Contributed by Dr Kate Gatenby, specialist registrar, and Dr Klaus Witte, senior lecturer and honorary consultant cardiologist, division of cardiovascular medicine and diabetes, University of Leeds.
Section 1: Epidemiology and aetiology
Chronic heart failure (CHF) is a common syndrome of symptoms of exercise intolerance due to breathlessness or fatigue, in the presence of left ventricular (LV) dysfunction.1
It affects up to 1 million adults in the UK, but the prevalence increases with age such that around 10 per cent of patients over 80 years old have CHF.
Despite recent advances in medical and device therapies, the condition remains associated with an annual mortality rate approaching 10-15 per cent per year, and a poor overall quality of life punctuated by frequent readmissions to hospital.
CHF costs the NHS almost £1 billion per year (>1.8 per cent of health expenditure).
Diastolic heart failure
Traditionally the term CHF applies to a syndrome associated with left ventricular systolic dysfunction (LVSD). However, a large proportion of mostly older and more commonly female patients with symptoms of exercise intolerance and signs of congestion do not have significant ventricular systolic dysfunction. These patients are sometimes labelled as having 'diastolic heart failure'.
This term remains controversial and many patients have other contributing causes for breathlessness, such as lung disease, lack of fitness and obesity.
Although some patients do have abnormalities of diastolic left ventricular function (impaired relaxation of the heart), this is also frequently seen in asymptomatic elderly patients. The management of patients with diastolic heart failure is much less clear than for those with LVSD. Furthermore, their outcome is generally better, although they do suffer similarly poor quality of life and hospitalisation rates.
This article will focus on recent developments in the management of CHF due to LVSD.
Ischaemic heart disease
Ischaemic heart disease (IHD) accounts for around two-thirds of all CHF, and most of the rest is due to isolated heart muscle weakness in the presence of normal coronary arteries, known as dilated cardiomyopathy (DCM).
Hypertension, alcohol and chronic valvular disease presently account for around 10 per cent of cases of CHF.
Identifying the aetiology is important in all cases, partly since non-ischaemic CHF has a better outcome than IHD, but also to explore potential treatments such as revascularisation or valvular surgery.
Section 2: Diagnosis
Patients presenting with breathlessness or fatigue that could be due to CHF should have a full physical examination.
Features suggestive of heart failure include signs of fluid overload, cardiac murmurs and extra sounds, and arrhythmia. Many patients will have a normal physical examination.
A 12-lead ECG is essential. If normal, heart failure is unlikely.2 Abnormalities such as arrhythmias (for example AF), left ventricular hypertrophy (LVH), ischaemia, evidence of previous infarction or conduction abnormalities such as left bundle branch block (LBBB) (see above) increase the likelihood that there is LVSD.
Blood tests should be performed in order to exclude anaemia, renal dysfunction or thyroid disease, and spirometry can help identify patients with airways disease, which may co-exist.
N-terminal brain natriuretic peptide (NT-pro BNP) is increasingly being measured in primary care. BNP is released by cardiomyocytes in response to stretch and is raised in CHF.
Although a normal value for BNP is a useful negative predictor, especially in the presence of a normal ECG,3 BNP can also be raised in acute sepsis, pneumonia, renal failure, hypertension and COPD.
Transthoracic echocardiography should be organised for most patients. If performed and interpreted by an experienced technician or physician, this simple non-invasive test will establish the presence of LVSD and give information about possible causes, such as valve disease (see section 3).
While many GPs have access to community echocardiography, it is important to consider why a patient has developed cardiac failure and to attempt to establish the aetiology.
Subsequent tests, which may only be provided in secondary care, aim to establish aetiology and prognosis of LVSD. These include coronary angiography to determine whether there is coronary artery disease and its severity, Holter monitoring to look for dysrhythmias, and an assessment of exercise capacity such as a six-minute walk test or cardiopulmonary exercise testing to measure peak oxygen uptake.
Section 3: Pharmacological treatment
The focus of treatment for CHF has moved away from fluid management toward addressing the neurohormonal activation seen in CHF, with the aims not only of improving symptoms but also prognosis.
Although diuretics are often useful to control fluid overload, they are not associated with prognostic benefit and the lowest dose necessary to prevent or treat congestion should be prescribed.
Usually loop diuretics suffice, although occasionally combination therapy with thiazide diuretics is necessary. NSAIDs cause fluid retention and should be avoided if possible.
Most patients should be prescribed an ACE inhibitor and a cardioselective beta-blocker. Patients with an adverse reaction to an ACE inhibitor (most commonly a persistent noctural cough) can be switched to an ARB. ACE inihibitor-induced renal failure is rare.
Most patients have a small increase in serum creatinine. Increases of more than 15-20 per cent can be treated first by reducing ACE inhibitor doses.
Despite early concerns that beta-blockers would be poorly tolerated in CHF, most patients, even the elderly,4 will tolerate high dosages provided small starting dosages are used and slowly increased.
