Dyslipidaemia & Cholesterol

📋 Key Information Summary

📋

Dyslipidaemia — abnormal LDL-cholesterol, HDL-cholesterol, or triglycerides — is a leading modifiable risk factor for atherosclerotic cardiovascular disease (ASCVD) in Australia.
Classification includes primary (genetic, e.g. familial hypercholesterolaemia) and secondary (dietary, metabolic, drug-induced) causes.
Absolute cardiovascular risk assessment using the Australian Absolute CVD Risk Calculator (derived from the Framingham Risk Equation) should guide treatment thresholds, not LDL-C alone.
All adults aged ≥45 years (≥30 years for Aboriginal and Torres Strait Islander peoples) should have a baseline lipid panel and CVD risk assessment.
Lifestyle modification — Mediterranean-style diet, ≥150 min/week moderate-intensity exercise, smoking cessation, and weight management — is first-line for all patients.
High-intensity statins (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) are first-line pharmacotherapy for elevated absolute CVD risk or established ASCVD.
Ezetimibe is the preferred second-line agent when LDL-C target is not achieved on maximum tolerated statin; PBS Authority Required.
PCSK9 inhibitors (evolocumab, alirocumab) are PBS-listed for very high-risk patients with inadequate response to maximised oral therapy.
Familial hypercholesterolaemia (FH) affects ~1 in 250 Australians and mandates early, aggressive LDL-C lowering; cascade screening of first-degree relatives is essential.
LDL-C targets: <1.8 mmol/L (high risk), <1.4 mmol/L (very high risk with ASCVD), ≥50% reduction from baseline when absolute targets are not feasible.
Statins are generally safe; baseline LFTs and CK are not routinely required but should be checked if symptoms arise (myalgia, unexplained fatigue).
Aboriginal and Torres Strait Islander peoples experience higher rates of premature CVD and should be screened from age 30 with lower treatment thresholds.
Pregnancy and breastfeeding are contraindications for statins and ezetimibe; bile-acid sequestrants are the only lipid-lowering agents considered safe in pregnancy.
Combination lipid-lowering therapy (statin + ezetimibe ± PCSK9 inhibitor) is recommended in stepwise fashion when LDL-C targets are not met.

🎧 Audio Brief

Why Your Cholesterol Number Isn't Enough

A short clinical audio briefing generated from this article — perfect for the commute or ward round.

Introduction & Australian Epidemiology

Dyslipidaemia is a disorder characterised by abnormal concentrations of lipoproteins in the blood, including elevated low-density lipoprotein cholesterol (LDL-C), low high-density lipoprotein cholesterol (HDL-C), elevated triglycerides (TG), or a combination of these abnormalities. It is one of the most important modifiable risk factors for atherosclerotic cardiovascular disease (ASCVD), which remains the leading cause of death in Australia, accounting for approximately 27% of all deaths annually.

According to the Australian Bureau of Statistics (ABS) National Health Survey, approximately 6.0 million Australian adults (34%) have total cholesterol levels ≥5.5 mmol/L, and an estimated 4.4 million have abnormal lipid profiles warranting clinical attention. Despite the widespread availability of effective lipid-lowering therapies, a significant treatment gap persists, with only 40–50% of high-risk Australians achieving guideline-recommended LDL-C targets.

The burden of dyslipidaemia is disproportionately borne by Aboriginal and Torres Strait Islander peoples, who experience cardiovascular mortality rates 1.5–2 times higher than non-Indigenous Australians, driven by earlier onset, higher prevalence of risk factors, and barriers to healthcare access.

Management of dyslipidaemia requires an integrated approach combining lifestyle interventions, cardiovascular risk stratification, and pharmacotherapy tailored to individual risk profiles. This guideline provides evidence-based recommendations for Australian primary care and specialist practitioners.

