Heart Failure with Reduced Ejection Fraction (HFrEF)

📋 Key Information Summary

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HFrEF is defined as heart failure symptoms with LVEF ≤40% on transthoracic echocardiography; BNP ≥100 pg/mL or NT-proBNP ≥300 pg/mL supports diagnosis and correlates with disease severity.
The four pillars of guideline-directed medical therapy (GDMT) are ARNI (or ACEi/ARB), beta-blocker, mineralocorticoid receptor antagonist (MRA), and SGLT2 inhibitor — all four should be initiated as early as tolerated, ideally within the first four weeks of diagnosis.
Sacubitril–valsartan (Entresto®) is PBS-listed as a Restricted Benefit for NYHA II–IV HFrEF and should replace ACEi/ARB when tolerated; it must not be used within 36 hours of an ACE inhibitor dose.
Three evidence-based beta-blockers reduce mortality in HFrEF: carvedilol (Dilatrend®), bisoprolol (not PBS-listed for HF), and metoprolol succinate (Betaloc CR®); start low and titrate every 2–4 weeks to maximum tolerated dose.
SGLT2 inhibitors (dapagliflozin 10 mg PO daily or empagliflozin 10 mg PO daily) are effective regardless of diabetes status; they are PBS-listed for HFrEF and should be initiated early in the GDMT pathway.
ICD implantation for primary prevention is indicated when LVEF remains ≤35% despite ≥3 months of optimised GDMT, NYHA II–III, and life expectancy >1 year; CRT (cardiac resynchronisation therapy) is indicated for LVEF ≤35% with QRS ≥150 ms (LBBB morphology preferred).
Patients with persistent NYHA III–IV symptoms despite maximal GDMT should be referred for advanced heart failure assessment including INTERMACS profiling and LVAD/transplant evaluation.
Fluid restriction (1.5–2 L/day) and daily weight monitoring are core non-pharmacological measures; a weight gain of >1.5 kg in 24 hours or >2 kg in a week warrants medical review for diuretic adjustment.
Aboriginal and Torres Strait Islander Australians experience HF at 1.5–2.5 times the rate of non-Indigenous Australians, with earlier onset and higher in-hospital mortality; culturally safe models of care, Telehealth access, and ACCHO-based follow-up improve outcomes.
Up-titration of GDMT requires regular review (every 1–2 weeks initially); renal function and electrolytes should be checked within 1–2 weeks of each dose change and within 2 weeks of hospital discharge.
Palliative care should be discussed early and integrated alongside active HF management for patients with refractory symptoms, frequent hospitalisations, or those declining advanced therapies.

Introduction & Australian Epidemiology

Heart failure with reduced ejection fraction (HFrEF) is a progressive clinical syndrome characterised by the heart's inability to pump blood effectively, resulting in elevated filling pressures, reduced cardiac output, and neurohormonal activation. HFrEF is specifically defined as heart failure with a left ventricular ejection fraction (LVEF) ≤40%, distinguishing it from heart failure with preserved ejection fraction (HFpEF, LVEF ≥50%) and heart failure with mildly reduced ejection fraction (HFmrEF, LVEF 41–49%).

In Australia, approximately 480,000 people live with heart failure, and this number is projected to exceed 600,000 by 2030 due to an ageing population and improving survival from acute cardiac events. Heart failure accounts for over 65,000 hospitalisations annually, with an average length of stay of 6–7 days, making it one of the leading causes of preventable hospitalisation under the National Healthcare Agreement benchmarks.

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Significant burden: The five-year mortality rate for HFrEF remains approximately 50%, comparable to many cancers. Despite advances in pharmacotherapy, one in four patients hospitalised with HF is readmitted within 30 days, highlighting gaps in guideline implementation and post-discharge care.

The Australian Institute of Health and Welfare (AIHW) reports that heart failure is the underlying or associated cause of death in approximately 10,000 Australians per year. The condition disproportionately affects Aboriginal and Torres Strait Islander Australians, people in rural and remote areas, and those of lower socioeconomic status. The National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (CSANZ) jointly publish clinical guidelines that align broadly with the European Society of Cardiology (ESC) 2021 and American Heart Association (AHA)/American College of Cardiology (ACC) 2022 frameworks, adapted for Australian practice.

Key aetiologies of HFrEF in the Australian context include ischaemic heart disease (the most common cause, accounting for approximately 60–70% of cases), dilated cardiomyopathy (idiopathic, familial, or toxin-related including alcohol), uncontrolled hypertension, valvular heart disease, myocarditis, peripartum cardiomyopathy, and tachycardia-mediated cardiomyopathy. Iron deficiency (with or without anaemia) is present in up to 50% of HFrEF patients and independently worsens outcomes.

