Dyslipidemia in general practice: what to test, who to treat, and what’s new

Dyslipidemia is common, under-screened, and still one of the most modifiable drivers of heart attack and stroke. Recent Australian data and newer ACC guidance have sharpened how we think about who to test, what numbers matter, and how low to go once treatment starts. This summary follows Dr Max Maffey’s CPD talk for GPs — plain language, clinically oriented, and organised for the consulting room.

Who to screen

Lipid problems are not rare. Roughly 60% of Australian adults aged 18 and over had abnormal lipids or were already on lipid-lowering therapy in recent national figures (2022–2024). About one in four Australian adults has an LDL cholesterol above 3.4 mmol/L.

Familial hypercholesterolaemia (FH) is also more common than many expect: heterozygous FH about 1 in 250; homozygous FH about 1 in 150,000–300,000. Many people are never screened at all — and that means missed chances to cut lifetime cardiovascular risk.

Premature CVD in a first-degree relative means male under 55 or female under 60. That history should lower your threshold to check lipids earlier.

What to test

The standard lipid profile

Order total cholesterol, HDL, triglycerides, and a calculated LDL. Fasting is not required for most patients. LDL changes little with a meal, and fasting versus non-fasting results give almost the same prognostic information.

Fasting still helps when triglycerides are high. If triglycerides are above about 4.5 mmol/L, the usual LDL equations break down — ask for a measured LDL instead.

LDL remains the most important number in day-to-day practice. Trial after trial (primary and secondary prevention) shows a strong, roughly linear link: the lower the achieved LDL, the fewer cardiovascular events.

Lipoprotein(a) — measure once

Lp(a) is an LDL-like particle with apo(a) stuck onto apoB100. More than 90% of the level is genetic (LPA locus). It does not meaningfully drift over a lifetime, so one measurement is enough for most people.

Levels tend to be highest in Black and South Asian populations, then White, and lower in East Asian groups. Higher Lp(a) clearly tracks with atherosclerotic CVD and also with aortic stenosis risk. Risk rises in a roughly linear way — from about 1.2× around 75 mg/dL toward about 4× at very high levels (Australian labs often report mg/dL).

ApoB — counting the particles

Think of ApoB as the number of atherogenic “trucks” on the road (LDL, VLDL, Lp(a) each carry one ApoB). LDL cholesterol is more like the cargo weight.

In most people ApoB and LDL move together. ApoB is more useful when there is discordance — especially on a statin, or in diabetes, high triglycerides, and metabolic disease, where particles can be cholesterol-depleted.

One study pattern worth remembering: high LDL but low non-HDL / ApoB → no excess MI or mortality; low LDL but high ApoB / non-HDL → excess risk. When ApoB is used as a treatment marker, targets are often discussed in the same numerical framework as LDL goals (for example secondary prevention aiming under about 1.4).

Who to treat — primary prevention

Start with a formal risk estimate, then layer clinical judgement.

• Australian ASCVD risk calculator: ages 45–79 (diabetes from 35; Indigenous from 30); reports 5-year CVD risk. Treat high risk; carefully consider intermediate risk with modifiers.
• Newer US calculator: 10-year risk. A statin may be considered above about 3% 10-year ASCVD risk (balancing number-needed-to-treat against new diabetes risk), typically when LDL is in the 1.8–4.9 range.

Statin intensity, calcium score & special groups

Statin intensity (quick reference)

Intermediate risk

Treat case by case. Useful risk modifiers include chronic inflammatory disease (lupus, rheumatoid arthritis, psoriasis), high Lp(a), high triglycerides, and a persistent LDL of 4.1–4.9.

High-risk primary prevention

Use a high-intensity statin. Aim for more than 50% LDL reduction, LDL under 1.8, and non-HDL under 2.6.

Coronary calcium score

CAC is reasonable in intermediate-risk patients and some borderline cases.

• Score >0 → lipid-lowering is recommended (calcified plaque usually means soft plaque is nearby too).
• Score ≥100 or ≥75th percentile → treat as high risk; aim LDL under 1.8.
• Once you are treating: do not repeat CAC. Scores often rise as plaque stabilises and calcifies — more anxiety, little benefit.
• If you are not treating yet: you may repeat in about 5 years.

