📋 Key Information Summary
- Heart failure with reduced ejection fraction (HFrEF) is defined as LVEF ≤ 40 % and is also termed systolic heart failure; it is characterised by impaired ventricular contraction and is the most evidence-rich phenotype for disease-modifying pharmacotherapy.
- Heart failure with preserved ejection fraction (HFpEF) (LVEF ≥ 50 %), historically called diastolic heart failure, results from impaired ventricular relaxation and increased stiffness; treatment focuses on managing congestion, comorbidities, and SGLT2 inhibitors (empagliflozin, dapagliflozin).
- HFmrEF (LVEF 41–49 %) represents a mid-range group; current Australian guidelines recommend ACEi/ARB, beta-blocker, and SGLT2 inhibitor therapy.
- NYHA functional classification (Class I–IV) guides prognosis, drug titration, and referral pathways and should be documented at every review.
- Ischaemic heart disease remains the leading cause of heart failure in Australia; hypertension, atrial fibrillation, valvular disease, and cardiomyopathy are other major aetiologies.
- B-type natriuretic peptide (BNP ≥ 100 pg/mL) or NT-proBNP ≥ 300 pg/mL is the recommended first-line investigation; echocardiography is mandatory to confirm diagnosis, classify phenotype, and identify underlying structural causes.
- First-line HFrEF drug therapy consists of an ACE inhibitor (or ARB), a beta-blocker (carvedilol, bisoprolol, or metoprolol succinate), a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and an SGLT2 inhibitor — collectively the "four pillars".
- Ace inhibitor dose should be titrated to the maximum tolerated evidence-based dose; blood pressure, renal function, and potassium must be checked 1–2 weeks after initiation or dose change.
- Beta-blockers must be initiated at low dose in stable, euvolaemic patients and up-titrated slowly — they are contraindicated in acute decompensation.
- Loop diuretics (furosemide, bumetanide) provide symptomatic relief of congestion but do not improve survival; dose is adjusted to maintain euvolaemia.
- Spironolactone / eplerenone reduces mortality in NYHA II–IV HFrEF; monitor potassium closely (risk of hyperkalaemia especially if eGFR < 30 mL/min/1.73 m²).
- Consider sacubitril–valsartan (Entresto®) as a replacement for ACEi in patients who remain symptomatic (NYHA II–III) on optimised ACEi therapy; a 36-hour washout is required when switching from an ACEi.
- Aboriginal and Torres Strait Islander Australians experience heart failure at 1.7–2.4 times the rate of non-Indigenous Australians, with younger age of onset, higher mortality, and significant barriers to specialist access in rural and remote areas.
- Self-management support including daily weight monitoring, fluid restriction (1.5–2 L/day), sodium restriction (< 2 g/day), and an action plan for weight gain ≥ 2 kg in 48 hours reduces readmissions.
Introduction & Australian Epidemiology
Chronic heart failure (CHF) is a complex clinical syndrome arising from structural or functional cardiac abnormalities that impair ventricular filling or ejection. It is characterised by cardinal symptoms — dyspnoea, fatigue, and fluid retention — and is the final common pathway of many cardiovascular diseases. In Australia, heart failure affects an estimated 480,000–600,000 individuals, with prevalence increasing sharply with age; approximately 1–2 % of the adult population is affected, rising to > 10 % in those aged over 75 years.
Each year in Australia there are approximately 60,000–70,000 hospitalisations where heart failure is the principal diagnosis, making it one of the leading causes of preventable hospital admissions. The Australian Institute of Health and Welfare (AIHW) reports that heart failure contributed to over 12,000 deaths in 2021, and the five-year mortality rate following diagnosis remains approximately 50 %, comparable to many cancers.
The burden of heart failure is not evenly distributed. Aboriginal and Torres Strait Islander Australians experience heart failure at rates 1.7–2.4 times higher than non-Indigenous Australians, with onset at a significantly younger age and substantially higher mortality. Socioeconomic disadvantage, geographic remoteness, and reduced access to guideline-directed medical therapy and specialist cardiology services compound this disparity.