Diagnostic Criteria

Echocardiographic Assessment

Transthoracic echocardiography (TTE) is the cornerstone of HFrEF diagnosis and should be performed in all patients with suspected heart failure. The diagnosis of HFrEF requires:

LVEF ≤40% measured by modified Simpson's biplane method (preferred) or other validated quantitative technique
Assessment of left ventricular dimensions (LVEDD, LVESD) and wall thickness
Diastolic function grading (E/e' ratio, left atrial volume index, tricuspid regurgitation velocity)
Evaluation for regional wall motion abnormalities suggesting ischaemic aetiology
Assessment of right ventricular function (TAPSE, RV S') and pulmonary artery systolic pressure
Valvular assessment for underlying structural causes or secondary regurgitation
Estimation of filling pressures and volume status

A repeat echocardiogram should be performed 3–6 months after initiating GDMT to assess treatment response, and again if there is a significant clinical change (e.g., new murmur, clinical deterioration, or before considering device therapy). An LVEF improvement to >40% (HFimpEF) does not remove the diagnosis of HFrEF; patients should continue all GDMT indefinitely as cardiac remodelling may reverse with treatment withdrawal.

BNP / NT-proBNP Interpretation

Natriuretic peptides are essential for both diagnosis and prognostication. Australian laboratories routinely offer both BNP and NT-proBNP. Results should be interpreted in the clinical context, noting that obesity, atrial fibrillation, renal function, and age significantly influence levels.

Biomarker	Exclusion Threshold (rule out HF)	Diagnosis Favourable	Notes
BNP	<100 pg/mL	≥100 pg/mL	Less affected by age and renal function than NT-proBNP; affected by neprilysin inhibitors (sacubitril)
NT-proBNP	<300 pg/mL	≥300 pg/mL	Higher thresholds in older adults; renal impairment raises levels independent of HF
NT-proBNP (age-adjusted)	<125 pg/mL (<75 years); <450 pg/mL (≥75 years)	Above age-specific thresholds	ESC 2021 age-adjusted cut-offs improve specificity in elderly patients

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Critical: BNP is unreliable in patients taking sacubitril–valsartan (Entresto®) as neprilysin inhibition raises BNP levels. Use NT-proBNP for monitoring in patients on ARNI therapy. Always interpret natriuretic peptides alongside clinical assessment and echocardiography — no single value is diagnostic in isolation.

Aetiology Determination

Identifying the underlying cause of HFrEF is essential for guiding specific therapy and prognosis. A structured approach to aetiology determination should include:

Investigation	Purpose	Availability / MBS
Coronary angiography (invasive or CTCA)	Exclude ischaemic aetiology; consider if angina, regional wall motion abnormalities, or ischaemic risk factors present	Available in all tertiary centres; MBS items for CT coronary angiography and invasive angiography
Cardiac MRI (CMR)	Tissue characterisation (oedema, fibrosis, infiltration); differentiate ischaemic vs non-ischaemic; detect myocarditis, sarcoidosis, ARVC	Available at major metropolitan centres; MBS item 63448 (cardiac MRI with contrast)
Iron studies (ferritin, transferrin saturation)	Iron deficiency assessment — ferritin <100 µg/L or 100–299 µg/L with transferrin saturation <20%	Widely available; MBS item 66591 (iron studies)
Thyroid function tests	Exclude thyroid dysfunction as reversible cause	Widely available; MBS item 66719
FBC, renal function, LFTs, glucose, lipids	Baseline organ function, comorbidity screening	Widely available
Genetic testing / family screening	Suspected familial dilated cardiomyopathy (≥2 affected family members, young onset, conduction disease, skeletal myopathy)	Referral to genetics service; available through state genetics services
Endomyocardial biopsy	Suspected giant cell myocarditis, eosinophilic myocarditis, cardiac amyloidosis (when non-invasive testing inconclusive), cardiac transplant rejection	Tertiary centre referral only; limited availability
99mTc-DPD / PYP scintigraphy	Transthyretin cardiac amyloidosis screening	Available at selected nuclear medicine centres; MBS item 61323
Sleep study (polysomnography)	Screen for obstructive sleep apnoea, a common comorbidity that worsens HF outcomes	Available in sleep laboratories and home-based testing; MBS item 12203 / 12250

All patients should have a comprehensive history and examination to identify potential reversible and treatable causes including alcohol excess, recreational drug use (cocaine, methamphetamine), chemotherapy exposure (anthracyclines, trastuzumab), autoimmune conditions, and infective aetiologies (Chagas disease in relevant populations).

Guideline-Directed Medical Therapy (GDMT)

Guideline-directed medical therapy for HFrEF has evolved into a four-pillar approach based on landmark randomised controlled trials demonstrating mortality and hospitalisation benefits. The four pillars are: (1) ARNI (or ACEi/ARB), (2) beta-blocker, (3) mineralocorticoid receptor antagonist (MRA), and (4) SGLT2 inhibitor. All four should be initiated in hospitalised patients before discharge where feasible and in outpatients as early as possible after diagnosis.

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Sequencing strategy: Current evidence supports rapid initiation of all four pillars, with the DAPA-HF, EMPEROR-Reduced, and PARADIGM-HF trials showing consistent benefits independent of initiation order. A practical approach is to initiate 1–2 agents from different pillars at each clinic visit (every 1–2 weeks), titrating to target doses over 8–12 weeks. Initiation in hospital before discharge is encouraged and safe with appropriate monitoring.

