and identifies high-risk relatives before they develop CVD โ€” every GP FH identification potentially saves multiple lives through family screening.

7
Treat

Treatment โ€” Primary vs Secondary Prevention (different doses & targets)

NICE CKS / NG238 treat the two groups differently โ€” the starting dose and the treatment target both change depending on whether there is established CVD.

Primary preventionNo established CVD ยท QRISK3-led
WhoQRISK3 โ‰ฅ10% (age 25โ€“84); type 1 diabetes (>40y, >10y duration, nephropathy or other risk); CKD; consider at age โ‰ฅ85. Don't rule out if QRISK <10% but informed preference or risk underestimated (HIV, severe mental illness, recently stopped smoking).
StartAtorvastatin 20 mg OD (high-intensity). CKD: 20 mg for primary & secondary.
WhenQRISK 10โ€“20%: may trial lifestyle ~3 months first (shared decision). โ‰ฅ20%: offer promptly.
Target at 2โ€“3 months>40% reduction in non-HDL cholesterol. No absolute LDL target for primary prevention.
If target not metCheck adherence, diet, dose timing โ†’ up-titrate atorvastatin (to 40 then 80 mg) if judged higher risk; consider switching to rosuvastatin; add ezetimibe.
Secondary preventionEstablished CVD ยท no risk score
WhoEstablished atherosclerotic CVD: MI / ACS, angina, stroke / TIA, peripheral arterial disease, coronary or other arterial revascularisation. High-risk by definition โ€” do not calculate QRISK3.
StartAtorvastatin 80 mg OD (high-intensity). Lower dose only if drug interactions, high adverse-effect risk, or patient preference.
WhenImmediately at diagnosis โ€” do not delay (including ACS); offer lifestyle changes alongside.
Target at 2โ€“3 monthsLDL โ‰ค2.0 mmol/L or non-HDL โ‰ค2.6 mmol/L. (NICE NG238 / QOF).
If target not metOptimise adherence/diet, up-titrate to 80 mg โ†’ add ezetimibe (can add even if target met, to lower risk further) โ†’ inclisiran / PCSK9 inhibitor (evolocumab, alirocumab) / bempedoic acid per NICE TA & lipid pathway.
Statin intolerant โ€” both groups
Lower dose / alternate-day โ†’ ezetimibe
Confirm true intolerance (rechallenge โ€” most myalgia is nocebo). Try a lower dose or alternate-day rosuvastatin 5 mg; if intolerant to โ‰ฅ2 statins use ezetimibe 10 mg OD monotherapy and refer to lipid clinic for add-on (bempedoic acid, PCSK9i / inclisiran).

Escalation when target not met โ€” step up only after rechecking non-HDL at 2โ€“3 months. GP / primary care Refer to secondary care

Step 1Optimise before escalating โ€” confirm adherence & correct dose timing, reinforce diet/lifestyle, and exclude/treat secondary causes (hypothyroidism, alcohol, drugs). Roughly half of apparent non-response is adherence. Recheck non-HDL at 2โ€“3 months.
Step 2Maximise the statin โ€” titrate atorvastatin 20 โ†’ 40 โ†’ 80 mg OD to the highest tolerated dose (โ‰ˆ40โ€“55% LDL fall at 80 mg). Secondary-prevention patients should already be on 80 mg. Each step: recheck at 2โ€“3 months.
Step 3Switch to a more potent statin โ€” if insufficient or partly intolerant, switch to rosuvastatin 10 โ†’ 20 โ†’ 40 mg OD (most potent per mg; rosuvastatin 20 mg โ‰ˆ atorvastatin 40โ€“80 mg). Useful where 80 mg atorvastatin not tolerated.
Step 4Add ezetimibe 10 mg OD โ€” first add-on, on top of the max tolerated statin. Further ~15โ€“20% LDL (โ‰ˆ21% non-HDL) reduction. Add even if target met in secondary prevention to lower risk further (NICE).
Step 5Bempedoic acid โ€” where a statin is contraindicated/not tolerated and ezetimibe alone is inadequate: bempedoic acid 180 mg OD, or fixed-dose Nustendi (bempedoic 180 mg / ezetimibe 10 mg) OD. Oral, primary care (NICE TA694).
Step 6Inclisiran 284 mg SC โ€” secondary prevention only (established ASCVD) with LDL-C โ‰ฅ2.6 mmol/L despite maximum tolerated statin ยฑ ezetimibe. Doses at 0 & 3 months, then 6-monthly. Can be given in primary care/community (NICE TA733).
ReferSecondary care (lipid clinic) for a PCSK9 inhibitor โ€” specialist-initiated: evolocumab 140 mg SC every 2 weeks (or 420 mg monthly) or alirocumab 75โ€“150 mg SC every 2 weeks (~50โ€“60% further LDL fall). NICE TA393/394 thresholds โ€” persistent LDL despite max tolerated therapy: FH without CVD >5.0; CVD high-risk >4.0; CVD very-high-risk >3.5 mmol/L.
ReferAlso refer to the lipid clinic if: confirmed or possible FH (genetic testing + cascade), intolerance to โ‰ฅ3 statins with persistently high LDL, triglycerides >10 mmol/L (pancreatitis risk), or diagnostic uncertainty / complex mixed dyslipidaemia.

