#heart-failure #guideline #HFrEF #HFpEF #foundational-medical-therapy #decompensated-heart-failure #cardiac-amyloidosis

2026 ESC Guidelines for the Management of Heart Failure

Authors, Journal, Affiliations, Type, DOI

Authors: Lars Køber (Rigshospitalet and Herlev-Gentofte Hospital, Copenhagen) and Marianna Adamo (University of Brescia) — joint chairpersons and corresponding authors; Anne-Christine Ruwald and Daniela Tomasoni — Task Force co-ordinators
Journal: European Heart Journal (2026) 47, 5346–5457
Affiliations: ESC Task Force with the special contribution of the Heart Failure Association; endorsed by the European Association for Cardio-Thoracic Surgery (EACTS)
Type: ESC Clinical Practice Guideline — replaces the 2021 ESC HF guideline and its 2023 focused update
DOI: https://doi.org/10.1093/eurheartj/ehag100

Overview

The 2026 ESC guideline rewrites the classification of heart failure rather than merely updating its treatment. HFmrEF is abolished: HF failure is now divided into two phenotypes only — HFrEF at LVEF <50% and HFpEF at LVEF ≥50% — on the argument that patients at LVEF 41–49% resemble HFrEF in aetiology, pathophysiology and treatment response. The ACC/AHA stages A–D are adopted for the first time, and "acute heart failure" is replaced throughout by decompensated heart failure (DHF). Treatment terminology is rebuilt as well: "GDMT" gives way to FMT (foundational medical therapy — Class I with proven morbidity or mortality benefit in the general HF population), AMT (additional medical therapy) and GDIT (guideline-directed interventional therapy).

The therapeutic consequence is the guideline's headline change: SGLT2 inhibitors and MRAs are now Class I, Level A for all symptomatic HF regardless of ejection fraction, making MRA a foundational HFpEF drug. Elsewhere the revision is a mix of upgrades supported by new trials — LVAD to Class I, mitral TEER to Class I, continuous inotropes and remote PA monitoring to IIa, TTR silencers and stabilizers to I/A — and deliberate downgrades where evidence weakened, notably CRT instead of RV pacing for AV block (I→IIa) and catheter ablation for AF in HF (IIa/B→IIa/C, narrowed to HFrEF).

Keywords

Guidelines · European Society of Cardiology · heart failure · HFrEF · HFpEF · decompensated heart failure · advanced heart failure · stages of heart failure · heart failure phenotypes · prevention · pharmacotherapy · foundational medical therapy · additional medical therapy · guideline-directed interventional therapy · cardiac resynchronization therapy · implantable cardioverter-defibrillator · aetiology · diagnosis · comorbidities · cardiac amyloidosis

Key Takeaways

Definition and classification — what changed

HF is redefined as two phenotypes. HFrEF: LVEF <50% plus symptoms and/or signs. HFpEF: LVEF ≥50% plus symptoms and/or signs plus objective evidence of structural/functional abnormality consistent with diastolic dysfunction or raised filling pressures, supported by raised natriuretic peptides.
HFmrEF has been removed. The Task Force cites similar aetiology, similar pathophysiology (reduced contractility rather than increased stiffness), similar treatment response, and the risk that LVEF 41–49% deteriorates over time.
HFpEF now additionally requires that LVEF has never previously been <50% — a new criterion that excludes recovered-EF patients from the HFpEF label.
Stages A–D adopted, aligned with the 2022 AHA/ACC/HFSA guideline, to bring prevention and early detection into the framework.
Improved LVEF is defined as an absolute rise of ≥10% reaching at least >40%; these patients have a better prognosis but should remain on optimal therapy except in selected cases.
New treatment nomenclature. FMT = Class I, proven morbidity/mortality benefit in unselected HF (HFrEF: beta-blocker, ACE-I/ARNI/ARB, MRA, SGLT2-I; HFpEF: MRA, SGLT2-I). AMT = Class IIa/IIb, or Class I for symptoms/QoL only, or Class I in a specific subset. GDIT = all recommended devices and interventions. GDMT now covers FMT plus AMT.
Decompensated HF replaces acute HF: acute or gradual onset of symptoms and/or signs severe enough to require urgent attention and treatment initiation or intensification, whether that ends in admission, an ED visit or an unplanned ambulatory visit. Worsening HF is the deterioration; DHF is the requirement for treatment modification.