Pillar 1: ARNI / ACEi / ARB

Sacubitril–valsartan (Entresto®), a combined neprilysin inhibitor and ARB, is the preferred first-line agent based on the PARADIGM-HF trial (20% relative risk reduction in cardiovascular death or HF hospitalisation vs enalapril). It is PBS-listed as a Restricted Benefit for chronic heart failure (NYHA II–IV) with LVEF ≤40% on optimised background therapy. An ACEi or ARB remains appropriate when ARNI is not tolerated or not accessible.

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Sacubitril–Valsartan (ARNI)

Entresto® · Combined neprilysin inhibitor / ARB

Starting dose 24/26 mg PO BD (50 mg tablet); if previously on low-dose ACEi/ARB or SBP 95–110 mmHg, start 49/51 mg BD (100 mg tablet)

Target dose 97/103 mg PO BD (200 mg tablet) — titrate every 2–4 weeks

Renal adjustment No adjustment required for eGFR ≥20 mL/min/1.73m²; caution below this threshold

Key contraindication Must not be administered within 36 hours of last ACEi dose (risk of angioedema); avoid with aliskiren in diabetes

PBS status PBS Restricted Benefit

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Enalapril (ACEi alternative)

Renitec® · ACE inhibitor

Starting dose 2.5 mg PO BD

Target dose 10–20 mg PO BD

Renal adjustment Start at 2.5 mg daily if eGFR <30; monitor potassium and creatinine within 1–2 weeks

PBS status ✔ PBS General Benefit

Pillar 2: Beta-Blockers

Only three beta-blockers have demonstrated mortality benefit in HFrEF: carvedilol (COPERNICUS, US Carvedilol HF trials), bisoprolol (CIBIS-II), and metoprolol succinate (MERIT-HF). Other beta-blockers, including atenolol and metoprolol tartrate, should not be used for this indication. Beta-blockers should be initiated at low dose once the patient is euvolaemic and haemodynamically stable, then titrated upward every 2–4 weeks to maximum tolerated dose.

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Carvedilol

Dilatrend® · Non-selective beta / alpha-1 blocker

Starting dose 3.125 mg PO BD

Target dose 25 mg PO BD (50 mg BD if body weight ≥85 kg)

Renal adjustment None required

PBS status ✔ PBS General Benefit

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Metoprolol Succinate (controlled release)

Betaloc CR® · Selective beta-1 blocker

Starting dose 23.75 mg PO daily (quarter of 95 mg tablet)

Target dose 190 mg PO daily

PBS status ✔ PBS General Benefit

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Bisoprolol

Not PBS-listed for HF · Selective beta-1 blocker

Starting dose 1.25 mg PO daily

Target dose 10 mg PO daily

PBS status ✘ Not PBS for HF (private script or GP co-payment)

Pillar 3: Mineralocorticoid Receptor Antagonists (MRAs)

Spironolactone and eplerenone reduce mortality and hospitalisation in HFrEF (RALES, EMPHASIS-HF trials). MRAs should be initiated once serum potassium is <5.0 mmol/L and eGFR is ≥30 mL/min/1.73m². Hyperkalaemia and worsening renal function are the most common adverse effects requiring monitoring.

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Spironolactone

Aldactone® · Non-selective MRA

Starting dose 12.5–25 mg PO daily

Target dose 25–50 mg PO daily

Renal adjustment Avoid if eGFR <30 mL/min/1.73m²; use with caution if eGFR 30–59 (monitor K⁺ closely)

Side effects Gynaecomastia (up to 10%), breast tenderness; consider eplerenone if bothersome

PBS status ✔ PBS General Benefit

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Eplerenone

Inspra® · Selective MRA

Starting dose 25 mg PO every other day (25 mg daily if eGFR >50)

Target dose 50 mg PO daily

Renal adjustment 25 mg every other day if eGFR 30–50; avoid if eGFR <30

PBS status PBS Authority Required

Pillar 4: SGLT2 Inhibitors

SGLT2 inhibitors (dapagliflozin and empagliflozin) have demonstrated robust reductions in the composite of cardiovascular death or HF hospitalisation in the DAPA-HF and EMPEROR-Reduced trials, respectively. Benefits were consistent regardless of diabetes status, and these agents should be considered foundational therapy in all HFrEF patients. They are now PBS-listed for HFrEF independently of diabetes.

