Defining heart failure
Diagnosing heart failure
Managing chronic HF
NICE recommendations
Other potential therapies for HF






Heart failure (HF) is a complex clinical syndrome of symptoms and signs that suggest the action of the heart is impaired.1 However, the signs and symptoms may be difficult to elicit or non-specific, particularly in elderly individuals with comorbidities, and some primary care practitioners may need to increase confidence in their ability to accurately identify affected patients.2

A systematic approach to history taking, examination and referral helps to improve the accuracy of HF diagnosis and ensure that patients receive appropriate referral for specialist assessment and evidence-based therapies at target doses.

NICE1,3 and the European Society of Cardiology (ESC)4 have recently updated their guidance on the diagnosis and management of acute and chronic HF.


Defining heart failure

The ESC defines HF as a clinical syndrome characterised by typical symptoms (such as dyspnoea, fatigue and ankle swelling), which may be accompanied by other signs (such as elevated jugular venous pressure, pulmonary crackles and peripheral oedema), caused by a structural and/or functional cardiac abnormality, resulting in reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.4

HF is generally a chronic condition.5 A treated patient is considered to be ‘stable’ if their symptoms and signs have remained unchanged for at least one month.4 If chronic HF deteriorates, with episodes of worsening symptoms and signs necessitating more frequent visits to the GP or hospitalisation, the patient is said to be ‘decompensated’.5 Acute AF is the sudden development or worsening of signs and symptoms. It is a life-threatening condition that requires immediate medical attention and often urgent hospital admission. Congestive HF is acute or chronic HF, with evidence of volume overload.4

HF is historically described on the measurement of left ventricular ejection fraction (LVEF). HF patients may have preserved LVEF ≥50% (HFpEF), reduced LVEF <40% (HFrEF), or EF in the ‘grey area’ between 40–49% (HFmrEF). HFrEF remains the best understood in terms of pathophysiology, diagnosis and treatment.4


Diagnosing heart failure

The ESC definition restricts itself to the stages at which clinical symptoms are evident. However, prior to this, patients may present with asymptomatic structural or functional cardiac abnormalities (left ventricular systolic or diastolic dysfunction), which are precursors of HF. Recognition of these precursors is important, because they are associated with poor outcomes, and starting treatment at this early stage may reduce mortality in patients with left ventricular systolic dysfunction (LVSD).4

The identification of an underlying cardiac cause is central to a HF diagnosis. While a myocardial abnormality causing systolic and/or diastolic ventricular dysfunction, is the most common cause, HF may also result from abnormalities of the valves, endocardium, pericardium, heart rhythm and conduction, with more than one of these factors often being present.4

Differentiating patients with HF on the basis of LVEF is important due to differences in demographics, aetiologies, comorbidities and therapeutic response.4

NICE make the following recommendations for the diagnosis of HF, via a careful and detailed history, clinical examination and appropriate tests.1

An electrocardiogram (ECG) should be performed and the following tests considered to assess potential aggravating factors and/or rule out other disorders that may present similarly:1

  • Chest x-ray
  • Blood tests
    • full blood count
    • fasting lipids
    • fasting glucose
    • liver function tests
    • thyroid function tests
    • electrolytes, urea and creatinine
    • estimated glomerular filtration rate (eGFR)
    • Urinalysis
    • Peak flow or spirometry.
Atherosclerotic vascular disease
Metabolic syndrome
Renal insufficiency
Physical inactivity
Genetic (family history of cardiomyopathy)

Serum natriuretic peptides (B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NTproBNP)) should be measured in patients with suspected HF, who have not had a previous myocardial infarction (MI).

For those with new suspected acute HF, a single measurement of BNP or NTproBNP should be taken, and the following thresholds used to rule out a HF diagnosis:

  • B-type natriuretic peptide <100 ng/litre
  • N-terminal pro-B-type natriuretic peptide <300 ng/litre

Regarding serum natriuretic peptides, it is important to bear in mind that:1

  • Levels may be reduced in obese patients and those receiving treatment with diuretics, ACE inhibitors, beta-blockers, ARBs and aldosterone antagonists
  • High levels may result from causes other than HF. These include left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia [including pulmonary embolism], renal dysfunction (GFR <60ml/min), sepsis, chronic obstructive pulmonary disease (COPD), diabetes mellitus, age >70 years and cirrhosis of the liver
  • A BNP level <100 pg/ml (29pmol/litre) or an
    NTproBNP level <400pg/ml (47pmol/litre) in an untreated patient, means a diagnosis of HF is unlikely
  • The level does not differentiate between HF with LV systolic dysfunction and HFpEF.