The economic burden is substantial: heart failure costs the Australian health system an estimated .7 billion annually, with hospital admissions accounting for the majority of expenditure. Strategies that improve adherence to guideline-directed medical therapy (GDMT), facilitate early diagnosis, and optimise transitional care from hospital to community have been shown to reduce readmissions and improve quality of life.
Systolic vs Diastolic Heart Failure
The classification of heart failure by left ventricular ejection fraction (LVEF) is fundamental to guiding therapy. The 2021 European Society of Cardiology (ESC) and 2023 American Heart Association/American College of Cardiology (AHA/ACC) guidelines classify heart failure into three phenotypes based on echocardiographic LVEF:
| Feature | HFrEF (Systolic) | HFmrEF (Mid-Range) | HFpEF (Diastolic) |
|---|---|---|---|
| LVEF | ≤ 40 % | 41–49 % | ≥ 50 % |
| Primary abnormality | Impaired myocardial contraction (reduced systolic function) | Mixed; may transition between HFrEF and HFpEF | Impaired myocardial relaxation and increased ventricular stiffness (diastolic dysfunction) |
| Typical patient | Male, post-MI, dilated cardiomyopathy | Older, ischaemic aetiology, comorbid AF | Older female, hypertension, obesity, diabetes, atrial fibrillation, renal impairment |
| Echocardiographic features | Dilated LV, global hypokinesis, raised LVEDP | Intermediate findings | Normal or small LV cavity, LVH, impaired relaxation (E/A ratio < 1), raised E/e′ ratio (> 14), LA enlargement |
| Proportion of HF cases | ~50 % | ~10–15 % | ~40–50 % (increasing with an ageing population) |
| Mortality benefit from GDMT | Strong evidence for all four pillars | Emerging evidence; beta-blockers, ACEi/ARB, SGLT2i recommended | SGLT2i (empagliflozin, dapagliflozin) — first class with mortality/morbidity benefit; diuretics for congestion; treat comorbidities |
Pathophysiology of Systolic Heart Failure (HFrEF)
In HFrEF, the underlying problem is impaired myocardial contractility. This leads to reduced stroke volume and cardiac output, triggering compensatory neurohormonal activation:
- Renin–angiotensin–aldosterone system (RAAS) activation — angiotensin II causes vasoconstriction, sodium retention, and myocardial fibrosis; aldosterone promotes fluid retention and potassium loss.
- Sympathetic nervous system (SNS) activation — catecholamines increase heart rate and contractility acutely but cause cardiomyocyte apoptosis, arrhythmias, and beta-receptor downregulation chronically.
- Natriuretic peptide release — BNP and ANP provide counter-regulatory vasodilation and natriuresis but are overwhelmed by RAAS/SNS dominance.
- Ventricular remodelling — progressive LV dilatation, eccentric hypertrophy, and interstitial fibrosis worsen function and increase mortality.
Pathophysiology of Diastolic Heart Failure (HFpEF)
In HFpEF, the myocardium contracts normally but relaxation is impaired and ventricular compliance is reduced. The underlying mechanisms include:
- Myocardial stiffness — driven by cardiomyocyte hypertrophy, titin hypophosphorylation, and interstitial collagen deposition.
- Systemic microvascular inflammation — endothelial dysfunction reduces nitric oxide availability, impairing cGMP–PKG signalling in cardiomyocytes.
- Increased left atrial pressure — during exertion or tachycardia, the stiff ventricle cannot adequately fill at low pressures, causing pulmonary congestion despite a normal ejection fraction.
- Comorbidity-driven pathophysiology — obesity, diabetes, hypertension, atrial fibrillation, and chronic kidney disease each contribute to the inflammatory milieu.
NYHA Functional Classification & Causes
NYHA Functional Classification
The New York Heart Association (NYHA) functional classification remains the most widely used system for grading symptom severity in heart failure. It should be assessed and documented at every clinical encounter, as it guides therapy intensity, prognosis, and access to services (e.g., cardiac rehabilitation, advanced therapies, palliative care referral).