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Dapagliflozin

Forxiga® · SGLT2 inhibitor

Dose 10 mg PO once daily (no titration needed)

Renal adjustment Initiate if eGFR ≥20 mL/min/1.73m²; may continue below this threshold if already on therapy; HF benefit persists across eGFR range

Key considerations Ensure adequate hydration; may cause transient eGFR dip (haemodynamic, reversible); monitor for genital mycotic infections; euglycaemic DKA is rare but important in T1DM (contraindicated in T1DM)

PBS status PBS Authority Required (for HFrEF; also available for T2DM)

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Empagliflozin

Jardiance® · SGLT2 inhibitor

Dose 10 mg PO once daily

Renal adjustment Same as dapagliflozin — initiate if eGFR ≥20 mL/min/1.73m² for HF indication

PBS status PBS Authority Required

Diuretics for Volume Management

Loop diuretics (furosemide, bumetanide) are essential for managing congestion but do not improve mortality. They should be prescribed at the lowest dose that maintains euvolaemia. In patients with diuretic resistance, sequential nephron blockade with the addition of metolazone (2.5–5 mg PO daily/alternate days) or thiazide diuretic is recommended, with close electrolyte monitoring.

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Furosemide

Lasix® · Loop diuretic

Starting dose (mild congestion) 20–40 mg PO daily

Acute decompensation 40–80 mg IV stat then 10–20 mg/hr infusion or repeated boluses; bioavailability of oral furosemide is ~50%, so IV dose ≈ ½ oral equivalent

Renal adjustment Higher doses required with impaired renal function (up to 250 mg IV); consider continuous infusion for refractory oedema

PBS status ✔ PBS General Benefit

Additional Pharmacotherapy

For patients who remain symptomatic on optimised four-pillar GDMT, additional agents to consider include:

Ivabradine (Coralan®): Indicated when HR ≥70 bpm despite maximally tolerated beta-blocker (or if beta-blocker contraindicated), LVEF ≤35%, and in sinus rhythm. Dose: 5 mg BD, titrate to 7.5 mg BD. PBS Authority Required.
Hydralazine + isosorbide dinitrate: Consider as add-on therapy in patients who cannot tolerate ACEi/ARB/ARNI (e.g., severe renal impairment, hyperkalaemia) or as an adjunct in self-identified African American patients (A-HeFT trial). Not commonly used in Australian practice.
Intravenous iron (ferric carboxymaltose — Ferinject®): For iron-deficient HFrEF patients (ferritin <100 or ferritin 100–299 with TSAT <20%). The AFFIRM-AHF and IRONMAN trials demonstrated reduction in HF hospitalisation. Dose: 500–1000 mg IV per infusion, with repeat dosing guided by iron studies at 4–6 weeks. PBS-listed for iron deficiency with chronic heart failure.
Vericiguat (Verquvo®): Oral soluble guanylate cyclase stimulator for patients with worsening HF on optimised GDMT (VICTORIA trial). Not yet PBS-listed in Australia; available via compassionate access or private script in selected cases.

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Treatment target: All four GDMT pillars should be initiated and titrated to maximum tolerated doses within 8–12 weeks. Doses do not need to reach target to confer benefit — any dose is better than no dose — but clinical outcomes improve incrementally with higher doses. Document target doses and reasons for deviation at each review.

Device Therapy

Implantable Cardioverter-Defibrillator (ICD) — Primary Prevention

ICD implantation for primary prevention of sudden cardiac death is indicated in patients with HFrEF who meet all of the following criteria:

LVEF ≤35% despite ≥3 months of optimised GDMT (documented at ≥4 weeks after most recent dose change or hospitalisation)
NYHA functional class II or III (ambulatory)
Expected survival with good functional status >1 year
Sinus rhythm preferred (benefit less clear in atrial fibrillation, individualised decision)

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Do not implant early: ICD implantation should NOT be performed within 40 days of acute myocardial infarction or within 3 months of a new diagnosis of non-ischaemic cardiomyopathy, as LVEF may improve with GDMT. Re-assess LVEF with echocardiography before device consideration. Up to 30% of patients will have LVEF improvement to >35% on GDMT, potentially avoiding ICD implantation.

ICD — Secondary Prevention

ICD implantation is indicated for secondary prevention in survivors of cardiac arrest due to ventricular fibrillation or sustained ventricular tachycardia (VT) not due to a reversible cause, or in patients with spontaneous sustained VT with structural heart disease or haemodynamic compromise. These indications apply regardless of LVEF once the acute event has been managed.

Cardiac Resynchronisation Therapy (CRT)

CRT with biventricular pacing (CRT-P) or CRT combined with defibrillator (CRT-D) improves symptoms, reduces hospitalisation, and reduces mortality in selected patients with HFrEF and electrical dyssynchrony.

Indication	QRS Criteria	LVEF	NYHA	Rhythm
Class I (strongest)	≥150 ms, LBBB morphology	≤35%	II–IV (ambulatory)	Sinus rhythm
Class IIa	≥150 ms, LBBB	≤35%	II–IV	Atrial fibrillation (consider AV node ablation)
Class IIa	130–149 ms, LBBB	≤35%	II–IV	Sinus rhythm
Class IIb	≥150 ms, non-LBBB	≤35%	II–IV	Sinus rhythm
Class III (not indicated)	<130 ms	Any	Any	Any

CRT-D is generally preferred over CRT-P for patients who also meet primary prevention ICD criteria. CRT-P alone may be appropriate for elderly patients, those with significant comorbidities, or those who decline a defibrillator. Conduction system pacing (His bundle pacing or left bundle branch area pacing) is an emerging alternative to conventional CRT when coronary sinus lead placement is not feasible.