Other primary-prevention groups

• Low calculated risk but LDL stuck at 4.1–4.9: consider a moderate statin.
• LDL >4.9: ignore the calculator — this is high risk. Use maximally tolerated statin. Target under 2.6 (or under 1.8 if extra risk factors).
• Primary prevention with LDL already under 1.8: no clear benefit from further lipid-lowering for primary prevention.
• Very high LDL: check secondary causes (thyroid function, urine / nephrotic syndrome, medications). Consider FH referral if LDL is around ≥5.

Adherence, intolerance & diet myths

The best regimen fails if the script sits in the drawer. Non-adherence is about 24% by 6 months and about 50% by 5 years. Secondary prevention patients do a bit better — but still need follow-up and plain talk about why the tablet matters.

True statin intolerance is around 9%. Serious adverse effects are uncommon:

• Myopathy ≈ 0.5% over 5 years
• Rhabdomyolysis ≈ 0.01%
• New diabetes ≈ 0.5–1%
• Symptomatic myalgia often quoted around 1%

Higher risk of trouble: higher dose, female sex, age over 65. Sometimes start softer and uptitrate.

Diet — helpful, not usually enough alone

A healthy diet has many cardiovascular benefits, but the direct LDL drop is often modest — on average around 0.3 mmol/L comparing vegetarian/vegan patterns with an omnivore diet. Hyper-responders exist (for example a carnivore-style diet pushing LDL into double digits). A Mediterranean diet does not always drop LDL much either. For high-risk patients, diet alone is not enough — medication is usually still needed.

Secondary prevention & what’s new

Practical sequence:

1. High-intensity statin
2. If still not under 1.4 → add ezetimibe (event-reduction data from around 2015)
3. If still not under about 1.8 → consider a PCSK9 agent (PBS criteria apply; discuss with cardiology)

PCSK9 and related therapies

• Monoclonal antibodies (e.g. evolocumab / Repatha): about 50–60% LDL reduction; fortnightly subcutaneous injection; PBS pathways for FH and some non-familial indications.
• Inclisiran (Leqvio): siRNA; dose at 0, 3 months, then every 6 months in clinic. Lowers LDL; cardiovascular outcome data still pending. Private cost roughly A$3,500/year.
• Oral PCSK9 (enlicitide — recent FDA): about 57% LDL drop at 24 weeks, plus about 25% Lp(a) reduction.
• VERVE-102 base editing: one-time PCSK9 gene edit; early data ~60% LDL reduction sustained to 18 months.
• Pelacarsen: antisense therapy against Lp(a); about 80% Lp(a) reduction; phase 3 outcome trials ongoing.

Triglycerides — a practical approach

Triglyceride-rich lipoproteins contribute to CVD risk. When triglycerides climb into the teens (around 10–11+), pancreatitis risk rises — often driven by chylomicrons and frequently polygenic.

Unlike LDL, lifestyle can cut triglycerides by more than 70% in good responders. Focus on:

• Cutting simple/processed carbs and added sugar
• Limiting total fat (even “good” fats add up when TG is very high)
• Limiting or stopping alcohol
• Weight loss of 5–10%
• Screening for diabetes, hypothyroidism, and nephrotic syndrome

For very high triglycerides: eliminate added sugars, keep fat around 10–15% of calories, no alcohol, and involve a dietitian.

Medicines for high triglycerides

• Statin: 10–30% TG reduction plus proven CV benefit.
• Fenofibrate: 30–50% TG reduction (prefer over gemfibrozil because of interactions / rhabdomyolysis risk). Fibrates lower TG but do not improve CV outcomes in the same way.
• OTC fish oil: not recommended as a CV strategy.
• Icosapent ethyl (Vascepa): can lower TG and CV events in select high-risk patients, but raises AF hospitalisation risk and has a narrow PBS niche (LDL 1–2.6, TG 1.5–3.5, established CVD) — hard to fit many patients.

Take-home messages for clinic

1. Screen earlier when family history, Indigenous status, diabetes, or premature CVD clues are present — and remember how common abnormal lipids are.
2. LDL still leads decision-making; add Lp(a) once in a lifetime and use ApoB when particles and cargo disagree.
3. Match statin intensity to risk; use CAC selectively; do not re-scan calcium once treatment has started.
4. Secondary prevention now aims under 1.4 — escalate with ezetimibe then PCSK9 when needed.
5. For high triglycerides, lifestyle is powerful; use medicines to prevent pancreatitis and to deliver CV benefit where evidence exists.

Dr Kotha · Gold Coast · dyslipidemia.drkotha.com