1. Definition and clinical relevance
Absolute cardiovascular disease (CVD) risk is the probability that a person will experience a fatal or non-fatal cardiovascular event (myocardial infarction, stroke, or related death) over a defined future period, typically five years. Rather than treating individual risk factors in isolation, the absolute risk framework integrates multiple variables simultaneously, producing a single number that guides treatment intensity. For an Australian intern, this framework is the foundation of preventive cardiology in general practice: it determines who gets a statin, who needs blood pressure medication, and how aggressively lifestyle modification should be pursued. Errors in risk stratification lead directly to under-treatment of high-risk patients or unnecessary medication in low-risk ones.
2. Key values, thresholds, scoring systems
Absolute 5-year CVD risk categories
| Risk category | 5-year CVD event probability | Typical action |
|---|---|---|
| Low | Less than 10% | Lifestyle advice, reassess in 2 years |
| Moderate | 10 to 15% | Lifestyle modification, consider pharmacotherapy |
| High | Greater than 15% | Lifestyle plus pharmacotherapy recommended |
Automatic high-risk conditions (treat as high risk regardless of calculated score)
Certain clinical states confer high risk without needing a formal calculation: established atherosclerotic CVD (prior MI, stroke, TIA, peripheral arterial disease), diabetes with end-organ damage or duration greater than 10 years, moderate-to-severe chronic kidney disease (eGFR below 45 mL/min/1.73 m^2), familial hypercholesterolaemia, and systolic blood pressure persistently at or above 180 mmHg.
Lipid targets
| Lipid | Target (high-risk or established CVD) | General population |
|---|---|---|
| LDL-C | Less than 1.8 mmol/L (very high risk) or less than 2.0 mmol/L (high risk) | Less than 3.0 mmol/L |
| Total cholesterol | Less than 4.0 mmol/L | Less than 5.5 mmol/L |
| HDL-C | Greater than 1.0 mmol/L (men), greater than 1.2 mmol/L (women) | Aim to raise if low |
| Triglycerides | Less than 2.0 mmol/L | Less than 2.0 mmol/L |
| Non-HDL-C | Less than 2.5 mmol/L (high risk) | Less than 3.5 mmol/L |
Blood pressure targets
| Population | Target |
|---|---|
| General hypertension | Below 140/90 mmHg |
| Diabetes or CKD | Below 130/80 mmHg |
| Established CVD | Below 130/80 mmHg |
Diabetes glycaemic targets
Fasting glucose ideally 4.0 to 6.0 mmol/L; HbA1c at or below 7% (53 mmol/mol) for most patients. Optimal glycaemic control contributes meaningfully to CVD risk reduction.
LDL-C reduction and mortality
Each 1 mmol/L fall in LDL-C is associated with roughly a 10% reduction in all-cause mortality, making lipid-lowering one of the highest-yield interventions in preventive medicine.
3. Approach: presentation and differential
Who to screen
CVD risk assessment is opportunistic and systematic. Prioritise:
Adults aged 45 years and over (or 35 years and over for Aboriginal and Torres Strait Islander peoples), anyone with a first-degree relative with premature CVD, patients with diabetes, hypertension, obesity, chronic kidney disease, or a personal history of dyslipidaemia. Smoking status, physical inactivity, and poor diet compound risk substantially.
History: red flags and risk factor elicitation
Take a structured history covering: chest pain (exertional or rest), dyspnoea, claudication, TIA symptoms (transient focal neurology), erectile dysfunction (an early marker of systemic atherosclerosis), and family history of premature CVD (first-degree relative with MI or stroke before age 60). Document all modifiable risk factors: smoking pack-years, alcohol intake (excessive alcohol independently raises blood pressure and triglycerides), physical activity level, and dietary pattern.
Examination findings
Measure blood pressure in both arms on at least two separate occasions before diagnosing hypertension. A single elevated reading is insufficient. Calculate BMI and waist circumference. Examine for xanthelasma, corneal arcus before age 45, tendon xanthomata (suggesting familial hypercholesterolaemia), and signs of peripheral arterial disease (absent pulses, bruits). Auscultate the epigastric region for renal artery bruits if secondary hypertension is suspected.