Lipid Physiology & Classification

Lipoprotein Metabolism

Lipids are transported in the bloodstream as components of lipoproteins — spherical particles comprising a hydrophobic core of cholesterol esters and triglycerides surrounded by a hydrophilic shell of phospholipids, free cholesterol, and apolipoproteins. Understanding lipoprotein metabolism is essential for rational classification and treatment of dyslipidaemia.

The two principal metabolic pathways are:

Exogenous pathway: Dietary cholesterol and triglycerides are absorbed from the gut and incorporated into chylomicrons. Lipoprotein lipase (LPL) on capillary endothelium hydrolyses triglycerides, generating chylomicron remnants that are cleared by hepatic LDL-receptor-related protein (LRP).
Endogenous pathway: The liver synthesises very-low-density lipoproteins (VLDL), which are progressively converted by LPL and hepatic lipase to intermediate-density lipoproteins (IDL) and then LDL. LDL delivers cholesterol to peripheral tissues and is ultimately cleared via hepatic LDL receptors. PCSK9 promotes degradation of LDL receptors, reducing LDL clearance.

Lipoprotein Classification

Lipoprotein	Primary Lipid	Key Apolipoprotein	Role	Clinical Significance
Chylomicrons	Triglycerides (85%)	ApoB-48	Transport dietary fat	Elevated in familial chylomicronaemia syndrome
VLDL	Triglycerides (55%)	ApoB-100	Transport hepatic TG	Elevated in metabolic syndrome, diabetes
IDL	Cholesterol/TG	ApoB-100	Intermediate particle	Elevated in familial dysbetalipoproteinaemia
LDL	Cholesterol (50%)	ApoB-100	Deliver cholesterol to tissues	Primary atherogenic particle; target of therapy
HDL	Cholesterol (20%)	ApoA-I	Reverse cholesterol transport	Low HDL-C is an independent CVD risk factor
Lp(a)	Cholesterol	ApoB-100 + Apo(a)	Prothrombotic, proatherogenic	Genetically determined; emerging therapy target

Classification of Dyslipidaemia

Dyslipidaemia may be classified by aetiology or by Fredrickson (WHO) phenotype:

Category	Examples
Primary (genetic)	Familial hypercholesterolaemia (FH), familial combined hyperlipidaemia, familial dysbetalipoproteinaemia (Type III), familial chylomicronaemia syndrome, polygenic hypercholesterolaemia
Secondary (acquired)	Diabetes mellitus, hypothyroidism, nephrotic syndrome, chronic kidney disease, cholestatic liver disease, obesity, excess alcohol, drugs (corticosteroids, isotretinoin, antiretrovirals, cyclosporin)

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Clinical pearl: Always exclude secondary causes (particularly hypothyroidism and nephrotic syndrome) before attributing dyslipidaemia to a primary genetic disorder. A TSH and urine albumin-to-creatinine ratio (ACR) should be performed in all newly diagnosed patients.

Cardiovascular Risk Assessment

Absolute CVD Risk Assessment

The cornerstone of dyslipidaemia management in Australia is absolute cardiovascular risk assessment rather than treatment based on isolated lipid values. The National Vascular Disease Prevention Alliance (NVDPA) recommends using the Australian Absolute CVD Risk Calculator, derived from the Framingham Risk Equation and calibrated to the Australian population.

Risk assessment should be performed for:

All adults aged 45–79 years without known CVD
Aboriginal and Torres Strait Islander adults aged 30–79 years
Adults with diabetes aged ≥60 years (or ≥50 years if ATSI)
Adults with eGFR <60 mL/min/1.73 m² or albuminuria

Risk Categories & LDL-C Targets

Low Risk

<10% 5-year CVD risk

No diabetes, no CKD stage 3+, normal lipids or mildly elevated LDL-C.

LDL-C target: <3.0 mmol/L; Lifestyle first-line; Pharmacotherapy if LDL-C ≥5.0 mmol/L

Moderate Risk

10–15% 5-year CVD risk

One or more risk factors (smoking, hypertension, family history, low HDL-C, CKD).