Causes and Aetiologies of Heart Failure
Identifying the underlying aetiology is essential, as many causes are reversible or amenable to specific treatment. In Australia, the most common aetiologies include:
| Category | Causes | Specific Considerations |
|---|---|---|
| Ischaemic | Coronary artery disease, prior MI, ischaemic cardiomyopathy | Leading cause in Australia (~60–70 % of HFrEF); assess viability for revascularisation |
| Valvular | Aortic stenosis, mitral regurgitation, rheumatic heart disease | Rheumatic heart disease disproportionately affects Aboriginal and Torres Strait Islander Australians |
| Hypertensive | Chronic hypertension leading to LVH and diastolic dysfunction | Most common contributor to HFpEF; aggressive BP control is essential |
| Cardiomyopathy | Dilated (idiopathic), peripartum, alcohol-related, tachycardia-mediated, infiltrative (amyloid, sarcoid), hypertrophic (HCM) | Consider genetic referral for familial DCM; cardiac amyloidosis (ATTR) is increasingly recognised |
| Arrhythmic | Persistent atrial fibrillation, chronic tachycardia | Rate control or rhythm control may improve LVEF |
| Drug/toxin | Anthracyclines, trastuzumab, alcohol, methamphetamine, cocaine | Methamphetamine-related cardiomyopathy is an increasing concern in Australia |
| Other | Thyroid disease, iron overload (haemochromatosis), peripartum cardiomyopathy, myocarditis (viral, immune), congenital heart disease | Iron overload: check ferritin and transferrin saturation; treat with venesection or chelation |
Investigation of Heart Failure
Investigation of suspected heart failure follows a structured approach: (1) confirm the diagnosis, (2) determine the phenotype (HFrEF, HFmrEF, HFpEF), (3) identify the underlying aetiology, and (4) assess severity and comorbidities.
Essential First-Line Investigations
Second-Line & Specialist Investigations
Drug Therapy — Guideline-Directed Medical Therapy (GDMT)
Modern HFrEF management is built on four evidence-based pharmacological "pillars", each with independent mortality and/or morbidity benefit. These should be initiated as early as possible after diagnosis and up-titrated to maximum tolerated evidence-based doses. HFmrEF and HFpEF management has a growing evidence base, particularly with SGLT2 inhibitors.
Pillar 1: RAAS Inhibition — ACE Inhibitors, ARBs, and ARNI
Pillar 2: Evidence-Based Beta-Blockers
Pillar 3: Mineralocorticoid Receptor Antagonists (MRAs)
Pillar 4: SGLT2 Inhibitors
Diuretics — Symptomatic Congestion Management
Loop diuretics are the mainstay of decongestion therapy and are essential for symptom relief but have not been shown to reduce mortality. The goal is to maintain euvolaemia at the lowest effective dose. Thiazide diuretics may be added for diuretic resistance.
Additional Therapies
Device Therapy (Brief Overview)
Device therapy is an important adjunct to pharmacotherapy in selected patients:
- Implantable Cardioverter-Defibrillator (ICD): Indicated for primary prevention in HFrEF with LVEF ≤ 35 % after ≥ 3 months of optimised GDMT, NYHA II–III, and life expectancy > 1 year. Requires LBBB with QRS ≥ 150 ms for CRT-D benefit.
- Cardiac Resynchronisation Therapy (CRT): Indicated for HFrEF with LVEF ≤ 35 %, LBBB with QRS ≥ 150 ms (Class I), QRS 130–149 ms (Class IIa), NYHA II–IV despite optimised GDMT, and sinus rhythm. CRT-P or CRT-D.
- Referral to advanced HF service: Consider for refractory NYHA III–IV despite maximised GDMT and devices, for assessment of heart transplantation, left ventricular assist device (LVAD), or palliative care planning.
Special Populations
Pregnancy
Paediatrics
Elderly (≥ 75 years)
Renal Impairment
Hepatic Impairment
Immunocompromised
Heart failure burden among Aboriginal and Torres Strait Islander Australians is disproportionately high, with onset at a younger age, more advanced disease at presentation, and substantially higher mortality compared with non-Indigenous Australians. Culturally safe, community-centred approaches are essential to improving outcomes.
📚 References
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