Summary

Heart Failure (HF) is a complex clinical syndrome characterised by the heart's inability to pump blood at a rate sufficient to meet the metabolic demands of tissues, or to do so only at elevated filling pressures. It represents the final common pathway for most cardiac diseases and carries a prognosis worse than many cancers, with 5-year mortality rates of 50-75% for advanced disease. The syndrome is defined by a constellation of symptoms (dyspnoea, fatigue, ankle swelling) and signs (elevated JVP, pulmonary crackles, peripheral oedema) resulting from structural or functional cardiac abnormalities. Modern classification divides HF by ejection fraction: HFrEF (EF ≤40%), HFmrEF (EF 41-49%), and HFpEF (EF ≥50%), each with distinct pathophysiology and treatment implications. The introduction of disease-modifying therapies (ACEi/ARBs, Beta-blockers, MRAs, SGLT2i, ARNI) has revolutionised outcomes for HFrEF, reducing mortality by up to 50% when used in combination. [1,2,3]

Key Facts

• Definition: Clinical syndrome with symptoms/signs of HF + objective evidence of cardiac dysfunction (structural/functional)
• Prevalence: 1-2% of adult population in developed countries; rises to >10% in those >70 years [PMID: 33504513]
• Incidence: 5-10 per 1000 person-years; lifetime risk ~20% at age 40
• Mortality: 1-year mortality 20-30% for new diagnosis; 5-year mortality 50-75% [PMID: 28455343]
• Morbidity: Leading cause of hospitalisation in >65s; high readmission rates (25% at 30 days)
• Peak Demographics: Bimodal - younger males (DCM, IHD); older females (HFpEF)
• Pathognomonic Feature: None - diagnosis is clinical + imaging (Echo EF, NTproBNP)
• Gold Standard Investigation: Transthoracic Echocardiography (TTE)
• First-line Treatment: GDMT quadruple therapy (ACEi/ARNi + BB + MRA + SGLT2i)
• Prognosis Summary: With optimal GDMT, 5-year survival >60% for HFrEF; without treatment <30%

Clinical Pearls

Diagnostic Pearl: BNP <100 pg/mL or NTproBNP <300 pg/mL effectively EXCLUDES acute heart failure (NPV >95%). A raised level does NOT confirm HF - needs clinical + echo correlation.

Examination Pearl: "Cold and Wet" is the worst prognosis profile - hypoperfusion (cold peripheries, confusion, low SBP) + congestion (oedema, crackles). These patients may need inotropes.

Treatment Pearl: "Start Low, Go Slow, But Get There" - titrate GDMT to maximum tolerated doses. Most mortality benefit is at target dose, not just initiation.

Pitfall Warning: Do NOT stop beta-blockers during acute decompensation unless cardiogenic shock. Reduce dose if needed, but discontinuation worsens outcomes.

Mnemonic: FACES for HF symptoms: Fatigue, Activities limited, Chest congestion/cough, Edema, Shortness of breath.

Why This Matters Clinically

Heart Failure is the cardiovascular epidemic of the 21st century. With an ageing population and improved survival from acute MI, the prevalence continues to rise exponentially. It is the most common reason for hospital admission in those over 65, with each admission costing healthcare systems thousands and increasing subsequent mortality risk by 30-40%. Medico-legally, failure to optimise GDMT or investigate the underlying cause is increasingly scrutinised. For examinations, HF is a favourite viva topic encompassing pathophysiology, pharmacology, and clinical acumen - expect detailed questioning on EF categories, GDMT rationale, and prognosis. [4,5]

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Structured Approach

General:

• Respiratory distress (tachypnoea, accessory muscle use, tripod position)
• Pallor (anaemia as exacerbating factor)
• Cyanosis (peripheral or central)
• Cachexia (cardiac cachexia in chronic severe HF)
• State of hydration (wet vs dry)
• Perfusion status (warm vs cold)

Vital Signs:

• Pulse: rate (tachycardia), rhythm (AF), character (pulsus alternans in severe LV failure)
• Blood pressure: may be low (cardiogenic shock) or high (acute HTN crisis)
• Respiratory rate: typically elevated (>20/min)
• Oxygen saturation: may be reduced (target >94%, or 88-92% if COPD)