Differential: causes of dyslipidaemia
Primary (genetic) causes include familial hypercholesterolaemia (autosomal dominant, LDL-C typically above 5.0 mmol/L), familial combined hyperlipidaemia, and familial hypertriglyceridaemia. Secondary causes to exclude before attributing dyslipidaemia to primary disease: hypothyroidism, type 2 diabetes, nephrotic syndrome, chronic kidney disease, cholestatic liver disease, and medications (corticosteroids, atypical antipsychotics, thiazides at high dose, ciclosporin).
4. Investigations
Bedside
Blood pressure (bilateral, seated, two readings separated by two minutes), BMI, waist circumference, resting ECG if symptomatic or age over 40 with multiple risk factors.
Bloods
| Test | Purpose |
|---|---|
| Fasting lipid panel (total cholesterol, LDL-C, HDL-C, triglycerides, non-HDL-C) | Baseline risk stratification, treatment target monitoring |
| Fasting glucose and HbA1c | Diagnose or exclude diabetes; glycaemic contribution to CVD risk |
| eGFR and urine albumin:creatinine ratio | CKD as independent risk factor and statin dosing consideration |
| TFTs (TSH) | Exclude hypothyroidism as secondary cause of dyslipidaemia |
| LFTs and CK | Baseline before starting a statin; monitor if symptoms develop |
| FBC, UEC | General metabolic assessment |
A non-fasting lipid panel is acceptable for initial screening; a fasting sample is preferred when triglycerides are elevated or when precise LDL-C calculation is needed (Friedewald equation is unreliable when triglycerides exceed 4.5 mmol/L, requiring direct LDL-C measurement).
Imaging and special tests
Coronary artery calcium (CAC) scoring by CT can reclassify patients in the intermediate-risk band (10 to 15%) and may support or defer statin initiation. It is not routine but is useful when the patient and clinician are uncertain about pharmacotherapy. Carotid intima-media thickness and ankle-brachial index are adjuncts in selected cases.
5. Management
Lifestyle modification (all risk categories)
Lifestyle change is first-line for low and moderate risk and is concurrent with pharmacotherapy for high risk. Key targets: smoking cessation (the single most impactful modifiable intervention), dietary saturated fat reduction with replacement by unsaturated fats, increased soluble fibre and plant sterol intake (plant sterols 2 to 3 g/day from fortified foods can reduce LDL-C by approximately 10%), regular aerobic exercise (at least 150 minutes of moderate-intensity activity per week), weight reduction if BMI is elevated, and alcohol reduction to within recommended limits.
Pharmacotherapy: statins
Statins are the first-line lipid-lowering agent for CVD risk reduction. They are indicated in all patients with established CVD (secondary prevention) and in high-risk primary prevention patients.
Commonly used statins and typical doses:
| Statin | Starting dose | Maximum dose | Notes |
|---|---|---|---|
| Rosuvastatin | 5 to 10 mg orally daily | 40 mg daily | High-intensity option; renally excreted, dose-reduce in CKD |
| Atorvastatin | 10 to 20 mg orally daily | 80 mg daily | High-intensity option; hepatically metabolised |
| Pravastatin | 20 to 40 mg orally daily | 80 mg daily | Preferred in drug interactions; less CYP3A4 involvement |
| Simvastatin | 10 to 20 mg orally daily | 40 mg daily | Avoid 80 mg dose due to myopathy risk |
Statin therapy for primary prevention in patients over 75 years requires individualised discussion: benefit is present in those with multiple risk factors or diabetes, but polypharmacy and frailty must be weighed.
Monitoring: Check LFTs and CK at baseline. Routine ongoing LFT monitoring is not required in asymptomatic patients. If a patient develops myalgia, check CK. Statin-induced myopathy ranges from mild myalgia (common, CK normal or mildly elevated) to rhabdomyolysis (rare, CK greater than 10 times upper limit of normal with renal impairment). Cease the statin and reassess if CK is markedly elevated.
Statin intolerance: Try an alternative statin at a lower dose or alternate-day dosing. If true intolerance is confirmed, ezetimibe is the next agent.
Add-on lipid-lowering therapy
Ezetimibe 10 mg orally daily inhibits intestinal cholesterol absorption and reduces LDL-C by a further 15 to 20% when added to a statin. It is PBS-listed for patients with established CVD or familial hypercholesterolaemia who do not reach target on statin alone.
