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Heart Failure

Dr Rajesh Varma

Definition

Heart failure (HF) is a complex syndrome in which the ability of the heart to maintain the circulation of blood is impaired as a result of a structural or functional impairment of ventricular ejection or ventricular filling. 

Prevalence

HF affects 1-2% of adults in developed countries.

  • 1 in 35 people 65–74 years of age.

  • 1 in 15 people 75–84 years of age.

  • Just over 1 in 7 people 85 years of age or older.

Pathophysiology and Pharmacotherapy

Heart failure is classified into two main categories with either a reduced (HFrEF) or preserved (HFpEF) ejection fraction [left ventricular ejection fraction (LVEF)].
Heart failure midrange ejection fraction (HFmrEF) has been recognised by European Society of Cardiology ESC.

HFrEF assigned to LVEF < 40%

HFpEF assigned to LVEF ≥ 50% with evidence of diastolic dysfunction (restrictive left ventricular filling) or structural cardiac changes

HFmrEF for LVEF 40-50%

In both HFrEF and HFpEF the heart fails to pump adequately, causing activation of:

  • Natriuretic peptide system (such as BNP, ANP). These are endogenous cardio-protective peptides which cause vasodilation/hypotension, reduced sympathetic tone, natriuresis/diuresis, reduced vasopressin/aldosterone and reduced myocardial hypertrophy/fibrosis.
    Two laboratory assays: N-terminal pro B type NP, B type NP

    Natriuretic peptides are broken down by the enzyme Neprilysin: Sacubitril is a Neprilysin Enzyme Inhibitor

  • Sympathetic nervous system activation. Adrenaline/Noradrenaline activate alpha-1, beta-1, beta-2 receptors, causing vasoconstriction, activation of Renin-Angiotensin-Aldosterone System (RAAS), increased vasopressin, increased heart rate and increased contractility.

    Cardio-selective beta-blockers (bisoprolol, carvedilol, nebivolol) reduce the effects of sympathetic nervous system activation.

  • Renin-Angiotensin-Aldosterone System (RAAS) activation. Increased angiotensin II acts on AT-1 Receptors located in adrenal, renal and vascular systems leading to vasoconstriction, increased sympathetic tone, increased aldosterone and increased myocardial hypertrophy/fibrosis.

    RAAS inhibitors (ACE-I, ARB, MRA) reduce the effects of RAAS activation.

There is strong evidence for pharmacological intervention to reduce morbidity and mortality of HFrEF, but not for HFpEF

Causes

Myocardial disease:

Coronary artery disease
Hypertension
Cardiomyopathies:
Familial, Infective, Immune-mediated, Toxins (alcohol or cocaine), Pregnancy, Infiltrative (sarcoidosis, amyloidosis, haemochromatosis, connective tissue disease)

Valvular heart disease (for example aortic stenosis).
Pericardial disease: Constrictive pericarditis, Pericardial effusion.
Congenital heart disease
Arrhythmias (for example atrial fibrillation and other tachyarrythmias).
High output states: Anaemia, Thyrotoxicosis, Phaeochromocytoma, Septicaemia, Liver failure, Arteriovenous shunts, Paget's disease, Thiamine (vitamin B1) deficiency.
Volume overload: End-stage chronic kidney disease.Nephrotic syndrome.
Obesity
Drugs: Alcohol, Cocaine, Pioglitazone, Steroids, NSAIDs, Non-dihydropyridine CCBs like verapamil, TCAs, pseudoephedrine (decongestant), [Beta-blockers]

Differential diagnosis

Shortness of breath:
COPD/Asthma
Pulmonary embolism
Lung cancer

Peripheral oedema:
Venous insufficiency (dependent oedema)
Nephrotic syndrome
Drugs (dihydropyridine CCBs like amlodipine, NSAIDs)
Hypoalbuminaemia (from renal or hepatic disease)
Pelvic tumour

Other conditions:
Obesity
Severe anaemia
Thyroid disease
Bilateral renal artery stenosis

Complications

Arrhythmias: Atrial fibrillation and Ventricular arrhythmias
Depression: Major depressive disorder is present in up to 20% of people with heart failure
Cachexia
Chronic kidney disease
Sexual dysfunction
Sudden cardiac death

Prognosis

50% of  heart failure cases die within 5 years of diagnosis
40% of people admitted to hospital with heart failure die or are re-admitted within 1 year.

Signs

Raised jugular venous pressure (highly predictive for HF, but not always present)
Tachycardia, Atrial fibrillation
A laterally displaced apex beat,
Heart murmurs +/- 3rd/4th heart sounds (gallop rhythm)
Tachypnoea, basal crepitations, and pleural effusions
Oedema (legs, sacrum), ascites, hepatomegaly

Symptoms

Breathlessness
Orthopnoea
Fluid retention
Fatigue
Light headedness or syncope

New York Heart Association (NYHA) functional classification of symptoms.
Class I — no limitation of physical activity.
Class II — slight limitation of physical activity
Class III — marked limitation of physical activity.
Class IV — unable to carry out any physical activity without discomfort.

Primary care investigations

  1. 12-lead ECG

  2. Bloods: NT-proBNP, FBC, U&Es, LFTs, TFTs, Lipids, HBA1C, FBC

  3. Urinalysis

  4. CXR

  5. Consider peak flow and spirometry

Assessment

  1. Arrange admission if the person has severe symptoms.

  2. For pregnant women (or women who have given birth within 6 months) with suspected heart failure, either arrange emergency admission (based on clinical judgement) or seek immediate specialist advice.