Cardiovascular Examination:

• JVP assessment (cm above sternal angle) - elevated in congestion
• Apex beat location and character
• Heart sounds - S3 (HFrEF), S4 (HFpEF), murmurs (valvular disease)
• Hepatojugular reflux - press on liver, watch JVP rise

Respiratory Examination:

• Percussion: stony dull = effusion; dull = consolidation
• Auscultation: bibasal crackles (pulmonary oedema), reduced breath sounds (effusion)

Abdominal Examination:

• Hepatomegaly (tender in acute congestion)
• Ascites (shifting dullness)

Peripheral Examination:

• Pitting oedema (ankles, sacrum)
• Peripheral perfusion (capillary refill, temperature)

Special Tests

Test	Technique	Positive Finding	Sensitivity/Specificity
Hepatojugular reflux	Firm pressure on liver for 30 sec, observe JVP	JVP rises >3cm and sustained	70%/85% for elevated RA pressure
Raised JVP	Measure height above sternal angle at 45°	>4cm above sternal angle	70%/90%
S3 gallop	Listen at apex with bell, left lateral decubitus	Low-pitched early diastolic sound	40%/95% for elevated LVEDP
Displaced apex	Palpate apex in expiration	Lateral to mid-clavicular line	60%/90% for cardiomegaly
Capillary refill	Blanch nailbed, measure time to refill	>2 seconds indicates hypoperfusion	50%/70% for low cardiac output
Pitting oedema	Press skin over tibia/sacrum for 5 sec	Indentation remains	Non-specific (many causes)

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Natural History

Without treatment, heart failure is a relentlessly progressive condition. Historical data from the Framingham Heart Study showed median survival of only 1.7 years for men and 3.2 years for women after diagnosis. Mortality is highest in the first year after diagnosis (20-30%) and subsequently follows an annual mortality rate of 10% for mild HF (NYHA I-II) to 50% for severe HF (NYHA IV). Half of deaths are sudden (arrhythmic), and half are from progressive pump failure.

The trajectory of HF differs from malignancy - rather than a steady decline, patients often experience repeated acute decompensations with incomplete recovery, creating a "sawtooth" pattern of decline.

Mortality Comparison

Heart failure has a prognosis comparable to or worse than many cancers:

Condition	5-Year Survival
HFrEF (no GDMT)	20-25%
HFrEF (with GDMT)	50-60%
Breast cancer	90%
Prostate cancer	98%
Colorectal cancer	65%
Lung cancer	20%
Pancreatic cancer	10%

Outcomes with Treatment

Variable	Outcome
1-year mortality	10-20% (optimised GDMT) vs 30-40% (untreated)
5-year mortality	40-50% (with GDMT) vs 70-80% (untreated)
Hospitalisation rate	20-25% per year (1-2 admissions/patient/year)
CRT response	60-70% are responders; 15-20% super-responders (EF normalises)
LVAD bridge-to-transplant	80% successful bridge
Cardiac transplant 1-year survival	85-90%
Cardiac transplant 10-year survival	50-60%

Prognostic Scores

MAGGIC Risk Score (Meta-Analysis Global Group in Chronic HF):

• Validated in >39,000 patients
• Variables: EF, age, creatinine, NYHA class, SBP, BMI, medications, diabetes, smoking
• Predicts 1-year and 3-year mortality
• Available online: calculator for clinical use

Seattle Heart Failure Model:

• Estimates 1, 2, and 3-year survival
• Includes pharmacological and device therapy
• Useful for advanced HF decision-making (transplant/LVAD evaluation)
• Variables: Age, sex, NYHA, EF, ischaemic aetiology, medications, devices, labs

INTERMACS Profiles (Advanced HF):

Profile	Description	1-Year Survival without MCS
1	Critical cardiogenic shock	<50%
2	Progressive decline on inotropes	50-60%
3	Stable but inotrope-dependent	60-70%
4	Resting symptoms, frequent hospitalisations	70-80%
5-7	Variable limitation, ambulatory	>80%

Prognostic Factors

Good Prognosis:

• Younger age (<65 years)
• Higher EF (HFpEF > HFmrEF > HFrEF for mortality)
• Preserved renal function (eGFR >60 mL/min)
• Sinus rhythm
• Toleration of maximum GDMT doses
• NYHA Class I-II
• Response to CRT (especially super-responders)
• Normal blood pressure (not requiring dose reduction of GDMT)
• No significant comorbidities (DM, CKD, COPD)
• Good functional capacity (6MWT >350m, peak VO2 >14 mL/kg/min)
• Low BNP/NTproBNP levels on therapy
• Recovery of EF on treatment (HFimpEF)

Poor Prognosis:

• Very low EF (<20%)
• Persistent NYHA Class III-IV symptoms despite GDMT
• Atrial fibrillation (especially new-onset)
• Persistently elevated natriuretic peptides despite treatment
• Cardiorenal syndrome (worsening creatinine, eGFR <30)
• Hyponatraemia (<135 mmol/L) - marker of neurohormonal activation
• Cardiac cachexia
• Recurrent hospitalisations (≥2 in past year)
• Ventricular arrhythmias
• Right ventricular dysfunction
• Inability to tolerate GDMT (hypotension, AKI, bradycardia)
• High MAGGIC or Seattle score
• Low 6MWT (<300m) or peak VO2 (<12 mL/kg/min)
• Elevated troponin (ongoing myocyte injury)
• High sST2 or galectin-3 levels (fibrosis biomarkers)

Mode of Death

Understanding mode of death helps guide preventive strategies:

Mode	Proportion	Risk Factors	Prevention
Sudden cardiac death	40-50% (early/mild HF)	NSVT, low EF, prior arrest	ICD, GDMT
Progressive pump failure	20-30% (advanced HF)	Low EF, NYHA IV, refractory	LVAD, transplant, palliative
Other CV (MI, stroke)	10-15%	Atherosclerosis	Secondary prevention
Non-CV	15-20% (older, comorbid)	Malignancy, infection, renal	Address comorbidities

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Key Guidelines

1. ESC Guidelines for Heart Failure (2021) — Comprehensive diagnostic and treatment recommendations. Introduced quadruple therapy as first-line. European Heart Journal [PMID: 34447992]

2. AHA/ACC/HFSA Guideline for HF Management (2022) — US perspective with staging system. Endorses SGLT2i for all EF categories. [PMID: 35363499]

3. NICE NG106: Chronic Heart Failure (2018, updated 2023) — UK guidance; emphasises integrated care, specialist HF nurses. NICE

4. BSH Guidelines on Device Therapy (2022) — ICD and CRT indications. [PMID: 35485232]

Landmark Trials

PARADIGM-HF (2014) — Sacubitril/Valsartan vs Enalapril in HFrEF

• 8442 patients, EF ≤40%, NYHA II-IV
• 20% reduction in CV death or HF hospitalisation (HR 0.80)
• Clinical Impact: ARNI became standard of care for HFrEF
• [PMID: 25176015]

DAPA-HF (2019) — Dapagliflozin in HFrEF (with or without diabetes)

• 4744 patients, EF ≤40%
• 26% reduction in worsening HF or CV death (HR 0.74)
• Clinical Impact: SGLT2i added to GDMT regardless of diabetes
• [PMID: 31535829]

EMPEROR-Preserved (2021) — Empagliflozin in HFpEF

• 5988 patients, EF >40%
• 21% reduction in CV death or HF hospitalisation
• Clinical Impact: First therapy proven effective in HFpEF
• [PMID: 34449189]

COPERNICUS (2001) — Carvedilol in severe HFrEF

• 2289 patients, EF <25%, NYHA IV
• 35% reduction in mortality
• Clinical Impact: Beta-blockers safe and effective even in severe HF
• [PMID: 11386263]

RALES (1999) — Spironolactone in severe HFrEF

• 1663 patients, EF ≤35%, NYHA III-IV
• 30% reduction in mortality
• Clinical Impact: MRA became standard of care
• [PMID: 10471456]

EMPHASIS-HF (2011) — Eplerenone in mild HFrEF

• 2737 patients, EF ≤35%, NYHA II
• 37% reduction in CV death or HF hospitalisation
• Clinical Impact: Extended MRA indication to milder symptoms
• [PMID: 21073363]

CONSENSUS (1987) — Enalapril in severe HFrEF

• 253 patients, NYHA IV
• 40% reduction in mortality at 6 months
• Clinical Impact: First proof that ACEi reduce mortality in HF
• [PMID: 2883575]

