📋 Key Information Summary
- Foundation of management: Absolute cardiovascular risk (ACVR) assessment using the Australian CV Risk Calculator is required for all adults ≥45 years (≥30 for Aboriginal and Torres Strait Islander peoples) before initiating lipid-lowering therapy.
- Risk categories: Low (<10% 5-year CVD risk), Moderate (10–15%), High (15–30%), and Very High (>30% or established atherosclerotic CVD, diabetes with microalbuminopathy, CKD eGFR <45, familial hypercholesterolaemia).
- First-line pharmacotherapy: Statins (atorvastatin, rosuvastatin preferred) are the cornerstone of lipid-lowering therapy for both primary and secondary prevention.
- PBS prescribing: Statin initiation requires Authority Required (streamlined) approval. Prescribers must document ACVR category and baseline lipid levels on the authority application.
- LDL-C targets: High/very-high risk: LDL-C <2.0 mmol/L; moderate risk: LDL-C <2.5 mmol/L. At least 50% reduction from baseline is the minimum therapeutic goal.
- Non-pharmacological measures: Diet (Mediterranean/DASH pattern), ≥150 min/week moderate-intensity exercise, weight loss (target BMI <30), smoking cessation, and alcohol moderation are essential first-line interventions for all patients.
- Severe hypertriglyceridaemia: Triglycerides ≥5.6 mmol/L require urgent management with fibrates (fenofibrate) and dietary fat restriction to reduce pancreatitis risk.
- Icosapent ethyl (Vascepa®): PBS-listed for residual cardiovascular risk in patients with TG 1.5–5.6 mmol/L despite maximally tolerated statin therapy.
- Statin intolerance: Confirm with rechallenge or cross-over trial. Alternatives include ezetimibe (PBS Authority Required in combination), PCSK9 inhibitors (specialist-initiated), and bempedoic acid.
- Familial hypercholesterolaemia (FH): Suspect if LDL-C >4.9 mmol/L, tendon xanthomas, or premature CVD in first-degree relatives. Refer to lipid specialist. Cascade screening of family members is essential.
- Monitoring: Lipid panel at 6–8 weeks after initiation/change, then every 3–12 months. LFTs at baseline; CK only if symptoms of myopathy. Annual lipid review for stable patients.
- ATSI priority: Aboriginal and Torres Strait Islander Australians have 2–3× the CVD burden of non-Indigenous Australians. Begin CV risk assessment from age 30. Ensure culturally safe communication and address barriers to access in remote communities.
- Drug interactions: Check for interactions with protease inhibitors (HIV/HCV), cyclosporine, verapamil, diltiazem, gemfibrozil, and azole antifungals — these may increase statin toxicity risk.
Introduction & Australian Epidemiology
Dyslipidaemia refers to an abnormal concentration of one or more plasma lipids — total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). It is a major modifiable risk factor for atherosclerotic cardiovascular disease (ASCVD), which remains the leading cause of death in Australia, accounting for approximately 42,000 deaths annually (AIHW, 2023).
In Australian general practice, dyslipidaemia management has evolved from a single risk-factor approach to an integrated absolute cardiovascular risk (ACVR) framework. This approach estimates the cumulative probability of a cardiovascular event over 5 years based on age, sex, smoking status, blood pressure, lipid levels, diabetes status, and eGFR. The National Vascular Disease Prevention Alliance (NVDPA) guidelines and the Royal Australian College of General Practitioners (RACGP) Red Book provide the clinical framework used in Australian primary care.
| Statistic | Value | Source |
|---|---|---|
| Australians with elevated cholesterol (≥5.5 mmol/L) | ~3.7 million (15% of adults) | ABS National Health Survey 2022 |
| Proportion of adults on lipid-lowering medication | ~20% of adults ≥45 years | AIHW 2023 |
| CVD as proportion of all deaths | ~25% | AIHW Leading Causes of Death 2022 |
| Prevalence of familial hypercholesterolaemia | 1 in 250 (estimated) | National FH Foundation Australia |
| CVD burden in ATSI Australians vs non-Indigenous | 2.3× higher age-standardised rate | AIHW Indigenous Health Report 2023 |
Despite the widespread availability of effective lipid-lowering therapies, undertreatment remains a significant issue. Only an estimated 30–40% of high-risk Australians achieve their LDL-C targets. Barriers include therapeutic inertia, statin intolerance concerns, patient misconceptions about statins, and inconsistent use of ACVR calculators in general practice.
This guideline provides a practical, evidence-based approach to the assessment, investigation, and management of dyslipidaemia in Australian primary care, with specific attention to PBS prescribing requirements, Australian risk stratification tools, and health equity considerations for Aboriginal and Torres Strait Islander communities.
Risk Categories & PBS Prescribing Guidelines
Absolute Cardiovascular Risk (ACVR) Assessment
All Australian adults should have their absolute cardiovascular risk assessed using the Australian Cardiovascular Risk Calculator (available at cvdcheck.org.au), based on the Framingham Risk Score recalibrated for the Australian population. The calculator integrates age, sex, systolic blood pressure, total cholesterol, HDL-C, smoking status, diabetes status, and eGFR.