Wearable Cardioverter-Defibrillator (WCD)

A wearable cardioverter-defibrillator (LifeVest®) provides temporary protection against sudden cardiac death during the "window of opportunity" before ICD implantation may be indicated. Indications include:

LVEF ≤35% within the first 40 days post-MI
Newly diagnosed non-ischaemic cardiomyopathy within the first 3–9 months of GDMT initiation
Bridge to transplant or LVAD (where ICD is not yet implanted)
Patients with a temporary indication who have contraindications to implantation (e.g., active infection)

WCD availability in Australia is limited to major centres. Adherence is the primary barrier — patients must wear the device ≥20 hours/day for it to be effective. Average wear time in clinical practice is 15–18 hours/day.

Advanced Heart Failure & Transplantation

Defining Advanced Heart Failure

Advanced (or stage D) heart failure is characterised by severe symptoms (NYHA III–IV) despite maximally tolerated GDMT, device therapy where appropriate, and treatment of reversible factors. Patients typically experience recurrent hospitalisations (≥2 in 12 months for HF), worsening renal function, intolerance to GDMT, hypotension, hyponatraemia, and increasing diuretic requirements. Referral to an advanced heart failure specialist centre should not be delayed — early referral improves outcomes for patients who may benefit from transplantation or mechanical circulatory support.

INTERMACS Profiles

The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) profiles classify advanced HF patients by acuity, guiding urgency for mechanical circulatory support and transplantation listing.

Profile 1

Critical Cardiogenic Shock

"Crash and burn" — escalating inotropes, deteriorating vital organs, often on mechanical ventilation or ECMO

Setting: ICU — emergent MCS or transplant if available

Profile 2

Progressive Decline

"Sliding on inotropes" — inotrope-dependent with declining function despite therapy

Setting: ICU / HDU — urgent LVAD assessment

Profile 3

Stable but Inotrope-Dependent

"Dependent stability" — stable on continuous inotropes, recurrent haemodynamic instability if weaned

Setting: Advanced HF unit — LVAD / transplant evaluation

Profile 4

Resting Symptoms

"Frequent flyer" — comfortable at rest but minimal exertion causes symptoms, recurrent hospitalisations

Setting: Advanced HF clinic — active transplant / LVAD workup

Profile 5–6

Exertion Intolerant / Exertion Limited

Tolerates minimal to light activity; comfortable at rest; frequent HF decompensations

Setting: Advanced HF clinic — transplant listing assessment

Profile 7

Advanced NYHA III

"Placeholder" — close to listing threshold; significant limitation but stable

Setting: HF clinic — ensure optimal GDMT and devices before listing

Left Ventricular Assist Device (LVAD)

Durable LVAD therapy (predominantly the HeartMate 3™ centrifugal-flow pump) is indicated as bridge to transplant (BTT) or as destination therapy (DT) for patients with advanced HF who are not transplant candidates. In Australia, LVAD implantation is performed at specialised centres in major cities (Royal Prince Alfred Hospital, St Vincent's Hospital Sydney, Alfred Hospital Melbourne, Prince Charles Hospital Brisbane, Fiona Stanley Hospital Perth).

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LVAD outcomes: The MOMENTUM 3 trial demonstrated 2-year survival of approximately 80% with the HeartMate 3 device. Quality of life improvements are substantial for most patients, although ongoing complications including bleeding (especially GI bleeding), stroke, driveline infection, and right ventricular failure require specialist management. Over 150 LVADs are implanted annually in Australia.

Heart Transplantation

Cardiac transplantation remains the gold standard for advanced HFrEF, with median post-transplant survival exceeding 13 years in Australia. Indications include severe refractory HF with poor prognosis despite maximal medical and device therapy, and absence of significant contraindications.

Absolute contraindications include active malignancy (excluding low-risk skin cancers), active substance abuse, severe irreversible pulmonary hypertension (PVR >5 Wood units unresponsive to vasodilator testing), active systemic infection, and significant psychosocial barriers to adherence.

Australian transplant centres: Heart transplantation is performed at seven nationally accredited centres — St Vincent's Hospital Sydney, Royal Prince Alfred Hospital Sydney, Alfred Hospital Melbourne, Royal Melbourne Hospital, Prince Charles Hospital Brisbane, Fiona Stanley Hospital Perth, and Royal Adelaide Hospital. Approximately 100–120 heart transplants are performed annually in Australia, with wait-list times ranging from 3–12 months depending on blood group, body size, and clinical urgency (Status 1 listing for high-acuity patients).