Epidemiology and prognosis

Prevalence 1–3% of adults, with European estimates of 12–58 cases per 1000 people; incidence 2–13 per 1000 person-years in Europe, from <1/1000 at ages 45–54 to >12/1000 above 74.
Age-adjusted incidence has fallen over three decades, but crude incidence is rising with population ageing, and incidence in younger adults is stagnant or increasing.
Nearly half of all HF in population samples is HFpEF. Mean onset: HFpEF 77 years, 55% female; HFrEF 72 years, 71% male.
Five-year overall survival remains <60%. Contemporary Danish data: 5-year mortality 15% under age 65 and 39% at 65–79.
Advanced HF affects 5.1–7.7% of patients with HF (Framingham) and carries >40% one-year mortality on medical therapy.
DHF: in-hospital death 3–10%, 20–30% at one year, >50% at five years; one-year rehospitalisation 35–44%; up to 50% of patients require treatment intensification in the ED or an outpatient setting.

Prevention and stage B

Diabetes, hypertension, obesity and smoking account for approximately 50% of all HF events overall — 75–80% below age 55, 30–40% above 75.
SGLT2-I Class I/A in T2DM at risk of HF (multiple ASCVD risk factors or established ASCVD) and in T2DM with CKD; finerenone Class I/A in T2DM with CKD.
GLP-1 RA Class IIa/A in T2DM with at least one additional CV risk factor; statin IIa/A in high ASCVD risk.
Strict blood pressure control to SBP <130 mmHg, Class I/A, in hypertension or stage B HF.
Stage B: ACE-I or ARB Class I/A if LVEF ≤40%; beta-blocker Class I/B1 if LVEF <50%; eplerenone Class I/B1 after MI with LVEF ≤40% plus HF or diabetes.
REDUCE-AMI argues against routine beta-blockade after MI with preserved LVEF. Risk scores: AHA PREVENT-HF, ESC SCORE2-HF and ESC SMART2-HF.

Diagnosis

Age-adjusted NT-proBNP thresholds replace the single cut-off: ≥125 pg/mL under 50 years, ≥250 pg/mL at 50–74, ≥500 pg/mL at 75 or older; BNP >35 pg/mL. The single <125 pg/mL rule-out is retained in prose but more than 75% of healthy people over 80 exceed it.
Urine albumin-to-creatinine ratio added to baseline investigations alongside eGFR, per KDIGO.
Simplified HFpEF echocardiographic criteria (Table 10): LV mass index ≥95 g/m² (female) or ≥115 g/m² (male), or relative wall thickness >0.42; LA volume index >34 mL/m² in sinus rhythm or >40 mL/m² in AF; E/e′ >9 at rest (≥15 more specific, less sensitive); estimated systolic PA pressure >35 mmHg or TR velocity >2.8 m/s. Probability rises with the number of abnormal parameters.
HFpEF diagnostic gold standard is invasive haemodynamic exercise testing — PCWP ≥15 mmHg at rest, ≥25 mmHg with exercise, or LVEDP ≥16 mmHg at rest — but it is reserved for diagnostic uncertainty because it is expensive and unavailable in many centres.
Cardiac amyloidosis: serum and urine immunofixation, serum free light chains and DPD/PYP/HMDP bone scintigraphy as initial testing, Class I/B. Genetic testing in cardiomyopathy Class I/C. ¹⁸F-FDG-PET for suspected cardiac sarcoidosis IIa/C. Endomyocardial biopsy IIa/C.
Review the proportion of RV pacing in all patients with a CIED and de novo or worsening HFrEF, IIa/C — new. Electrical cardioversion as a diagnostic tool in persistent AF IIb/C.
Viability testing to select patients for revascularisation: the guideline states the evidence is lacking.