When to perform ACVR assessment: All adults ≥45 years (≥30 years for Aboriginal and Torres Strait Islander peoples). Reassess every 2 years for low-risk patients, or earlier if new risk factors develop. Do not use the calculator in patients who already have established ASCVD, familial hypercholesterolaemia, or CKD eGFR <45 — these patients are automatically classified as high or very high risk.
Australian CV Risk Categories
Low
<10% 5-year CVD risk
Lifestyle advice as first-line. Pharmacotherapy generally not indicated unless LDL-C >4.0 mmol/L with additional risk factors, or patient preference after informed discussion.
Setting: GP — lifestyle focus, reassess in 2 years
Moderate
10–15% 5-year CVD risk
Lifestyle measures + consider statin therapy if LDL-C remains elevated after 3–6 months of non-pharmacological intervention. Patient discussion about risk–benefit is essential.
Setting: GP — shared decision-making on statin initiation
High
15–30% 5-year CVD risk
Statin therapy strongly recommended in addition to lifestyle modification. PBS-subsidised statin prescribing available. Target LDL-C <2.0 mmol/L.
Setting: GP — initiate statin, refer if target not achieved on combination therapy
Very High Risk (Clinically Determined): Patients with any of the following are automatically classified as very high risk regardless of calculated ACVR: established ASCVD (prior MI, stroke, PAD, ACS), type 2 diabetes with microalbuminopathy or eGFR 30–59, CKD with eGFR <45, familial hypercholesterolaemia, or a calculated 5-year risk >30%. Target LDL-C: <1.4 mmol/L (or ≥50% reduction from baseline).
PBS Prescribing Requirements for Statins
The Pharmaceutical Benefits Scheme (PBS) requires Authority Required (streamlined) approval for statin prescribing. The prescriber must document the clinical indication on the authority application. The key criteria are:
- Secondary prevention: Patient has established ASCVD (documented ischaemic heart disease, ischaemic cerebrovascular disease, or peripheral arterial disease). Streamlined authority is straightforward.
- Primary prevention — high risk: Calculated ACVR ≥15% over 5 years (or ≥10% with additional risk factors such as strong family history, elevated Lp(a), South Asian ethnicity, CKD).
- Familial hypercholesterolaemia: Authority Required (may require phone approval in some states). Document diagnosis using Dutch Lipid Clinic Network criteria or genetic testing.
- Diabetes: Most adults with diabetes aged ≥45 years qualify for PBS-subsidised statin therapy.
PBS Authority Process: For streamlined authority, the prescriber enters the indication code when writing the prescription (e-prescribing or paper). Phone approval via PBS Authority (1800 888 333) is required for indications not covered by streamlined codes, such as complex familial hypercholesterolaemia or paediatric statin use.
When to Refer
- Suspected familial hypercholesterolaemia (LDL-C >4.9 mmol/L, family history of premature CVD, tendon xanthomas)
- Failure to reach lipid targets on maximal tolerated combination therapy
- Confirmed statin intolerance (unable to tolerate any statin after structured rechallenge)
- Need for PCSK9 inhibitor initiation (specialist initiation required for PBS)
- Severe hypertriglyceridaemia (TG >11.3 mmol/L) or recurrent pancreatitis
- Paediatric patients with significant dyslipidaemia
Clinical Presentation & Diagnostic Criteria
Classification of Dyslipidaemia
Dyslipidaemia is broadly classified as primary (genetic/familial) or secondary (acquired). Most patients in Australian general practice have a mixed or secondary aetiology. The Fredrickson/WHO classification remains useful for characterising lipid phenotypes:
| Phenotype | Key Lipid Abnormality | Common Causes |
|---|---|---|
| Type IIa (Familial hypercholesterolaemia) | ↑↑ LDL-C; normal TG | LDLR, APOB, PCSK9 mutations |
| Type IIb (Combined hyperlipidaemia) | ↑ LDL-C + ↑ TG | Metabolic syndrome, familial combined |
| Type III (Dysbetalipoproteinaemia) | ↑↑ TC + ↑↑ TG (broad β-band) | APOE2/E2 homozygosity (rare) |
| Type IV (Hypertriglyceridaemia) | Normal/↑ LDL-C; ↑↑↑ TG | Metabolic syndrome, alcohol, diabetes |
| Type V (Mixed hypertriglyceridaemia) | ↑↑ TG + ↑ TC (chylomicrons + VLDL) | Alcohol, uncontrolled diabetes, drugs |
Secondary Causes to Exclude
Before diagnosing primary dyslipidaemia, always screen for secondary causes. The most common contributors in Australian practice are:
- Hypothyroidism: Elevated TC and LDL-C — check TSH in all patients with newly identified hypercholesterolaemia
- Type 2 diabetes / metabolic syndrome: Characteristic pattern of ↑TG, ↓HDL-C, small dense LDL
- Chronic kidney disease: ↑TG, ↑TC (particularly in nephrotic syndrome)
- Medications: Thiazide diuretics, β-blockers (non-selective), isotretinoin, corticosteroids, antiretroviral protease inhibitors, immunosuppressants (cyclosporine, tacrolimus), oestrogen-containing HRT
- Alcohol excess: ↑TG (often severe); ↓HDL-C with heavy use
- Obesity and physical inactivity
- Cholestatic liver disease / primary biliary cholangitis: ↑TC with lipoprotein X
- Pregnancy: Physiological rise in lipids — do not diagnose dyslipidaemia in pregnancy
Clinical Features Suggesting Familial Hypercholesterolaemia
Suspect FH if: LDL-C >4.9 mmol/L (adults) or >3.5 mmol/L (children); tendon xanthomas (Achilles, extensor tendons of hands); arcus cornealis <45 years; xanthelasma; or premature ASCVD in the patient or first-degree relatives (<55 years men, <65 years women). Use the Dutch Lipid Clinic Network (DLCN) criteria to score likelihood of FH (score ≥6 = definite FH).