SOLVD-Treatment (1991) — Enalapril in HFrEF

• 2569 patients, EF ≤35%
• 16% reduction in mortality
• Clinical Impact: Established ACEi as cornerstone therapy
• [PMID: 2057034]

CIBIS-II (1999) — Bisoprolol in HFrEF

• 2647 patients, EF ≤35%, NYHA III-IV
• 34% reduction in all-cause mortality
• Clinical Impact: Confirmed beta-blocker mortality benefit
• [PMID: 9925425]

MERIT-HF (1999) — Metoprolol CR/XL in HFrEF

• 3991 patients, EF ≤40%, NYHA II-IV
• 34% reduction in mortality
• Clinical Impact: Extended beta-blocker evidence base
• [PMID: 10376614]

DELIVER (2022) — Dapagliflozin in HFpEF

• 6263 patients, EF >40%
• 18% reduction in worsening HF or CV death
• Clinical Impact: Confirmed SGLT2i benefit across EF spectrum
• [PMID: 36027570]

Evidence Strength

Intervention	Level	Key Evidence
ACEi in HFrEF	1a	CONSENSUS, SOLVD
Beta-blocker in HFrEF	1a	COPERNICUS, MERIT-HF, CIBIS-II
MRA in HFrEF	1a	RALES, EMPHASIS-HF
ARNI in HFrEF	1b	PARADIGM-HF
SGLT2i in HFrEF	1a	DAPA-HF, EMPEROR-Reduced
SGLT2i in HFpEF	1a	EMPEROR-Preserved, DELIVER
ICD primary prevention	1a	SCD-HeFT, MADIT-II
CRT	1a	CARE-HF, COMPANION, MADIT-CRT
IV iron for deficiency	1a	FAIR-HF, AFFIRM-AHF
Hydralazine-Isosorbide	1b	V-HeFT, A-HeFT
Exercise training	1a	HF-ACTION
Remote monitoring	1b	TIM-HF2

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What is Heart Failure?

Heart failure means your heart muscle has become weaker and can't pump blood around your body as well as it should. Think of your heart as a pump - in heart failure, the pump isn't working efficiently. This doesn't mean your heart has stopped or is about to stop - it's still working, just not as strongly as normal.

When the heart pumps less effectively, fluid can build up in your lungs (making you breathless) and in your legs (causing swelling). You might also feel very tired because your muscles aren't getting enough blood.

Why does it matter?

If left untreated, heart failure can get progressively worse. Each time you end up in hospital, it can weaken your heart further. The good news is that modern medications can help your heart pump better, reduce fluid build-up, and significantly improve how long you live and how well you feel.

How is it treated?

1. Tablets: You'll likely be on 4 main types of tablets - these work together to protect your heart, reduce strain, and prevent fluid build-up. It's very important to take these every day.
2. Lifestyle changes: Limiting salt and fluids, weighing yourself daily, staying active, and avoiding alcohol.
3. Devices: Some people benefit from special pacemakers that help the heart beat more efficiently, or defibrillators that can treat dangerous heart rhythms.

What to expect

• It may take several weeks/months to find the right doses of medications
• You should gradually feel less breathless and have more energy
• You'll need regular blood tests to monitor kidney function and electrolytes
• A specialist heart failure nurse will support you

When to seek help

• Sudden worsening of breathlessness
• Weight gain of more than 2kg (4lbs) in 3 days
• Swelling in legs getting much worse
• Feeling very dizzy or fainting
• Chest pain

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Common Exam Questions

Questions that frequently appear in examinations:

1. MRCP: "A 72-year-old man with a history of MI presents with worsening breathlessness and ankle swelling. His echocardiogram shows EF 30%. What is the optimal medical therapy?"

