Dr Andrew Clark (left) and Dr John Cleland advocate widespread uptake of the new ESC guidelines to give patients with CHF the benefits of best practice


   

For guidelines to command the wide support of those who are applying them in clinical practice, they must be based upon respected judgment of the available evidence. In the field of chronic heart failure (CHF) there is a large number of trials available to guide practice.

The first set of European guidelines for the diagnosis and assessment of heart failure was published in 1995.1 The European Society of Cardiology Guidelines for the management of CHF have been published more recently (see below).2

Extract from the summary of the European Society of Cardiology's guidelines for the diagnosis and management of heart failure
extract from esc guidelines

A collegiate approach

There are problems in the interpretation of clinical trial evidence. Clinical trials cannot be all inclusive: the more restrictive the inclusion criteria the less generally applicable will be the results, and the more broad the criteria the less specific can be the question answered. The Task Force of the Working Group on Heart Failure took advice and opinions from the Working Group as a whole and from the chairmen of the other European Society of Cardiology Working groups; therefore the present guidelines represent the results of a collegiate approach.

The need for guidelines

It is generally thought that nothing can be done for the patient with heart failure, and clinicians are often reluctant to make best use of the available treatments, even in highly specialised centres.3

CHF is important because it is common, and is likely to become more so as the population ages (figure 1, below). Furthermore, improvements in the management of myocardial infarction mean that patients who would previously have died are now surviving to develop heart failure. Heart failure accounts for some 5% of acute hospital admissions,4 and makes major demands on general practice.5 The cost to the health service was estimated at £358 million in 1990-91.6 Most of these costs come from the need for repeated hospital admissions. About 30% of patients with heart failure are hospitalised each year,6 and individual patients may need multiple admissions.

Figure 1: The incidence of chronic heart failure from the Framingham study.13 Note the dramatic increase with age.
graph

High morbidity and mortality

CHF also carries a very high morbidity and mortality. Of common chronic conditions, CHF is associated with the greatest level of symptoms.7

Because the symptoms are severe and prognosis is poor, treatments can be tested in relatively small numbers of patients over relatively short periods of time to obtain relevant results relating to mortality, morbidity and potential cost implications.

Therapy has striking effect

There is now a wealth of evidence from clinical trials that modern therapy can have a striking effect in CHF. Despite this, therapies are not making their way into practice, and some treatments are still being used which are of little or no value, or are even dangerous.

Guidelines should depend upon trial evidence and guide the physician towards the best treatment for individual patients. They should not be too prescriptive – there are always patients for whom specific treatments may be inappropriate – and they should not be ashamed of noting where there is a lack of evidence for a particular treatment, nor of being firm where common treatments are shown to be deleterious.

Guidelines also suggest lines for future enquiry by defining current best practice, and provide a yardstick against which we can all measure our practice.

The clinical trials

CHF is the area par excellence for which solid evidence for the benefit of treatment exists. The aims of treatment must be to improve symptoms, to improve morbidity, and to reduce mortality. There are several areas that need to be addressed.

Diagnosis: A sound diagnosis of heart failure is the basis of good therapy. Studies have shown that the diagnosis of heart failure by clinical means alone is flawed. Clinical symptoms and signs are a good mechanism for alerting a doctor to a diagnosis of heart failure, but wrongly attributing symptoms to heart failure can lead to inappropriate and dangerous therapy.1

Diagnosis of heart failure relies heavily on echocardiography. It is widely available and non-invasive. Open access echo services are becoming increasingly available. However, a normal 12-lead electrocardiogram appears to indicate a low likelihood of heart failure,8 and may be a means of identifying patients in whom echocardiography is not required.

Role of primary care teams: The accurate diagnosis of heart failure is heavily dependent on primary care teams. It is important to have a high index of suspicion for CHF, particularly when a patient with known ischaemic heart disease presents with breathlessness. In addition, it is important to try to establish the underlying cause of heart failure. This is important prognostically, and may guide treatment.

Some studies suggest that some therapies are of benefit in specific conditions: thus, for example, amlodipine may benefit patients with non-ischaemic cardiomyopathy. In a small number of patients there may be a correctable abnormality, such as haemochromatosis or thyroid disease.