Physical Examination Findings
- Tendon xanthomas (pathognomonic for FH)
- Xanthelasma (yellowish plaques on eyelids — non-specific)
- Corneal arcus (arcus senilis — significant if <45 years)
- Eruptive xanthomas (creamy papules — severe hypertriglyceridaemia)
- Lipemia retinalis (milky retinal vessels — TG >11.3 mmol/L)
- Hepatosplenomegaly (severe hypertriglyceridaemia)
Investigations
Baseline Lipid Assessment
A fasting lipid panel (9–12 hour fast) is the standard for cardiovascular risk assessment and treatment monitoring. Non-fasting lipid panels are acceptable for initial screening and routine follow-up (TC, LDL-C, HDL-C, non-HDL-C are reliable non-fasting; TG is less reliable if non-fasting).
Essential
Fasting lipid panel
Total cholesterol, LDL-C (direct or calculated via Friedewald), HDL-C, triglycerides. Fasting 9–12 hours preferred; non-fasting acceptable if TG not the primary concern. Available via any Australian pathology provider. MBS Item 66825.
Essential
ACVR calculation
Use Australian CV Risk Calculator (cvdcheck.org.au). Requires: age, sex, smoking status, systolic BP, TC, HDL-C, diabetes status, eGFR. Free, validated for Australian population.
Essential
Thyroid function (TSH)
Screen all patients with newly identified hypercholesterolaemia for hypothyroidism. MBS Item 66716.
Essential
Renal function (eGFR, uACR)
eGFR required for ACVR calculation and to classify CKD (high/very high risk). Urine albumin:creatinine ratio (uACR) for diabetic nephropathy screening. MBS Items 66503, 66528.
Available
Liver function tests (LFTs)
Baseline before statin initiation. Repeat only if clinically indicated (symptoms of hepatotoxicity). Routine monitoring of LFTs on statins is no longer recommended. MBS Item 66512.
Available
HbA1c, fasting glucose
Screen for diabetes if not known. Required for ACVR calculation. MBS Item 66555.
Available
Creatine kinase (CK)
Baseline CK recommended before statin initiation (particularly in patients >70 years, Asian background, hypothyroidism, or on interacting medications). Repeat only if myalgia/myopathy symptoms develop. MBS Item 66525.
Referral / Specialist
Lipoprotein(a) [Lp(a)]
Once-in-a-lifetime measurement. Elevated Lp(a) (>0.5 g/L or >125 nmol/L) is an independent, genetically determined CV risk factor. May upgrade risk category. Available through major Australian pathology providers (extra cost — not routinely MBS-rebated).
Referral / Specialist
Apolipoprotein B (ApoB)
Alternative to LDL-C for risk stratification and treatment monitoring. Target ApoB <0.80 g/L (high risk) or <0.65 g/L (very high risk). Useful when TG >4.5 mmol/L (Friedewald formula unreliable). Available in Australian pathology (additional cost).
Specialist
Genetic testing for FH
LDLR, APOB, PCSK9 gene sequencing. Available through specialised genetics services. MBS Item 73288 (requires clinical geneticist referral). Essential for cascade screening of family members.
Treatment Goals & Non-Pharmacological Measures
Lipid Targets by Risk Category
| Risk Category | 5-year CVD Risk | LDL-C Target | Non-HDL-C Target | Triglycerides |
|---|---|---|---|---|
| Low | <10% | <3.0 mmol/L | <3.8 mmol/L | <2.0 mmol/L |
| Moderate | 10–15% | <2.5 mmol/L | <3.3 mmol/L | <2.0 mmol/L |
| High | 15–30% | <2.0 mmol/L | <2.6 mmol/L | <1.7 mmol/L |
| Very High | >30% / established ASCVD | <1.4 mmol/L (or ≥50% reduction) | <2.0 mmol/L | <1.7 mmol/L |
Non-Pharmacological Measures
Lifestyle modification is the foundation of dyslipidaemia management for all patients, regardless of risk category or use of pharmacotherapy. Australian evidence-based dietary and lifestyle guidelines include the NHMRC Australian Dietary Guidelines, the Heart Foundation's position statements, and Exercise and Sports Science Australia (ESSA) recommendations.
