Secondary Prevention of CVD

📋 Key Information Summary

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Secondary CVD prevention reduces recurrent events by 25–50% through integrated lipid, blood pressure, glycaemic, and antiplatelet management.
LDL-C target <1.8 mmol/L for most patients with established ASCVD; consider <1.4 mmol/L for very high-risk patients (ACS ≤12 months, polyvascular disease, or DM with target organ damage).
High-intensity statin therapy (atorvastatin 80 mg or rosuvastatin 40 mg) is first-line; add ezetimibe if LDL-C target not achieved after 6–8 weeks.
PCSK9 inhibitors (evolocumab, alirocumab) are indicated when maximally tolerated statin + ezetimibe fails to reach target — available on PBS Authority Required.
Bempedoic acid (Nexletol®) is a non-statin option for statin-intolerant patients; PBS-listed with Authority Required status.
Target BP <130/80 mmHg for secondary CVD prevention; ACEi/ARB + CCB is preferred first-line combination.
ACE inhibitors (or ARBs) are strongly recommended post-MI, in HFrEF, and in diabetic patients; add beta-blockers for post-MI and HFrEF.
HbA1c target ≤53 mmol/mol (7.0%) in most CVD patients with T2DM; individualise for frailty and hypoglycaemia risk.
SGLT2 inhibitors (empagliflozin, dapagliflozin) reduce cardiovascular death and HF hospitalisation — recommended regardless of glycaemic status in patients with established CVD or HF.
GLP-1 receptor agonists (semaglutide, liraglutide) reduce MACE in T2DM with ASCVD; preferred second-line after metformin in this population.
Long-term aspirin 100 mg daily remains standard for secondary prevention; extended DAPT (aspirin + ticagrelor or clopidogrel) is guided by ischaemic vs bleeding risk balance.
Aboriginal and Torres Strait Islander Australians have 1.7× the cardiovascular mortality rate of non-Indigenous Australians; culturally safe follow-up and medication access are essential.

Introduction & Australian Epidemiology

Cardiovascular disease (CVD) remains the leading cause of death in Australia, responsible for approximately 42,900 deaths in 2022 and accounting for 25% of all deaths nationally. Patients who survive an acute cardiovascular event — myocardial infarction (MI), ischaemic stroke, or peripheral arterial disease (PAD) — face a substantially elevated risk of recurrent events. Evidence consistently demonstrates that comprehensive secondary prevention reduces recurrent cardiovascular events by 25–50% and all-cause mortality by 20–30%.

Secondary prevention of CVD encompasses a multifactorial approach targeting modifiable risk factors: dyslipidaemia, hypertension, diabetes mellitus, platelet activation, smoking, physical inactivity, and obesity. The Australian Institute of Health and Welfare (AIHW) reports that only 30–40% of Australians with established CVD achieve guideline-recommended targets for lipid control, blood pressure, and glycaemic management, highlighting a significant evidence-to-practice gap.

This guideline addresses the four pillars of pharmacological secondary prevention: lipid management, blood pressure control, diabetes management, and antiplatelet therapy, with specific reference to Australian PBS availability, MBS item numbers, and national cardiovascular guidelines.

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Key Australian statistic: Cardiovascular disease costs the Australian health system an estimated $11.8 billion annually. Secondary prevention is among the most cost-effective interventions in medicine — every dollar spent on optimal pharmacotherapy after ACS saves an estimated $5–7 in downstream hospitalisation costs.

Lipid Management

LDL-C Targets in Secondary Prevention

Elevated low-density lipoprotein cholesterol (LDL-C) is the primary lipid target in secondary CVD prevention. The relationship between LDL-C and recurrent cardiovascular events is log-linear, with no lower threshold identified below which benefit ceases. Current Australian and international guidelines recommend stratified LDL-C goals based on residual cardiovascular risk.

Risk Category	Criteria	LDL-C Target
High risk	Established ASCVD (prior MI, ischaemic stroke, PAD, revascularisation)	<1.8 mmol/L
Very high risk	ACS ≤12 months, polyvascular disease, DM + target organ damage, FH + ASCVD, recurrent events despite optimal therapy	<1.4 mmol/L
Extreme risk	Recurrent ACS within 2 years on maximally tolerated statin + ezetimibe, or ACS with multi-vessel disease + DM	<1.0 mmol/L (consider)

Statin Intensity Selection

High-intensity statin therapy is the cornerstone of lipid management in secondary prevention. In Australia, the two principal high-intensity statins are atorvastatin 80 mg and rosuvastatin 40 mg. Where these doses are not tolerated (myalgia, elevated transaminases), moderate-intensity statin therapy combined with ezetimibe is preferred over low-intensity monotherapy.

