Key slides heart_failure_notes

Heart Failure: Notes for key slides
Slide 1: Chronic heart failure
The following slides look at the key issues for the management and treatment of chronic heart failure (CHF)
due to left ventricular systolic dysfunction (LVSD), the most common type of CHF. Other types of heart
failure (HF) for example, diastolic HF, asymptomatic HF, acute HF, or HF due to non-cardiac causes are not
covered by this slide set.
Most of the information on the slides and in these notes is taken from:
• NICE Full Guideline 05. Chronic heart failure, 2003.1
• Scottish Intercollegiate Guidelines Network (SIGN). Management of chronic heart failure, 2007.2
• European Society of Cardiology (ESC) Guidelines. Heart failure guideline 2008.3
• MeReC bulletin. Chronic heart failure February 2008.4
These notes are intended to support you in using these slides, but we recommend you are familiar with these
essential references.
Slide 2: What is the prognosis, and what are the costs to the NHS?
HF occurs when the heart does not pump enough blood to support the needs of the body.1
It is associated
with a progressive decline in quality of life and ultimately death, although the speed of decline for individual
patients will vary and is difficult to predict. Prognosis in HF is significantly worse than several common
cancers, including breast and prostate cancer.1,2
Guidelines emphasise that prognosis is discussed with patients and carers in a sensitive, open and honest
manner. Patients should have access to the support of healthcare professionals and be advised of the local
patient support groups that they can access.
Estimates of mortality rates vary between 26–75% of patients, who receive a diagnosis of HF dying within 5
years. One-third of deaths are preceded by a major ischaemic event and between one-quarter and one-half
of cases, ventricular arrhythmia leads to sudden death.1
HF affects about 1% of men and women in the UK. However, the prevalence increases steeply with age, up
to 15% in patients above the age of 85 years. The number of patients with HF is set to rise in the next 20
years, due to the combined effects of improvements made to survival after a heart attack and the general
ageing of the population.5
The prevalence and incidence of HF is such that the average GP will look after
around 30 patients with HF and suspect another 10 of having it each year. Nearly all of these will be in
patients over the age of 65 years.1
This resource has been produced with the support of a number of NHS individuals and organisations. It is intended as a template from which you can
produce local versions adapted to your own local needs.

HF also carries a major burden for health services. It has been estimated to cost the NHS about £625 million
per year; much of this due to the high rate of hospital admissions and readmissions. It is one of the most
common causes of emergency admission.6
Slide 3: Diagnosis of HF
There is no individual sign or symptom that is sensitive or specific enough to diagnose HF. Patients will
often present with symptoms, such as fatigue, shortness of breath, and/or ankle swelling, which are
suggestive of HF however, there are many other conditions that can cause these symptoms. Individual
symptoms and signs of HF are poorly predictive of HF. Only about 1 in 4 patients suspected of having HF,
because of presenting symptoms, are actually confirmed as having HF on further investigations.1
For HF to be diagnosed there needs to be evidence of cardiac dysfunction. There are useful tests, in
particular electrocardiogram (ECG) and B-type natriuretic peptide (BNP) testing, that can be used to help
assess the likelihood of a patient having HF.
This slide shows the diagnosis algorithm for HF taken from the NICE guideline which highlights an
appropriate sequence to follow when investigating suspected HF. Where patients have signs and symptoms
that suggest HF, ECG and/or BNP testing should be carried out, alongside other tests to exclude other
conditions that may be causing the symptoms. If a patient has both a normal ECG and normal BNP levels, it
is very unlikely that they have HF. However, if one of these tests is abnormal it does not mean that the
patient definitely has HF, but it does increase the likelihood to a level that justifies further evaluation by
echocardiography as appropriate. This can then confirm diagnosis of HF, help identify the cause, and so
direct management and treatment.1
Slide 4: Improving the quality of care
In addition to recommendations by NICE, SIGN and ESC, NHS Improvement6
has published a practical
guide for commissioning services to improve the care of patients with HF. This stresses that a co-ordinated
multidisciplinary approach across primary and secondary care is needed to improve the uptake of evidence-
based medicines and reduce hospital admissions and duration of stay, which is associated with high financial
cost.
This slide lists the key aspects of treatment that should be considered for a patient with HF. There are many
evidence-based interventions that can be used to alleviate symptoms and improve outcomes for people with
HF. They include behavioural modification (for example, smoking cessation, dietary changes, and exercise),
drug treatments, such as angiotensin-converting enzyme inhibitors (ACEIs) and beta blockers, and specialist
interventional procedures, such as cardiac resynchronisation therapy, for which there is now specific NICE
guidance.
Slide 5: Drug treatment of HF