1
Dietary Modification
Adopt a Mediterranean or DASH-style eating pattern. Reduce saturated fat to <7% of total energy. Replace with monounsaturated (olive oil, avocado) and polyunsaturated fats (nuts, seeds, oily fish). Increase soluble fibre (oats, legumes, psyllium — 10–25 g/day). Limit trans fats (avoid commercially fried foods, some margarines). Add plant sterols/stanols (2 g/day) — available in margarine and yoghurt products — for a 6–10% LDL-C reduction.
2
Physical Activity
≥150 minutes/week of moderate-intensity aerobic exercise (brisk walking, cycling, swimming) or ≥75 minutes/week of vigorous activity. Resistance training 2–3 times/week. Exercise improves HDL-C (+5–10%), reduces TG (−10–20%), and reduces LDL-C (−5–10%). Refer to ESSA-accredited exercise physiologist if available (Medicare-funded for patients with chronic disease under Team Care Arrangements).
3
Weight Management
Target BMI <30 kg/m² (or waist circumference <94 cm men, <80 cm women). A 5–10% weight loss can reduce LDL-C by 5–8% and TG by 20–30%. Refer to GP Management Plan (GPMP, MBS Item 721) for structured weight management. Consider bariatric surgery referral for BMI ≥40 (or ≥35 with comorbidities).
4
Smoking Cessation
Smoking lowers HDL-C and increases oxidised LDL. Cessation improves HDL-C by ~0.1 mmol/L and substantially reduces CV risk. Offer NRT, varenicline (Champix® — PBS-listed), or bupropion (Zyban®). Refer to Quitline (13 7848) or state-based smoking cessation services.
5
Alcohol Moderation
Limit to ≤10 standard drinks/week and ≤4 on any one day (NHMRC 2020 guidelines). Heavy alcohol intake raises TG significantly. Patients with hypertriglyceridaemia should be counselled to abstain.
Expected lipid effects of combined lifestyle modification: LDL-C reduction of 10–15%, HDL-C increase of 5–10%, TG reduction of 20–30%. These effects are additive to pharmacotherapy and may reduce the statin dose required.
Statins & Lipid-Lowering Drugs
First-Line: HMG-CoA Reductase Inhibitors (Statins)
Statins are the most effective and well-studied class of lipid-lowering agents. The Cholesterol Treatment Trialists' (CTT) Collaboration meta-analysis demonstrates that every 1.0 mmol/L reduction in LDL-C reduces major vascular events by ~22% and all-cause mortality by ~10%. In Australian practice, atorvastatin and rosuvastatin are the preferred agents due to their superior potency, longer half-lives, and convenient once-daily dosing.
Atorvastatin
Lipitor® · Generic available · High-intensity statin
Adult dose
Start 20–40 mg PO once daily; range 10–80 mg. Can be taken at any time of day. High intensity: 40–80 mg.
Paediatric dose
10–17 years: 10 mg once daily; max 20 mg (for FH). TGA-approved from age 10.
Renal adjustment
No dose adjustment required in renal impairment.
Hepatic adjustment
Contraindicated in active liver disease or unexplained persistent transaminase elevation.
Key interactions
CYP3A4 substrate. Caution with erythromycin/clarithromycin, azole antifungals, protease inhibitors (HIV), diltiazem, verapamil, grapefruit juice (large quantities). Max 20 mg with cyclosporine. Avoid with gemfibrozil (use fenofibrate if fibrate needed).
LDL-C reduction
36–51% (dose-dependent; 20 mg: ~37%, 40 mg: ~43%, 80 mg: ~51%)
PBS status
✔ PBS Authority Required (Streamlined)
Rosuvastatin
Crestor® · Generic available · High-intensity statin
Adult dose
Start 5–10 mg PO once daily; range 5–40 mg. High intensity: 20–40 mg.
Paediatric dose
6–17 years: 5–20 mg once daily (for FH). TGA-approved from age 6 (homozygous FH from age 7).
Renal adjustment
CrCl <30 mL/min: max 10 mg/day. Start at 5 mg.
Hepatic adjustment
Contraindicated in active liver disease. Caution in heavy alcohol use.
Key interactions
Not CYP3A4-metabolised (fewer interactions than atorvastatin). Caution with cyclosporine (max 5 mg), atazanavir/ritonavir (max 10 mg), lopinavir/ritonavir (max 10 mg). Gemfibrozil increases levels — avoid combination.
LDL-C reduction
41–55% (dose-dependent; 10 mg: ~41%, 20 mg: ~48%, 40 mg: ~55%)
PBS status
✔ PBS Authority Required (Streamlined)
Simvastatin
Zocor® · Generic available · Moderate-intensity statin
Adult dose
10–40 mg PO once daily (evening dose preferred). Max 80 mg — note TGA safety advisory against 80 mg due to myopathy risk.
Renal adjustment
CrCl <30 mL/min: start 5 mg; max 20 mg.
LDL-C reduction
26–38% (40 mg: ~31–38%)
PBS status
✔ PBS General Benefit / Authority Required
Pravastatin
Pravachol® · Generic available · Low-to-moderate-intensity statin
Adult dose
10–40 mg PO once daily (evening or at bedtime).