Palliative Care in HFrEF

Palliative care should be integrated early and concurrently with active HF management, not reserved for the terminal phase. Key triggers for palliative care referral include:

NYHA III–IV symptoms despite optimised GDMT and devices
≥2 HF hospitalisations in 12 months
Declining or ineligible for advanced therapies (transplant, LVAD)
Patient preference to focus on quality of life
Significant non-cardiac comorbidities limiting prognosis

Advance care planning discussions, including documentation of resuscitation preferences (Advance Care Directive / substitute decision-maker designation), should be initiated at the time of device consideration or when prognosis is anticipated to be limited. Symptom management with opioids for refractory dyspnoea, anxiolytics for breathlessness-associated anxiety, and management of fluid overload with intermittent subcutaneous furosemide infusions (in community palliative care settings) should be considered. Australian palliative care services are accessible via referral through state-based palliative care networks and community palliative care teams.

Monitoring & Follow-up

Clinical Assessment Schedule

A structured, multidisciplinary approach to follow-up reduces readmissions and improves mortality. Heart failure nurse-led titration clinics and telehealth models have been shown to improve GDMT uptake in Australian settings (NHFA/CSANZ 2024 guidance).

Week 1–2

Post-discharge or new diagnosis review. Assess volume status, weight trend, vital signs, symptoms. Review medication adherence. Check renal function and electrolytes (within 7 days of discharge or last medication change). Initiate first GDMT agents. Provide self-management education.

Week 2–4

Second or third clinic visit. Titrate first medications and initiate additional GDMT pillars. Re-check renal function and electrolytes. Review fluid and sodium restriction compliance. Evaluate for orthostatic hypotension.

Month 1–3

Continue GDMT up-titration toward target doses. Repeat echocardiography at 3 months if newly diagnosed or if clinical status changed. Iron studies at baseline and recheck at 4–6 weeks if IV iron administered. BNP/NT-proBNP trajectory assessment.

Month 3–6

Reassess NYHA class, 6-minute walk test (if available), functional capacity. Confirm all four GDMT pillars at maximum tolerated dose. Evaluate for ICD/CRT consideration if LVEF remains ≤35%. Cardiopulmonary exercise testing if transplant evaluation being considered.

Every 3–6 months (ongoing)

Stable patients: clinic or telehealth review every 3–6 months. Review symptoms, weight, medication adherence, self-management. Renal function and electrolytes every 3–6 months (more frequently with diuretic dose changes or MRA/ACEi/ARNI dose adjustments). Annual echocardiography optional if clinically stable.

Medication Titration Protocol

Systematic up-titration is critical — the majority of Australian HF patients are sub-optimally dosed, particularly beta-blockers and ACEi/ARB/ARNI. The following protocol applies:

Medication	Titration Interval	Key Monitoring	Stop/Revert Criteria
ARNI / ACEi / ARB	Every 2–4 weeks	BP, K⁺, Cr within 1–2 weeks of each dose change	SBP <90 mmHg, K⁺ >5.5 mmol/L, Cr rise >30% from baseline, symptomatic hypotension
Beta-blockers	Every 2–4 weeks	HR (target 55–70 bpm at rest), BP, symptoms	HR <50 bpm, SBP <90, worsening HF symptoms (may need to reduce diuretic first before halting beta-blocker uptitration)
MRAs	Single dose step (12.5 → 25 → 50 mg)	K⁺ and Cr at 3 days, 1 week, and 1 month after initiation; then every 3–6 months	K⁺ >5.5 mmol/L, eGFR <30 mL/min/1.73m²
SGLT2 inhibitors	No titration (fixed dose)	eGFR at 2–4 weeks (expect transient dip); BP; symptoms of volume depletion	eGFR decline >30% sustained (unusual); symptomatic hypotension

Remote Monitoring

Remote monitoring strategies are increasingly incorporated into Australian HF care models:

Structured telephone support: Regular nurse-led phone calls (weekly initially, then monthly) for symptom assessment, weight review, and medication titration. Multiple Australian RCTs (e.g., TIM-HF2-equivalent programs) demonstrate reduced readmissions. Funded through state heart failure programs and Medicare chronic disease management items.
Telehealth video consultations: Particularly valuable in rural and remote Australia where specialist access is limited. Medicare Benefits Schedule items for telehealth have been expanded post-COVID and remain available for cardiologist and GP reviews.
Implantable haemodynamic monitoring: CardioMEMS™ (pulmonary artery pressure monitoring) is available in selected Australian centres. The CHAMPION trial demonstrated a 37% reduction in HF hospitalisation. Access is currently limited to research or compassionate use in most jurisdictions.
Patient self-management education: Daily weight monitoring, fluid restriction adherence (typically 1.5–2 L/day), sodium restriction (<2 g/day), exercise prescription (cardiac rehabilitation), and recognition of decompensation signs (weight gain >1.5 kg in 24 hours, increasing dyspnoea, oedema).

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Common pitfall: Failure to up-titrate GDMT due to transient hypotension, mild renal function changes, or asymptomatic bradycardia. The most effective GDMT optimisation programs use nurse-led titration protocols with physician oversight, achieving target doses in 70–80% of patients vs 30–40% with usual care. Document reasons for sub-target dosing at every visit.