LDL-C target: <2.5 mmol/L; Consider statin therapy; Lifestyle + pharmacotherapy

High Risk

>15% 5-year CVD risk

Multiple risk factors, diabetes with microalbuminuria, CKD stage 3+, or calculated risk >15%.

LDL-C target: <1.8 mmol/L (or ≥50% reduction); High-intensity statin indicated

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Very high risk (secondary prevention): Patients with established ASCVD (prior MI, stroke, PVD, ACS), familial hypercholesterolaemia, or diabetes with target organ damage require LDL-C <1.4 mmol/L and ≥50% reduction. Early combination therapy (statin + ezetimibe ± PCSK9 inhibitor) should be considered.

Risk Enhancers

Family history of premature CVD (first-degree male <55 years, female <65 years)
LDL-C ≥4.9 mmol/L (suggestive of familial hypercholesterolaemia)
Triglycerides ≥2.3 mmol/L despite lifestyle measures
Lipoprotein(a) ≥50 mg/dL (consider measurement in intermediate-risk patients)
Coronary artery calcium (CAC) score ≥100 Agatston units (MBS item 57360 — specialist only)
High-sensitivity CRP ≥2.0 mg/L
Ankle-brachial index <0.9
South Asian, Pacific Islander, or Aboriginal and Torres Strait Islander ethnicity

Pharmacological Treatment

Lifestyle Modification (All Patients)

Lifestyle intervention is the foundation of dyslipidaemia management and should be continued alongside all pharmacotherapy:

Diet: Mediterranean-style diet rich in vegetables, fruits, legumes, whole grains, nuts, olive oil, and fish; reduce saturated fat to <7% of total energy intake; increase soluble fibre (≥10 g/day); limit alcohol to ≤2 standard drinks/day
Exercise: ≥150 minutes/week moderate-intensity or ≥75 minutes/week vigorous-intensity aerobic activity
Weight: Target BMI 18.5–24.9 kg/m²; waist circumference <94 cm (men), <80 cm (women)
Smoking: Complete cessation — reduces ASCVD risk by 25–50% within 1–5 years

Statins (HMG-CoA Reductase Inhibitors)

Statins remain the first-line pharmacotherapy for elevated LDL-C. They reduce LDL-C by inhibiting hepatic cholesterol synthesis, upregulating LDL receptor expression, and increasing LDL clearance. Meta-analyses demonstrate a 22% reduction in major vascular events per 1.0 mmol/L LDL-C reduction.

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Atorvastatin

Lipitor® · Generic · HMG-CoA reductase inhibitor

Adult dose Moderate intensity: 10–20 mg PO daily; High intensity: 40–80 mg PO daily

Paediatric dose FH: 10 mg PO daily (≥10 years); max 20 mg/day (10–17 years)

LDL-C reduction 40–50% (moderate); 50–60% (high intensity)

Renal adjustment No dose adjustment required

Key interactions CYP3A4 substrate — caution with clarithromycin, itraconazole, grapefruit juice; increased myopathy risk with gemfibrozil

PBS status ✔ PBS General Benefit

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Rosuvastatin

Crestor® · Generic · HMG-CoA reductase inhibitor

Adult dose Moderate intensity: 5–10 mg PO daily; High intensity: 20–40 mg PO daily

Paediatric dose FH: 5–10 mg PO daily (≥10 years); max 20 mg/day

LDL-C reduction 45–55% (moderate); 55–65% (high intensity)

Renal adjustment eGFR <30 mL/min: max 10 mg/day; haemodialysis: max 10 mg/day

Key interactions Not CYP3A4-dependent — fewer drug interactions; caution with cyclosporin (max 5 mg/day)

