Heart failure has never had a single, globally agreed definition — until now. In June 2026, four of the world's leading cardiovascular societies published a Second Universal Definition of Heart Failure, co-authored by the AHA, ACC, ESC, and World Heart Federation, with collaboration from the HFSA, HFA, and JHFS.[1] The consensus appeared simultaneously in Circulation, JACC, and the European Heart Journal, and was covered in the August 11 issue of JAMA as clinical news for American physicians.
The stakes are practical. An estimated 64 million people worldwide live with heart failure, yet the label itself has been applied inconsistently — with "preserved ejection fraction" defined anywhere from EF ≥40% to ≥55% depending on which guideline you consulted. Different definitions made cross-trial comparisons unreliable, left borderline patients in limbo, and created confusion in clinical documentation. The new document fixes that.
Heart failure is now defined as a clinical syndrome caused by structural or functional cardiac abnormality, producing symptoms and signs due to inadequate cardiac output or elevated intracardiac pressures.[1] Critically, a natriuretic peptide elevation is now required for a diagnosis of HFpEF when resting hemodynamics are uncertain — moving "preserved EF" away from purely clinical gestalt toward an objective biomarker anchor. The threshold: BNP ≥35 pg/mL or NT-proBNP ≥125 pg/mL.
The staging framework reaffirms the four-stage A–D continuum and centers Stage B — "pre-HF" — as the critical window for intervention. Stage B includes anyone with structural disease (LVH, regional wall motion abnormalities, elevated filling pressures) or biomarker elevation who has no symptoms yet. Treating physicians are directed to act here, not after symptoms arrive.
What Changed from the 2021 Definition
The 2021 ESC Heart Failure Guidelines and the 2022 AHA/ACC/HFSA Guideline each defined HFpEF slightly differently. The new document harmonizes the cutpoint at EF ≥50% for HFpEF and 40–49% for HFmrEF. It also formally incorporates the category of "HFrecEF" — improved EF — as a distinct phenotype, not a recovery state. Patients with previously reduced EF who respond to therapy but then stop medications often relapse: recognizing HFrecEF as a permanent phenotype underscores that treatment is indefinite.[1]
The document also formally endorses SGLT2 inhibitors across all EF categories — the only drug class to have demonstrated benefit in HFrEF, HFmrEF, HFpEF, and HFrecEF in randomized trials.[2]
Clinical Context
Heart failure affects approximately 6.7 million Americans, with nearly half carrying a preserved EF diagnosis. The definitional ambiguity around HFpEF has historically made it harder to prove treatment benefit in trials — trials that enrolled EF ≥40% included very different patients from those enrolling EF ≥55%. The harmonized cutpoint should improve future trial comparability.
Your 68-year-old with exertional dyspnea, an EF of 52%, and an NT-proBNP of 145 pg/mL now unambiguously has HFpEF under this definition — no more hedging. Stage B patients in your clinic without symptoms deserve optimization of RAAS, blood pressure, and weight now, not after they decompensate. And any patient whose EF improved on guideline therapy still has HFrecEF and still needs lifelong treatment.
Limitations
A consensus definition is not a guideline. Specific drug choices, targets, and monitoring frequencies require reference to the 2022 AHA/ACC/HFSA Guideline and the 2023 ESC Focused Update. The biomarker threshold for HFpEF (NT-proBNP ≥125 pg/mL) will misclassify some obese patients, who run lower natriuretic peptide levels even with elevated filling pressures.
References
[1] Metra M, et al. AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026). Circulation. 2026. DOI: 10.1161/CIR.0000000000001455. [Full Text]
[2] Packer M, et al. Cardiovascular and Renal Outcomes with Empagliflozin in Heart Failure (EMPEROR-Reduced). N Engl J Med. 2020;383(15):1413-1424. PMID: 32865377. [PubMed]