Foundational and additional medical therapy

SGLT2-I Class I/A and MRA Class I/A in all symptomatic HF, independent of LVEF.
For HFpEF, the MRA recommendation explicitly covers steroidal (spironolactone) and non-steroidal (finerenone) agents; for HFrEF the evidence rests on steroidal MRAs only.
The Task Force accepts the primary composite endpoints where individual mortality was not reduced — in HFpEF the SGLT2-I and MRA benefits are driven by HF hospitalisation.
HFrEF FMT: beta-blocker I/A; ACE-I or ARNI I/A; switching ACE-I/ARB to ARNI I/B1; ARB if ACE-I/ARNI not tolerated I/A.
Uptitration at least every 1–2 weeks to target doses, Class I/C; continuation at the highest tolerated doses lifelong, Class I/C, including after LVEF improvement.
Additional therapy in HFrEF: cardiac glycoside IIa/B1 (upgraded from IIb), ivabradine IIa/B1 (or IIa/C if beta-blocker intolerant), hydralazine/ISDN IIa/B2 in self-identified Black patients and IIb/C if renin-axis therapy not tolerated, vericiguat IIb/B1 at LVEF <45%, gradual FMT discontinuation IIb/C in complete remission after a reversible cause.
HFpEF: ACE-I/ARB/ARNI IIb/C only. ARNI may be considered at lower LVEF on the basis of a PARADIGM-HF/PARAGON-HF meta-analysis showing benefit below LVEF 60–65%.
Loop diuretics are Class I/A for congestion with explicit acknowledgement that this reflects clinical acceptance rather than a randomised trial. Dynamic individualised dosing is Class I/A.
Potassium binders: no recommendation — insufficient evidence for clinical benefit, and REALIZE-K showed a signal toward more HF deterioration with sodium zirconium cyclosilicate.
Target doses are tabulated (Table 11) for ACE-Is, ARNI, ARBs, beta-blockers, steroidal and non-steroidal MRAs, SGLT2-Is, digoxin, digitoxin, ivabradine and vericiguat.

Device therapy

ICD: secondary prevention I/A; primary prevention in ischaemic HFrEF with LVEF ≤35% after ≥3 months of FMT I/B1; non-ischaemic IIa/B1. Not recommended within 40 days of MI (III/B1) or in NYHA IV unless a candidate for CRT, LVAD or transplant (III/C). Wearable defibrillator IIb/C.
CRT: LBBB with QRS ≥150 ms in sinus rhythm, LVEF ≤35% — I/A. LBBB 130–149 ms — IIa/C (previously Class I at ≥120 ms); non-LBBB ≥150 ms — IIa/C; non-LBBB 130–149 ms — IIb/C; QRS <130 ms — III/A.
CRT instead of RV pacing for high-degree AV block — IIa/B1, downgraded from Class I/A.
Upgrade to CRT in a paced or ICD patient who develops worsening HF with a significant RV pacing burden — IIa/B1, supported by BUDAPEST-CRT Upgrade (≥20% RV pacing, QRS ≥150 ms; HR 0.27).
Conduction system pacing: no recommendation. No RCT with patient-centred outcomes exists in HFrEF.