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Atorvastatin

Lipitor® / Generic · HMG-CoA reductase inhibitor

Adult dose 40–80 mg PO nocte (high intensity: 80 mg)

Paediatric dose 10–20 mg PO daily (≥10 years, heterozygous FH under specialist care)

LDL-C reduction 39–55% (dose-dependent)

Renal adjustment No dose adjustment required

Hepatic adjustment Contraindicated in active liver disease; use with caution in Child-Pugh A–B

PBS status ✔ PBS General Benefit

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Rosuvastatin

Crestor® / Generic · HMG-CoA reductase inhibitor

Adult dose 20–40 mg PO daily (high intensity: 40 mg)

Paediatric dose 5–20 mg PO daily (≥10 years, FH specialist care)

LDL-C reduction 45–63% (dose-dependent)

Renal adjustment Start 5 mg if eGFR <30 mL/min; max 10 mg in severe CKD

Hepatic adjustment Contraindicated in active liver disease

PBS status ✔ PBS General Benefit

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Pravastatin

Pravachol® / Generic · HMG-CoA reductase inhibitor (moderate intensity)

Adult dose 40–80 mg PO nocte

LDL-C reduction 25–35%

Renal adjustment Start 10 mg if eGFR <30 mL/min

Hepatic adjustment Contraindicated in active liver disease

PBS status ✔ PBS General Benefit

Ezetimibe

Ezetimibe reduces LDL-C by inhibiting intestinal cholesterol absorption via NPC1L1 blockade. It provides an additional 15–25% LDL-C reduction when added to statin therapy and is recommended as the first add-on agent when statin monotherapy fails to achieve target. The IMPROVE-IT trial demonstrated a modest but significant reduction in cardiovascular events when ezetimibe was added to simvastatin in post-ACS patients.

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Ezetimibe

Ezetrol® / Generic · Cholesterol absorption inhibitor

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

LDL-C reduction 15–25% (add-on to statin); ~18% monotherapy

Renal adjustment No dose adjustment required

Hepatic adjustment Not recommended in moderate–severe hepatic impairment

PBS status ✔ PBS General Benefit (combination with statin in ASCVD)

PCSK9 Inhibitors

Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are monoclonal antibodies that significantly reduce LDL-C by 50–70% when added to maximally tolerated statin ± ezetimibe. The FOURIER trial (evolocumab) and ODYSSEY OUTCOMES trial (alirocumab) demonstrated significant reductions in MACE in patients with established ASCVD. In Australia, PBS access requires Authority Approval and is restricted to patients with ASCVD who have not achieved target LDL-C despite maximally tolerated statin + ezetimibe.

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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 50–70% (add-on to statin ± ezetimibe)

Renal adjustment No dose adjustment required

Hepatic adjustment No dose adjustment; use with caution in severe impairment

PBS status Authority Required (ASCVD + LDL-C above target on max statin + ezetimibe)

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Alirocumab

Praluent® · PCSK9 monoclonal antibody

Adult dose 75 mg SC every 2 weeks (titrate to 150 mg if needed)

LDL-C reduction 45–65% (dose-dependent)

Renal adjustment No dose adjustment required

Hepatic adjustment No dose adjustment; use with caution in severe impairment

PBS status Authority Required (same criteria as evolocumab)

Bempedoic Acid

Bempedoic acid (Nexletol®) is an ATP citrate lyase inhibitor that reduces LDL-C by 15–25% and is approved for use as monotherapy or add-on therapy. It is activated in the liver (not muscle), which accounts for its lower myalgia risk compared with statins. The CLEAR Outcomes trial demonstrated a 13% relative reduction in MACE in statin-intolerant patients. It is available in Australia as a combination with ezetimibe (Nexlizet®).