This is the treatment algorithm for HF due to LVSD published in the MeReC Bulletin (2008).4
It broadly
follows the NICE HF guideline algorithm, with the exception of including the use of angiotensin-2 receptor
antagonists (A2RAs), such as candesartan, as an alternative to spironolactone, for those patients who
remain symptomatic subsequent to optimised therapy with ACEIs and beta blockers. This is consistent
with SIGN guidance (2007) and ESC guidance (2008), which considered evidence subsequent to that
considered for the NICE guideline when it was developed in 2003. At the time of preparing this slide set in
November 2008, the NICE HF guidance from 2003 has not been updated.
All NICE, SIGN and ESC guidelines recommend the use of ACEIs and beta blockers as first- and second line
drug treatments, unless they are contraindicated or not tolerated. Whereas previously diuretics and perhaps
digoxin would have occupied these places, these are now recommended as symptomatic treatments to be
added in defined circumstances. Most patients will need a diuretic to control symptoms. Digoxin can also be
considered for those patients in sinus rhythm who remain symptomatic, despite optimised drug treatment
with an ACEI and beta blocker.
Spironolactone or an A2RA can be considered as options in addition to ACEI and beta blocker treatment
when patients remain symptomatic despite optimal therapy. These are both associated with an increased
risk of adverse side effects and are recommended to be initiated by specialists. Eplerenone might be
considered as an alternative where spironolactone cannot be tolerated due to gynaecomastia.
For all drug treatments refer to dose, titration and monitoring information in NICE and SIGN guidelines.
Slide 6: ACEIs in HF
All patients with confirmed HF due to LVSD should be considered for ACEI treatment (before beta blocker
therapy is initiated). This recommendation is based on evidence from systematic reviews of randomised
controlled trials (RCTs) which demonstrate that ACEIs improve symptoms, reduce the risk of hospitalisation
for HF and increase life expectancy compared with placebo.
The key results of the two largest of these studies are shown on this slide. Both show impressive numbers
needed to treat (NNT) for improving survival. The SOLV-D study suggests that for patients with mild or
moderate HF, for every 22 patients treated, one patient is saved from dying over 41 months, whereas the
CONSENSUS study in patients with severe HF identified a NNT of just seven over a period of 6 months.
Data from shorter-term, placebo-controlled RCTs indicate a clear reduction in mortality within the first 3
months. They also show that ACEIs improve symptoms and quality of life. ACEIs should therefore be
prescribed for everyone with LVSD, unless they are specifically contraindicated or not tolerated.
ACEI treatment should be initiated at an appropriate dose and titrated upwards at short intervals to the
optimal tolerated or target dose (refer to dose and titration information in NICE and SIGN guidelines). The
NICE guideline takes the view that some dose of ACEI is better than no ACEI in those patients who cannot
tolerate the target dose.

