Clinical Review: Heart failure

Dr Rajiv Sankaranarayanan, a cardiology specialty registrar in electrophysiology, North West Deanery, and British Heart Foundation Clinical Research Fellow.

Cardiomyopathy may be a cause of heart failure (Photograph: SPL)
Cardiomyopathy may be a cause of heart failure (Photograph: SPL)

Section 1: Epidemiology and aetiology
Heart failure (HF) occurs when abnormal cardiac function causes the heart to fail to pump enough blood to match the metabolic demands of tissues under normal filling pressure.

The prevalence of HF in the UK has been shown to be 8.3 per 1,000 population in a large GP survey (list size about 250,000).1 The UK incidence of a clinical diagnosis of HF by GPs in a general practice population of about 700,000 was found to be 9.3 per 1,000 person-years.2

The prevalence of HF is rising with the ageing population and improved treatments mean more people survive ischaemic events. The cost of HF to the NHS is estimated to be as much as 2% of total NHS expenditure, because it is present in up to 10% of inpatients and is the cause of up to 5% of acute admissions.3

IHD and hypertension are the two main causes of HF in the developed world.4 AF is another common association, and valve disease and cardiomyopathies can each account for up to 10% of cases.4 Other causes may be endocrine (thyroid disorders, diabetes, adrenal disorders), toxins (alcohol, recreational drugs), nutritional (thiamine deficiency), infiltrative (sarcoidosis, amyloidosis, haemochromatosis), peripartum cardiomyopathy and end stage renal failure. Increased metabolic load on the heart may lead to high-output HF.

The term 'acute' HF is discouraged, because it is an umbrella term covering a variety of presentations. This classification has been superseded by three types according to presentation: new-onset HF, transient (episodic or recurrent) HF and chronic (persistent symptoms) HF.

Systolic and diastolic HF
Cardiac ejection fraction (EF), measured using echocardiography, has for years been a surrogate measure of the systolic function of the heart. It refers to the fraction of the cardiac end-diastolic volume that is ejected with each heartbeat. An EF ?55% is consistent with normal systolic function. The term diastolic HF - often replaced by 'preserved' or 'normal' EF (HFPEF or HFNEF) - is increasingly recognised, because up to half of patients presenting with symptoms of HF can have a normal or near-normal EF.

Raised JVP may be a sign of HF (Photograph: SPL)

Section 2: Making the diagnosis
Detailed history taking to elicit the aetiology is paramount. Typical signs include tachycardia, hypotension, raised JVP, ankle and sacral oedema, displaced apex beat, third heart sound, murmurs, lung crepitations and signs of pleural effusion.

However, in early HF presentation, clinical examination may be normal and the GP should consider the diagnosis based on the history and investigations. There is poor correlation between symptom severity and prognosis, but it is useful to stage symptom severity using NYHA or ACC/AHA classifications to gauge the patient's response to treatment.

The NICE guidelines offer a succinct diagnostic algorithm for diagnosis of HF, depending on the presence or absence of previous MI.5

Presence of previous MI
If history and examination are indicative of possible HF, the patient needs to be referred for specialist assessment and echocardiography.

If the echocardiogram does not show an abnormality consistent with HF (systolic or HFPEF), serum B-type natriuretic peptides (BNP) should be measured. If levels are raised (see below for interpretation of levels), consider a diagnosis of HFPEF. If levels are normal, HF is unlikely. BNP can be used in this way to diagnose diastolic HF, as recommended in the NICE guidelines, as long as false positive causes of raised BNP are excluded.

Absence of previous MI
If history and examination are suggestive of possible HF, the next step is to measure BNP or N-terminal pro-B-type natriuretic peptide (NT-proBNP).

If the levels are high (BNP ≥400pg/ml or NT-proBNP >2,000pg/ml), patients should be referred for specialist assessment and Doppler echocardiography within two weeks. If BNP ≥100-400pg/ml or NT-proBNP 400-2,000pg/ml, specialist assessment and echocardiography should take place within six weeks. If the levels are normal (BNP ≤100pg/ml), HF is unlikely and other diagnoses should be considered.