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Bempedoic Acid

Nexletol® · ATP citrate lyase inhibitor

Adult dose 180 mg PO daily (with or without food)

LDL-C reduction 15–25% (monotherapy); 25–35% (with ezetimibe)

Renal adjustment Not recommended if eGFR <30 mL/min

Hepatic adjustment Use with caution in moderate–severe hepatic impairment

Key caution May increase serum uric acid → gout; may cause tendinopathy/tendon rupture

PBS status Authority Required (statin-intolerant patients with ASCVD or FH)

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Statin intolerance: True statin intolerance (myalgia with elevated CK, or symptoms reproducible with rechallenge) affects ~5–10% of patients. A structured statin rechallenge protocol and identification of the highest tolerated statin dose is recommended before switching to non-statin therapy. N-of-1 trials with blinded rechallenge can be helpful.

Lipid-Lowering Stepwise Approach

1

High-intensity statin

Atorvastatin 80 mg or rosuvastatin 40 mg. Recheck lipid panel at 6–8 weeks.

2

Add ezetimibe 10 mg

If LDL-C above target on maximum tolerated statin. Recheck at 6–8 weeks.

3

Add PCSK9 inhibitor

If still above target on statin + ezetimibe. Apply for PBS Authority.

4

Consider bempedoic acid

For statin-intolerant patients or as additional LDL-C–lowering agent.

Blood Pressure Control

Blood Pressure Targets in CAD

Hypertension is the most prevalent modifiable risk factor for recurrent cardiovascular events. In patients with established coronary artery disease (CAD), ischaemic stroke, or PAD, the target blood pressure is <130/80 mmHg, consistent with the 2023 ESH guidelines, AHA/ACC guidance, and the Australian Clinical Practice Guidelines for the Management of Hypertension. A systolic target of 120–129 mmHg may be beneficial in high-risk patients if tolerated, supported by the SPRINT trial and subsequent meta-analyses.

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Diastolic threshold caution: Avoid reducing diastolic BP below 60 mmHg, particularly in patients with significant coronary stenosis, as this may compromise coronary perfusion and paradoxically increase ischaemic risk.

Antihypertensive Selection in Secondary Prevention

The choice of antihypertensive agent in secondary CVD prevention is guided by comorbidities and evidence from landmark trials. ACE inhibitors (or ARBs if intolerant) are the preferred first-line agents given their mortality benefit post-MI and in heart failure with reduced ejection fraction (HFrEF). Beta-blockers have a strong evidence base post-MI and in HFrEF, while calcium channel blockers and thiazide-like diuretics are effective add-on agents.

Drug Class	Preferred Agent	Indication in CVD	Key Considerations
ACE inhibitor	Ramipril, perindopril, enalapril	Post-MI, HFrEF, DM, CKD	Monitor K⁺ and eGFR at 1–2 weeks; contraindicated in bilateral RAS, pregnancy
ARB	Candesartan, valsartan, telmisartan	ACEi intolerance (cough), HFrEF, post-MI	Same monitoring as ACEi; do NOT combine with ACEi
Beta-blocker	Metoprolol succinate, bisoprolol, carvedilol	Post-MI (12+ months), HFrEF, rate control	Prefer evidence-based agents for HFrEF (bisoprolol, carvedilol, metoprolol succinate)
Calcium channel blocker	Amlodipine, lercanidipine	Add-on therapy, angina, elderly	Avoid verapamil/diltiazem in HFrEF; amlodipine safe in HFrEF
Thiazide-like diuretic	Indapamide, chlorthalidone	Resistant hypertension, volume overload	Monitor electrolytes (Na⁺, K⁺, uric acid); prefer indapamide in elderly
Mineralocorticoid receptor antagonist	Spironolactone, eplerenone	HFrEF, resistant hypertension, post-MI with LVSD	Monitor K⁺ closely; avoid if eGFR <30; gynaecomastia risk with spironolactone

Combination Therapy Strategies

Most patients with established CVD will require ≥2 antihypertensive agents to achieve target BP. Australian guidelines recommend the following combination approaches:

First-line combination: ACEi (or ARB) + dihydropyridine CCB (e.g., perindopril + amlodipine) — preferred in most patients with CAD
Second-line combination: ACEi/ARB + CCB + thiazide-like diuretic — for resistant hypertension
Third-line / resistant HT: Add spironolactone 25 mg (PATHWAY-2 trial demonstrated superiority over doxazosin and bisoprolol in resistant hypertension)
Single-pill combinations (SPCs): Improve adherence by 20–30%. Available Australian SPCs include perindopril/amlodipine, perindopril/indapamide, irbesartan/amlodipine, and candesartan/amlodipine — all PBS-listed
Post-MI: ACEi + beta-blocker is the foundational combination; add CCB or diuretic if BP remains above target

