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Health condition · Clinically reviewed

Heart failure, the four pillars, SGLT2 inhibitors and when devices or transplant fit.

A syndrome, not a single disease. Modern UK care combines four disease-modifying drugs, careful monitoring and, for the right patients, devices, valve work or transplantation.

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A radiographer guides a patient onto the bed of an advanced 3 Tesla MRI scanner in a London imaging suite

Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE NG106, ESC 2021 and the trials that shaped modern heart-failure care.

  • 03

    Current for 2026

    Reflects the four-pillar approach for HFrEF and the newer SGLT2 evidence in HFpEF.

Key facts

Heart failure at a glance.

The essentials, in plain English. What heart failure is, how it is grouped by ejection fraction, and how it is treated in the UK today.

  • What it is

    A clinical syndrome of breathlessness, fatigue and fluid overload caused by cardiac dysfunction, not a single disease.

  • How common

    Around a million people in the UK live with heart failure and it remains a major cause of hospital admission.

  • Three EF phenotypes

    HFrEF (LV EF 40 per cent or less), HFmrEF (41 to 49 per cent) and HFpEF (50 per cent or more) each have their own treatment mix.

  • Acute vs chronic

    Chronic heart failure managed in the community can decompensate acutely and needs urgent hospital care.

  • Four pillars

    For HFrEF, ARNI or ACE inhibitor, beta-blocker, MRA and an SGLT2 inhibitor are all started early.

  • Practice-changing

    DAPA-HF, EMPEROR-Reduced, EMPEROR-Preserved and DELIVER extended SGLT2 inhibitors across the EF spectrum.

Why this guide matters

A syndrome, treated with a plan.

Heart failure is common, treatable and, with the right combination of medicines, devices and follow-up, often stable for years. The three points below shape the rest of the page.

  • Ejection fraction guides therapy

    HFrEF, HFmrEF and HFpEF share symptoms but respond to different drug and device mixes. Echocardiography is the first test that changes management.

  • The four pillars save lives

    For HFrEF, ARNI or ACE inhibitor, beta-blocker, MRA and SGLT2 inhibitor together reduce hospital admissions and death. Start early, uptitrate steadily.

  • Look for the treatable causes

    Ischaemia, hypertension, valve disease, cardiac amyloid and iron deficiency all have specific treatments. Chasing the cause changes outcomes.

How the diagnosis is made

From first breathlessness to a clear plan.

The steps a UK GP and cardiologist will normally follow, in order, so you know what to expect and why each investigation is being done.

  1. 01

    Assessing

    History and risk factors

    Breathlessness on exertion, orthopnoea, paroxysmal nocturnal dyspnoea, ankle swelling, prior MI, hypertension, alcohol, chemotherapy and family history.

  2. 02

    Assessing

    Examination

    Raised JVP, a third heart sound gallop, lung crackles and peripheral oedema all support the diagnosis at the bedside.

  3. 03

    Assessing

    NT-proBNP and urgent referral

    Per NICE NG106, NT-proBNP above 400 pg/mL prompts specialist review and above 2000 pg/mL prompts a two-week pathway.

  4. 04

    Confirming

    ECG and chest X-ray

    A normal ECG makes heart failure less likely. Chest X-ray looks for cardiomegaly, pulmonary oedema and effusions.

  5. 05

    Confirming

    Transthoracic echocardiogram

    The gold-standard test, sizing chambers, measuring ejection fraction and screening for valve disease. Read more on the /tests/echocardiogram/ page.

  6. 06

    Confirming

    Ischaemic and structural workup

    Coronary CT angiography or invasive angiography, cardiac MRI for tissue characterisation and, where indicated, PYP scanning for cardiac amyloid.

  7. 07

    Preparing

    Baseline bloods and comorbidities

    FBC, U and Es, LFTs, TFTs, HbA1c, iron studies and ferritin, plus assessment of sleep apnoea, obesity and diabetes.

Typical timeline: from first symptoms to an echo and a starter plan in weeks, not months.

Symptoms

What heart failure actually feels like.

The classic mix of breathlessness, fatigue and fluid retention, plus the features that mean it is time to escalate.

  • Breathlessness on exertion

    Reduced exercise tolerance is often the first change, with stairs, hills and hurrying becoming harder over weeks to months.

  • Orthopnoea

    Difficulty breathing lying flat that eases when propped up. Patients often add pillows without realising why.