Decompensated heart failure

Four clinical categories: decompensated left-sided HF, decompensated right-sided HF, acute pulmonary oedema, and cardiogenic shock.
Rule-out thresholds NT-proBNP <300 pg/mL, BNP <100 pg/mL, MR-proANP <120 pg/mL; age-related rule-in >450 (<50 y), >900 (50–74 y), >1800 (>74 y); NT-proBNP >5000 pg/mL implies very high risk and generally warrants admission.
Cardiogenic shock is critical end-organ hypoperfusion from primary cardiac dysfunction; no specific blood pressure threshold, and lactate >2 mmol/L is required as biochemical evidence. SCAI stages A to E.
Intravenous loop diuretics Class I/A; short-term IV acetazolamide or oral hydrochlorothiazide IIa/B1 (new, ADVOR and CLOROTIC — decongestion only, no hard-endpoint benefit); urinary sodium-guided diuretic therapy IIb/B1 (PUSH-AHF, ENACT-HF).
Satisfactory diuretic response is defined as urine sodium ≥70 mEq/L at 2 hours or urine output ≥100 mL/h over the first 6 hours.
In-hospital SGLT2-I after initial stabilisation — Class I/B1, new (EMPULSE, SOLOIST-WHF).
Rapid FMT initiation and uptitration before discharge with frequent visits over the first 6 weeks — Class I/B2 (STRONG-HF). The prose calls the traditional sequential approach "suboptimal" and prefers simultaneous implementation, but explicitly declines to recommend a number or sequence of drug classes because no RCT exists.
Vasodilators IIb/C only when SBP >110 mmHg; inotropes IIb/C; vasopressors IIb/C with norepinephrine first line; routine opiates III/C.
Temporary MCS: Shock Team Class I/C; microaxial flow pump in selected STEMI-related shock without risk of hypoxic brain injury IIa/B1 (DanGer Shock, HR 0.74); temporary MCS in unselected MI shock III/B1; IABP in unselected shock III/B1. No RCT evidence in non-infarct-related shock, and VA-ECLS has no mortality benefit (ECLS-SHOCK, RR 0.98).
No recommendation on anticoagulation for thromboembolism prophylaxis in DHF — no trial exists.

Advanced heart failure

Definition (Table 14) requires all of: NYHA III–IV; severe cardiac dysfunction by at least one criterion (LVEF ≤30%, isolated RV failure, non-operable severe valve or congenital disease, or high natriuretic peptides with severe diastolic dysfunction); ≥2 unplanned visits or hospitalisations in 12 months, or ≥1 low-output episode needing inotropes; and severe exercise limitation (6-minute walk <300 m or peak VO₂ <12–14 mL/kg/min). A low LVEF is common but not required — HFpEF and restrictive cardiomyopathies qualify.
Early consultation with an advanced HF centre — Class I/A. Cardiopulmonary exercise testing and right heart catheterisation are Class I/C as part of transplant and LVAD evaluation.
Durable MCS (LVAD) — Class I/C, upgraded from IIa, across bridge-to-transplant, bridge-to-candidacy, bridge-to-recovery and destination therapy. Contemporary 2-year survival is comparable to transplantation: MOMENTUM 3 reported 79% at 2 years and 58.4% at 5 years.
Histopathological examination of explanted heart tissue in non-ischaemic HF — IIa/C, new.
Continuous inotropes IIa/C, upgraded from IIb. Down-titration of beta-blockers or ivabradine IIa/C when hypoperfusion persists. Kidney replacement therapy IIa/C; ultrafiltration IIb/C.
Heart transplantation Class I/C and remains the gold standard despite never having been tested in an RCT; post-transplant one-year survival 80–90%, median survival around 12.5 years.