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Perindopril

Coversyl® / Generic · ACE inhibitor

Adult dose 5–10 mg PO daily (post-MI: start 2 mg, titrate to 8 mg)

Renal adjustment Start 2.5 mg daily if eGFR 30–60; avoid if eGFR <15 or anuria

PBS status ✔ PBS General Benefit

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Metoprolol Succinate

Betaloc® CR / Generic · Beta-1 selective blocker

Adult dose Post-MI: 50–200 mg PO daily (controlled release); HFrEF: start 23.75 mg, titrate to 190 mg daily

Renal adjustment No dose adjustment required

PBS status ✔ PBS General Benefit

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Amlodipine

Norvasc® / Generic · Dihydropyridine CCB

Adult dose 5–10 mg PO daily

Renal adjustment No dose adjustment required

PBS status ✔ PBS General Benefit

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Spironolactone

Aldactone® / Generic · Mineralocorticoid receptor antagonist

Adult dose 25–50 mg PO daily (resistant HT: 25 mg daily)

Renal adjustment Avoid if eGFR <30 mL/min or K⁺ >5.0 mmol/L

PBS status ✔ PBS General Benefit

Diabetes Management in CVD

HbA1c Targets in Cardiovascular Disease

Diabetes mellitus confers a 2–4-fold increased risk of cardiovascular events and is present in 25–35% of patients hospitalised with acute coronary syndromes in Australia. Glycaemic management in secondary CVD prevention focuses not only on HbA1c reduction but increasingly on cardiovascular risk reduction through agent-specific effects.

The recommended HbA1c target for most patients with T2DM and established CVD is ≤53 mmol/mol (≤7.0%). This target should be individualised: less intensive targets (≤64 mmol/mol / ≤8.0%) may be appropriate for patients with limited life expectancy, significant comorbidities, recurrent severe hypoglycaemia, or advanced frailty.

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Paradigm shift: Current guidelines recommend SGLT2 inhibitors and GLP-1 receptor agonists be prioritised for their cardiovascular benefits independent of glucose-lowering effect, even in patients with well-controlled HbA1c. Cardiovascular protection is the primary goal, with glycaemic control as a secondary benefit.

SGLT2 Inhibitors — Cardiovascular Benefits

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have transformed cardiovascular management in diabetes. The EMPA-REG OUTCOME, CANVAS, DECLARE-TIMI 58, and CREDENCE trials collectively demonstrated reductions in major adverse cardiovascular events (MACE), cardiovascular death, and heart failure hospitalisation. These benefits extend to patients without diabetes, as shown in DAPA-HF and EMPEROR-Reduced.

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Empagliflozin

Jardiance® · SGLT2 inhibitor

Adult dose 10 mg PO daily (may increase to 25 mg)

Key CV evidence EMPA-REG: 38% reduction in CV death; 14% reduction in 3-point MACE

Heart failure evidence EMPEROR-Reduced/Preserved: 21–25% reduction in HF hospitalisation/CV death

Renal adjustment Initiate if eGFR ≥20 mL/min; glycaemic efficacy reduced below eGFR 45

Key caution Euglycaemic DKA risk; hold peri-operatively; monitor for genital mycotic infections

PBS status Restricted Benefit (T2DM + ASCVD or HF; or HFrEF regardless of DM status)

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Dapagliflozin

Forxiga® · SGLT2 inhibitor

Adult dose 10 mg PO daily

Key CV evidence DECLARE-TIMI 58: 17% reduction in HF hospitalisation/CV death composite

Heart failure evidence DAPA-HF: 26% reduction in worsening HF/CV death; DELIVER: similar in HFpEF

Renal evidence DAPA-CKD: 39% reduction in sustained eGFR decline regardless of DM status

Renal adjustment Initiate if eGFR ≥20 mL/min

PBS status Restricted Benefit (T2DM + ASCVD/HF, or HFrEF, or CKD with albuminuria)

GLP-1 Receptor Agonists — Cardiovascular Outcomes

GLP-1 receptor agonists (GLP-1 RAs) have demonstrated significant reductions in MACE in patients with T2DM and established ASCVD. The LEADER trial (liraglutide) showed a 13% reduction in 3-point MACE and 22% reduction in cardiovascular death. The SUSTAIN-6 and PIONEER-6 trials established semaglutide's cardiovascular safety profile, while the SELECT trial demonstrated MACE reduction in overweight/obese patients without diabetes.