  • Paroxysmal nocturnal dyspnoea

    Waking one or two hours after falling asleep, gasping for breath and needing to sit up or stand at a window.

  • Ankle and leg oedema

    Pitting swelling that worsens through the day. Read more on the /conditions/edema/ page.

  • Fatigue and weight change

    Deep tiredness, poor recovery from small tasks and unexplained weight gain from fluid retention.

  • Cough and frothy sputum

    A persistent cough, sometimes with pink frothy sputum, can be the first sign of pulmonary oedema.

  • Palpitations and syncope

    Atrial fibrillation and ventricular arrhythmias are common. Blackouts warrant urgent cardiology review.

  • NYHA class I to IV

    Symptoms are graded from I (no limitation) to IV (symptoms at rest) and guide both prognosis and treatment intensity.

Treatment

How heart failure is treated in the UK.

Four disease-modifying drug classes for HFrEF, SGLT2 inhibitors across the EF spectrum, and devices, valve procedures or transplantation when the medicines alone are not enough.

  • ARNI or ACE inhibitor

    Sacubitril/valsartan (Entresto) is preferred for HFrEF following PARADIGM-HF, with ramipril or an ARB as alternatives.

  • Beta-blocker

    Bisoprolol, carvedilol or nebivolol (older patients), titrated slowly to the highest tolerated dose.

  • MRA

    Spironolactone or eplerenone reduces mortality in HFrEF. Finerenone is increasingly used where indicated.

  • SGLT2 inhibitor

    Dapagliflozin (DAPA-HF, DELIVER) and empagliflozin (EMPEROR-Reduced, EMPEROR-Preserved) benefit patients across the EF range. See /treatments/sglt2-inhibitor-clinic/.

  • Loop diuretic

    Furosemide or bumetanide for symptomatic relief of congestion. Dose is titrated against weight and symptoms, not fixed for life.

  • Ivabradine and hydralazine/ISDN

    Ivabradine when heart rate stays above 70 in sinus rhythm. Hydralazine with isosorbide dinitrate for African-Caribbean patients or ACE intolerance.

  • IV iron for iron deficiency

    Following FAIR-HF and AFFIRM-AHF, intravenous iron improves symptoms and reduces admissions. See /treatments/iv-iron-heart-failure-clinic/.

  • Device therapy

    Primary-prevention ICDs and cardiac resynchronisation for eligible patients. See /treatments/subcutaneous-icd/.

Advanced options

When medicines are not enough.

Revascularisation for ischaemic disease (see coronary angioplasty and coronary artery bypass), TAVI or MitraClip for valve disease (see TAVR/TAVI clinic), CRT for LBBB with reduced EF, LVAD implantation and heart transplantation at specialist commissioned centres such as Papworth, Harefield and Freeman.

Specific therapies

When cause dictates treatment.

Tafamidis is NICE-approved for ATTR cardiac amyloidosis (see tafamidis clinic). Patisiran, inotersen and vutrisiran target hereditary ATTR. Mavacamten (Camzyos) is licensed for obstructive hypertrophic cardiomyopathy. Cardiac rehabilitation (see cardiac rehab), vaccinations and palliative input sit alongside the disease-modifying medicines.

What this guide is based on

The sources behind every claim on this page.

UK national guidance, European Society of Cardiology guidelines and the landmark trials that changed practice, current at the time of last review.

Key references

Guidelines and trials we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or cardiologist knows your heart, your comorbidities and your medicines and can tell you which parts apply to you. If symptoms change quickly, get seen.

  • NICE. Chronic heart failure in adults: diagnosis and management (NG106).

  • European Society of Cardiology. 2021 Guidelines for the diagnosis and treatment of acute and chronic heart failure.

  • PARADIGM-HF, DAPA-HF, EMPEROR-Reduced, EMPEROR-Preserved and DELIVER trial publications.

  • NICE technology appraisal on tafamidis (TA696) for wild-type or hereditary transthyretin amyloid cardiomyopathy.

Red flags

When heart failure needs urgent attention.

Most chronic heart failure is managed in the community. These are the situations that are not, and where same-day or specialist care matters.

  • Acute pulmonary oedema

    Sudden severe breathlessness at rest, cold sweats and pink frothy sputum. Call 999. This is a medical emergency.

  • Cardiogenic shock

    Cold, clammy, hypotensive and confused. Immediate hospital care and inotropic or mechanical support are needed.

  • Rapid weight gain

    More than 2 kg in three days usually means fluid overload and warrants a diuretic review with the heart-failure team.