PBS status ✔ PBS General Benefit

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Simvastatin

Zocor® · Generic · HMG-CoA reductase inhibitor

Adult dose Moderate intensity: 20–40 mg PO daily (max 80 mg — rarely used due to myopathy risk)

LDL-C reduction 30–40% (moderate intensity)

Renal adjustment eGFR <30 mL/min: initiate 5 mg daily; titrate with caution

Key interactions CYP3A4 substrate — avoid with diltiazem, verapamil, amiodarone; contraindicated with gemfibrozil

PBS status ✔ PBS General Benefit

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Pravastatin

Pravachol® · Generic · HMG-CoA reductase inhibitor

Adult dose Moderate intensity: 40 mg PO daily

LDL-C reduction 30–35% (moderate intensity)

Renal adjustment Significant renal impairment: initiate 10 mg daily

Key advantage Minimal CYP metabolism — fewer drug interactions; preferred when polypharmacy is a concern

PBS status ✔ PBS General Benefit

⚠️

Statin-associated muscle symptoms (SAMS): Occur in 5–10% of patients. If myalgia develops, check CK. CK >5× ULN warrants temporary cessation. Consider switching to a hydrophilic statin (rosuvastatin, pravastatin), alternate-day dosing, or dose reduction. Concomitant gemfibrozil significantly increases myopathy risk — use fenofibrate instead if fibrate therapy is required.

Ezetimibe

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Ezetimibe

Ezetrol® · Generic · Cholesterol absorption inhibitor

Mechanism Inhibits NPC1L1 transporter in the small intestine, reducing dietary and biliary cholesterol absorption

Adult dose 10 mg PO daily (with or without food)

LDL-C reduction 18–20% monotherapy; 15–20% additional when added to statin

Renal/hepatic No dose adjustment required; avoid in moderate–severe hepatic impairment

PBS status ⚠ PBS Authority Required

PBS Authority criteria for ezetimibe: patient must be on maximum tolerated statin dose with documented intolerance or inadequate LDL-C response, OR statin-intolerant with documented trial of at least two statins. The combination tablet rosuvastatin/ezetimibe (Rosuzet®) is also PBS-listed under restricted conditions.

PCSK9 Inhibitors

PCSK9 inhibitors are monoclonal antibodies that bind and inhibit PCSK9, preventing degradation of hepatic LDL receptors and dramatically increasing LDL clearance. They are reserved for very high-risk patients with inadequate LDL-C reduction on maximised oral therapy.

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Evolocumab

Repatha® · PCSK9 monoclonal antibody

Adult dose 140 mg SC every 2 weeks OR 420 mg SC monthly

LDL-C reduction 55–60% additional reduction on background statin therapy

Evidence FOURIER trial: 15% reduction in MACE; 20% reduction in CV death/MI/stroke in very high risk

PBS status ⛔ PBS Authority Required (Specialist)

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Alirocumab

Praluent® · PCSK9 monoclonal antibody

Adult dose 75 mg SC every 2 weeks; may increase to 150 mg SC every 2 weeks

LDL-C reduction 50–60% additional reduction on background statin therapy

Evidence ODYSSEY OUTCOMES: 15% reduction in MACE post-ACS; greatest benefit in LDL-C ≥2.6 mmol/L

PBS status ⛔ PBS Authority Required (Specialist)

PBS Authority criteria for PCSK9 inhibitors: patient must have ASCVD or FH; be on maximum tolerated statin + ezetimibe for ≥3 months; and have LDL-C persistently above target. Prescribing is restricted to cardiologists, endocrinologists, or lipid specialists.