2. MRCP: "Which patients with heart failure are candidates for CRT? Describe the ECG criteria."

3. PACES: "Examine this patient's cardiovascular system" (Signs of heart failure - JVP, S3, oedema, murmurs)

4. MCQ: "Which of the following medications reduces mortality in HFrEF?" (Answer: All of quadruple therapy)

5. Viva: "Discuss the pathophysiology of heart failure and the rationale for GDMT"

Viva Points

Opening Statement:

"Heart failure is a clinical syndrome characterised by symptoms and signs of fluid overload and/or inadequate tissue perfusion, resulting from structural or functional cardiac abnormality. It is classified by ejection fraction into HFrEF (≤40%), HFmrEF (41-49%), and HFpEF (≥50%). The cornerstone of treatment for HFrEF is quadruple guideline-directed medical therapy: ACEi/ARNI, beta-blockers, MRAs, and SGLT2 inhibitors."

Key Facts to Mention:

• Prevalence 1-2%, rising to >10% in over 70s
• Neurohormonal activation (SNS, RAAS) drives progression
• Echocardiography is mandatory for diagnosis and classification
• BNP/NTproBNP excellent for exclusion (high NPV)
• GDMT reduces mortality by up to 50% in HFrEF

Classification to Quote:

• "The ESC 2021 classification divides HF into HFrEF, HFmrEF, and HFpEF based on ejection fraction"
• "NYHA classes I-IV describe functional limitation"
• "ACC/AHA stages A-D describe disease progression"

Evidence to Cite:

• "PARADIGM-HF showed ARNI superior to ACEi with 20% reduction in CV death/HF hospitalisation"
• "DAPA-HF demonstrated SGLT2i benefit in HFrEF regardless of diabetes status - 26% reduction in primary endpoint"
• "RALES established MRAs with 30% mortality reduction in severe HFrEF"

Structured Answer Framework:

1. Definition and Classification (30 seconds)
2. Epidemiology and Aetiology (30 seconds)
3. Clinical Features (45 seconds)
4. Investigations (30 seconds)
5. Management - GDMT and Devices (60 seconds)
6. Prognosis (30 seconds)

Common Mistakes

What fails candidates:

• ❌ Calling it "congestive cardiac failure" without knowing the EF classification
• ❌ Not knowing the quadruple therapy components and their mechanism
• ❌ Forgetting that SGLT2 inhibitors work regardless of diabetes status
• ❌ Not mentioning device therapy (CRT/ICD) indications
• ❌ Confusing ARNI with ACEi - they cannot be given together

Dangerous Errors to Avoid:

• ⚠️ Stopping beta-blockers during acute decompensation (reduce dose, don't stop)
• ⚠️ Missing hyperkalaemia with ACEi + MRA combination
• ⚠️ Not recognising cardiogenic shock (needs ICU, inotropes)

Outdated Practices (Do NOT mention):

• Digoxin as first-line therapy — Now only for rate control in AF + HF
• High-dose diuretics alone — No mortality benefit; GDMT essential
• Routine bed rest — Exercise training is beneficial

Examiner Follow-Up Questions

Expect these follow-up questions:

1. "What would you do if the patient's potassium rises to 5.8mmol/L on ACEi and MRA?"

   • Answer: Review dietary intake, check for AKI, consider reducing MRA dose, use potassium binders (patiromer/sodium zirconium cyclosilicate) if need to continue both agents

2. "What is the evidence for SGLT2 inhibitors in HFpEF?"

   • Answer: EMPEROR-Preserved and DELIVER trials showed 20-25% reduction in CV death/HF hospitalisation. First therapies proven effective in HFpEF.

3. "How would you manage acute pulmonary oedema?"

   • Answer: Sit upright, oxygen, IV furosemide 40-80mg, GTN if SBP >110, consider NIV/CPAP. If not responding: escalate to ICU for inotropes/vasopressors.

4. "What are the contraindications to beta-blockers in HF?"

   • Answer: Cardiogenic shock, severe hypotension, heart block (without pacemaker), severe bradycardia. NOT acute decompensation - can continue at reduced dose.

5. "Describe the mechanism of action of Sacubitril/Valsartan (ARNI)"

   • Answer: Dual mechanism - Sacubitril inhibits neprilysin (enhances natriuretic peptides → vasodilation, natriuresis), Valsartan blocks AT1 receptor (reduces vasoconstriction, aldosterone). Combined effect: reduced preload/afterload, reverse remodelling.

6. "What is the role of digoxin in heart failure management?"

   • Answer: No mortality benefit. Reduces hospitalisations. Used for rate control in AF + HF, or symptomatic HFrEF in sinus rhythm despite maximal GDMT. Target level 0.5-1.0 ng/mL.