Renal adjustment
CrCl <30 mL/min: start 10 mg; max 20 mg.
LDL-C reduction
20–34% (40 mg: ~34%)
PBS status
✔ PBS General Benefit
Statin-associated muscle symptoms (SAMS): Myalgia (muscle pain without CK elevation) occurs in 5–10% of patients. True myopathy (CK >10× ULN) is rare (~1:10,000). Rhabdomyolysis is very rare. If myalgia develops: (1) check CK, (2) rule out hypothyroidism and interacting drugs, (3) consider statin rechallenge at lower dose or alternate-day dosing, (4) switch to an alternative statin (rosuvastatin or pravastatin are often better tolerated), or (5) use the Statin Myalgia Clinical Index Score (SMCS) to assess likelihood of true SAMS.
Second-Line: Ezetimibe (Cholesterol Absorption Inhibitor)
Ezetimibe
Ezetrol® · Generic available · Cholesterol absorption inhibitor
Adult dose
10 mg PO once daily, at any time of day, with or without food.
Paediatric dose
10–17 years: 10 mg once daily (in combination with a statin for FH).
Renal adjustment
No dose adjustment.
Hepatic adjustment
Not recommended in moderate-to-severe hepatic impairment (Child-Pugh B or C).
LDL-C reduction
~18% monotherapy; 12–15% additional when added to a statin. IMPROVE-IT trial showed improved CV outcomes with combination.
PBS status
✔ PBS Authority Required (Streamlined) — in combination with maximally tolerated statin for high/very-high risk patients not at LDL-C target
PCSK9 Inhibitors (Monoclonal Antibodies)
PCSK9 inhibitors provide substantial LDL-C reductions (50–60%) in combination with statins. They are PBS-listed for patients with established ASCVD or heterozygous FH who have not reached LDL-C targets on maximally tolerated statin + ezetimibe therapy. Initiation requires specialist authorisation.
Evolocumab
Repatha® · PCSK9 monoclonal antibody
Adult dose
140 mg SC every 2 weeks, or 420 mg SC once monthly. Self-administered prefilled pen/syringe.
LDL-C reduction
~60% (add-on to statin); ~40% as monotherapy. FOURIER trial: 15% reduction in CV events.
PBS status
✔ PBS Authority Required (Specialist initiation)
Alirocumab
Praluent® · PCSK9 monoclonal antibody
Adult dose
75 mg SC every 2 weeks (initial); may increase to 150 mg SC every 2 weeks if LDL-C response insufficient. Self-administered pen.
LDL-C reduction
~45–60% (add-on to statin). ODYSSEY OUTCOMES: 15% reduction in MACE in recent ACS patients.
PBS status
✔ PBS Authority Required (Specialist initiation)
Statin Intolerance Management Algorithm
1
Confirm Symptom Attribution
Use the Statin Myalgia Clinical Index (SMCS). Exclude hypothyroidism (TSH), vitamin D deficiency, and interacting medications. Check CK (if elevated >4× ULN, do not rechallenge). A nocebo effect is present in up to 50% of statin-intolerant patients.
2
Rechallenge with Low-Dose or Alternate-Day Statin
Try a different statin at low dose (e.g., rosuvastatin 5 mg or pravastatin 10 mg). Alternate-day dosing of long half-life statins (rosuvastatin, atorvastatin) is an option. ~70% of patients tolerate rechallenge.
3
If Unable to Tolerate Any Statin
Add ezetimibe 10 mg monotherapy (18% LDL-C reduction). Consider bempedoic acid (if available — TGA-approved in Australia) for additional 18% reduction. Refer for PCSK9 inhibitor assessment if target not achieved.
Fibrates, Fish Oils & Other Agents
Fibrates
Fibrates are PPARα agonists that primarily lower triglycerides (−30–50%) and raise HDL-C (+5–15%). They have a modest effect on LDL-C. Their main role in Australian practice is management of severe hypertriglyceridaemia (TG >5.6 mmol/L) to reduce pancreatitis risk, and as adjunctive therapy for atherogenic dyslipidaemia (high TG, low HDL-C) in patients at residual cardiovascular risk.
Fenofibrate
Lipidil® · Lipidil EZ/SUPRA · Fibrate
Adult dose
145 mg (micronised) PO once daily with food, or 160 mg (non-micronised). SUPRA: 160 mg once daily (equivalent).
Renal adjustment
eGFR 30–59: start 67 mg (Lipidil); max 135 mg. eGFR <30: contraindicated. Avoid if on dialysis.
Hepatic adjustment
Contraindicated in hepatic impairment (including primary biliary cholangitis).
Key interactions
Potentiates warfarin (monitor INR). Can increase creatinine (reversible tubular effect — monitor). Do NOT combine with gemfibrozil. May increase risk of rhabdomyolysis with statins — fenofibrate is the only fibrate safe to combine with statins (lower interaction risk than gemfibrozil).
TG reduction
~30–50%. HDL-C increase: ~5–15%. FIELD and ACCORD trials — CV benefit in subgroup with high TG/low HDL-C.