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Semaglutide (injectable)

Ozempic® · GLP-1 receptor agonist

Adult dose 0.25 mg SC weekly ×4 weeks → 0.5 mg weekly → 1.0 mg weekly (titrate over 8–12 weeks)

Key CV evidence SUSTAIN-6: 26% reduction in 3-point MACE; SELECT: 20% reduction in MACE in non-diabetic obesity

Weight effect Mean weight loss 4–6 kg (T2DM); 10–15% in obesity

Renal adjustment No dose adjustment; caution in severe CKD

Key caution GI side effects (nausea, vomiting); contraindicated in personal/family history of MTC or MEN2

PBS status Restricted Benefit (T2DM + established ASCVD; or HbA1c above target on metformin)

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Liraglutide

Victoza® · GLP-1 receptor agonist

Adult dose 0.6 mg SC daily ×1 week → 1.2 mg daily → 1.8 mg daily (titrate over 2–4 weeks)

Key CV evidence LEADER: 13% reduction in MACE; 22% reduction in CV death

Renal adjustment No dose adjustment; caution in severe CKD

PBS status Restricted Benefit (T2DM + CVD; or dual/triple therapy failure)

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Practical tip: SGLT2 inhibitors and GLP-1 RAs have complementary mechanisms and can be safely combined. In patients with T2DM + established ASCVD, current guidelines support early initiation of both agents in addition to metformin, regardless of baseline HbA1c. Cardiovascular protection is the primary treatment goal.

Antiplatelet Therapy

Long-Term Aspirin Therapy

Low-dose aspirin (75–100 mg daily) remains the foundation of long-term antiplatelet therapy in secondary CVD prevention. Aspirin irreversibly acetylates cyclooxygenase-1 (COX-1), inhibiting thromboxane A₂ production and platelet aggregation. Evidence from the Antithrombotic Trialists' (ATT) Collaboration meta-analysis confirms a 25% proportional reduction in serious vascular events with aspirin in secondary prevention, with benefits clearly outweighing the modest increase in major bleeding risk.

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Aspirin (low-dose)

Cartia® / Cardiprin® / Generic · COX-1 inhibitor

Adult dose 75–100 mg PO daily (enteric-coated preferred)

Duration Indefinite (lifelong) in secondary prevention

Renal adjustment Use with caution in severe CKD (increased bleeding risk)

Key caution GI bleeding risk; consider PPI co-prescription in high-risk patients

PBS status ✔ PBS General Benefit

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Clopidogrel

Plavix® / Iscover® / Generic · P2Y12 inhibitor

Adult dose 75 mg PO daily (loading: 300–600 mg for ACS/PCI)

Duration 12 months post-ACS (with aspirin); indefinite if aspirin-intolerant

Renal adjustment No dose adjustment required

Key caution CYP2C19 poor metabolisers (~2–5% Caucasians, ~15–20% East Asians) have reduced efficacy

PBS status ✔ PBS General Benefit

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Ticagrelor

Brilinta® · P2Y12 inhibitor (reversible)

Adult dose 90 mg PO BD (maintenance); 180 mg loading dose. Extended: 60 mg BD post-12 months

Key CV evidence PLATO: Superior to clopidogrel in ACS (16% relative reduction in CV death/MI/stroke); PEGASUS-TIMI 54: Extended DAPT benefit 1–3 years post-MI

Renal adjustment No dose adjustment; caution in severe CKD (limited data)

Key caution Dyspnoea (common, usually self-limiting); avoid with strong CYP3A4 inhibitors; bleeding risk higher than clopidogrel

PBS status Restricted Benefit (ACS; Authority Required for extended DAPT >12 months)

Extended Dual Antiplatelet Therapy (DAPT)

Standard DAPT following ACS consists of aspirin + a P2Y12 inhibitor (clopidogrel or ticagrelor) for 12 months. The decision to extend DAPT beyond 12 months requires careful assessment of ischaemic versus bleeding risk.

