Decision support only — use with ESC 2026, NHFA/CSANZ, eTG/PBS and your cardiology service. ESC 2026 defines HFpEF as symptomatic HF with LVEF ≥50% plus objective evidence of raised filling pressure/structural disease. EF alone is not the diagnosis. Confirm HF, identify a treatable cause, then use SGLT2 inhibition + an MRA, dynamic diuresis and phenotype-directed care. Verify doses, renal function, potassium and subsidy locally.
ESC 2026 change HFpEF now has two Class I drug classes
SGLT2 inhibitors remain foundational. The major change is a Class I A recommendation for an MRA in symptomatic HF irrespective of LVEF, using a steroidal MRA or a steroidal/non-steroidal MRA in HFpEF. That recommendation is broader than Australian guidance and PBS access: finerenone's positive HF trial does not itself create a local HFpEF subsidy.
1 Treatment — evidence first, then phenotype
SGLT2 inhibitor I Adapagliflozin / empagliflozin
Evidence: EMPEROR-Preserved and DELIVER reduced worsening-HF events across preserved EF, irrespective of diabetes.
Foundation for symptomatic HFpEF. Minimal titration and early benefit; counsel sick-day withholding and genital infection/euglycaemic DKA risk. Do not oversell a proven mortality effect.
MRA I Anew ESC foundation
Evidence: FINEARTS-HF (finerenone) reduced total worsening-HF/CV-death events (RR 0.84), driven by fewer worsening-HF events; CV death alone was not reduced.
Use steroidal MRA or finerenone as appropriate. Check K⁺/eGFR at baseline, again within about 1–2 weeks, and after titration; follow local protocol. TOPCAT spironolactone was neutral overall and doubled hyperkalaemia; the new class recommendation is broader than that single trial.
Congestion I Adynamic loop-diuretic dosing
Clinical congestion: oedema, raised JVP, orthopnoea, pulmonary congestion or rapid weight gain.
Titrate loop diuretic to euvolaemia, then the lowest effective dose. Improves symptoms/exercise capacity and can reduce HFH. Reduce for symptomatic hypotension, AKI or genuine intravascular depletion, not merely because EF is preserved.
Obesity phenotype IIa BLVEF ≥45% · BMI ≥30
Evidence: STEP-HFpEF (semaglutide) improved symptoms, exercise function and weight; SUMMIT (tirzepatide) also reduced worsening-HF events. Neither establishes a clear mortality benefit.
Consider semaglutide or tirzepatide regardless of diabetes to reduce weight and improve exercise capacity/QoL. Use alongside structured nutrition and activity support; access/cost and tolerability are often the limiting step.
ESC 2026 ACEi/ARB/ARNI may be considered in symptomatic HFpEF to reduce HFH IIb C, but they are not a third foundation: PARAGON-HF, I-PRESERVE and PEP-CHF were neutral overall, while CHARM-Preserved showed only modest HFH benefit. Use when another indication exists or after phenotype-level discussion. ESC has removed “HFmrEF”: LVEF <50% now sits in the HFrEF pathway.
2 Diagnose it — objective evidence, not EF alone
The definition
- Three partsHF symptoms/signs + LVEF ≥50% + objective evidence of raised filling pressure or cardiac structural/functional abnormality.
- New bandsESC 2026: HFrEF <50% · HFpEF ≥50%. The former HFmrEF label has been removed.
- Echo supportLV mass index ≥95 g/m² (women) or ≥115 (men), relative wall thickness >0.42, LAVI >34 mL/m² in sinus rhythm (>40 in AF), E/e′ >9, sPAP >35 mmHg or TR velocity >2.8 m/s.
- BaselineFBC; eGFR + UACR; electrolytes; LFT; TSH; HbA1c; lipids; ferritin + TSAT; ECG; CXR; natriuretic peptide and transthoracic echo ESC I C.
When it's not obvious
- ScoresH2FPEF and HFA-PEFF estimate probability when the diagnosis is uncertain.
- BNP trapNatriuretic peptides may be deceptively low in obesity; AF, age and CKD push them up. Interpret the number, don't worship it.