PBS status
✔ PBS General Benefit
Gemfibrozil
Lopid® · Fibrate
Adult dose
600 mg PO BD, 30 minutes before morning and evening meals.
Renal adjustment
eGFR <30: contraindicated.
Key interactions
Must NOT be combined with statins (significantly increased risk of rhabdomyolysis via UGT interaction). Prefer fenofibrate if statin co-prescription is needed.
PBS status
✔ PBS General Benefit
Omega-3 Fatty Acids & Icosapent Ethyl
Icosapent ethyl
Vascepa® · Purified EPA ethyl ester
Adult dose
2 g PO BD (4 g/day total) with food.
Indication
Residual cardiovascular risk reduction in patients on maximally tolerated statin with (a) established ASCVD OR (b) diabetes with ≥1 additional CV risk factor, AND fasting TG 1.5–5.6 mmol/L. Based on REDUCE-IT trial (25% RRR in MACE).
Key points
NOT equivalent to over-the-counter fish oil supplements (which contain mixed EPA/DHA and have NOT shown CV benefit — STRENGTH trial negative). Pure EPA product only. Monitor for AF (increased risk in REDUCE-IT).
PBS status
✔ PBS Authority Required — specialist initiation; GP can continue prescribing
Over-the-counter fish oil supplements: Standard fish oil (containing EPA + DHA mix) is available without prescription in Australia. The STRENGTH trial (omega-3 carboxylic acids) and VITAL trial showed no significant CV event reduction with mixed EPA/DHA products. Only pharmaceutical-grade icosapent ethyl (pure EPA, 4 g/day) has demonstrated CV outcome benefit. Advise patients that OTC fish oil is not a substitute for Vascepa®.
Bempedoic Acid
Bempedoic acid
Nilemdo® · ACL inhibitor (upstream of HMG-CoA reductase)
Adult dose
180 mg PO once daily.
LDL-C reduction
~18% as monotherapy; ~15–18% add-on to statin. CLEAR Outcomes trial showed 13% reduction in MACE in statin-intolerant patients.
Key advantages
Not associated with myalgia (prodrug activated in the liver, not in skeletal muscle). Good option for statin-intolerant patients. Also available in combination with ezetimibe (Nustendi®).
Key points
May increase serum uric acid (caution in gout). Can increase tendon rupture risk (TGA warning). Not for use with cyclosporine.
PBS status
Not PBS-listed (as of current schedule). Private prescription — approx. –100/month. TGA-registered.
Other Agents
| Agent | Mechanism | Indication | Notes |
|---|---|---|---|
| Bile acid sequestrants (cholestyramine, colestipol) | Bind bile acids → ↑ hepatic LDL receptor expression | Adjunct to statins; useful in pregnancy (not systemically absorbed) | LDL-C reduction 15–25%. GI side effects (constipation, bloating). Can ↑ TG. Must be taken 1h before or 4h after other medications (impairs absorption). |
| Inclisiran (Leqvio®) | siRNA targeting PCSK9 mRNA | LDL-C reduction in HeFH or ASCVD with elevated LDL-C despite max therapy | SC injection every 6 months (after initial loading at 0, 3, 6 months). ~50% LDL-C reduction. TGA-approved. Not yet PBS-listed in Australia — specialist-initiated private script (~,000–,000/year). |
| Lomitapide (Juxtapid®) | MTP inhibitor → ↓ VLDL assembly | Homozygous FH (specialist use only) | LDL-C reduction 40–50%. Significant hepatic steatosis risk. Requires TGA Special Access Scheme. Restricted to lipid clinics. |
| Evinacumab (Evkeeza®) | Anti-angiopoietin-like 3 (ANGPTL3) antibody | Homozygous FH | IV infusion every 4 weeks. ~47% LDL-C reduction independent of LDL receptor function. Limited availability in Australia. |
Quick Reference: Choosing Lipid-Lowering Therapy
High LDL-C (primary target)
Atorvastatin 40–80 mg or Rosuvastatin 20–40 mg
Ongoing
Add ezetimibe if not at target → then PCSK9 inhibitor via specialist
Severe hypertriglyceridaemia (TG >5.6)
Fenofibrate 145 mg daily + dietary fat restriction
Ongoing
Treat to prevent pancreatitis. Rule out secondary causes (alcohol, diabetes, drugs)
Residual CV risk (TG 1.5–5.6 despite statin)
Icosapent ethyl 2 g BD
Ongoing
PBS Authority. Pure EPA only — not interchangeable with OTC fish oil
Statin intolerance
Ezetimibe ± Bempedoic acid 180 mg daily
Ongoing
Rechallenge statin first (alternate-day rosuvastatin). Refer for PCSK9 inhibitor if needed
High LDL-C in pregnancy
Cholestyramine (bile acid sequestrant)
Throughout pregnancy
All statins are contraindicated in pregnancy (Category X). Discontinue statin 3 months pre-conception
Monitoring
Monitoring Schedule
Baseline (before starting therapy)
Fasting lipid panel, LFTs, CK (if risk factors for myopathy), TSH, eGFR, uACR, HbA1c (if diabetic), ACVR calculation. Document all results.