Cardiovascular comorbidities

Atrial fibrillation coexists in more than half of patients with HF, and HF in more than a third with AF. Anticoagulation is guided by CHA₂DS₂-VA (sex category removed), Class I/A: score ≥2 is an indication, score 1 should be considered an indication. DOACs preferred over VKAs (I/B1) except with mechanical valves or moderate-severe mitral stenosis. Anticoagulate all patients with HCM or cardiac amyloidosis and AF regardless of score.
Rate control: lenient target (resting HR <110 bpm) should be the initial strategy; beta-blockers are Class I/C first line in stable HFrEF with AF (upgraded from IIa). Digoxin IIa/C when rate remains high or beta-blockers are not tolerated. AV node ablation plus CRT IIa/B1 in severely symptomatic permanent AF with poor rate control and ≥1 HFH. IV amiodarone or digoxin IIb/C in haemodynamically unstable HFrEF with AF. Urgent cardioversion I/C in DHF with rapid rates and instability.
Catheter ablation for AF: IIa/C, restricted to selected HFrEF patients who meet all three criteria — high AF burden, less than one year of continuous persistent AF, and a clear cause–effect relationship between AF and HF. This narrows and downgrades the 2021 recommendation (IIa/B).
Revascularisation: for persistent angina despite FMT and antianginals, revascularisation is Class I/C (upgraded from IIa). For outcome benefit in HFrEF with LVEF ≤35% and multivessel disease, CABG is IIa/B1 — and the Task Force explicitly acknowledges that this conflicts with the 2024 ESC chronic coronary syndromes guideline, which gives CABG Class I.
Aortic stenosis: valve intervention I/B1 in severe high-gradient AS regardless of LVEF, and in low-flow low-gradient AS with HFrEF. DapaTAVI (n=1,222, HF plus ≥1 risk factor) reduced death or worsening HF at one year by 28%, mainly through worsening HF events — supporting SGLT2-I in this setting.
Secondary mitral regurgitation: mitral TEER is Class I/B1 (upgraded from IIa) in haemodynamically stable symptomatic HFrEF with persistent severe ventricular secondary MR despite optimised FMT and CRT, meeting the Table 19 criteria (LVEF 20–50%, LVESD ≤70 mm, sPAP ≤70 mmHg, ≥1 HFH or BNP ≥300/NT-proBNP ≥1000, no advanced HF, no severe RV dysfunction). TEER outside those criteria for symptom relief is IIb/C. A new atrial-versus-ventricular secondary MR classification is introduced.
Tricuspid regurgitation: severe TR affects 9–20% in both phenotypes; three transcatheter trials showed QoL benefit without reducing death or HFH at one year, and all were unblinded.
Hypertension: no RCT has tested specific targets in HF. In HFrEF, non-dihydropyridine CCBs and central sympatholytics (moxonidine) are contraindicated; asymptomatic hypotension should be accepted to maintain FMT doses. In HFpEF, preserve preload reserve and avoid hypotension.
Stroke: stroke risk appears independent of rhythm (2.0 per 100 patient-years in sinus rhythm versus 2.87 in AF), and no trial supports routine anticoagulation in HFrEF in sinus rhythm.

Non-cardiovascular comorbidities

Obesity: the obesity-related HFpEF phenotype accounts for 30–40% of HFpEF in Europe and 60–70% in North America. Semaglutide or tirzepatide IIa/B1 for symptomatic HF, LVEF ≥45% and BMI ≥30 kg/m² regardless of diabetes status; bariatric surgery IIb/C at BMI ≥35 when structured lifestyle change plus weight-reducing medication has failed. Adjust peak VO₂ for lean body mass rather than body weight.
Diabetes: SGLT2-Is recommended in all HF with T2DM independent of HbA1c; not indicated in type 1 diabetes because of ketoacidosis risk (2–3%). Saxagliptin and thiazolidinediones increase HF hospitalisation by about 30% and are contraindicated.
CKD: 30–40% of chronic HF patients, up to 50% in HFpEF. FMT should be initiated and maintained in CKD — relative risk reduction is unchanged and absolute benefit is greater. A creatinine rise of <50% above baseline with eGFR still >15 mL/min/1.73 m² is acceptable and should not prompt interruption.
Iron deficiency — the definition has changed. The 2021 definition (ferritin <100 ng/mL, or 100–299 with TSAT <20%) is criticised as unreliable; the Task Force now supports TSAT <20% alone as more sensitive, more specific and better at identifying IV iron responders. IV iron is I/B1 for symptoms and QoL and IIa/B1 to reduce HFH, in HFrEF only. Erythropoiesis-stimulating agents are contraindicated after RED-HF.
Lung disease and sleep-disordered breathing: prefer cardioselective beta-blockers (bisoprolol, metoprolol succinate, nebivolol); do not stop beta-blockers during a COPD exacerbation. ASV IIb/C in predominant obstructive sleep apnoea — new — but III/A in predominant central sleep apnoea after SERVE-HF. ADVENT-HF was neutral for outcomes in a mostly obstructive population.
Anxiety, depression and frailty: assessment IIa/C. Depression affects 20% of patients and impairs FMT adherence; CBT has the best evidence, SSRIs are safe but no better than placebo, tricyclics should be avoided.
Vaccination IIa/C; NSAIDs and COX-2 inhibitors III/B2.