Special Populations

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Pregnancy

Contraindicated in pregnancy: ACEi, ARB, ARNI, MRA, SGLT2 inhibitors — all are teratogenic (Category D). Women of childbearing potential should receive contraception counselling when initiated on GDMT.

Peripartum cardiomyopathy: Defined as LVEF ≤45% in the last month of pregnancy or within 5 months postpartum. Management includes bromocriptine (2.5 mg PO BD for 2 weeks then 2.5 mg daily for 6 weeks — evidence from the IPAC registry and small RCTs), hydralazine, and diuretics. Recovery of LVEF occurs in ~50% of cases within 6–12 months.

Breastfeeding: ACEi/ARB (enalapril, losartan) are considered compatible with breastfeeding; ARNI and SGLT2 inhibitors lack safety data — avoid.

Anticoagulation: Warfarin is teratogenic in the first trimester; use LMWH or dose-adjusted unfractionated heparin in early pregnancy if anticoagulation required (e.g., peripartum cardiomyopathy with LVEF <30%).

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Paediatrics

Aetiology differs: Paediatric HF is most commonly due to congenital heart disease, dilated cardiomyopathy (genetic or myocarditis), or acquired conditions (Kawasaki disease, rheumatic heart disease in ATSI communities).

Carvedilol: 0.05 mg/kg/dose PO BD, titrate to 0.3 mg/kg/dose BD (max 25 mg BD if >35 kg). Evidence is extrapolated from adult trials; modest benefit in paediatric dilated cardiomyopathy.

Enalapril: 0.1 mg/kg/dose PO BD, titrate to 0.25–0.5 mg/kg/dose BD (max 10 mg BD).

SGLT2 inhibitors: Not approved in patients <18 years for HF indication; ongoing trials.

Diuretics: Furosemide 0.5–2 mg/kg/dose PO/IV BD–TDS; spironolactone 0.5–1 mg/kg/day PO in divided doses.

Referral: All paediatric HF should be managed by or in consultation with a paediatric cardiologist. Mechanical circulatory support (Berlin Heart EXCOR®) is available at paediatric cardiac transplant centres in Melbourne and Sydney.

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Elderly (≥75 years)

Prevalence increases with age: >10% of Australians aged ≥75 years have heart failure, often with multiple comorbidities (atrial fibrillation, CKD, COPD, frailty).

GDMT tolerability: Lower starting doses and slower titration are often necessary. Monitor closely for hypotension, falls risk, renal impairment, and electrolyte disturbances. Beta-blockers and ARNI/ACEi are still indicated but target doses may be lower.

Polypharmacy: Review all medications for potential interactions and deprescribe where appropriate. NSAIDs and certain antihistamines should be avoided.

Device therapy: ICD and CRT decisions should consider frailty, cognitive status, and patient goals. CRT-P may be preferred over CRT-D in the very elderly or frail.

Frailty assessment: Use validated tools (Clinical Frailty Scale, Fried criteria) to guide treatment intensity and care planning.

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Renal Impairment

Cardiorenal syndrome: HF and CKD commonly coexist (~50% of HF patients have CKD stage 3+). Worsening renal function during GDMT initiation does not necessarily mandate discontinuation — a mild rise in creatinine (up to 30%) is acceptable and expected.

ARNI: No dose adjustment for eGFR ≥20. Use cautiously below eGFR 20; limited data.

MRA: Avoid spironolactone/eplerenone if eGFR <30 mL/min/1.73m² (hyperkalaemia risk).

SGLT2 inhibitors: Can be initiated at eGFR ≥20 for HF indication (not dialysis); HF benefit is independent of kidney function.

Diuretics: Higher doses of loop diuretics may be required; consider adding metolazone for diuretic resistance.

Dialysis patients: HFrEF management in dialysis-dependent patients is challenging; beta-blockers (particularly carvedilol) have evidence of benefit. Avoid ACEi/ARB if hyperkalaemia is recurrent. Specialist nephrology–cardiology co-management is recommended.

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Hepatic Impairment

Cardiac hepatopathy: Congestive hepatopathy (passive congestion) and acute cardiogenic liver injury are common in severe HF. LFT derangement is common and does not contraindicate GDMT.

Cautions: Sacubitril–valsartan: limited data in severe hepatic impairment (Child-Pugh C); use with caution. Carvedilol: bioavailability is increased in cirrhosis — start at lowest dose. Spironolactone: used therapeutically in cirrhosis for ascites, but monitor K⁺ carefully in combined HF-liver disease.

Alcohol-related cardiomyopathy: Abstinence is essential — LVEF may recover partially or completely. Refer to alcohol and other drug services. Cardiac MRI may demonstrate mid-wall fibrosis.

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Immunocompromised

Transplant recipients: Heart transplant patients require lifelong immunosuppression (typically tacrolimus, mycophenolate, prednisolone). Develop a chronic immunosuppressive cardiomyopathy in a proportion of cases — manage with standard GDMT with attention to drug interactions.