Other Lipid-Lowering Agents

Agent	Mechanism	Primary Effect	Dose	PBS Status
Fenofibrate	PPARα agonist	↓ TG 30–50%, ↑ HDL-C 10–20%	145 mg PO daily	✔ PBS General Benefit
Bempedoic acid	ACL inhibitor (upstream of HMG-CoA)	↓ LDL-C 15–25%	180 mg PO daily	⛔ Not PBS listed
Icosapent ethyl	Purified EPA (omega-3)	↓ TG 20–30%, anti-inflammatory	2 g PO BD (with food)	⛔ Not PBS listed
Inclisiran	siRNA targeting PCSK9 mRNA	↓ LDL-C 50%	284 mg SC at 0, 3 months, then 6-monthly	⛔ Not PBS listed (TGA approved)
Cholestyramine	Bile acid sequestrant	↓ LDL-C 15–25%	4 g PO BD–QDS	✔ PBS General Benefit

Stepwise Approach to LDL-C Lowering

1

Lifestyle + High-Intensity Statin

Atorvastatin 40–80 mg or rosuvastatin 20–40 mg daily. Recheck lipids at 6–8 weeks.

2

Add Ezetimibe 10 mg daily

If LDL-C remains above target on maximum tolerated statin. Combination provides additive 15–20% LDL-C reduction.

3

Add PCSK9 inhibitor

For very high-risk patients (ASCVD, FH) not at LDL-C target on statin + ezetimibe. Specialist initiation required.

4

Consider inclisiran or bempedoic acid

For refractory cases or statin-intolerant patients. Access via clinical trial, private prescription, or special access scheme.

Management of Hypertriglyceridaemia

Elevated triglycerides are independently associated with residual cardiovascular risk. Management is stratified by severity:

Mild (1.7–2.3 mmol/L): Lifestyle modification; address metabolic syndrome, alcohol, diabetes
Moderate (2.3–5.6 mmol/L): Lifestyle + statin first; consider fenofibrate addition if TG remains ≥2.3 mmol/L on statin (ACCORD Lipid, FIELD subanalyses)
Severe (≥5.6 mmol/L): Priority is prevention of pancreatitis — fibrate first-line; strict dietary fat restriction (<20 g/day); consider icosapent ethyl if available; urgent investigation for familial chylomicronaemia if TG >11.3 mmol/L

Familial Hypercholesterolaemia

Overview

Familial hypercholesterolaemia (FH) is an autosomal dominant genetic disorder affecting approximately 1 in 250 Australians (heterozygous FH, HeFH) and 1 in 300,000 (homozygous FH, HoFH). It is caused by loss-of-function mutations in the LDLR (≥90%), APOB (~5–10%), or PCSK9 (<5%) genes, resulting in markedly elevated lifelong LDL-C levels and accelerated atherosclerosis.

Without treatment, men with HeFH have a 50% risk of a coronary event by age 50, and women a 30% risk by age 60. Early diagnosis and treatment can normalise life expectancy.

Diagnostic Criteria

The Dutch Lipid Clinic Network (DLCN) criteria or Simon Broome criteria are used. In Australia, DLCN score ≥6 (probable/definite FH) triggers referral and cascade screening:

Criterion	Points
First-degree relative with premature CAD (<55 M, <65 F)	+1
First-degree relative with LDL-C >95th percentile	+1
Personal history of premature CAD	+2
Tendon xanthoma or arcus cornealis <45 years	+6
LDL-C >8.5 mmol/L	+8
LDL-C 6.5–8.4 mmol/L	+5
LDL-C 5.0–6.4 mmol/L	+3
DNA mutation in LDLR, APOB, or PCSK9	+8

Interpretation: 0–2 = unlikely; 3–5 = possible; 6–8 = probable; >8 = definite FH.

Cascade Screening

✅

Mandatory cascade screening: Every confirmed or probable FH case requires contact-tracing of first-degree relatives (parents, siblings, children). In Australia, genetic testing for FH-causing mutations is available through public genetics services and the FH Australasia Network (FHAN). Lipid testing of children of affected parents should occur from age 2 (or earlier if HoFH is suspected).