Serum levels are also useful to assess the patient's prognosis and monitor the efficacy of treatment.

For a diagnosis of HFPEF, all of the following criteria must be met:4

  • Signs and/or symptoms of chronic HF.
  • Normal or only mildly abnormal LV systolic function (LVEF ≥45-50%).
  • Evidence of diastolic dysfunction (abnormal LV relaxation or diastolic stiffness).

Routine tests include FBC, renal function including electrolytes and eGFR (these have to be monitored serially during initiation and uptitration of therapy such as diuretics, ACE inhibitors or ARBs), TFTs and LFTs, glucose, fasting lipids and urinalysis. Troponin measurement should only be considered if a recent acute coronary syndrome is suspected to have led to HF.

ECG is mandatory in all patients because it can provide evidence of a previous MI or associated arrhythmias such as AF. ECG features such as presence of left bundle branch block (LBBB) and QRS duration are essential in decision-making regarding implantation of ICD or cardiac resynchronisation therapy (CRT). Chest X-ray is also mandatory. It helps to assess for pulmonary congestion and cardiomegaly, and to rule out pulmonary causes of dyspnoea. Lung function tests may be considered.

Echocardiography provides information on systolic and diastolic function, valvular pathology and pulmonary pressures. Radionuclide imaging or cardiac MRI can be used to assess EF. Cardiac MRI also helps to differentiate between aetiologies such as ischaemia, inflammation or infiltration.

If ischaemia is suspected as the cause of HF, further tests, such as coronary angiography, myocardial perfusion imaging, CT angiography and stress echocardiography, can also be considered.

The role of the GP
Despite the increasing availability of more accurate diagnostic tests for HF, there can be delays in accessing these tests.

A large cohort of patients in the community with a diagnosis of HF made by a GP using a clinical approach showed that the accuracy of diagnosis can be comparable to that of cardiologists using defined diagnostic criteria.2

GPs can make an early clinical diagnosis and influence the outcome by early initiation of life-saving therapy.

Section 3: Managing the condition
Management should focus on relieving symptoms, improving quality of life and prolonging survival through a combination of lifestyle measures, pharmacological and non-pharmacological interventions.

HF management is prolonged and many of the treatments have side-effects, so it is important for patients and their carers to be fully involved in decisions. Lifestyle modifications include smoking cessation and restriction of salt intake (less than 2-3g per day fluid and alcohol complete avoidance of in cases alcohol-related cardiomyopathy.

Physical training as part of a supervised cardiac rehabilitation programme has been shown to have beneficial effects. Advice should also be provided regarding sexual activity, air travel and the importance of annual influenza vaccination.

GPs play an important part in reinforcing lifestyle advice and they can be an important bridge between the patient and secondary or tertiary care.

HFPEF is known to confer a similar prognosis to that for HF with impaired EF, but there is as yet no proven drug which is known to improve survival in this cohort of patients. It is important, therefore, to control the causative comorbidity, such as hypertension, diabetes or ischaemia, aggressively.

HF with impaired EF
Combinations of beta-blockers, ACE inhibitors and aldosterone antagonists at maximum tolerated doses are defined as optimal medical therapy.

If the patient is asymptomatic, cardioselective beta-blockers and ACE inhibitors/ARBs (if ACE inhibitor intolerant) are initiated and uptitrated to their maximum tolerated doses. If the patient is symptomatic and has evidence of fluid overload, diuretics are added.

Aldosterone receptor antagonists are added if the patient continues to exhibit NYHA Class 2-4 symptoms, but require close monitoring of renal function and electrolytes.

Ivabradine, a new HF drug, should be considered after a cardiologist's advice if the patient is intolerant to beta-blockers or their heart rate remains suboptimally controlled, at >70 beats per minute (bpm). Other drugs include combinations of nitrate and hydralazine (if ACE inhibitors/ARBs are contraindicated) and digoxin.