- Provoke itDiastolic stress echo or exercise right-heart catheter when resting data are equivocal.
3 Don't miss the treatable cause hiding as "HFpEF"
Cardiac amyloidosis — actively look
- SuspectOlder man, bilateral carpal tunnel or spinal stenosis, LVH on echo with low/normal ECG voltages, apical-sparing on strain.
- ConfirmSerum + urine immunofixation and serum free light chains, with DPD/PYP/HMDP scintigraphy when ATTR is suspected ESC I B. If any monoclonal test is abnormal, the scan cannot establish ATTR: involve an amyloid/haematology service and pursue tissue typing where indicated.
- WhyATTR is treatable (tafamidis) — and increasingly common with age.
The other mimics
- CMRUse contrast-enhanced CMR when cardiomyopathy is suspected or aetiology remains uncertain ESC I C.
- HCMHypertrophic cardiomyopathy — assess obstruction and refer for phenotype-specific therapy.
- ConstrictionConstrictive pericarditis — surgically correctable; look for it.
- ValveSevere AS or MR can masquerade — echo carefully.
- OtherInfiltrative (sarcoid), high-output states. "HFpEF" is a label, not a final diagnosis.
4 The traps & the whole patient
Don't harm
- VolumeAim for euvolaemia. Excess diuresis can cause hypotension, AKI or true intravascular depletion, but fear of “preload dependence” should not leave a congested patient wet.
- MRA safetyHyperkalaemia and renal dysfunction are predictable. Check baseline K⁺/eGFR, repeat within about 1–2 weeks and after dose changes, and review interacting drugs.
- NSAIDsAvoid NSAIDs/COX-2 inhibitors: fluid retention, renal injury and more HFH ESC III B.
- PH-HFpEFDisproportionate pulmonary hypertension or RV dysfunction → clarify haemodynamics and refer. Do not empirically start PAH-specific therapy for presumed group 2 PH.
- Don't anchorDon't settle on "HFpEF" before excluding the treatable mimics above.
The whole patient
- ComorbidityTreat hypertension, AF (rate/rhythm + anticoagulation), obesity, CAD, CKD, diabetes and sleep-disordered breathing. Beta-blockers are for a specific indication, not routine HFpEF disease modification.
- ProgramMultidisciplinary HF program I B, self-management education I A and personalised exercise/cardiac rehab I B.
- BariatricBMI ≥35 with persistent obesity despite structured lifestyle + medication: metabolic surgery may be considered IIb C.
- FollowTrack symptoms, volume, BP, rhythm, renal function/K⁺, weight and functional capacity; reassess the diagnosis when the course does not fit.
Sources.
Primary source: 2026 ESC Guidelines for the management of heart failure (Eur Heart J, 28 Aug 2026; doi:10.1093/eurheartj/ehag100), mapped to NHFA/CSANZ Australian guidance, eTG and PBS restrictions; ESC/ERS 2022 pulmonary hypertension guideline for PH-LHD; ESC cardiac amyloidosis diagnostic statement.
Seminal and update trials: EMPEROR-Preserved (empagliflozin) and DELIVER (dapagliflozin); FINEARTS-HF (finerenone); TOPCAT and Aldo-DHF (spironolactone); PARAGON-HF (sacubitril/valsartan), CHARM-Preserved (candesartan), I-PRESERVE (irbesartan), PEP-CHF (perindopril); STEP-HFpEF/STEP-HFpEF DM (semaglutide) and SUMMIT (tirzepatide).
Caveats: ESC 2026 is ahead of Australian adoption. FINEARTS-HF was positive for recurrent worsening-HF/CV-death events but not CV death alone; TOPCAT was neutral for its primary outcome. SGLT2i and MRA benefits are chiefly fewer HF events, not a licence to promise survival benefit. At the latest official Australian listing, finerenone PBS subsidy was for CKD with T2DM rather than HFpEF; incretin access for obesity/HFpEF remained indication- and funding-dependent. Recheck PBS at prescribing. HFpEF is a clinical/imaging diagnosis, not an EF result.