Angiotensin-converting enzyme inhibitors: ACE inhibitors have repeatedly been shown to confer a mortality benefit on patients with all grades of heart failure,9,10 and for the present these must be regarded as essential for the management of many patients. ACE inhibitors show benefits in all three goals of patient care: to improve symptoms, to improve morbidity and to reduce mortality.

However, it is important to appreciate that they have only been demonstrated to work for patients with systolic dysfunction. A minority of patients have heart failure with preserved systolic function, and ACE inhibitors have not been shown conclusively to benefit such patients. This emphasises the need for adequate diagnosis of heart failure.

The issue of which ACE inhibitor and in which dose has not been resolved to everyone's satisfaction. Pending definitive evidence from trials, the target dose for ACE inhibitor should be the target dose used in the mortality trials (table 1).

Table 1: Target doses for ACE inhibitors
Trial Drug Target dose
CONSENSUS9 Enalapril

20 mg bd

SOLVD10 Enalapril

10 mg bd

SAVE14 Captopril

50 mg tds

AIRE15 Ramipril

5 mg bd

TRACE16 Trandolapril

4 mg od

ATLAS17 Lisinopril up to 35 mg od

ACE = angiotensin-converting enzyme; od = once a day; bd = twice a day; tds = three times a day; CONSENSUS, SOLVD and ATLAS were heart failure studies; SAVE, AIRE and TRACE were post-infarction studies.

Other therapies: Diuretics and digoxin have not been so convincingly associated with a mortality benefit (table 2), and guidelines to some extent reflect the balance of contemporary opinion. Diuretic treatment has not been subjected to mortality trials. No-one would doubt the symptomatic benefit of diuretics, yet their use is associated with neurohormonal activation, known to be an adverse prognostic feature.

Table 2: Treatments available for chronic heart failure

Treatment Symptoms Hospitalisation Prognosis
Diuretics +++ +

?

ACE inhibitor ++ ++ +++
Digoxin + ++ (-)
Beta-blockers (+) + +++

+ suggests a beneficial effect on a given variable, – a negative one. Some studies report an adverse effect on symptoms with beta-blockers. The effect of digoxin on mortality is still not certain.

The role of digoxin, in use for centuries for heart failure, is still not clear-cut, despite the recent DIG trial.11 Although the digoxin-treated patients had fewer admissions to hospital, there was no effect on mortality. There are suggestions that while deaths due to worsening heart failure were reduced, deaths due to arrhythmia were increased. Doubts still linger about the safety of digoxin.

Beta-blockade: The use of beta-blockers for heart failure is likely to prove a ticklish problem. The accumulating evidence is strongly in favour of their widespread use,12 although every doctor was taught at medical school not to use beta-blockers for patients with CHF. Patients with CHF are potentially very sensitive to the introduction of beta-blockers and the general rule is to introduce very small doses, and increase the dose very slowly. For the present, beta-blockers should only be prescribed under expert supervision.

Adjunctive treatment

We need to recognise that the evidence base for many therapies is lacking, including those used in heart failure. Traditionally, for example, patients with CHF have been told to "take it easy", whereas recent evidence suggests that the converse may be the correct approach.

Other lifestyle changes need to be considered carefully for individual patients – should the patient be recommended to take early retirement from a job they dislike and are not dependent upon financially, or can they continue a job they greatly enjoy? Avoiding being overweight and abstaining from smoking, particularly in patients with ischaemic heart disease, is important.

Other active treatments are still being investigated. Positive inotropic agents have been a disappointment, but other agents acting on the renin-angiotensin system may have a role in the future. Other drugs, such as calcium-channel blockers and antiarrhythmics are best avoided unless there is a specific indication.

Implications for general practice

CHF is so common that it is unrealistic to expect all, or even most, patients to be seen by hospital specialists. The burden of care is likely to fall on GPs. The use of guidelines will help GPs to aim for the best possible treatment, and give them confidence in defining therapeutic aims.