  • Syncope or sustained arrhythmia

    Blackouts, prolonged palpitations or documented VT need urgent cardiology assessment for arrhythmia and device therapy.

  • Suspected cardiac amyloidosis

    Unexplained HFpEF with carpal tunnel, low voltages on ECG or apical sparing on echo warrants a PYP scan and specialist review.

  • Chemotherapy-related dysfunction

    Anthracycline or trastuzumab exposure with a falling ejection fraction needs cardio-oncology input, not watchful waiting.

  • Postpartum breathlessness

    Peripartum cardiomyopathy can present in the last month of pregnancy or the first months after delivery and needs urgent echo.

  • End-stage symptoms

    NYHA IV symptoms despite optimal therapy warrant an early conversation about advanced options and palliative support.

  • Suspected endocarditis or myocarditis

    Fever, new murmur or a viral prodrome with a falling EF needs same-day hospital assessment.

Living with it

A treatable condition, with a clear rhythm.

Four things that make the biggest difference day to day: a daily weight, taking the four pillars, cardiac rehabilitation and staying on top of vaccinations.

A quiet reminder

Small, steady habits change the trajectory.

A weight chart, a labelled dosette and a rehab class do more for prognosis than any single scan.

  1. 01 Daily weight

    Weigh yourself each morning

    A sudden rise of more than 2 kg in three days is a red flag. Keep a written or app-based diary the team can review.

  2. 02 Medicines

    Do not skip the four pillars

    ARNI, beta-blocker, MRA and SGLT2 inhibitor together reduce hospitalisation and death. Ask before stopping any of them.

  3. 03 Rehab

    Cardiac rehabilitation matters

    Supervised exercise improves symptoms, mood and prognosis. Read more on /treatments/cardiac-rehabilitation-programme/.

  4. 04 Vaccines

    Keep vaccinations up to date

    Annual flu, pneumococcal, COVID and RSV vaccinations lower the chance of an admission that pushes the heart back into decompensation.

Frequently asked

Everything we get asked about heart failure.

Quick answers on ejection fraction, the four pillars, SGLT2 inhibitors, devices and cardiac amyloid.

  • What is heart failure?

    Heart failure is a clinical syndrome, not a single disease. The heart cannot fill or empty well enough to meet the body’s demands at normal filling pressures, which causes breathlessness, fatigue and fluid overload. It is graded by ejection fraction (HFrEF, HFmrEF and HFpEF) and by NYHA class.

  • How is heart failure diagnosed?

    Diagnosis combines a suggestive history and examination with an NT-proBNP blood test and a transthoracic echocardiogram. Per NICE NG106, an NT-proBNP above 400 pg/mL prompts specialist referral and above 2000 pg/mL prompts a two-week pathway. Cardiac MRI, coronary imaging and, where indicated, PYP scanning refine the underlying cause.

  • What are the four pillars of HFrEF treatment?

    For heart failure with reduced ejection fraction, modern care starts all four disease-modifying drug classes early: an ARNI (sacubitril/valsartan) or ACE inhibitor, a beta-blocker, a mineralocorticoid receptor antagonist and an SGLT2 inhibitor such as dapagliflozin or empagliflozin. A loop diuretic is added for symptomatic congestion.

  • Do SGLT2 inhibitors help HFpEF too?

    Yes. The EMPEROR-Preserved and DELIVER trials showed empagliflozin and dapagliflozin reduce cardiovascular death and heart-failure hospitalisation in HFpEF, regardless of diabetes. SGLT2 inhibitors are now recommended across the ejection-fraction spectrum.

  • When are devices or transplant considered?

    An ICD is considered for primary prevention when the LV ejection fraction stays below 35 per cent despite optimal therapy. Cardiac resynchronisation is added when there is left bundle branch block with a reduced EF. LVAD implantation and heart transplantation are reserved for advanced heart failure and delivered at specialist commissioned centres such as Papworth, Harefield, Freeman and other UK transplant units.

  • What is cardiac amyloidosis and why does it matter?

    Cardiac amyloidosis is an under-recognised cause of HFpEF, especially in older men. Suspect it with carpal tunnel syndrome, low voltages on ECG or apical sparing on echo. A PYP scan and free light chains screen sort ATTR from AL disease. Tafamidis (Vyndamax/Vyndaqel) is a NICE-approved disease-modifying therapy for ATTR. See /treatments/tafamidis-cardiac-amyloid-clinic/.

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