7. "How would you investigate a new diagnosis of heart failure?"

   • Answer: Echo (essential), ECG, CXR, BNP/NTproBNP, FBC, U&Es, LFTs, TFTs, iron studies, HbA1c. Consider coronary angiography if ischaemic aetiology suspected. Cardiac MRI if aetiology unclear.

8. "What are the indications for cardiac transplantation?"

   • Answer: Refractory NYHA III-IV symptoms despite optimal GDMT and devices, peak VO2 <12-14ml/kg/min, recurrent hospitalisations, inotrope-dependent. Age typically <70, no irreversible organ damage, good psychosocial support.

Additional Viva Scenarios

Scenario 1: Acute Decompensated Heart Failure

"A 68-year-old man with known HFrEF (EF 25%) presents with worsening dyspnoea over 3 days. He stopped taking his medications 2 weeks ago. BP 105/70, HR 110 irregular, SpO2 88% on air. JVP elevated 8cm, bilateral crackles, and pitting oedema to knees."

Approach:

• This is acute decompensated HF with AF, congestion, and precipitant (non-adherence)
• ABC approach: oxygen to target SpO2 94%, IV access, monitoring
• Immediate: IV furosemide 80-120mg (1.5-2x home dose), consider GTN if SBP >110
• Investigations: ECG (AF vs sinus), BNP, troponin, U&Es, CXR
• Identify/treat precipitants: AF rate control (beta-blocker if not shocked)
• Do NOT stop beta-blocker - reduce dose if necessary
• Anticoagulation for AF: DOAC once stable
• Restart/optimise GDMT before discharge

Scenario 2: New Diagnosis of Heart Failure

"A 55-year-old woman presents with progressive exertional dyspnoea over 6 months. No significant PMH. Echo shows dilated LV with EF 30%. How would you investigate?"

Approach:

• New onset HFrEF without obvious cause - need aetiological workup
• Basic: FBC (anaemia), U&Es, LFTs, TFTs, iron studies, HbA1c, lipid profile
• Coronary assessment: CTCA or invasive angiography (IHD most common cause)
• Cardiac MRI: Assessment for infiltrative disease, myocarditis, viability
• Genetics: Consider if family history of HF/SCD (DCM screening)
• Specific tests: Amyloid typing if suspected, HIV, autoimmune screen
• Consider endomyocardial biopsy if diagnosis unclear

Scenario 3: Refractory Heart Failure

"A 62-year-old man with HFrEF (EF 20%) remains NYHA III despite maximum tolerated GDMT. CRT-D in situ. Recurrent admissions. What are the options?"

Approach:

• Refractory HF - Stage D
• Confirm optimal GDMT: tolerating target doses?
• Review CRT: pacing percentage >98%? Consider upgrade to CRT-D if only ICD
• Advanced therapies:
  • LVAD (bridge to transplant or destination therapy)
  • Cardiac transplantation (if eligible)
• Palliative care: If not candidate for advanced therapies - symptom control, advance care planning

HFpEF - Detailed Management

Heart failure with preserved ejection fraction (HFpEF) represents 50% of HF cases but historically lacked effective therapies. Key points for examinations:

Diagnosis:

• Symptoms + Signs of HF
• EF ≥50% on echo
• Evidence of diastolic dysfunction (E/e' >15, elevated LA volume index, raised BNP)
• Rule out other causes of dyspnoea (lung disease, anaemia)

H2FPEF Score (diagnostic probability):

• Heavy (BMI >30): +2
• Hypertensive (≥2 agents): +1
• AF: +3
• Pulmonary hypertension (PASP >35): +1
• Elder (>60): +1
• Filling pressures (E/e' >9): +1
• Score ≥6 = high probability HFpEF

Management of HFpEF:

• SGLT2 inhibitors: EMPEROR-Preserved and DELIVER showed benefit - NOW FIRST-LINE
• Diuretics: For congestion (no mortality benefit)
• Treat comorbidities: HTN, AF, DM, obesity
• Exercise training: Improves functional capacity
• Other GDMT (ACEi, BB, MRA): No mortality benefit in HFpEF, but may use for comorbidities

Emerging Evidence:

• GLP-1 agonists: STEP-HFpEF (semaglutide) showed improvement in symptoms/function in obese HFpEF
• Weight loss: Significant benefit in obese HFpEF

Specific Aetiologies and Their Management

1. Ischaemic Cardiomyopathy (Most Common - 50-60%):

• Revascularisation if viable myocardium (PCI or CABG)
• Viability assessment with MRI or nuclear imaging
• Secondary prevention: Aspirin, statin, optimal BP/glucose control

2. Dilated Cardiomyopathy (DCM):

• Familial (20-35%): Genetic testing, family screening
• Alcohol-related: Abstinence can lead to full recovery
• Tachycardia-induced: Rate control → potential complete recovery
• Peripartum: 50% recover within 6 months; LVAD/transplant if not
• Inflammatory/myocarditis: Consider immunosuppression if biopsy-proven

3. Hypertensive Heart Disease:

• Aggressive BP control
• May present as HFpEF (diastolic dysfunction)
• Regression of LVH with treatment

4. Valvular Heart Disease:

• Surgical or transcatheter intervention when indicated
• Timing crucial: before irreversible LV dysfunction

5. Cardiotoxic Drugs (Anthracyclines):

• Prevention: Dexrazoxane
• Monitoring: Serial echo/MUGA during treatment
• Early GDMT if EF drops

Special Populations

Heart Failure in the Elderly:

• Polypharmacy concerns
• Start GDMT at lower doses, titrate slowly
• Higher risk of adverse effects (AKI, hypotension)
• Goals may be symptom control rather than mortality reduction
• Consider frailty assessment

Heart Failure in Pregnancy:

• Peripartum cardiomyopathy: Presents late pregnancy to 6 months postpartum
• ACEi/ARB/ARNI contraindicated - use hydralazine/nitrates
• Beta-blockers: Metoprolol, labetalol safe
• Anticoagulation: LMWH (warfarin teratogenic first trimester, avoid DOACs)
• Delivery: Vaginal preferred unless obstetric indication for c-section
• Bromocriptine: May aid recovery (reduces prolactin-induced angiogenesis)

Heart Failure in Renal Impairment:

• Cardiorenal syndrome: Type 1 (acute HF → AKI), Type 2 (chronic HF → CKD)
• Dose adjust: ACEi, digoxin, spironolactone
• SGLT2i: Safe (and beneficial) down to eGFR 20
• Tolerate modest rise in creatinine (up to 30% from baseline) when initiating ACEi
• Avoid NSAIDs

Heart Failure with Atrial Fibrillation:

• Present in 30-40% of HF patients
• Worsens prognosis
• Rate control: Beta-blockers preferred (also GDMT)
• Rhythm control: Consider if symptomatic despite rate control
• Anticoagulation: DOACs preferred (CHA2DS2-VASc score typically ≥2)
• Ablation: May improve symptoms and EF (especially tachycardia-mediated)

Device Therapy - Extended Details

ICD (Implantable Cardioverter Defibrillator):

Primary Prevention Criteria:

• EF ≤35% despite ≥3 months optimal GDMT
• Expected survival >1 year with good functional status
• NYHA II-III
• Ischaemic: ≥40 days post-MI, ≥3 months post-revascularisation
• Non-ischaemic: ≥3 months on optimal GDMT

Secondary Prevention:

• Survived VT/VF arrest
• Sustained VT with haemodynamic compromise
• Sustained VT with EF ≤35%

Contraindications:

• Expected survival <1 year
• Incessant VT/VF
• Severe psychiatric disease
• NYHA IV not candidate for advanced therapies

CRT (Cardiac Resynchronisation Therapy):

Strongest Indication (LBBB + QRS >150ms):

• EF ≤35%
• LBBB morphology
• QRS ≥150ms
• NYHA II-IV despite optimal GDMT
• Response rate: ~70%; super-response (EF normalises): ~20%

Moderate Indication:

• LBBB with QRS 130-149ms
• Non-LBBB with QRS ≥150ms

Not Recommended:

• QRS <130ms
• RV pacing requirement >40% (consider upgrade from pacemaker to CRT)

Technical Aspects:

• LV lead placed via coronary sinus into lateral/posterolateral vein
• Complications: LV lead dislodgement (5%), phrenic nerve stimulation, coronary sinus dissection
• Programming: Aim for biventricular pacing >98%

LVAD (Left Ventricular Assist Device)

Indications:

• Bridge to transplant (BTT): Awaiting transplant
• Bridge to decision (BTD): Assess transplant candidacy
• Destination therapy (DT): Not transplant candidate

Patient Selection:

• Refractory HF (INTERMACS profile 1-4)
• Adequate RV function (RV failure = poor outcome)
• No severe comorbidities that would limit survival/quality of life
• Adequate home support and ability to manage device

Complications:

• Pump thrombosis: 8% per patient-year
• Stroke: 10% per patient-year
• Driveline infection: 20% per patient-year
• GI bleeding: Common (acquired von Willebrand syndrome)
• RV failure: May require temporary RVAD support

Outcomes:

• 2-year survival: 70-80% (comparable to transplant short-term)
• Significant improvement in functional status

Monitoring and Follow-Up

Parameters to Monitor:

• Weight: Daily (patient); report if >2kg gain in 3 days
• Heart rate and BP: Each visit
• Renal function (U&Es): After dose changes, then 6-monthly
• Potassium: After ACEi/MRA dose changes
• NTproBNP: Prognostic; target 30% reduction from baseline
• Iron studies: Annually (treat if ferritin <100 or TSAT <20%)
• Echo: If clinical change; not routinely repeated if stable

Titration Schedule:

• Review every 2-4 weeks until target doses achieved
• Check U&Es 1-2 weeks after dose changes
• Don't increase dose if: symptomatic hypotension, AKI, hyperkalaemia

Heart Failure Nurse Specialist:

• Telephone monitoring
• Home visits for vulnerable patients
• Rapid access clinic
• Patient education
• Reduces hospitalisations by 25%

Quality Improvement in Heart Failure

Key Performance Indicators:

• % patients on ACEi/ARB/ARNI
• % patients on beta-blocker
• % patients on MRA
• % patients on SGLT2i
• % at target doses
• 30-day readmission rate
• Length of stay

Discharge Checklist:

• GDMT initiated/optimised
• Oral diuretic dose established
• Weight and BP checked
• U&Es checked post-diuretic adjustment
• Patient education (daily weights, fluid restriction, when to call)
• Follow-up arranged (HF nurse within 2 weeks, cardiology within 6 weeks)
• ICD/CRT referral if indicated
• Cardiac rehabilitation referral
• Smoking cessation advice
• Vaccinations up to date

Summary Comparison Tables

HFrEF vs HFpEF Comparison:

Feature	HFrEF (EF ≤40%)	HFpEF (EF ≥50%)
Prevalence	50% of HF	50% of HF
Demographics	Younger, male predominant	Older, female predominant
Aetiology	IHD, DCM	HTN, obesity, AF, DM
Echo findings	Dilated LV, reduced EF	Normal LV size, diastolic dysfunction
BNP levels	High	Elevated but may be lower than HFrEF
Prognosis	Worse mortality	Better mortality but high morbidity
GDMT proven	ACEi/ARNI, BB, MRA, SGLT2i	SGLT2i only (EMPEROR-Preserved, DELIVER)
Diuretics	For congestion	For congestion
Devices	CRT/ICD if criteria met	No role

Neurohormonal Antagonism - Mechanism Summary:

Drug Class	Targets	Mechanism	Mortality Evidence
ACEi	RAAS	Blocks ACE → ↓Ang II, ↓aldosterone	CONSENSUS, SOLVD
ARB	RAAS	Blocks AT1 receptor → ↓vasoconstriction	CHARM, Val-HeFT
ARNI	Neprilysin + AT1	↑Natriuretic peptides + ↓Ang II	PARADIGM-HF
Beta-blocker	SNS	Blocks β1 receptors → ↓HR, ↓remodelling	COPERNICUS, MERIT-HF
MRA	RAAS	Blocks mineralocorticoid receptor → ↓fibrosis	RALES, EMPHASIS-HF
SGLT2i	Multiple	↓preload, ↓afterload, metabolic effects	DAPA-HF, EMPEROR-Reduced

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Last Reviewed: 2025-12-27 | MedVellum Editorial Team

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and current guidelines.