Muscle symptoms: Check CK if symptomatic. CK >4ร— ULN: stop statin. CK <4ร—: continue and review. Most "statin myalgia" is nocebo effect โ€” trial of different statin or rechallenge important.

Each mmol/L reduction in LDL-C reduces major CV events by ~22% (Cholesterol Treatment Trialists). Atorvastatin is first-line over simvastatin because of fewer drug interactions and better potency per mg. High-intensity statin in secondary prevention reduces CV events by 25โ€“35% over 5 years (NNT ~15โ€“20). Ezetimibe added to statin gives additional 6โ€“7% CV event reduction (IMPROVE-IT trial). The nocebo effect accounts for 70โ€“80% of reported statin intolerance โ€” rechallenge with a different statin leads to successful treatment in most patients.

8
Lifestyle

Non-Pharmacological Interventions โ€” Foundation of Treatment

Mediterranean diet Olive oil, oily fish โ‰ฅ2ร—/week, legumes, nuts, vegetables, wholegrains. Reduces LDL by 0.3โ€“0.5 mmol/L, CV events by 30% (PREDIMED trial). Single most evidence-based dietary intervention.
Saturated fat reduction Replace saturated fat (butter, red meat, full-fat dairy) with unsaturated (olive oil, avocado, oily fish). Each 1% SFA replaced by PUFA reduces LDL by 0.03 mmol/L.
Plant sterols/stanols 2 g/day (fortified spreads, yoghurt drinks, orange juice) reduces LDL by 10โ€“15%. Available OTC. Recommend alongside statin for additive effect.
Physical activity 150 min moderate intensity/week. Raises HDL by 0.08โ€“0.15 mmol/L, reduces TG by 20โ€“30%. Aerobic exercise most effective โ€” brisk walking, cycling, swimming.
Weight loss 5โ€“10 kg weight loss reduces LDL by 0.2โ€“0.3 mmol/L, TG by 20%, raises HDL. BMI reduction below 25 dramatically improves TC:HDL ratio.
Smoking cessation Smoking reduces HDL by 5โ€“10%. Cessation raises HDL within 6 months. NRT + varenicline. Refer to stop-smoking service โ€” 4ร— more effective than willpower alone.
Alcohol reduction Excess alcohol raises TG and LDL. Target <14 units/week with 2 alcohol-free days. High alcohol = secondary cause of hypertriglyceridaemia.
Dietary fibre Soluble fibre (oats, psyllium, beans) binds bile acids and reduces LDL by 0.2โ€“0.4 mmol/L. Porridge for breakfast is a simple, evidence-based recommendation.

The PREDIMED trial showed Mediterranean diet reduced major CV events by 30% over 5 years โ€” comparable to statin therapy โ€” without the medication burden. Combined lifestyle changes can reduce LDL by 1.0โ€“1.5 mmol/L without medication, which is equivalent to low-dose statin. The key message for patients is that lifestyle is not an optional add-on to statins โ€” it is a concurrent treatment that amplifies statin benefit and may be sufficient alone in low-to-moderate risk patients.

9
Safety

Follow-Up, Monitoring & Safety-Netting

3 months post-statin
Repeat fasting lipid profile + LFTs. Assess tolerance. Check LDL target achieved. Muscle symptom enquiry. If LDL not at target: intensify (increase dose or add ezetimibe)
1 year
Annual lipid profile. Annual LFTs. QRISK3 recalculation (changes with age/new diagnoses). Review lifestyle changes. Medication adherence check
Ongoing monitoring
LFTs annually on statin. No routine CK unless muscle symptoms. No routine lipid check more frequently than 6-monthly unless dose change
Statin safety
Stop statin if: ALT >3ร— ULN (persistent), CK >10ร— ULN, new-onset diabetes symptoms (statin slightly increases T2DM risk โ€” net CV benefit still clearly outweighs this). Restart at lower dose when resolved
Safety-net
Severe unexplained myalgia/weakness โ†’ stop statin, check CK same day. Jaundice โ†’ stop statin, urgent LFTs. Chest pain โ†’ 999 regardless of lipid treatment status
Pregnancy
Stop statin as soon as pregnancy confirmed โ€” teratogenic. Restart postnatally (not while breastfeeding). Use bile acid sequestrants if essential during pregnancy
Drug interactions
Simvastatin: avoid with clarithromycin, erythromycin, diltiazem, amiodarone (increases myopathy risk). Atorvastatin has fewer interactions. Check all new prescriptions

The 3-month lipid recheck is the critical intervention point โ€” studies show that patients not at target after 3 months need proactive intensification, not watchful waiting. Without intensification at 3 months, ~60% of high-risk patients remain above LDL target. Statin-associated muscle symptoms affect 5โ€“10% of patients in trials but much higher in clinical practice โ€” systematic re-examination (rechallenge, different statin, alternate dosing) recovers tolerable treatment in 80% of cases. Statins in pregnancy carry a risk of structural abnormalities โ€” women of childbearing age must be counselled and contraception discussed.

Educational use only. Based on: NICE NG238 (Cardiovascular disease risk assessment 2023), NICE CKS Lipid modification โ€” CVD prevention, NICE CG181, NICE TA385 (ezetimibe), TA393 (alirocumab), TA394 (evolocumab), TA694 (bempedoic acid), TA733 (inclisiran), Simon Broome FH criteria, QRisk3.org. Always check the current BNF and local lipid pathway; adapt to individual patient context.