Low Ischaemic Risk

Standard DAPT Duration

Simple PCI, no prior events, no DM, no high-risk features. May consider shortening to 3–6 months if high bleeding risk (DAPT score <2).

Setting: Aspirin monotherapy after 12 months (or 3–6 months if high bleeding risk)

Moderate Risk

Consider Extended DAPT

Prior MI 1–3 years ago with ≥1 risk factor (DM, multi-vessel disease, PAD, prior revascularisation, CKD). DAPT score ≥2.

Setting: Consider ticagrelor 60 mg BD + aspirin (PEGASUS regimen) for up to 36 months

High Ischaemic / Low Bleeding

Extended DAPT Recommended

Spontaneous MI with DM + multi-vessel disease, recurrent events, or complex PCI. LOW Bleeding score (HAS-BLED <3).

Setting: Ticagrelor 60 mg BD + aspirin for 36+ months; consider aspirin + clopidogrel if ticagrelor not tolerated

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Contraindication to extended DAPT: HAS-BLED score ≥3, history of intracranial haemorrhage, severe thrombocytopenia (<50 × 10⁹/L), active malignancy with high bleeding risk, or need for long-term anticoagulation (consider aspirin + anticoagulant monotherapy per AF guidelines — "dual pathway" with clopidogrel + anticoagulant for a limited period post-PCI in AF).

Bleeding vs Ischaemic Risk Assessment

The decision to intensify or de-escalate antiplatelet therapy requires integrated assessment using validated risk scores:

Ischaemic Risk Scores

DAPT Score: Integrates age, DM, MI at presentation, prior PCI/MI, stent diameter, smoking, CHF/LVEF <30%, paclitaxel stent, vein graft PCI. Score ≥2 favours extended DAPT.
GRACE Score: Predicts 6-month mortality post-ACS (age, HR, SBP, creatinine, cardiac arrest, ST deviation, biomarkers, Killip class).
Thrombolysis in Myocardial Infarction (TIMI) Risk Score: For unstable angina/NSTEMI.

Bleeding Risk Scores

HAS-BLED: Hypertension, abnormal renal/liver function, stroke, bleeding history, labile INR, elderly (>65), drugs/alcohol. Score ≥3 = high bleeding risk.
PRECISE-DAPT: Age, haemoglobin, WBC, creatinine clearance, prior bleeding. Score ≥25 suggests high bleeding risk and favours shorter DAPT.
ARC-HBR: Academic Research Consortium criteria for high bleeding risk (anatomical and clinical criteria).

Antiplatelet Therapy Post-Stroke

For secondary prevention following ischaemic stroke or TIA, dual antiplatelet therapy (aspirin + clopidogrel) for 21 days followed by clopidogrel monotherapy is supported by the CHANCE and POINT trials. For long-term secondary prevention, clopidogrel 75 mg monotherapy is preferred over aspirin based on the CAPRIE trial showing superior efficacy of clopidogrel in patients with recent ischaemic events.

Investigations & Monitoring

Baseline and Ongoing Investigations

Essential

Fasting lipid panel (TC, LDL-C, HDL-C, TG)

At baseline and 6–8 weeks after lipid therapy change; then every 6–12 months once stable. MBS Item 66549.

Essential

HbA1c

Every 3–6 months in T2DM; annually in non-diabetic patients with high risk factors. MBS Item 66551.

Essential

Serum creatinine, eGFR, electrolytes (Na⁺, K⁺)

Baseline and 1–2 weeks after ACEi/ARB initiation or dose change; then every 6–12 months. MBS Item 66500.

Essential

Blood pressure (clinic and home BP monitoring)

Every visit; home BP monitoring (HBPM) recommended. Medicare rebate for 24-hour ABPM (MBS Item 11606) when clinically indicated.

Available

hs-CRP

Consider for residual inflammatory risk assessment; informs colchicine therapy decisions. MBS Item 66544.

Available

Lipoprotein(a) [Lp(a)]

Once-lifetime measurement recommended for all patients with premature ASCVD; informs risk stratification. MBS Item 66811.

Available

Coronary artery calcium (CAC) score

CT-based; useful for risk reclassification in intermediate-risk patients. Not typically MBS-rebated for secondary prevention (imaging focus).