Non-pharmacological care
Non-pharmacological options require referral to tertiary care and include ICD, CRT (which prolongs survival and significantly improves symptoms), surgery (coronary revascularisation, valve repair or replacement, aneurysmectomy, LV assist device implant and cardiac transplantation).

According to NICE guidelines, CRT should be considered in patients with EF ≤35%, LBBB with QRS duration ≥150ms or if QRS duration is 120-149ms with evidence of mechanical dyssynchrony, and ongoing or recent NYHA3/4 symptoms while on optimal medical therapy.

Section 4: Prognosis
HF is a diagnosis that confers poor prognosis. One study has shown that HF had the lowest five-year survival rate of 25% when compared with common cancers (with the exception of lung cancer).6

Despite significant advances in management options, more than half of severe HF patients die within a year.7 Although HF is a chronic condition, there is a significant risk of sudden death and this makes prognostication difficult. Various clinical risk-scoring systems have been advocated to help predict individual prognosis, especially in patients admitted due to HF.

Accurate risk prediction is important because it helps to define the role of pharmacological and non-pharmacological therapies, as well as the need for palliative care.

Risk predictors used in the EFFECT risk tool include comorbidities (age, cerebrovascular disease, dementia, cirrhosis), clinical variables (respiratory rate, systolic BP) and blood results (blood urea nitrogen, Hb and serum sodium).8 However, renal function and systolic BP have been shown to be the most important risk predictors in acute HF.9

EF, the six-minute walk test10 and BNP have been shown to be strong independent predictors of the risk of hospital admission and of mortality. Newer methods of assessing arrhythmic risk include T-wave alternans, heart rate variability and baroreflex sensitivity, although as yet, none of these has been widely applied in mainstream clinical practice in the UK.

Patients with stable NYHA Class 1 symptoms who are well established on optimal medical therapy and understand self-care (dietary and fluid management) are usually discharged to GP follow-up with a plan for re-referral to hospital-based management in case of deterioration.

Patients can also be managed by HF specialist nurses in the community and this has been shown to improve quality of life and reduce readmissions.11

Section: 5 Case study
A 54-year-old white male presented to his GP with a three-month history of worsening exertional dyspnoea.

He is a current smoker with a 40 pack-year history and also had a positive family history of IHD. There was no history of hypertension, diabetes or hyperlipidaemia.

A detailed history revealed that the patient first developed dyspnoea on walking up slopes about three months before presentation; this had now progressed to dyspnoea on walking a mile on flat ground (NYHA Class 2).

There was no associated chest pain, cough or orthopnoea, but there had been five episodes in the past two weeks that were suggestive of paroxysmal nocturnal dyspnoea. His BP was 124/60mmHg and his pulse was 96bpm and regular.

Cardiorespiratory system examination showed a raised JVP of 5cm, normal apex but a third heart sound and bibasal lung crepitations. There was also mild pitting pedal oedema.

Presumed HF
ECG performed at the surgery showed normal sinus rhythm and poor progression of R waves, but no other significant abnormalities.

The GP made a presumptive diagnosis of HF, offered lifestyle advice and requested routine blood tests including BNP. The patient was started on furosemide 40mg twice daily and bisoprolol 1.25mg once daily, with a plan for follow-up later in the week with BNP results.

He was seen later in the week and reported improvement in his dyspnoea (NYHA Class 1); his JVP was now normal and there was no pedal oedema.

Routine bloods were within normal limits, but his BNP result was elevated, at 555pg/ml. The GP explained to the patient that this result was indicative of a diagnosis of HF and that he would require an echocardiogram in secondary care (within two weeks as recommended by NICE). The patient was started on an ACE inhibitor, with a plan to repeat renal function tests the following week.

