Heart failure

Ischaemic

Prior myocardial infarction, chronic coronary disease — the commonest cause of HFrEF

Hypertensive

Long-standing hypertension with concentric hypertrophy — a dominant cause of HFpEF

Valvular

Aortic stenosis, mitral regurgitation, rheumatic heart disease

Cardiomyopathies

Dilated (genetic, alcohol, peripartum), hypertrophic, restrictive, arrhythmogenic

Infiltrative / metabolic

Cardiac amyloidosis, haemochromatosis, sarcoidosis, thyrotoxicosis, thiamine deficiency

Toxic / drug-induced

Anthracyclines, trastuzumab, immune checkpoint inhibitors, alcohol, cocaine

Arrhythmic / high output

Persistent tachyarrhythmia, severe anaemia, arteriovenous fistula, sepsis

• Affects roughly 1-2% of adults, rising above 10% over the age of 70.
• Half of prevalent cases have preserved ejection fraction, and that proportion is growing.
• Heart failure is a leading cause of hospital admission in adults over 65 and readmission is common within 30 days.

• Coronary disease, hypertension, diabetes, obesity, atrial fibrillation, CKD, valve disease, sleep apnoea, harmful alcohol, cardiotoxic chemotherapy, family history of cardiomyopathy.

Normal physiology → mechanism → tissue change → clinical picture

1. 1Normal physiology: stroke volume adapts to preload (Frank-Starling), afterload and contractility.
2. 2Mechanism: myocyte loss or stiffening reduces output or raises filling pressures.
3. 3Compensation: sympathetic activation and renin-angiotensin-aldosterone activation preserve pressure but increase afterload, sodium retention and fibrosis.
4. 4Tissue change: adverse remodelling — dilatation in HFrEF, concentric hypertrophy and interstitial fibrosis in HFpEF.
5. 5Clinical manifestation: congestion (dyspnoea, orthopnoea, oedema) and hypoperfusion (fatigue, cool peripheries, renal dysfunction).

HFrEF

Dilated chambers, thin walls, myocyte hypertrophy with slippage, replacement fibrosis

HFpEF

Concentric hypertrophy, interstitial and perivascular fibrosis, microvascular rarefaction

Amyloid

Congo red positive apple-green birefringence; increased wall thickness with low voltage ECG

Chronic congestion

Nutmeg liver, pulmonary haemosiderosis with heart-failure cells

• Exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
• Fatigue and exercise intolerance
• Ankle swelling, abdominal distension, early satiety
• Nocturnal cough, weight gain from fluid
• Palpitations or syncope suggesting arrhythmia

• Raised JVP, hepatojugular reflux
• Displaced apex, third heart sound, murmurs of valve disease
• Bibasal crackles, pleural effusion
• Peripheral and sacral oedema, tender hepatomegaly, ascites
• Narrow pulse pressure, cool peripheries and hypotension in advanced low-output states

1. 1Assess symptoms and signs, then measure natriuretic peptide (BNP/NT-proBNP) — a normal level makes heart failure unlikely.
2. 2Perform ECG, chest radiograph and bloods (FBC, renal function, glucose/HbA1c, thyroid, iron studies, liver enzymes).
3. 3Transthoracic echocardiography to determine ejection fraction, chamber size, valve function and filling pressures.
4. 4Classify HFrEF / HFmrEF / HFpEF and assign NYHA class.
5. 5Seek the underlying cause and precipitant: ischaemia, arrhythmia, valve disease, infiltration, non-adherence, NSAIDs, infection.
6. 6Start disease-modifying therapy early and titrate; decongest in parallel where congested.
7. 7Consider advanced imaging, cardiac MRI, coronary assessment or biopsy for unexplained cardiomyopathy.

• Symptoms and/or signs of heart failure PLUS objective evidence of cardiac dysfunction (echocardiographic abnormality or raised natriuretic peptide).
• HFrEF: LVEF ≤ 40%. HFmrEF: LVEF 41-49%. HFpEF: LVEF ≥ 50% with evidence of raised filling pressures.
• Rule-out thresholds in the non-acute setting: NT-proBNP < 125 pg/mL or BNP < 35 pg/mL make the diagnosis unlikely.

Initial

• BNP or NT-proBNP, ECG, chest radiograph, FBC, renal function and electrolytes, liver enzymes, TSH, HbA1c, iron studies, urinalysis.

Confirmatory

• Transthoracic echocardiography — the key confirmatory test.

Severity

• NYHA class, six-minute walk or peak VO2, serial natriuretic peptide, renal function trend.

Aetiology

• Cardiac MRI for infiltration/inflammation, coronary angiography or CT for ischaemia, bone scintigraphy and free light chains for amyloid, genetic testing in familial cardiomyopathy.

Monitoring

• Daily weight, fluid balance, potassium and creatinine after each up-titration, blood pressure and heart rate, device interrogation.

COPD / asthma

Rule in: obstructive spirometry, smoking history, no orthopnoea. Rule out: raised BNP with echo abnormality.

Pulmonary embolism

Rule in: acute pleuritic pain, RV strain, raised D-dimer. Rule out: chronic progressive congestion.