Specialist

Echocardiography

Post-MI to assess LVEF; monitor HFrEF patients. MBS Item 55118 (transthoracic echo).

Specialist

Stress testing / CT coronary angiography

For assessment of recurrent ischaemia or new symptoms. MBS Item 63350 (stress echo) / MBS Item 57360 (CTCA).

Special Populations

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Pregnancy

Statins — Contraindicated in pregnancy (Category X in Australian categorisation). Discontinue at least 1 month before planned conception or immediately upon confirmed pregnancy.
ACEi/ARBs — Teratogenic (Category D); must be ceased before conception. Switch to methyldopa or labetalol for BP control.
SGLT2 inhibitors — Contraindicated in pregnancy. Cease before conception.
GLP-1 RAs — Not recommended in pregnancy; discontinue at least 2 months before planned conception (semaglutide).
Aspirin — Low-dose (100 mg) is safe in pregnancy for pre-eclampsia prevention; continue for secondary CVD prevention if high risk, after individual risk–benefit assessment.
Women of reproductive age with established CVD should receive pre-conception counselling and be managed jointly by cardiology and obstetric medicine.

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Paediatrics

Statins — Limited to heterozygous familial hypercholesterolaemia (FH) under specialist supervision from age 10 years. Atorvastatin 10–20 mg or rosuvastatin 5–20 mg.
Ezetimibe — May be used from age 10 years in FH (specialist indication).
Aspirin — Low-dose aspirin (2–5 mg/kg/day) in paediatric patients post-Kawasaki disease with coronary artery aneurysms (secondary CVD prevention in children).
ACEi/ARBs — Use in paediatric hypertension (enalapril, losartan) with weight-based dosing; monitor growth and renal function.
Secondary CVD prevention in paediatrics is rare and typically relates to Kawasaki disease, congenital heart disease, or FH. Always involve paediatric cardiology.

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Elderly (≥75 years)

Statins — Benefit persists but with reduced relative risk reduction. Intensity may be reduced if frailty, polypharmacy, or myalgia limit high-intensity therapy. Continue if previously tolerated.
BP targets — Individualise; SBP <130 mmHg may cause orthostatic hypotension and falls. Consider <140/90 mmHg as pragmatic target if frail. SPRINT showed benefit in fit elderly.
Antiplatelet therapy — Increased bleeding risk (HAS-BLED); GI protection with PPI recommended. Consider risk–benefit of continuing DAPT beyond 12 months.
SGLT2i / GLP-1 RA — Limited data in very elderly (>80 years); use with caution, especially SGLT2i (volume depletion, falls).
Regular medication review to reduce polypharmacy-related harm. Falls risk assessment with BP management changes.

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Renal Impairment

Statins — Atorvastatin (no renal dose adjustment) preferred in CKD. Rosuvastatin: start 5 mg, max 10 mg if eGFR <30. Pravastatin: start 10 mg in severe CKD.
ACEi/ARBs — Essential for cardiorenal protection; monitor K⁺ and creatinine at 1–2 weeks. Accept up to 30% rise in creatinine from baseline. Avoid in bilateral renal artery stenosis.
SGLT2i — Can be initiated at eGFR ≥20 mL/min for cardiorenal benefits. Glycaemic efficacy reduced below eGFR 45 but organ-protective benefits persist (DAPA-CKD, EMPA-KIDNEY).
Antiplatelet agents — Increased bleeding risk in advanced CKD; no specific dose adjustments for aspirin, clopidogrel, or ticagrelor.
Patients on dialysis have been excluded from most CVD prevention trials. Extrapolate with caution and individualise care.

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Hepatic Impairment

Statins — Contraindicated in active liver disease or unexplained persistent transaminase elevation. Use cautiously in Child-Pugh A; avoid in Child-Pugh B–C.
Ezetimibe — Not recommended in moderate–severe hepatic impairment.
ACEi/ARBs — Use with caution; no specific dose adjustment but monitor for hepatotoxicity (rare with ACEi).
GLP-1 RAs — Limited data; caution in severe hepatic impairment.
Non-alcoholic fatty liver disease (NAFLD) is common in CVD patients; statins are safe and may reduce liver fibrosis progression.

