Heart Failure with Preserved Ejection Fraction (HFpEF)

HFpEF — formerly called diastolic heart failure — is the syndrome of heart failure in a patient whose ejection fraction is normal. The ventricle is stiff and fills poorly at high pressure rather than emptying weakly. It accounts for roughly half of all heart failure, and four-year mortality is around 32%: lower than HFrEF, but a long way from benign.

For a reduced ejection fraction, see Heart Failure with Reduced Ejection Fraction, which also covers the shared history, examination and non-drug management in more detail.

The single most important change since these notes were written: HFpEF is no longer a condition with no disease-modifying treatment. It now has a first-line drug class with mortality and hospitalisation evidence, a second, and a third for the obesity phenotype.

Diagnosis

The Australian guideline requires all three of the following:

Component	Requirement
Clinical	Symptoms ± signs of heart failure
LVEF	≥50%
Objective evidence	Relevant structural heart disease — LV hypertrophy or left atrial enlargement — and/or diastolic dysfunction with demonstrated high filling pressure

HFpEF has always been harder to pin down than HFrEF, because the objective marker that defines the other half of the syndrome — the ejection fraction — is by definition normal, leaving non-specific symptoms and signs. Treat it as a diagnosis to be positively established, not a label applied to any breathless older patient with a normal echo.

High filling pressure can be demonstrated by:

• Echocardiography — at least three of: septal e′ <7 cm/s or lateral e′ <10 cm/s; average E/e′ >14; left atrial volume index >34 mL/m²; tricuspid regurgitation velocity >2.8 m/s.
• Natriuretic peptides — using the rule-in thresholds (BNP >400; NT-proBNP >450 under 50 years, >900 at 50–75, >1800 over 75). Remember obesity lowers natriuretic peptides and AF and renal impairment raise them — a mid-range value in an obese patient does not exclude HFpEF.
• Invasive measurement — PCWP ≥15 mmHg, or LV end-diastolic pressure >16 mmHg.
• Exercise testing — worth considering when suspicion persists despite a resting study that does not meet criteria, since filling pressures may only rise on exertion. It also gives an objective measure of exercise capacity and can assess for ischaemia.

An LVEF of 41–49% is not HFpEF under the Australian classification — see the mildly reduced band.

Before settling on HFpEF, exclude the treatable mimics

“HFpEF” is a syndrome, not an aetiology, and several specific diagnoses hide inside it:

• Cardiac amyloidosis — increasingly recognised and now treatable with transthyretin stabilisers. Suspect with marked LVH not explained by blood pressure, low-voltage ECG despite LVH on echo, bilateral carpal tunnel syndrome, or intolerance of usual heart failure drugs.
• Hypertrophic cardiomyopathy — see Cardiomyopathies.
• Constrictive pericarditis — potentially curable surgically.
• Valvular disease, particularly aortic stenosis and mitral regurgitation.
• High-output states — anaemia, thyrotoxicosis, arteriovenous fistula.
• Non-cardiac causes of the same symptoms — chronic lung disease, obesity itself, deconditioning, renal or hepatic disease, pulmonary hypertension.

Who gets it

Older patients, more often women, and almost always with an accumulation of comorbidities: hypertension (the dominant driver), obesity, atrial fibrillation, diabetes, chronic kidney disease and sleep apnoea. Prevalence rises steeply with age. These comorbidities are not incidental — treating them is much of the treatment.

Management

1. SGLT2 inhibitor — first-line for everyone

Dapagliflozin or empagliflozin 10mg daily, regardless of diabetes status. This is the change that broke the therapeutic deadlock: EMPEROR-Preserved was the first adequately powered HFpEF outcome trial to meet its primary endpoint, and DELIVER confirmed it. SGLT2 inhibitors are now strongly recommended in heart failure regardless of ejection fraction.

PBS-wise, empagliflozin has been listed since 1 November 2023 for chronic heart failure with an LVEF >40%, and dapagliflozin since 1 March 2024 for HFpEF. The same practical points apply as in HFrEF — sick-day plan for euglycaemic ketoacidosis, cease three days before surgery, expect a small early eGFR dip, counsel about genitourinary infection, and reduce the loop diuretic by 25–50% at initiation if euvolaemic.

2. Finerenone — the emerging second pillar

FINEARTS-HF (2024) was the first trial to show clear benefit from a mineralocorticoid receptor antagonist in heart failure with an LVEF ≥40%, reducing the composite of cardiovascular death and worsening heart failure events by about 16%, with the benefit driven by fewer worsening-heart-failure events — and it held in patients already taking an SGLT2 inhibitor. Finerenone is a non-steroidal MRA, pharmacologically distinct from spironolactone and eplerenone.

The 2025 international guidance now recommends finerenone as a second pillar in HFpEF, with spironolactone suggested where finerenone is unavailable. In Australia, finerenone’s subsidised indication has been diabetic kidney disease rather than heart failure — confirm current PBS status before prescribing for this indication. Monitor potassium and renal function as for any MRA.

3. GLP-1 receptor agonists — for the obesity phenotype

For patients whose HFpEF sits on a background of obesity, semaglutide (STEP-HFpEF) and tirzepatide (SUMMIT) produced large improvements in symptoms, physical limitation, exercise capacity and weight, with SUMMIT also showing a reduction in worsening heart failure events or cardiovascular death. These are strongly recommended in obesity-related HFpEF to reduce weight and improve symptoms and quality of life. This is a genuinely distinct treatment target — the obesity is part of the disease, not a bystander. See Obesity.

4. ARNI — selectively

Sacubitril/valsartan is recommended in HFpEF where the LVEF sits at the lower end of the preserved range, particularly in women — the subgroups in which the trial evidence was most favourable. It is not a treatment for all HFpEF.

5. Treat the drivers — still the backbone

• Hypertension — the single most important target. See Hypertension.
• Atrial fibrillation — rate and rhythm control matter more here than in HFrEF, because a stiff ventricle depends on atrial contraction and adequate filling time. See Atrial Fibrillation.
• Obesity — weight loss improves symptoms and exercise capacity.
• Sleep apnoea — see Obstructive Sleep Apnoea.
• Ischaemia, diabetes, CKD and anaemia/iron deficiency — each treated on its own merits, and each worsens HFpEF when neglected.

6. Congestion — and the cautions specific to HFpEF

Loop diuretics relieve congestion and remain the mainstay for symptom control, but a stiff ventricle is preload-dependent, so it is easy to overshoot:

• Diuretics — over-diuresis drops cardiac output and blood pressure and causes renal impairment. Use the lowest effective dose and down-titrate once euvolaemic.
• Nitrates and other venodilators — reduce preload and cardiac output; routine use is not beneficial.
• Hydralazine — may provoke dynamic LV outflow obstruction.
• Digoxin — no role unless required for AF rate control.

7. Non-drug care

As for HFrEF: education, a heart failure action plan, daily weights, moderate fluid and salt restriction, vaccination, depression screening, review within 7 days of hospital discharge, and HMR/GPMP/Team Care Arrangements. Exercise training is particularly worthwhile in HFpEF — supervised programs improve exercise capacity and quality of life; refer to cardiac rehabilitation or an exercise physiologist.

Referral

Refer for cardiology assessment to confirm the diagnosis where it rests on borderline criteria, when an infiltrative or hypertrophic cardiomyopathy is suspected, for persisting symptoms despite treating the drivers, and for consideration of the newer agents where PBS access is unclear. The gold standard for a confident HFpEF diagnosis remains specialist assessment with echocardiography, and increasingly exercise or invasive haemodynamic testing.