6–8 weeks after initiation or dose change
Repeat fasting lipid panel to assess response and LDL-C target achievement. Check LFTs only if clinically indicated (symptoms of hepatotoxicity — new guidelines do NOT mandate routine LFT monitoring on statins). Ask about muscle symptoms. Assess adherence.
3 months
If not at target: titrate statin dose, add ezetimibe, or switch to more potent statin. Recheck lipid panel at 6–8 weeks after any change.
6 months
Confirm stability. Reassess ACVR if risk factors have changed. Discuss ongoing lifestyle measures. Address adherence barriers.
Annually (ongoing)
Fasting lipid panel. Reassess ACVR (if primary prevention). Review medication adherence. Screen for side effects. Update GPMP/TCA if applicable. Consider need for therapy escalation or de-escalation.
Key Monitoring Parameters
| Parameter | Frequency | Action Thresholds |
|---|---|---|
| LDL-C | 6–8 weeks post-change, then 3–12 monthly | Not at target → escalate therapy |
| Triglycerides | With lipid panel | TG >5.6: initiate fibrate urgently. TG >11.3: admit for pancreatitis risk reduction |
| LFTs (ALT/AST) | Baseline only (routine monitoring no longer recommended) | >3× ULN persistent: withhold statin, investigate |
| CK | Baseline (high-risk patients); PRN if myalgia | >4× ULN without symptoms: monitor closely. >10× ULN: stop statin immediately |
| eGFR / uACR | Annually (more often in CKD) | Declining eGFR → review fenofibrate dose (contraindicated <30), rosuvastatin dose (max 10 if <30) |
| Fasting glucose / HbA1c | Annually | New-onset diabetes on statin: do NOT discontinue statin (benefits outweigh risks) |
Statin-related new-onset diabetes: Statins increase diabetes risk by ~9–12% (higher with intensive-dose regimens). This is a class effect. The absolute CV benefit of statins far outweighs the diabetes risk in high/very-high risk patients. Do NOT discontinue statin therapy if diabetes develops — manage diabetes concurrently.
Special Populations
Pregnancy & Breastfeeding
All statins — CONTRAINDICATED
Category X (TGA). Discontinue at least 3 months before planned conception. Statins cross the placenta and may affect fetal lipid metabolism and development. The 2021 FDA labeling change removed the absolute contraindication, but Australian guidelines (TGA, RANZCOG) continue to recommend avoidance.
Ezetimibe — NOT recommended
Insufficient safety data in pregnancy. Discontinue pre-conception.
Fibrates — NOT recommended
Avoid in pregnancy.
Cholestyramine
Safe in pregnancy (not systemically absorbed). Can be used for LDL-C reduction if pharmacotherapy is essential. May impair absorption of fat-soluble vitamins and other medications. Take other medications 1 hour before or 4 hours after.
PCSK9 inhibitors — NOT recommended
Insufficient data. Discontinue pre-conception. IgG antibodies may cross the placenta.
Breastfeeding: Statins are present in breast milk. Avoid during breastfeeding. Lifestyle measures are the mainstay. If high-risk, discuss individualised risk–benefit with lipid specialist.
Paediatric Patients
Familial hypercholesterolaemia in children
Atorvastatin TGA-approved from age 10 (10–20 mg). Rosuvastatin from age 6 (5–20 mg). Simvastatin from age 10. Pravastatin from age 8. Ezetimibe from age 10 (in combination). Always combine with lifestyle intervention. Refer to paediatric lipid specialist for initiation and ongoing management.
Target LDL-C in paediatric FH
LDL-C <3.5 mmol/L (or ≥50% reduction from baseline). Reassess at age 18 for transition to adult lipid service.
Non-FH dyslipidaemia in children
Lifestyle modification is the mainstay. Statins are not routinely recommended for non-FH paediatric dyslipidaemia. Refer if lifestyle measures fail after 6–12 months.
Universal lipid screening is not recommended in Australia. Targeted screening for children with: family history of premature CVD, familial hypercholesterolaemia, obesity, diabetes, chronic kidney disease, or chronic inflammatory conditions. Test fasting lipid panel from age 2 if family history positive.
Elderly (≥75 years)
Statins in the elderly
Secondary prevention: Continue statins — benefit persists. Primary prevention: Individualise decision. Absolute risk is high but competing mortality reduces absolute benefit. Start at lower doses (rosuvastatin 5 mg, atorvastatin 10–20 mg). Monitor for myopathy (higher risk due to polypharmacy, renal decline, sarcopenia). STOPP/START criteria recommend statin review in frail elderly.
De-escalation considerations
In patients with limited life expectancy (<1–2 years), significant frailty, or high polypharmacy burden, consider deprescribing statins. Discuss goals of care. The decision to stop is appropriate when treatment burden outweighs benefit.
CK considerations
Baseline CK recommended in all patients >70 years before starting statins. Sarcopenia may mask myopathy symptoms — have a low threshold for CK measurement if function declines.