Treatment of Heterozygous FH

LDL-C target: <2.5 mmol/L (no ASCVD) or <1.8 mmol/L (with ASCVD) or <1.4 mmol/L (very high risk); ≥50% reduction from baseline
First-line: High-intensity statin (atorvastatin 80 mg or rosuvastatin 40 mg daily)
Second-line: Add ezetimibe 10 mg daily
Third-line: Add PCSK9 inhibitor (evolocumab or alirocumab) — specialist-initiated, PBS Authority
Referral: All patients with probable/definite FH should be referred to a lipid specialist or cardiologist
Paediatric FH: Lifestyle from age 2; statin therapy from age 8–10 years (atorvastatin 10 mg) with paediatric endocrinologist/cardiologist guidance

Treatment of Homozygous FH

Homozygous FH (HoFH) is a medical emergency in paediatrics. LDL-C is typically >13 mmol/L without treatment. Management requires:

Maximised oral therapy (statin + ezetimibe)
PCSK9 inhibitor (limited efficacy due to absent LDL receptors — only ~20% LDL-C reduction in HoFH)
Lipoprotein apheresis — available at major tertiary centres (MBS item 13700); typically weekly or fortnightly
Lomitapide (Juxtapid®) — microsomal triglyceride transfer protein inhibitor; TGA approved but not PBS listed; available via Special Access Scheme
Evkeeza® (evinacumab) — anti-ANGPTL3 antibody; TGA registered; not yet PBS listed; ~50% LDL-C reduction in HoFH

Investigations

Baseline Lipid Profile

A fasting lipid panel (12-hour fast) is preferred but non-fasting samples are acceptable for initial screening. LDL-C may be calculated (Friedewald equation) or directly measured if triglycerides >4.5 mmol/L.

✔ MBS Available

Fasting lipid panel (total cholesterol, LDL-C, HDL-C, TG)

MBS item 66815; Fasting preferred; repeat 6–8 weeks after therapy initiation

✔ MBS Available

Apolipoprotein B (ApoB)

MBS item 66824; Superior to LDL-C for residual risk assessment; useful when TG >2.3 mmol/L

✔ MBS Available

Lipoprotein(a) — Lp(a)

MBS item 66823; Measure once in lifetime for all patients; recommended in intermediate risk, premature CVD, or family history of FH

Specialist

Genetic testing for FH (LDLR, APOB, PCSK9)

Available through public genetics services; MBS item 73291 (genetic testing under specific criteria); Refer via FHAN

✔ MBS Available

Coronary artery calcium (CAC) score

MBS item 57360; Specialist referral; useful for reclassifying intermediate-risk patients; CAC = 0 → defer statin if low-risk features

✔ MBS Available

Liver function tests (LFTs)

Baseline before statin therapy not routinely recommended (RACGP); check if symptoms arise or pre-existing liver disease

✔ MBS Available

Creatine kinase (CK)

Check only if myalgia or muscle weakness develops during statin therapy; not required at baseline

✔ MBS Available

Thyroid function tests (TSH)

Exclude hypothyroidism as a secondary cause of dyslipidaemia

✔ MBS Available

Urine albumin-to-creatinine ratio (ACR)

Screen for nephrotic syndrome / diabetic nephropathy as secondary cause

✔ MBS Available

HbA1c / fasting glucose

Screen for diabetes — major secondary cause of dyslipidaemia

Monitoring

Post-Initiation Monitoring

6–8 weeks

Repeat fasting lipid panel after statin initiation or dose titration. Assess LDL-C response (expect ≥30–50% reduction). Check adherence. If myalgia present, check CK.

3 months

If not at target, add ezetimibe. Recheck lipids 6–8 weeks after addition. Consider LFTs if on high-dose statin + ezetimibe.

6–12 months

Annual lipid panel once stable and at target. Reassess absolute CVD risk. Review medication adherence and side effects. Address lifestyle factors.

Annually (ongoing)

Lipid panel, CVD risk reassessment, renal function, HbA1c (if diabetic), medication review, and screening for new ASCVD events.