If patients are truly not able to tolerate an ACEI, guidelines recommend switching to an A2RA. The most
common reason for intolerance is cough, which, at least according to clinical trials data should be fairly
infrequent. Approximately 6% of patients in the SOLV-D study discontinued treatment due to a cough. In
the ONTARGET trial which compared telmisartan, ramipril or both in patients at high risk of vascular events,
4.2% of patients in the ramipril group stopped treatment due to cough compared to 1.1% in the telmisartan
group. This is an absolute difference of 3.1% and a number needed to harm (NNH) of 32.7,8
However, the symptom of a cough is common in patients with CHF, many of whom also have smoking
related lung disease, so may not be due to ACEI treatment. Cough is also a symptom of pulmonary oedema
which should be excluded when a new or worsening cough develops.1
Slide 7: A2RAs in HF
Although ACEIs and A2RAs block the same common biochemical pathway, we should be careful not to
automatically assume that they will therefore generate the same clinical outcomes. In the less than 60 minute
presentation that accompanies this set of key slides there is more detail regarding the evidence from
individual RCTs regarding the use of A2RAs in HF.
This large meta-analysis summarises the position with these drugs in the management of HF. Taking data
on 38,000 patients from 24 placebo-controlled or active comparator trials it showed significant reductions in
mortality and hospital admissions for A2RAs (or ARBS as they are called in this table) compared with
placebo, as shown by the results outlines in red. However, there were no differences between ACEIs and
the A2RAs. These results are outlined in blue. Finally, the combination of an A2RA and an ACEI versus an
ACEI alone reduced hospitalisation but did not seem to affect mortality, as shown by the data outlined at the
bottom in green.
The commentary in evidence based medicine, from which these figures are drawn, sums this up well.
Basically A2RAs are effective drugs in CHF however, so too are ACEIs and these cost less than A2RAs.
A2RAs would have to be more effective or have a better safety profile than ACEIs for them to be used as an
alternative; this has not been shown to be the case. Guidelines state that A2RAs may provide an alternative
to ACEIs for patients intolerant of ACEIs (for example, because of cough).
Slide 8: ACEI plus A2RAs in HF
As seen on the table on the previous slide there is some evidence that the combination of an A2RA and an
ACEI versus an ACEI alone reduced hospitalisation but did not seem to affect mortality.
When adding an A2RA to an ACEI, the increased risk of serious side effects has to be considered. This
meta-analysis of patients with symptomatic LVSD considered studies where an A2RA was added to an
ACEI. The VALIANT trial is separated from the others as this was in patients with acute MI with symptomatic
LVSD. It can be seen that discontinuations from studies due to adverse events was significantly higher in
those patients taking the A2RAs in combination with ACEIs, compared with ACEIs alone. Hyperkalaemia,

renal dysfunction and symptomatic hypotension all occurred with greater frequency in patients with chronic
HF who received the combination.
Caution is advised when using a combination of ACEI and A2RA treatment in patients with CHF as there is
no evidence that adding an A2RA to previously optimised therapy will improve survival, and combination
treatment confers an increased risk of adverse events and drug discontinuation.4
Slide 9: Beta blocker treatment in HF
Traditional teaching prior to the 1990s was that beta blockers should be avoided in patients with HF. The
rationale was that the sympathetic nervous system was overactive and provided a crucial level of
compensation for the failing heart. To remove this by using a beta blocker would risk precipitating or
exacerbating HF. However, things have changed. More recent clinical studies have led beta blockers to
become well established now as a second or third-line option that can improve important outcomes for
patients with HF. This is a good example of why patient-oriented outcome data, like improving survival and
reducing hospitalisation, are needed to guide practice rather than relying on beliefs about mechanisms of
action and pathophysiological principles — disease oriented outcomes.
Beta blockers produce benefits in the medium to long-term. When they are first introduced, they can produce
decompensation with worsening of HF and hypotension. Therefore, beta blocker initiation in HF must be
carried out cautiously and requires some degree of expertise, but can be done in primary care. The dose
should be titrated upwards slowly towards the target dose.
The top-line statement on this slide is that beta blockers increase life expectancy in HF due to LVSD, across
all grades of the condition. They also reduce hospitalisations. However, there is limited evidence that not all
beta blockers are equal in this respect. The NICE guidelines recommend starting with a licensed drug. Those
currently licensed in the UK for HF are carvedilol and bisoprolol, which can be used in any grade of HF, and
nebivolol, which is only licensed for mild to moderate HF in the elderly. The consensus seems to be that the
better option is to use a licensed beta blocker, where there is evidence of a benefit, wherever possible. There
is no guidance on what to do if patients are already taking a beta blocker for angina or hypertension, such as
atenolol, which is not licensed for HF. It is a matter of clinical judgement whether or not clinicians continue to
prescribe the unlicensed drug, and assume a class effect, or switch to a licensed alternative.4
The key message is that beta blockers are now routinely recommended in all patients with HF due to LVSD,
in addition to ACEI, regardless of whether symptoms persist or not, unless contraindicated. Treatment
should be started at a low dose and gradually increased up to the target or highest tolerated dose.
Slide 10: Spironolactone in HF
There is evidence that the use of spironolactone in patients with moderate to severe HF due to LVSD can
increase life expectancy. The RALES study, as shown on this slide, found a relative reduction in death rate
at 2 years of around one-quarter. One life was saved for every nine patients treated. Spironolactone is a
potassium sparing diuretic but there were relatively few problems with hyperkalaemia in the trial, possibly