Accurate diagnosis is crucial

To implement the guidelines most effectively, an accurate initial diagnosis is crucial, and GPs will need to identify all their potential CHF patients. These will most readily be identified from a past history of myocardial infarction, and from regular prescriptions of diuretics. All such patients will need an initial assessment, probably by echocardiography in the first instance (although a normal 12-lead electrocardiogram may prove sufficient to exclude patients with heart failure8).

Once diagnosed as having heart failure, all patients with systolic dysfunction (who therefore must have had echocardiography) should be tried on an ACE inhibitor. They will need regular review after the initiation of treatment, particularly for evidence of renal impairment or symptomatic hypotension. The doses will need to be increased to recommended levels. Adjunctive symptomatic treatment with diuretics will be needed for most patients, and in many cases also a beta-blocker.

Benefits for patients

Heart failure is a common condition for which effective cost-effective therapy is available. It is very frustrating that we have been unable to apply this knowledge more broadly to date. Widespread uptake of the guidelines will give patients the benefit of best current practice.

One of the challenges in implementing the guidelines will be the close cooperation between primary and hospital care.

Some centres are introducing nurse practitioners with a specific brief to provide liaison between patients in the hospital and the community. This can only help bring improvements to patient care.

Conclusions

CHF is common and a major cause of morbidity and mortality in the community. Treatment to alleviate symptoms and reduce mortality is readily available in the shape of ACE inhibitors, but their use is critically dependent on an accurate diagnosis of systolic dysfunction.

Identifying and accurately diagnosing the patients will allow GPs to create a register of patients. The field of heart failure is an active research area and one that is constantly changing. New recommendations for heart failure treatment will surely follow.

References

  1. Cleland JGF, Erdmann E, Ferrari R et al. Guidelines for the diagnosis and assessment of heart failure. Eur Heart J 1995; 16: 741-51.
  2. The Task Force of the Working Group on Heart Failure of the European Society of Cardiology. The treatment of heart failure. Eur Heart J 1997; 18: 736-53.
  3. Clark AL, Coats AJS. The usage of angiotensin-converting enzyme inhibitors: influence of severity of heart failure on treatment regime. Br Med J 1995; 310: 973-4.
  4. Parameshwar J, Poole-Wilson PA, Sutton GC. Heart failure in a district general hospital. Br Heart J 1990; 64: 57-8.
  5. Parameshwar J, Shackell MM, Richardson A, Poole-Wilson PA, Sutton GC. Prevalence of heart failure in three general practices in north west London. Br J Gen Pract 1992; 42: 287-9.
  6. McMurray JJV, Hart W, Rhodes G. An evaluation of the cost of heart failure to the National Health Service in the UK. Br J Med Econ 1993; 6: 99-110
  7. Stewart AL. Greenfield S, Hays RD et al. Functional status and well-being of patients with chronic conditions. JAMA 1989; 262: 907-13.
  8. Davie AP, Francis CM, Love MP et al. Value of the electrocardiogram in identifying heart failure due to left ventricular systolic function. Br Med J 1996; 312: 222.
  9. The CONSENSUS trial study group. Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1991; 325: 303-10.
  10. The SOLVD investigators. Effects of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 352: 293-302.
  11. The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med 1997; 336: 525-33.
  12. Packer M, Bristow MR, Cohn JN et al. Effect of carvedilol on morbidity and mortality in chronic heart failure. N Engl J Med 1996; 334: 1349
  13. Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart J 1991; 121: 951-7.
  14. Pfeffer MA, Braunwald E, Moye LA, et al for the SAVE investigators. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction and myocardial infarction. Results of the Survival and Left Ventricular Enlargement Trial. N Engl J Med 1992; 327: 669-77.
  15. Acute Infarction Ramipril Efficacy (AIRE) investigators. Effects of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet 1993; 324: 821-8.
  16. Kober L, Torp-Pederson C, Carlsen JE et al for the TRACE study group. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 1995; 333: 1670-6.
  17. Packer M. The ATLAS trial. Presented to the 47th Scientific Session of the American College of Cardiology, Atlanta, Georgia, 1997.

Guidelines in Practice, November 1998, Volume 1
© 1998 MGP Ltd
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