Multidisciplinary management, rehabilitation and follow-up

Multidisciplinary HF management programme I/B1; education and self-management I/A; adherence interventions including health-literacy assessment and polypharmacy review I/B2.
Exercise training is now two Class I recommendations — within exercise-based cardiac rehabilitation (I/B1) and outside it on a long-term basis (I/B2). Cardiac rehabilitation in LVAD I/B1; in DHF IIa/B1, "as soon as safely possible".
Remote pulmonary artery pressure monitoring IIa/B1, upgraded from IIb and restricted to NYHA III with an HFH in the past 12 months. Non-invasive telemonitoring IIb/B1. Device-based monitoring has little evidence of outcome benefit.
Follow-up intervals by stage (Figure 22): stage A every 3–5 years, stage B annually, stage C every 6–12 months, stage D every 3–6 months. Routine biomarker-guided diuretic therapy is explicitly not supported, and the necessity of cardiologist-led follow-up is described as uncertain.
Palliative care: proactive discussion of trajectory, goals of care and advance care planning I/B1; access to an integrated palliative care multidisciplinary team I/B2.

Specific conditions

Pregnancy: pre-conception counselling I/C; switch non-selective to beta1-selective beta-blockers (metoprolol, bisoprolol) I/C; ACE-Is, ARBs, ARNIs, MRAs, ivabradine and SGLT2-Is are Class III in pregnancy — the explicit inclusion of SGLT2-Is is new. Management defers to the 2025 ESC guideline on cardiovascular disease in pregnancy.
Cardiac amyloidosis: suspect in HF with increased LV wall thickness and any red flag, particularly above age 65. Non-invasive diagnosis is accepted only for ATTR-CA (grade 2–3 diphosphonate uptake with no monoclonal protein). Treatment with a TTR silencer (vutrisiran) or stabiliser (tafamidis or acoramidis) in variant or wild-type ATTR-CA, NYHA I–III — Class I, Level A. Patisiran is described but excluded from the recommendation because APOLLO-B reported no morbidity or mortality data. No head-to-head or combination trial of silencers versus stabilisers exists. Anticoagulate AF in cardiac amyloidosis regardless of CHA₂DS₂-VA score; transoesophageal echo before cardioversion regardless of prior anticoagulation; avoid digoxin.
Adult congenital heart disease: HF accounts for 26–46% of deaths, with higher rates in complex lesions; management defers to the 2020 ESC ACHD guideline.