because patients most at risk of this were excluded from the study. Gynaecomastia was reported in 1 in 10
cases. In its 2003 guideline, NICE recommended the addition of spironolactone to the treatment of patients
who remain symptomatic despite optimised treatment with diuretics, ACEIs, beta blockers and perhaps
digoxin.
Spironolactone is an alternative to A2RAs for those patients whose symptoms are not adequately controlled
on optimised ACEIs and beta blockers. They should not be used together with an A2RA, in addition to ACEIs
and beta blockers. There is no evidence for the use of spironolactone in mild HF.
Eplerenone is the only aldosterone antagonist specifically licensed for use in people with recent MI. The
evidence for this comes from the EPHESUS study, which is discussed in the less than 60 minute section of
this topic. We don’t know how eplerenone would compare with spironolactone, as there have been no head
to head trials. Other than for use soon after an MI, both SIGN and ESC guidelines consider eplerenone as
an option for patients with HF who develop gynaecomastia with spironolactone.
Careful monitoring is important for all aldosterone antagonists because of the risk of hyperkalaemia.
Slide 11: Digoxin treatment in HF
The appropriate use of digoxin in patients with HF depends on whether a patient has sinus rhythm or atrial
fibrillation (AF). A systematic review which included the large DIG study found that, for those in sinus rhythm,
digoxin seems to reduce hospitalisation but didn’t affect overall mortality. NICE recommends that it can be
considered as an add-on treatment for patients in sinus rhythm who remain symptomatic despite taking
diuretics, ACEIs and beta blockers.1
Digoxin in patients with AF has an important role in controlling the heart rate to improve symptoms. In
patients with symptomatic HF and AF, digoxin may be used to slow a rapid ventricular rate. In patients with
AF and a reduced left ventricular ejection fraction digoxin can be used to control heart rate in addition to or
prior to a beta blocker.
It is important to use digoxin carefully as it is a drug with potentially very toxic adverse events, a narrow
therapeutic index, and, as it is excreted in an active form via the kidneys, must be used with caution in those
with impaired renal function.
Routine monitoring of digoxin is not recommended following initiation, but there are situations where levels
can be considered, for example, after a dose change, or when there are symptoms suggestive of toxicity,
etc. There is no evidence that routine monitoring improves outcomes.
Prescribers should be aware that lower doses may be necessary in elderly patients and in those with renal
impairment and that steady state may take longer to reach, also that certain drugs may increase digoxin
levels (these include amiodarone, verapamil, certain antibiotics, and quinidine).