Cardiologist review
The echocardiogram showed normal valve function but severely impaired LV systolic function with an EF of 35%. The GP then referred the patient for urgent outpatient cardiologist review. The patient remained at NYHA Class 1 and was reviewed in the cardiology outpatient clinic after 10 days, when his beta-blocker and ACE inhibitor doses were uptitrated.

Lifestyle advice was reiterated and the patient was followed up six-monthly, with stable symptoms. A repeat echocardiogram the following year showed an improved EF of 45%.

Section 6: Evidence base
Clinical trials

  • De Giulia F, Khawb KT, Cowie MR et al. Incidence and outcome of persons with a clinical diagnosis of heart failure in a general practice population of 696,884 in the United Kingdom. Eur J Heart Fail 2005; 7(3): 295-302. See the diagnostic algorithm in section 4.4, page 70.

This large population-based study of a UK GP practice population of about 700,000 assessed the incidence and outcome of HF based on clinical diagnosis by GPs. It showed that identification of HF by GPs is comparable to diagnosis by cardiologists using diagnostic criteria.


  • NICE. Clinical Guideline. Chronic heart failure: management of chronic heart failure in adults in primary and secondary care. NICE, London, 2010.
  • Dickstein K, Cohen-Solal A, Filippatos G et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Eur J Heart Fail 2008; 10(10): 933-89.

Information on all aspects of aetiopathogenesis, classification, diagnosis and management of HF.

  • Hunt SA, Abraham WT, Chin MH et al. ACC AHA Guidelines. 2009. Focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults. J Am Coll Cardiol 2009; 53(15): e1-e90.
  • SIGN. Management of chronic heart failure, Scottish Intercollegiate Guidelines Network. SIGN, 2007.


Click here to take a test on this article and claim a certificate on MIMS Learning


These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.

  • Audit your patients with HF, checking which patients have an identifiable cause of HF listed in the notes.
  • Ensure all patients are regularly reviewed, checking they are concordant with their medication.
  • Discuss with colleagues setting up an HF clinic at your practice.

1. Majeed A, Williams J, de Lusignan S et al. Management of heart failure in primary care after implementation of the National Service Framework for Coronary Heart Disease: a cross-sectional study. Public Health 2005; 119: 105-11.

2. De Giulia F, Khawb KT, Cowie MR et al. Incidence and outcome of persons with a clinical diagnosis of heart failure in a general practice population of 696,884 in the United Kingdom. Eur J Heart Fail 2005; 7(3): 295-302.

3. Stewart S, Jenkins A, Buchan S et al. The current cost of heart failure to the National Health Service in the UK. Eur J Heart Fail 2002; 4: 361-71.

4. Dickstein K, Cohen-Solal A, Filippatos G et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Eur J Heart Fail 2008; 10(10): 933-89.

5. NICE. Clinical Guideline. Chronic heart failure: management of chronic heart failure in adults in primary and secondary care. NICE, London, 2010.

6. Stewart S, MacIntyre K, Hole DJ et al. More 'malignant' than cancer? Five-year survival following a first admission for heart failure. Eur J Heart Fail 2001; 3(3): 315-22.

7. Graham I, Atar D, Borch-Johnsen K et al. European guidelines on cardiovascular disease prevention in clinical practice: executive summary. Eur Heart J 2007; 28: 2375-414.

8. Lee DS, Austin PC, Rouleau JL et al. Predicting mortality among patients hospitalized for heart failure: derivation and validation of a clinical model. JAMA 2003; 290: 2581-7.

9. Fonarow GC. Epidemiology and risk stratification in acute heart failure. Am Heart J 2008; 155(2): 200-7.

10. Bittner V, Weiner DH, Yusuf S et al. Prediction of mortality and morbidity with a 6-minute walk test in patients with left ventricular dysfunction. SOLVD Investigators. JAMA 1993; 270(14): 1702-7.

11. Stewart S, Blue L, Walker A et al. An economic analysis of specialist heart failure nurse management in the UK; can we afford not to implement it? Eur Heart J 2002; 23(17): 1369-78.

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