Nephrotic syndrome / CKD

Rule in: heavy proteinuria, hypoalbuminaemia. Rule out: raised JVP and echo dysfunction.

Cirrhosis with ascites

Rule in: stigmata of chronic liver disease, low JVP. Rule out: elevated filling pressures on echo.

Constrictive pericarditis

Rule in: pericardial calcification, septal bounce, discordant respiratory variation. Rule out: normal pericardium with reduced EF.

Anaemia / thyrotoxicosis

Rule in: high-output state with wide pulse pressure. Rule out: normal haemoglobin and thyroid function.

NYHA I

No limitation with ordinary activity

NYHA II

Slight limitation; symptoms with ordinary activity

NYHA III

Marked limitation; symptoms with minimal activity

NYHA IV

Symptoms at rest

ACC/AHA stages

A at risk, B structural change without symptoms, C symptomatic, D advanced/refractory

Acute decompensation

• Sit up, high-flow oxygen if hypoxaemic, IV loop diuretic (bolus or infusion), monitor urine output
• IV nitrate for hypertensive pulmonary oedema; non-invasive ventilation for respiratory distress
• Identify and treat the precipitant: ACS, arrhythmia, infection, anaemia, non-adherence
• Inotropes and mechanical support only for cardiogenic shock

HFrEF disease-modifying therapy

• ARNI (or ACEi/ARB), evidence-based beta-blocker, MRA and SGLT2 inhibitor — start all four early, in low doses, then titrate
• Loop diuretic titrated to the lowest dose maintaining euvolaemia
• Treat iron deficiency with IV iron; consider ivabradine, hydralazine-nitrate or vericiguat in selected patients

HFmrEF / HFpEF

• SGLT2 inhibitor for HFmrEF and HFpEF, plus diuretics for congestion and aggressive management of hypertension, atrial fibrillation, obesity and sleep apnoea.

Device / surgical

• ICD for primary prevention when LVEF ≤ 35% despite optimal therapy; CRT for LVEF ≤ 35% with LBBB and QRS ≥ 130 ms.
• Valve intervention, revascularisation, LV assist device or transplantation in advanced disease.

Supportive

• Cardiac rehabilitation, sodium and fluid advice, daily weights, vaccination, depression screening, structured heart-failure nurse follow-up, advance care planning in stage D.

Acute

• Acute pulmonary oedema, cardiogenic shock, arrhythmia, cardio-renal syndrome, electrolyte disturbance from diuretics.

Chronic

• Recurrent admissions, progressive functional decline, cardiac cachexia, hepatic congestion, thromboembolism, depression.

Late

• Sudden cardiac death, end-stage heart failure requiring transplant or palliative care.

• Historically about 50% five-year mortality; contemporary four-pillar therapy meaningfully improves survival and admissions.
• Estimated benefit of complete four-drug therapy in HFrEF is several additional years of event-free survival versus ACEi/beta-blocker alone.
• Poor prognostic markers: NYHA IV, low systolic pressure, hyponatraemia, renal impairment, persistently raised natriuretic peptides, recurrent admissions.
• Each hospitalisation marks a step down in trajectory — prevention of readmission is a therapeutic target.

• Treat hypertension to target and manage diabetes with SGLT2 inhibitors where indicated
• Rapid reperfusion in ACS limits infarct size and later heart failure
• Rate and rhythm control in atrial fibrillation; alcohol reduction; cardio-oncology surveillance
• Echocardiographic screening in familial cardiomyopathy relatives

• Review within 1-2 weeks of discharge; the early post-discharge period carries the highest readmission risk
• Up-titrate all four pillars every 2 weeks as tolerated, with renal function and potassium checks
• Repeat echocardiography at 3-6 months to reassess EF and device eligibility
• Structured education on daily weights, diuretic flexibility and when to call for help

Pregnancy

Peripartum cardiomyopathy; avoid ACEi/ARB/ARNI, MRA and SGLT2 inhibitors — use hydralazine, nitrates, beta-blockers with specialist input

Elderly / frail

Start low, go slow, watch orthostatic hypotension and falls; simplify regimens

CKD

Expect a 20-30% creatinine rise on RAAS or SGLT2 initiation — do not stop reflexively; monitor potassium

Diabetes

SGLT2 inhibitors are first-choice; avoid pioglitazone and saxagliptin

Atrial fibrillation

Anticoagulate per risk score; consider rhythm control including ablation in selected HFrEF

Amyloidosis

Beta-blockers and ACEi often poorly tolerated; refer for disease-specific therapy

• ESC heart failure guideline (2021 with 2023 focused update)
• ESC ACS guideline 2023 for post-infarction LV dysfunction

• SGLT2 inhibitor trials extended benefit across the whole ejection-fraction spectrum.
• Rapid in-hospital initiation and titration of all four pillars is safe and reduces early readmission.
• GLP-1 based therapy in obesity-related HFpEF is an active and promising area of evidence.

• ESC 2021/2023 heart failure guideline (guideline, Europe).
• DrZep editorial summary, demo dataset v0.1.