Summary of CHF treatment
Although there are limitations with the evidence base as in most areas of therapeutics, we should be able to
apply it to our patients with HF with a reasonable degree of confidence. Many of the interventions available
save lives, reduce hospitalisation and improve quality of life. Patient and carer education is crucial here and
should include the condition, medication, weight, fluid and alcohol, diet, nutrition and salt, smoking, sex,
physical activity, vaccination and travel.
In terms of drug treatment, where possible and appropriate, the NICE drug treatment algorithm should be
followed, aiming for target dose ACEIs or A2RAs and beta blockers, however some treatment is better than
none and not everyone will be able to tolerate the recommended doses. There is no evidence to support
using A2RAs over ACEIs, they should be reserved for genuine ACE intolerance (usually due to cough),
although working out if the cough is due to worsening HF or the ACEI can be difficult. It is probably better to
use a licensed beta blocker and do not forget to monitor closely, especially renal function and electrolytes.
Adding spironolactone or an A2RA to optimised ACEI and beta blocker treatment can be considered
(normally by specialists) for patients who are symptomatic. Eplerenone can be considered as an alternative
to spironolactone if gynaecomastia is a problem. Statins, aspirin or warfarin are indicated according to
cardiovascular risk, although there is no direct evidence for a benefit from trials in HF for these. Isosorbide
dinitrate and hydralazine should be considered for African-American patients or when ACEIs or A2RAs can’t
be used. Amiodarone may be used by specialists in certain circumstances.
Slide 13: Summary of CHF management
When managing the care of patients with CHF it is important to monitor for and manage comorbid conditions.
AF is commonly encountered in HF and can be both the cause and the consequence. Its onset is associated
with worsening symptoms, an increased risk of thromboembolic complications, and poorer long-term
outcomes.
Anaemia is common in HF and may account for some of the fatigue seen in people with the condition, one of
the predominant symptoms experienced by many. Whether doing anything about the anaemia affects the
outcome for patients with HF is not known, but it may well help improve some symptoms such as fatigue and
breathlessness. Correction of anaemia has not been established as routine therapy in HF.
Renal dysfunction is common in HF, and the prevalence increases with severity of HF, age, and history of
hypertension or diabetes. It is strongly linked to increased morbidity and mortality. As with anaemia it is
unclear if the renal impairment causes the increase in risk, or it is just a sign of more severe illness. The
cause of renal impairment should always be sought in order to detect potential reversible causes, including
drug-related causes. Possible causes include dehydration, ACEIs or A2RAs, or coincidental renal disease.
Depression tends to be more common in patients with HF than in the general population, and it should be
considered in all patients. There is insufficient evidence to support the use of specific antidepressants in HF
however, tricyclics are best avoided.

Palliative care needs should be considered in patients with advanced HF. The NICE guideline refers to
substantial evidence that there is considerable unmet needs of patients and carers in this area although
there is little evidence on how and how best to provide for it. Professionals in the HF team should have
palliative care skills or be able to access them.
NICE guidelines recognise the need for an integrated multidisciplinary approach to the support of people with
HF. SIGN specifically recommends that there should be a nurse-led home based service, and the
involvement of pharmacists with regard to their medication. NICE recognises the importance of local cardiac
support services. Healthcare professionals need to be aware of these and advise patients accordingly.
A review of HF services by the Healthcare Commission (2007),6
showed considerable improvement in
services since the publication of the NICE guidance in 2003. However with regard to recognition and
diagnosis fewer cases of HF were recorded than was expected from epidemiology surveys. There was wide
variation in both the proportion of patients recorded with HF, and in the proportion of patients who had their
diagnosis confirmed appropriately. Having an audited multidisciplinary approach with good communication,
clear treatment protocols and plans and easy access of patient and carers is commended by all the
guidelines.
References
1. National Institute for Health and Clinical Excellence (NICE). Chronic heart failure: Management of
chronic heart failure in adults in primary and secondary care. NICE Clinical Guideline No. 5. July 2003.
Available from: www.nice.org.uk [last accessed 16 December 2008].
2. Scottish Intercollegiate Guidelines Network (SIGN). Management of chronic heart failure. Guideline No.
95. February 2007. Available from: www.sign.ac.uk [last accessed 16 December 2008].
3. European Society of Cardiology (ESC). Guidelines for the diagnosis and treatment of acute and chronic
heart failure 2008. Available from: www.escardio.org [last accessed16 December 2008].
4. MeReC Bulletin. Chronic heart failure: overview of diagnosis and drug treatment in primary care
2008;18(3). Available from: www.npc.co.uk [last accessed 16 December 2008].
5. National Heart Failure Audit. NHS Information Centre 2008. Available from: www.ic.nhs.uk [last
accessed 17 December 2008].
6. Healthcare Commission. Pushing the boundaries. 2007. Available from: www.wales.nhs.uk [last
accessed 16 December 2008].
7. The ONTARGET investigators. Telmisartan, ramipril or both in patients at high risk for vascular events.
New Engl J Med 2008;358:1547–1559.
8. MeReC Rapid Review. ACE-I plus ARB misses the target. April 2008. Available from: www.npci.org.uk

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