NICE recommend that patients are referred to the specialist multidisciplinary HF team for:

  • The initial diagnosis of HF
  • The identification of the cause of their HF if not confirmed previously
  • The management of their HF if it:
    • is severe
    • fails to respond to treatment
    • can no longer be managed effectively at home
  • Assessment and advice on follow up if their HF is due to valve disease.

Patients with suspected HF and previous MI should receive urgent referral for transthoracic Doppler 2D ECG and specialist assessment within two weeks.1

Very high levels of serum natriuretic peptides are associated with a poor prognosis, so:

  • Patients with suspected HF and a BNP level >400 pg/ml (116pmol/litre) or an NTproBNP level >2000 pg/ml (236pmol/litre), should receive urgent referral for a transthoracic Doppler 2D ECG and specialist assessment within two weeks.1
  • Patients with suspected HF and a BNP level between 100–400 pg/ml (29–116pmol/litre) or an NTproBNP level between 400–2000pg/ml (47– 236pmol/litre), should be referred for transthoracic Doppler 2D ECG and specialist assessment within six weeks.1


Dyspnoea (exertional, nocturnal) Oedema
Fatigue/lethargy Elevated jugular venous pressure
Reduced exercise tolerance Crepitations or wheeze
Orthopnoea Displaced apex beat
Noctural cough Tachycardia
Wheeze Third heart sounds, murmurs
Anorexia Hepatomegaly
Confusion/delirium (elderly patients) Cachexia and muscle wasting

Managing chronic HF

Following a diagnosis of HF, routine evaluation should include regular weight measurement to check for signs of fluid retention, and assessment of pulse regularity to aid the early identification of AF (which is present in 35–45% of HF patients at diagnosis10).

Patient education is essential and should be delivered at every opportunity. An integrative approach, involving self-care, pharmacological therapies, and invasive therapies where appropriate, helps to reduce patient and partner anxiety, depression and fear. It also reduces hospital admissions and mortality, and improves functional status and quality of life.11

Lifestyle modification is important. Patients with HF should be advised to consume a healthy diet and reduce their salt intake if it is high. Smokers should be advised to quit and provided with support to do so. Advice on alcohol consumption should be tailored to each individual. GPs may need to broach the subject of sexual activity, as this is often not brought up by patients. Depressive symptoms should be identified and addressed. Patients should be offered a supervised group exercise-based rehabilitation programme.1 Formal daily step or distance counters can help monitor fitness.

Treatment strategies for HF aim to improve symptoms, reduce morbidity (with fewer hospital admissions and improvements in quality of life), and reduce mortality. There is now convincing evidence that treatment can improve prognosis as well as alleviate symptoms.

Current pharmacological therapies reflect an understanding of the compensatory mechanisms involved, and include diuresis, suppression of the overactive neurohormonal systems and improving contractility.

Dosing regimens need to be kept as simple as possible. Pharmacological therapies licensed specifically for HF should be chosen wherever possible.1


NICE recommendations on the pharmacologic treatment of HF due to LVSD

Diuretics should be used routinely to help relieve fluid retention and congestive symptoms, and titrated up and down as necessary following the introduction of other HF therapies.

First-line therapy is an angiotensin converting enzyme (ACE) inhibitor plus a beta-blocker. Use clinical judgement when deciding which drug to start first. The ACE inhibitor should be started at a low dose then titrated upwards at short intervals (eg. fortnightly), until the optimal tolerated/target dose is achieved. The beta-blocker should be introduced at a low dose and titrated up slowly.

An angiotensin receptor blocker (ARB) can be used as an alternative in patients unable to tolerate ACE inhibitors. For patients who are intolerant of ACE inhibitors and ARBs, seek specialist advice and consider hydralazine plus a nitrate as an alternative.

Sacubitril valsartan (Entresto), which inhibits neprilysin and blocks angiotensin II type I receptors via valsartan, is an effective treatment option for chronic HF, but should initiated by a HF specialist, where appropriate in patients with all of the following:12

  • New York Heart Association (NYHA) class II-IV symptoms
  • EF ≤35%
  • Already taking a stable dose of ACE inhibitor or ARB. 

Ivabradine (Procoralan), a heart rate lowering agent, may be used to treat chronic HF, after a fourweek stabilisation period on optimised standard therapy (ACE inhibitors, beta-blockers, aldosterone agonists), when initiated by a HF specialist, in patients with all of the following:13

  • NYHA class II-IV stable chronic HF with systolic dysfunction
  • In sinus rhythm with a heart rate of ≥75 beats per minute
  • EF ≤35%
  • Already taking standard therapy, or beta-blocker therapy is not tolerated or contraindicated.