Although beta-blocker use is associated with a small, asymptomatic reduction in FEV1, pat-ients with chronic airways disease and little wheeze should not be excluded from taking them.5
Concerns about symptoms of postural hypotension are often not realised, but in those with symptoms, the ACE inhibitor dosage can be reduced slightly to allow initiation of a beta-blocker. Modest dosages of both agents are probably preferable to the maximum dosage of one.
Intolerance or side-effects limiting uptitration of either ACE inihibitors or beta-blockers is an indication for specialist review.
Spironolactone has been shown to reduce mortality and hospitalisation rates in patients with more severe CHF and is recommended in patients with current or previous hospitalisations for CHF. It is also useful in patients with fluid overload as an adjunct to loop diuretics.
The major side-effect is hyperkalaemia, which is more common in those with more severe renal impairment, diabetes and those already taking high dosage ACE inhibitors or ARBs. Other side-effects include gynaecomastia, which should prompt a switch to an alternative anti-aldosterone agent, eplerenone.
Digoxin is useful for symptom control in patients with severe heart failure, or in addition to beta-blockers for the control of the ventricular response to AF. It is neutral in terms of mortality. Antiarrhythmic therapy with amiodarone is not associated with improved outcome and should not be used routinely.
Although patients with CHF are at a high risk of thromboembolism, aspirin is at best neutral in terms of prognosis, even in those with IHD, and may in fact counter some of the beneficial effects of ACE inhibitors.
Formal anticoagulation with warfarin is associated with a reduction in CHF hospitalisations and a trend to reduced mortality compared with aspirin. All patients with both heart failure and atrial arrhythmias should receive warfarin unless there are absolute contra-indications.
Section 4: Cardiac resynchronisation therapy
LBBB is common in CHF patients and associated with more severe LV dysfunction, more severe symptoms and an adverse prognosis.
LBBB reflects delayed ventricular activation proceeds through the left ventricle, resulting in dyssynchronous ventricular contraction.
A cardiac resynchronisation therapy (CRT) pacemaker simultaneously paces the heart from the apex of the right ventricle and the lateral LV wall,(see image) thereby 're-synchronising' left ventricular contraction. The pacemaker is inserted under local anaesthetic during a short (60-90 minute) low-risk procedure.
CRT can improve symptoms, reduce hospitalisation rate and reduce total mortality (both due to heart failure and sudden death) (see box).6,7 Emerging data suggest that early CRT (before CHF becomes severe) in patients with mild symptoms and LBBB can delay deterioration and improve prognosis.
Combined devices providing CRT and an implantable cardioverter defibrillator (ICD) function to reduce the risk of sudden arrhythmic death. Potential candidates are younger patients with few co-morbidities and stable NYHA class III symptoms.
The best predictor of potential benefit from CRT is a simple ECG demonstrating LBBB and hence a referral for CRT can easily be made from primary care. There is no upper age limit for CRT.
Patients are increasingly managed in the community. However, there have been many recent developments offering significant improvements in quality of life, hospitalisation and mortality for this malignant disease.
The primary care team should therefore have a low threshold for referring patients for specialist review and all newly-diagnosed patients should be considered for referral to a physician with a special interest in heart failure.
Simple markers of high risk that should prompt referral are shown in the box above.
NICE guidelines for cardiac resynchronisation
Cardiac resynchronisation therapy with a pacing device (CRT-P) is recommended as a treatment option for patients with heart failure who fulfill all of the following criteria:
- Currently or have recently experienced NYHA class III-IV symptoms.
Are in sinus rhythm:
- either with a QRS duration of 150ms or longer on a standard ECG
- or with a QRS 120-149ms estimated by ECG and mechanical dyssynchrony confirmed by echocardiography.
- Have a left ventricular ejection fraction of 35 per cent or less.
- Receiving optimal medical therapy.
Patients requiring referral to a specialist
- New onset or worsening of symptoms
- High-risk features (LBBB, renal impairment)
- Symptomatic hypotension
- Recent admission
- Onset of AF
- Symptomatic palpitations
- Resistance congestion
- Recurrent angina pectoris
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1. Witte K K, Clark A L. Why does chronic heart failure cause breathlessness and fatigue. Prog Cardiovasc Dis 2007; 5: 366-84.
2. Khan N K, Goode K M, Cleland J G et al; EuroHeart Failure Survey Investigators. Prevalence of ECG abnormalities in an international survey of patients with suspected or confirmed heart failure at death or discharge. Eur J Heart Fail 2007; 9: 491-501.
4. Witte K K, Clark A L. Carvedilol in the treatment of elderly patients with chronic heart failure. Clin Intervent Ageing 2008; 3: 1-16.
5. Witte K K, Clark A L. Beta-blockers and inspiratory pulmonary function in chronic heart failure. J Card Fail 2005; 11: 112-6.
6. Cleland J G, Daubert J C, Erdmann E et al. Cardiac Resynchronization-Heart Failure (CARE-HF) Study Investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1,539-49.
7. Cubbon R M, Witte K K. Clinical review: Cardiac resynchronisation therapy for heart failure with conduction delay. BMJ 2009; 338: 1,265-70.