Monitoring Parameters

Parameter	When to Check	Action Threshold
LDL-C	6–8 wk post-initiation; then annually	Not at target → escalate therapy
CK	Only if symptomatic (myalgia, weakness)	≥5× ULN → stop statin; investigate
ALT/AST	Only if symptoms or pre-existing liver disease	≥3× ULN → withhold statin; assess
HbA1c	Annually (statins may mildly ↑ HbA1c)	Monitor glucose if new-onset DM on statin
eGFR	Annually	Dose adjust rosuvastatin if eGFR <30

Special Populations

🤰 Pregnancy & Breastfeeding

Statins: Contraindicated in pregnancy (Category X). Discontinue at least 3 months before conception. Cholesterol is essential for foetal development.

Ezetimibe: Not recommended — limited human data; discontinue pre-conception.

PCSK9 inhibitors: Contraindicated — insufficient safety data in pregnancy.

Cholestyramine: Only lipid-lowering agent considered safe in pregnancy — does not cross placenta. Use if LDL-C is critically elevated (e.g., HoFH).

Pre-conception counselling: Essential for women with FH. Discontinue statins/ezetimibe pre-conception and resume after breastfeeding. Contraceptive advice is critical for women of childbearing age on statins.

👶 Paediatrics

Heterozygous FH: Lifestyle from age 2. Statin therapy from age 8–10 years (atorvastatin 10 mg daily; titrate to 20 mg). Paediatric lipid specialist referral recommended.

Homozygous FH: Diagnosis often in infancy. Lipoprotein apheresis from early childhood. Statin + ezetimibe as tolerated. Specialist tertiary centre management mandatory.

Familial chylomicronaemia: Strict fat restriction (<15–20 g/day) from diagnosis. Avoid drugs that raise TG (e.g., isotretinoin).

Note: Routine cholesterol screening in children is not recommended unless family history of premature CVD or FH.

👴 Elderly (≥75 years)

Evidence supports statin therapy for secondary prevention in patients up to age 85 with established ASCVD.

Primary prevention benefit diminishes with age but is supported for patients aged 75–85 with ≥2 risk factors.

Use lower starting doses; monitor for drug interactions and myopathy.

Reassess risk–benefit annually; consider deprescribing if limited life expectancy or frailty.

🫘 Chronic Kidney Disease

Statin therapy is recommended for all CKD patients on dialysis (SHARP trial: simvastatin 20 mg + ezetimibe 10 mg reduced major atherosclerotic events by 17%).

Rosuvastatin: Max 10 mg/day if eGFR <30 mL/min.

Simvastatin: Start 5 mg/day if eGFR <30 mL/min.

Ezetimibe: No dose adjustment required in CKD.

Fibrates may worsen renal function — use with caution; avoid gemfibrozil.

🫁 Hepatic Impairment

Active liver disease or unexplained persistent transaminase elevation → contraindication to all statins.

Non-alcoholic fatty liver disease (NAFLD) is NOT a contraindication — statins are safe and may improve liver histology.

Ezetimibe: Avoid in moderate–severe hepatic impairment.

PCSK9 inhibitors: No hepatic dose adjustment required.

🛡️ Immunocompromised / Transplant

Cyclosporin significantly increases statin exposure — max rosuvastatin 5 mg/day; avoid simvastatin and atorvastatin at high doses.

Tacrolimus: Lower statin doses recommended; monitor for myopathy.

HIV protease inhibitors (ritonavir) increase statin levels — prefer pravastatin or pitavastatin.

Statin–fibrate combination with calcineurin inhibitors requires specialist supervision.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Epidemiology

Aboriginal and Torres Strait Islander peoples experience cardiovascular disease mortality rates 1.5–2.0 times higher than non-Indigenous Australians, with onset approximately 10–20 years earlier. The AIHW reports that CVD accounts for 22% of the gap in life expectancy.