Specialist advice should be sought prior to initiating second-line treatments. If a patient remains symptomatic despite optimal first-line therapy, consider adding one of the following:

  • An aldosterone antagonist (particularly in patients with moderate to severe HF (NYHA class III–IV) and those who have had an MI in the past month)
  • An angiotensin II receptor antagonist (ARB) (particularly in patients with mild to moderate HF (NYHA class II-III)
  • Hydralazine plus a nitrate (particularly in patients with moderate to severe HF and of African or Caribbean origin).
Drug Monitoring
ACE inhibitors Check serum urea, creatinine, electrolytes and eGFR on initiation and after each titration
Beta-blockers Check heart rate, blood pressure and clinical status after each titration
Aldosterone agonists Closely monitor potassium and creatinine levels plus eGFR—If the patient develops hyperkalaemia or renal function decreases, seek specialist advice
ARBs Monitor serum urea, electrolytes, creatinine and eGFR for signs of renal impairment or hyperkalaemia
Amiodarone Six monthly clinical review, including liver and thyroid function tests and assessment of side effects

In patients with HF, the calcium channel blocker (CCB), amlodipine, can be used to treat comorbid hypertension and/or angina. Avoid verapamil, diltiazem and short-acting dihydropyridine.

Amiodarone should only be prescribed on the advice of a specialist. The need to continue this treatment should be regularly reviewed.

Anticoagulants should be considered for patients with HF in sinus rhythm and those with a history of thromboembolism, intracardiac thrombus or left ventricular aneurysm.

Patients with HF and atherosclerotic disease should receive aspirin 75–150mg once daily.

In patients with decompensation of chronic HF, intravenous inotropic agents (eg. dobutamine, milrinone or enoximone) can be considered for shortterm use, but only on specialist advice.


NICE recommendations on the pharmacologic treatment of HF due to valve disease.1

ACE inhibitors should not be used in patients suspected of having haemodynamically significant valve disease, until they have received specialist assessment.



All patients with chronic HF require careful monitoring.1 Clinical assessment should include functional capacity, fluid status, cardiac rhythm, cognitive function and nutritional status. Serum urea, electrolytes, creatinine and eGFR should be checked. Medication reviews should include the need for changes and possible side effects.

Monitoring frequency depends on the patient’s clinical status and HF stability. The interval should be short (days to a fortnight) if the clinical condition or medication has changed, but is required at least sixmonthly for stable patients with proven HF.

If a patient is admitted to hospital as a result of HF, specialist advice should be sought on their management plan.

Adults with acute AF should receive a follow-up clinical assessment by a member of the hospital or community-based HF team within two weeks of hospital discharge.14

The management of HF should be guided by clinical criteria, irrespective of age and gender. Older patients may have reduced tolerance to medication and require more intensive monitoring for side effects.1


Other potential therapies for HF

The EMPA-REG OUTCOME trial assessed the effect of empagliflozin, a novel anti-diabetic agent, on cardiovascular outcomes in 7,028 patients with type 2 diabetes mellitus. If found a 35% relative risk reduction in the rate of hospitalisation for HF, which was a prespecified secondary endpoint.15 Although better explanations for this benefit may emerge, the combination of blood pressure reduction and prevention of sodium and water retention with empagliflozin, might have been particularly effective in preventing or delaying the development of HF. Unfortunately, we do not know which type of HF the EMPA-REG patients experienced, but the high prevalence of previous MI and hypertension suggests that many patients may have had underlying LVSD.16



HF rates are continuing to rise in the UK, mainly due to an ageing population, improved survival in people with coronary heart disease, particularly after MI, and improved use of evidence-based therapies.17

The National Audit shows convincingly, that we are making good progress in managing these patients, but there is still room for improvement.18

Although a case of HF is usually identified in primary care, it should be managed by a multidisciplinary team, including GPs, cardiologists, specialist nurses and elderly care physicians with an interest in HF, with good links to cardiac rehabilitation and advanced HF units, as well as palliative care services.


Professor Mike Kirby, Visiting Professor to the University of Hertfordshire and The Prostate Centre London

Conflict of interest: Professor Kirby has received funding for research, conference attendance, lecturing and advice from companies including Astellas, Pfizer, Takeda, Bayer, MSD, BI, Lilly, GSK, AZ, Besins and Menarini.