Renal Impairment
Statins in CKD
CKD stages 1–3: Standard statin dosing (no adjustment for atorvastatin; rosuvastatin max 10 mg if eGFR <30). CKD stages 4–5 / dialysis: Atorvastatin preferred (no dose adjustment). Rosuvastatin max 10 mg. New initiation of statins in patients already on dialysis is NOT recommended (AURORA, 4D trials — no CV benefit), but continue if already established. Simvastatin: max 20 mg if CrCl <30. Pravastatin: max 20 mg if CrCl <30.
Fenofibrate in CKD
eGFR 30–59: reduce dose (start 67 mg, max 135 mg). eGFR <30: CONTRAINDICATED — risk of rhabdomyolysis and acute kidney injury. Monitor creatinine closely when combining with statins.
Ezetimibe in CKD
No dose adjustment. Safe in all stages including dialysis. SHARP trial showed benefit of simvastatin + ezetimibe in CKD (not on dialysis).
Hepatic Impairment
Statins
All statins are contraindicated in active liver disease (acute hepatitis, unexplained persistent transaminase elevation >3× ULN). In stable chronic liver disease (e.g., NAFLD/NASH, chronic hepatitis C with compensated cirrhosis): atorvastatin may be used cautiously — evidence suggests statins are safe and may even improve outcomes in compensated cirrhosis. Monitor LFTs. Atorvastatin is preferred as it has the most safety data in liver disease.
Ezetimibe
Not recommended in moderate-to-severe hepatic impairment (Child-Pugh B or C). Safe in mild impairment.
Fibrates
Contraindicated in primary biliary cholangitis and severe hepatic impairment. Fenofibrate can increase ALT/AST — monitor.
Immunocompromised / HIV
HIV patients on antiretroviral therapy (ART)
Protease inhibitors (PIs) significantly increase statin exposure via CYP3A4 inhibition. SAFE statins: pravastatin (no CYP3A4 metabolism), rosuvastatin (CYP2C9, max 10 mg with some PIs), pitavastatin (if available). AVOID: simvastatin and lovastatin with PIs (contraindicated). Atorvastatin: max 20 mg with most PIs. Integrase inhibitors (dolutegravir) have fewer interactions — standard statin dosing usually OK. Always check interaction databases (e.g., University of Liverpool HIV drug interactions).
Transplant recipients
Cyclosporine significantly increases statin levels. Max atorvastatin 20 mg, max rosuvastatin 5 mg, max simvastatin 20 mg with cyclosporine. Pravastatin is safest (max 20 mg). Fluvastatin also has a lower interaction profile. Monitor CK closely. Tacrolimus: lower interaction risk than cyclosporine — standard monitoring.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of cardiovascular disease, with age-standardised CVD mortality rates approximately 2.3 times higher than in non-Indigenous Australians. Cardiovascular disease remains the leading single cause of death among Indigenous Australians, contributing to the significant gap in life expectancy (AIHW, 2023). Dyslipidaemia is highly prevalent and frequently undertreated in Indigenous communities, particularly in remote and very remote areas.
Clinical recommendations for Indigenous health: (1) Begin ACVR assessment from age 30 (earlier if risk factors present). (2) Use the Australian CV Risk Calculator but recognise it may underestimate risk in some Indigenous populations — consider upgrading risk category for patients with multiple social determinants. (3) Prioritise once-daily medications and blister packs. (4) Involve Aboriginal Health Practitioners in health education and medication support. (5) Address the full cardiometabolic risk profile (smoking, diabetes, hypertension, obesity, physical inactivity, alcohol) in a holistic, culturally safe manner. (6) Refer to the Close the Gap PBS co-payment arrangements — most Indigenous Australians in remote areas access PBS medicines at no co-payment.
📚 References
- 1. National Vascular Disease Prevention Alliance. Guidelines for the Management of Absolute Cardiovascular Disease Risk. Melbourne: NVDPA; 2012. Available at: cvdcheck.org.au.
- 2. Royal Australian College of General Practitioners. Guidelines for Preventive Activities in General Practice (Red Book). 9th ed. Melbourne: RACGP; 2016 (updated 2018).
- 3. Cholesterol Treatment Trialists' 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. National Heart Foundation of Australia. Position Statement on Lipid Management. Melbourne: NHF; 2019 (updated 2021).
- 5. Australian Institute of Health and Welfare. Cardiovascular Disease in Australia. AIHW; 2023. Cat. no. CVD 88.
- 6. 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.
- 7. 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.
- 8. Bhatt DL, Steg PG, Miller M, et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia (REDUCE-IT). N Engl J Med. 2019;380(1):11–22.
- 9. Nicholls SJ, Lincoff AM, Garcia M, et al. Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events (STRENGTH). JAMA. 2020;324(22):2268–2280.
- 10. Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (SHARP). Lancet. 2011;377(9784):2181–2192.
- 11. Nissen SE, Lincoff AM, Brennan D, et al. Bempedoic acid and cardiovascular outcomes in statin-intolerant patients (CLEAR Outcomes). N Engl J Med. 2023;388(15):1353–1364.
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