Earlier screening

CVD risk assessment should commence at age 30 years (not 45) for Aboriginal and Torres Strait Islander adults, as recommended by the NVDPA and RACGP Red Book. Lipid screening and risk calculation should be incorporated into annual Aboriginal Health Checks (MBS item 715).

Lower treatment thresholds

Consider initiating statin therapy at lower absolute CVD risk thresholds in the context of social determinants, high background prevalence of metabolic syndrome, and limited access to specialist care. The 2020 NVDPA guidelines acknowledge that risk calculators may underestimate risk in this population.

Remote & rural access

Many Aboriginal and Torres Strait Islander communities, particularly in remote NT, WA, and QLD, have limited access to lipid specialists and PCSK9 inhibitor infusions. Telehealth lipid clinics (available through NT AHS and QLD Health) can facilitate specialist review. Lipoprotein apheresis is only available in metropolitan centres.

Cultural safety

Dietary advice must be culturally appropriate, recognise food insecurity, and avoid deficit-based language. Community-controlled health services (ACCHS) should lead lifestyle counselling. Use of Aboriginal Health Workers and Torres Strait Islander Health Practitioners as medication educators improves adherence.

Familial hypercholesterolaemia

FH may be underdiagnosed in Aboriginal and Torres Strait Islander populations due to lower screening rates. Cascade screening programmes should be integrated into ACCHS. Genetic testing access may be limited; clinical (DLCN) diagnosis should be used when genetic testing is unavailable.

Medication adherence

Factors affecting adherence include housing instability, transport barriers, health literacy, and distrust of mainstream health services. Blister-packed medications, pharmacist-led MedsCheck services (MBS item 900), and community pharmacy partnerships improve medication management.

Co-morbidities

High rates of type 2 diabetes (3× prevalence), chronic kidney disease, and rheumatic heart disease in Aboriginal and Torres Strait Islander communities necessitate integrated cardiometabolic management. Statin therapy should be prioritised in all Aboriginal and Torres Strait Islander adults with diabetes aged ≥30 years.

📚 References

1. National Vascular Disease Prevention Alliance. Absolute cardiovascular disease risk management — quick reference guide for health professionals. 2012 (endorsed by RACGP). Available at: cvdcheck.org.au
2. Heart Foundation of Australia. Position statement: Lipid management — summary of evidence. Heart Foundation; 2020.
3. Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670–1681.
4. Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease (FOURIER). N Engl J Med. 2017;376(18):1713–1722.
5. Schwartz GG, Steg PG, Szarek M, et al. Alirocumab and cardiovascular outcomes after acute coronary syndrome (ODYSSEY OUTCOMES). N Engl J Med. 2018;379(22):2097–2107.
6. Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection — SHARP). Lancet. 2011;377(9784):2181–2192.
7. Watts GF, Sullivan DR, Poplawski N, et al. Familial hypercholesterolaemia in Australasia: model of care, position statement and recommendations. Heart Lung Circ. 2011;20:S22.
8. Familial Hypercholesterolaemia Australasia Network (FHAN). Australian FH model of care. Available at: fhan.org.au
9. Australian Institute of Health and Welfare (AIHW). Cardiovascular disease in Aboriginal and Torres Strait Islander people. AIHW; 2023. Cat. no. CVD 87.
10. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice (Red Book). 10th ed. RACGP; 2024.
11. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR guideline on the management of blood cholesterol. J Am Coll Cardiol. 2019;73(24):e285–e350.
12. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS guidelines for the management of dyslipidaemias. Eur Heart J. 2020;41(1):111–188.
13. Australian Commission on Safety and Quality in Health Care (ACSQHC). Australian Atlas of Healthcare Variation Series. ACSQHC; 2023.
14. Pharmaceutical Benefits Scheme (PBS). Schedule of Pharmaceutical Benefits. Australian Government Department of Health. Available