Chemotherapy-induced cardiomyopathy: Anthracyclines (doxorubicin), trastuzumab, and immune checkpoint inhibitors can cause HFrEF. Trastuzumab-related cardiomyopathy is often reversible; immune checkpoint inhibitor myocarditis requires high-dose corticosteroids and cessation of immunotherapy.

HIV-associated cardiomyopathy: Manage with standard GDMT; check for drug interactions between antiretrovirals and HF medications (particularly with boosted protease inhibitors and calcium channel blockers/beta-blockers).

Chagas disease: Consider in patients from endemic regions (Central/South America) with unexplained dilated cardiomyopathy. Benznidazole (5 mg/kg/day PO for 60 days) for chronic Chagas requires infectious disease specialist guidance; cardiac management is standard GDMT.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience heart failure at a significantly higher rate than non-Indigenous Australians, with onset at a younger age (often 10–15 years earlier), more advanced disease at presentation, and higher in-hospital and post-discharge mortality. Rheumatic heart disease remains an important and preventable cause of HFrEF in many remote communities, alongside ischaemic heart disease, which accounts for the majority of HF cases.

Epidemiology

Heart failure hospitalisation rates are 1.5–2.5 times higher for Indigenous Australians compared with non-Indigenous Australians (AIHW 2023). Premature cardiovascular mortality (before age 55) is 3–5 times higher. RHD-related HF disproportionately affects children and young adults in Northern Territory and Far North Queensland communities.

Cultural safety

Care should be delivered in culturally safe environments with Aboriginal and Torres Strait Islander health workers and liaison officers integrated into the multidisciplinary heart failure team. Respect for family structures, sorry business obligations, and avoidance of shame-based communication are essential. Clear, plain-language education materials co-designed with Indigenous communities improve health literacy and medication adherence.

Remote and rural access

Specialist cardiology and heart failure services are concentrated in metropolitan centres. Telehealth, echocardiography via remote ultrasound (FOCUS/FATE protocols), visiting specialist services through RFDS and outreach programs, and training of remote area nurses in HF management are critical to closing the gap. Cardiac MRI and advanced device therapy (ICD/CRT implantation) require transfer to tertiary centres, creating logistical and cultural barriers.

Medication access

PBS co-payment barriers are reduced through the Close the Gap PBS co-payment program, which provides PBS medicines at a reduced co-payment for Indigenous Australians living in remote areas. Despite this, medication supply disruptions in remote communities (pharmacy stockouts, cold-chain limitations) affect SGLT2 inhibitor and ARNI availability. Long-acting injectable formulations where available may improve adherence.

Rheumatic heart disease

RHD causes significant morbidity in Indigenous Australians, particularly in the Northern Territory (incidence up to 150 per 100,000 in Aboriginal children). Secondary prophylaxis with 4-weekly benzathine penicillin G injections (2.4 MU IM) is the cornerstone of RHD prevention. Valve surgery for severe RHD-related HF often requires transfer from remote communities to urban centres (e.g., Royal Darwin Hospital, St Vincent's Hospital Sydney).

ACCHO-based models of care

Aboriginal Community Controlled Health Organisations (ACCHOs) play a vital role in HF screening, chronic disease management, cardiac rehabilitation, and palliative care. Integrated chronic care programs within ACCHOs that include dedicated HF nurses, visiting cardiologists, echocardiography access, and medication management programs have shown improved GDMT utilisation and reduced hospitalisations in pilot studies. Examples include Wuchopperen Health Service (Cairns), Aboriginal Medical Service Western Sydney, and Danila Dilba Health Service (Darwin).

Quick Reference — GDMT Summary

Pillar

Agent

Target Dose

Key Trial

ARNI (or ACEi/ARB)

Sacubitril–valsartan

97/103 mg BD

PARADIGM-HF

Beta-blocker

Carvedilol / bisoprolol / metoprolol CR

25 mg BD / 10 mg daily / 190 mg daily

COPERNICUS, CIBIS-II, MERIT-HF

MRA

Spironolactone / eplerenone

25–50 mg daily / 50 mg daily

RALES, EMPHASIS-HF

SGLT2 inhibitor

Dapagliflozin / empagliflozin

10 mg daily (both)

DAPA-HF, EMPEROR-Reduced

📚 References

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3. Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian Clinical Guidelines for the Management of Heart Failure 2018. Med J Aust. 2018;209(7):325–338.
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12. Australian Institute of Health and Welfare. Heart, stroke and vascular disease — Australian facts. AIHW, Canberra; 2023.
13. National Heart Foundation of Australia. Position Statement: SGLT2 inhibitors in heart failure. NHFA, Melbourne; 2022.
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15. Australian Government Department of Health. National Aboriginal and Torres Strait Islander Health Plan 2021–2031. Commonwealth of Australia; 2021.
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17. Bozkurt B, Coats AJS, Tsutsui H, et al. Universal definition and classification of heart failure: a report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee. Eur J Heart Fail. 2021;23(3):352–380.