  3. Suspected Heart Failure AND history of previous MI —> Urgent 2ww referral to cardiology (+echocardiography).
    DO NOT MEASURE NT-proBNP

  4. Suspected Heart Failure AND no previous MI

    NT‑proBNP level <400 ng/litre (47 pmol/litre) —> Heart failure UNLIKELY (high NPV of the threshold used by NICE for NT-proBNP)
    NT‑proBNP level 400- 2,000 ng/litre (47 to 236 pmol/litre) —> Referral to cardiology (+ echocardiography) within 6 weeks
    NT‑proBNP > 2,000 ng/litre (236 pmol/litre) —> Urgent 2ww referral to cardiology (+echocardiography)

    High serum NT-proBNP correlates to poor prognosis

  5. Consider commencement of loop diuretics treatment (Furosemide 20–40 mg od, Bumetanide 0.5–1.0 mg od) to provide symptomatic improvement of fluid overload, whilst awaiting specialist assessment.

Interpretation of natriuretic peptide levels

Natriuretic peptide levels may be reduced by:

  • BMI>35

  • Drugs including diuretics, ACEi, ARBs, BB, MRA.

  • African-Caribbean family origin.

Natriuretic peptide levels may be elevated by:

  • Age over 70 years.

  • Left ventricular hypertrophy, myocardial ischaemia, or tachycardia.

  • Right ventricular overload.

  • Hypoxia.

  • Pulmonary hypertension.

  • Pulmonary embolism.

  • Chronic kidney disease (eGFR<60)

  • Sepsis.

  • Chronic obstructive pulmonary disease (COPD).

  • Diabetes mellitus.

  • Liver cirrhosis.

Management following diagnosis of chronic heart failure

Pharmacotherapy

HFpEF
Diuretics low to medium dose diuretic, up to 80 mg furosemide (or equivalent)
No evidence of improved morbidity or mortality following use of ACE Inhibitor, ARB, MRA or Beta-Blocker.
Refer for specialist management

HFrEF
Diuretics low to medium dose loop diuretic
Aim to prescribe both ACE Inhibitor or ARB AND Beta-Blocker (bisoprolol, carvedilol, nebivolol licensed for treatment of HF) (may need to switch from previous BB)
Both ACE-I/ARB and BB reduce morbidity and mortality in HFrEF
One drug should be introduced at a time, adding the second drug once the person is stable on the first drug.
If the person is still symptomatic despite optimal treatment with an ACEi/ARB and BB, a referral for specialist management should be arranged.

Other Actions for all HF (HFpEF, HFrEF)

  1. Review drugs which may cause or worsen HF (pioglitazone, steroids, NSAIDs, Non-dihydropyridine CCBs like verapamil, TCAs, pseudoephedrine)

  2. Recommended loop diuretics include furosemide (most widely used), bumetanide, and torasemide.

  3. Consider Antiplatelet drug if angina/coronary heart disease and Statin

  4. Manage co-morbidities: Hypertension, atrial fibrillation, ischaemic heart disease, angina, diabetes, chronic kidney disease, COPD/Asthma, Gout

  5. Screen for anxiety/depression

  6. Supervised exercise-based rehabilitation programme

  7. Appropriate vaccinations (seasonal influenza and once-only pneumococcal)

  8. Avoid overuse of dietary salt

  9. Advice on maintaining a health weight if obese (BMI>30)

  10. Follow-up and advanced care planning should be offered, if appropriate.

  11. Women of child-bearing age should be given advice about contraception and pregnancy.

Secondary care management


For patients with HFrEF who remain symptomatic:

  • Adding Amlodipine (long-acting dihydropyridine CCB) for the treatment of co-morbid hypertension and/or angina in patients with heart failure

  • Adding on MRA (spironolactone if K<4.5)

  • Replace ACE-I/ARB with Angiotensin receptor neprilysin inhibitor ARNI for EF<35%
    (PARADIGM-HF trial used LVEF<40% and compared ARNI vs enalapril)
    Entresto ( Sacubitril / Valsartan)
    Start at 24/26 mg BD 3w, 49/51 mg BD 3w, 97/103mg BD as maximum tolerated dose

  • Add ivabradine for sinus rhythm with heart rate>75 and EF<35%

  • Add Hydralazine and Nitrate (especially if African-Caribbean descent)

  • Add Digoxin (reduced hospitalisations but no decrease in mortality)

Other specialist treatments

  • Cardiac resynchronisation therapy (biventricular pacing): in patients with prolonged QRS complex (QRS>130ms) or bundle-branch block and LVEF<35%

  • Implantable cardioverter defibrillator (ICD): in patients deemed at high-risk of ventricular arrhythmias

  • Intravenous iron therapy for iron-deficiency anaemia in heart failure

  • Sodum-glucose co-transporter-2 inhibitors (SGLT2-I) (such as empagliflozin)

  • Guanylate cyclase stimulation (such as Vericiguat)

  • Cardiac myosin activator (such as Omecamtiv mecarbil)

  • Long-term mechanical ventricular assist devices (LVAD) as a bridge to eventual cardiac transplantation

  • Interventional percutaneous edge-to-edge repair of mitral valve regurgitation (using MitraClip) that has arisen secondary to progressive dilatation and re-modelling of the left ventricle by heart failure process.