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Immunocompromised

HIV-positive patients — Higher CVD risk; statin–antiretroviral interactions (avoid simvastatin with PIs; pravastatin and atorvastatin preferred). Consult with infectious disease specialist.
Transplant recipients — Cardiovascular disease is the leading cause of death post-transplant. Statins (pravastatin preferred in renal transplant due to lower interaction with calcineurin inhibitors). Avoid rosuvastatin with cyclosporin.
Rheumatic disease on immunosuppression — Increased CVD risk from chronic inflammation. Statins considered safe; colchicine (0.5 mg daily) may provide dual anti-inflammatory and cardiovascular benefit (COLCOT, LoDoCo2).
Screen for cardiovascular risk factors at baseline and regularly in all immunocompromised populations. Rheumatoid arthritis, SLE, psoriasis, and HIV are independent CVD risk equivalents.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Australians experience cardiovascular disease at 1.7 times the rate of non-Indigenous Australians, with coronary heart disease mortality 1.8 times higher. The burden is particularly pronounced in remote and very remote communities, where access to specialist cardiology services, cardiac rehabilitation, and pharmacotherapy is limited. Cardiovascular disease accounts for approximately 25% of the life expectancy gap between Indigenous and non-Indigenous Australians.

Access barriers

Limited availability of cardiologists and lipidologists in remote NT, WA, and QLD communities. Patients may need to travel >500 km for specialist review. Telehealth MBS items (MBS Item 99202 video consultation) should be used to facilitate specialist input. Many remote communities have 2–4 week pharmacy stockout cycles, affecting medication adherence.

Pharmacotherapy gaps

Studies show Aboriginal and Torres Strait Islander patients are 30–40% less likely to receive statins post-ACS compared with non-Indigenous patients. PBS Remote Area Aboriginal Health Services can supply medications without co-payment for eligible patients — ensure prescriptions are written through these services where available.

Modifiable risk factors

Smoking rates are 2.5× higher in Aboriginal and Torres Strait Islander populations (39% vs 14% daily smoking prevalence). Diabetes prevalence is 3.5× higher. These compound cardiovascular risk and require culturally tailored smoking cessation (Tackling Indigenous Smoking programme) and diabetes management support.

Cardiac rehabilitation

Participation in cardiac rehabilitation post-ACS is significantly lower in Aboriginal and Torres Strait Islander patients. Culturally safe cardiac rehab programmes (e.g., those led by Aboriginal health workers through AMS/AHCs) should be prioritised. MBS cardiac rehab items (MBS Item 699) are available but underutilised.

Rheumatic heart disease

Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) remain endemic in remote NT, northern WA, and far north QLD. While RHD is distinct from atherosclerotic CVD, secondary prevention of RHD (benzathine penicillin G 4-weekly) is a priority cardiovascular intervention in these communities. Patients with RHD often have coexisting atherosclerotic CVD risk factors.

Cultural safety

Management plans should be developed in partnership with Aboriginal Community Controlled Health Services (ACCHS). Yarning-based consultations, use of Aboriginal health workers/ practitioners as care coordinators, and avoiding shame-based language improve medication adherence and follow-up attendance. Acknowledge that sorry business and kinship obligations may affect appointment attendance.

⚠️

Key recommendation: All Aboriginal and Torres Strait Islander patients with established CVD should have a GP Management Plan (GPMP — MBS Item 721) and Team Care Arrangement (TCA — MBS Item 723) to coordinate multidisciplinary secondary prevention. Coordinate with local Aboriginal health workers for medication adherence support and follow-up.

Quick Reference — Secondary Prevention Targets

LDL-C

High-intensity statin ± ezetimibe ± PCSK9i

Target: <1.8 mmol/L (high risk); <1.4 (very high risk)

Recheck 6–8 weeks post-change

Blood Pressure

ACEi/ARB + CCB ± diuretic ± beta-blocker

Target: <130/80 mmHg

Avoid DBP <60 mmHg in CAD

HbA1c (T2DM)

Metformin + SGLT2i + GLP-1 RA

Target: ≤53 mmol/mol (7.0%)

CV benefit agent-first strategy

Antiplatelet

Aspirin 100 mg + ticagrelor/clopidogrel

DAPT 12 months → aspirin lifelong

Extended DAPT if DAPT score ≥2

📚 References

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