Contradictions this source creates — flagged for the wiki

HFmrEF no longer exists as an ESC phenotype, while AHA/ACC 2022 retains HFmrEF (41–49%) and the wiki's HFrEF/HFpEF pages were built on the four-phenotype model.
MRA is Class I in HFpEF here but COR 2b in AHA 2022 — the largest transatlantic divergence created by this guideline, and it rests on a meta-analysis pooling TOPCAT and FINEARTS-HF rather than a positive trial of spironolactone in HFpEF.
CRT for LBBB 130–149 ms was Class I in 2021 and is IIa here, and the lower QRS boundary moved from 120 to 130 ms.
Catheter ablation for AF in HF is narrowed and its evidence level reduced (IIa/B → IIa/C, restricted to HFrEF), against a body of trial evidence (CASTLE-AF, CASTLE-HTx) that the 2021/2023 documents read more favourably.
CABG in HFrEF with LVEF ≤35% and multivessel disease is IIa/B1 here but Class I/B in the 2024 ESC chronic coronary syndromes guideline. The Task Force names the discrepancy and attributes it to differing populations and evidence grading rather than claiming resolution.
The iron deficiency definition changes to TSAT <20% alone, but every trial supporting the IV iron recommendation enrolled by the old ferritin-based definition. The guideline says this openly — it endorses the new definition while acknowledging the evidence base does not use it.
The ESC 2023 focused update gave SGLT2 inhibitors Class I, Level A in HFmrEF. That grade now has nowhere to live: HFmrEF is abolished and its patients are absorbed into HFrEF, where the recommendation rests on extrapolation because no trial has been performed exclusively at LVEF 41–49%.

Limitations of the document

The guideline states its own evidence gaps at length (Section 14): consensus on normal ejection fraction ranges; validation of the new improved-LVEF definition; whether SGLT2-I and MRA prevent HF in people without diabetes; the role of artificial intelligence in diagnosis; validation of the historical exercise PCWP cut-offs used for HFpEF; prospective validation of the age-related natriuretic peptide thresholds; RCTs comparing different MRAs and different GLP-1 RAs; optimal sequencing of FMT in both phenotypes; the role of potassium binders; ICD selection within subgroups; CRT efficacy in AF; CSP versus transvenous CRT; interatrial shunt devices; decongestion protocols in DHF; and the role of MCS in cardiogenic shock.
Several recommendations rest on Task Force judgement rather than randomised evidence, and the document says so explicitly — loop diuretics are graded I/A "due to clear clinical benefit" although no adequately powered trial exists or is likely to be conducted; the same footnote appears for dynamic diuretic dosing and for early referral to an advanced HF centre.
Only one recommendation could be made for heart transplantation (I/C), because the procedure has never been evaluated in an RCT.
The pooled MRA evidence in HFpEF is a meta-analysis, not a positive trial: TOPCAT's overall result was neutral and finerenone's FINEARTS-HF trial used LVEF >40%. The guideline acknowledges the LVEF ranges of the constituent trials do not map onto its new two-phenotype division.
The 2026 classification is not yet reflected in any trial's entry criteria, so every HFrEF recommendation at LVEF 41–49% is extrapolation — the guideline itself notes no large prospective RCT has been performed exclusively in that band.
Topics delegated elsewhere (cardio-oncology, pregnancy, myocarditis, valvular heart disease, chronic coronary syndrome, cardiomyopathies, CKD, AF, ventricular arrhythmia) are not covered in detail here, so this document cannot be used alone for those.
The source is a 94,000-word multi-column PDF conversion with OCR artefacts: some prose is split across columns, one recommendation table is embedded in a picture-text block, and the ECG-style figure legends are partially garbled. Numbers cited here were taken from readable prose and tables, not from figures.

Key Concepts Mentioned

Key Entities Mentioned

Wiki Pages Updated

wiki/sources/HF-ESC-2026.md (created)
wiki/sourceindex.md (updated)
wiki/wikiindex.md (updated — no new concept or entity page was required)
wiki/entities/Heart-Failure.md (updated — classification, staging, nomenclature, contradictions)
wiki/entities/HFrEF.md (updated — LVEF threshold, FMT nomenclature, device classes)
wiki/entities/HFpEF.md (updated — MRA to Class I, diagnostic criteria, HFmrEF removal)
wiki/concepts/Iron-Deficiency-in-HF.md (updated — TSAT <20% definition)
wiki/entities/Vericiguat.md (updated — VICTOR trial, LVEF <45%)
wiki/log.md (appended)