PCSK9 inhibitors (evolocumab, alirocumab) are injectable monoclonal antibodies that dramatically lower LDL-C (by 50 to 60%). They are reserved for familial hypercholesterolaemia and patients with established CVD who cannot achieve LDL-C targets despite maximally tolerated statin plus ezetimibe. PBS criteria are strict.
Fibrates (fenofibrate 145 mg orally daily, or gemfibrozil 600 mg orally twice daily) are used for moderate-to-severe isolated hypertriglyceridaemia. They are not effective at LDL-C reduction. Combining gemfibrozil with a statin substantially raises myopathy risk and should be avoided where possible; fenofibrate combined with a statin carries lower myopathy risk. Monitor LFTs with fibrate use and counsel about gallstone risk.
Omega-3 fatty acids (fish oil concentrate, up to 4 g/day of EPA/DHA) reduce triglycerides and are an adjunct in severe hypertriglyceridaemia (TG above 10 mmol/L warrants urgent treatment to prevent pancreatitis, using fibrate plus fish oil and, if needed, nicotinic acid).
Nicotinic acid raises HDL-C and lowers triglycerides but is poorly tolerated (flushing) and has fallen out of favour for routine use.
Blood pressure management
Treat hypertension with lifestyle measures first in mild cases. Pharmacotherapy is indicated when blood pressure remains above 140/90 mmHg after lifestyle change, or immediately in high-risk patients. Do not diagnose hypertension on a single reading: at least two follow-up measurements are required. Add one agent at a time and allow approximately four weeks between dose adjustments to assess effect. If hypertension is resistant to treatment, consider secondary causes (renal artery stenosis, primary hyperaldosteronism, phaeochromocytoma).
Aspirin
Aspirin is not recommended for primary prevention of CVD, even in high-risk individuals, because the bleeding risk offsets the modest benefit. It remains standard in secondary prevention.
Disposition and follow-up
Low risk: reassess in two years. Moderate risk: reassess in six to twelve months after lifestyle intervention. High risk: initiate pharmacotherapy, review lipids and blood pressure at six to eight weeks, then three-monthly until targets are reached, then six-monthly.
6. Australian-specific considerations
Aboriginal and Torres Strait Islander peoples experience CVD at significantly higher rates and at younger ages than non-Indigenous Australians. The standard risk calculator thresholds are adjusted: formal CVD risk assessment is recommended from age 35 rather than 45. Clinicians should be aware that calculated risk scores may underestimate true risk in this population. The MBS Item 715 (annual health assessment for Aboriginal and Torres Strait Islander peoples) provides a structured opportunity to assess CVD risk factors, arrange lipid and glucose testing, and initiate preventive management. Cultural safety, community engagement, and continuity of care are central to effective preventive cardiology in this context.
For patients with type 2 diabetes, the MBS chronic disease management items (721 GP Management Plan, 723 Team Care Arrangement) support multidisciplinary CVD risk reduction including dietitian and exercise physiologist input.
In rural and remote settings, access to pathology, specialist cardiology, and PCSK9 inhibitor prescribing may be limited. Telehealth consultation with a cardiologist or endocrinologist is available and should be used when complex lipid management (familial hypercholesterolaemia, statin intolerance, PCSK9 inhibitor initiation) is required. Point-of-care lipid testing is available in some remote primary care settings.
Familial hypercholesterolaemia is underdiagnosed in Australia. Cascade screening of first-degree relatives is recommended when a proband is identified.
Clinical pearls
- A 1 mmol/L reduction in LDL-C produces roughly a 10% fall in all-cause mortality: even modest lipid lowering in high-risk patients has meaningful survival benefit.
- Never diagnose hypertension from a single reading. Two or more elevated readings on separate occasions are required before committing a patient to a lifetime diagnosis and treatment.
- Patients with established CVD, familial hypercholesterolaemia, or diabetes with end-organ damage are automatically high risk and do not need a risk calculator score to justify statin therapy.
- Statin-induced myalgia is common and does not always mean the drug must be stopped permanently. Switching to a different statin, reducing the dose, or using alternate-day dosing resolves symptoms in many patients.
- Aspirin has no role in primary CVD prevention: the bleeding risk outweighs any benefit, even in those with a 5-year risk above 15%.
- Severe hypertriglyceridaemia (TG above 10 mmol/L) is a medical urgency because of pancreatitis risk: treat with a fibrate, fish oil, and alcohol cessation, not a statin.