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Heart failure - what you need to know

Cardiology GPSI Dr Ahmet Fuat answers GP Dr Pam Brown’s questions on BNP testing, choosing a loop diuretic, starting ß-blockers and the best ACE inhibitor dose

Cardiology GPSI Dr Ahmet Fuat answers GP Dr Pam Brown's questions on BNP testing, choosing a loop diuretic, starting ß-blockers and the best ACE inhibitor dose

1. Which symptoms and features of the history should make us consider heart failure in a patient with dyspnoea?

41218382The key to reduction of mortality, morbidity and cost of heart failure is accurate and early diagnosis of left ventricular systolic dysfunction (LVSD).

Unfortunately, heart failure is difficult to diagnose accurately on clinical grounds. This is mainly because of the non-specificity of the clinical symptoms and the non-sensitivity of the clinical signs, especially in elderly patients who often have multiple comorbidities and are on polypharmacy. This would suggest that to positively establish a diagnosis of heart failure in primary care, patients must be referred for cardiac imaging.

Medical history may provide useful clues in assessing patients with suspected HF.

A patient who has IHD, and in particular previous MI, is more likely to have objective evidence of LVSD than one who does not.

Hypertension, atrial fibrillation and diabetes mellitus also raise suspicions that a patient presenting with breathlessness or oedema may have HF.

A clinical response to treatment directed at heart failure alone is not sufficient for diagnosis.

2. What ECG changes should we look for in a patient suspected of heart failure? If the ECG is normal, how likely is it that the patient has heart failure?

There are no specific ECG changes that confirm heart failure. If ECG abnormalities, including previous MI, atrial fibrillation or flutter, left ventricular hypertrophy, bundle branch block or ischaemic changes are present, the patient needs to be referred for echocardiography.

All guidelines and NICE guidance for the diagnosis and management of heart failure caused by LVSD suggest that if a 12-lead ECG is normal then LVSD is very unlikely1.

This has led to suggestions that a normal ECG be used to screen out patients with suspected HF prior to referral for echocardiography. This advice appears to be largely based on a trial that suggested that LVSD is unlikely to be present if an ECG is normal. But these claims have been contradicted by other studies.

For this reason, the Scottish Health Technology assessment of the use of ECG and natriuretic peptides in suspected heart failure suggests that if the ECG is abnormal, refer. But if normal, and symptoms suggest HF, undertake BNP or NT proBNP assay2.

If this is also normal the chances of HF are slim. If positive, refer for echocardiography.

This stepwise approach seems sensible, given that natriuretic peptide assays are expensive and cost-effectiveness trials have not been conducted in primary care.

3. Should all patients with suspected HF have an echocardiogram and BNP test?

If heart failure is suspected, echocardiography is essential to clarify whether the patient has LVSD, to help establish aetiology and identify other cardiac abnormalities. Both NICE guidance and the NSF for CHD suggest echocardiography for all patients with suspected HF, but provision is limited.

NICE1 and European Society of Cardiology3guidelines suggest the use of natriuretic peptides in the diagnostic triage of patients with suspected HF.

They recommend that in clinical practice ECG and/or BNP or NT proBNP is used as a rule out test to exclude significant cardiac disease in primary care. Personally, I favour the Scottish HTA approach outlined above.

4. Are there any benefits from the use of loop diuretics other than furosemide – such as torasemide or bumetanide – in heart failure?

Despite the extensive clinical use of loop diuretics in heart failure, there are no large clinical trials on the effects on mortality.

Diuretics should be considered for patients with water retention, but renal function will need to be monitored regularly and the dose kept low.

Furosemide and bumetanide are the two commonly used loop diuretics. Some suggest GI absorption of bumetanide is less affected by gut oedema and hepatomegaly and has higher bioavailability. So it may be useful to switch to bumetanide if patients have fluid retention not responding to furosemide. A dose of bumetanide 1mg is roughly equivalent to furosemide 40mg.

Torasemide has theoretical advantages in that it has more predictable bioavailability – at 90% – and less renal excretion – 20% renal and 80% hepatic – compared with furosemide, which is 100% renal excreted.

It also may cause less potassium loss and induced diuresis is less brisk in the elderly.

Thiazide diuretics can be added to a loop diuretic in resistant fluid retention, but this is best monitored by someone skilled in the management of heart failure.

5. Which drugs reduce mortality rates in patients with heart failure and what are the mortality reductions?

The aims of treating HF are broadly similar in all published guidelines:

• improving symptoms or slowing their deterioration

• reducing mortality

• reducing the frequency of cardiac events and admissions to hospital

• avoiding adverse events from treatment

• improving end-of-life experience.

ACE inhibitors significantly reduce total mortality with consistent effects in a broad range of patients with HF.

They slow the progression to HF in patients with asymptomatic left ventricular dysfunction, improve symptoms and quality of life, enable reduction of the amount and dosage of other anti-HF drugs and reduce cardiac events and admissions. Meta-analyses suggest they cut mortality by 23-26% and hospitalisation by 27-35%.

European, UK and US guidelines reiterate that patients with symptomatic heart failure and evidence of impaired left ventricular function should receive an ACE inhibitor, unless contraindicated. Patients with a recent MI and evidence of left ventricular dysfunction should also receive an ACE inhibitor, even if asymptomatic.

There is strong evidence that adding ß-blockers to standard therapy with diuretics and ACE inhibitors in patients with moderate or severe HF reduces mortality and hospital admission rates.

A systematic overview of 24 trials found a 31% reduction in the odds of death among patients with HF treated with a ß-blocker4.

All patients should be considered for ACE inhibitors and ß-blockers unless there are compelling contraindications. Diuretics, digoxin and spironolactone should be considered in some patients.

6. In patients unable to tolerate ACE inhibitors, are ARBs as effective at reducing mortality in those with heart failure?

ACE inhibitors only partially block the renin-angiotensin system. ARBs act at the angiotensin II receptor site itself and may more completely block its pressor actions. Furthermore, unlike ACE inhibitors they do not inhibit bradykinin breakdown, and are also less likely to cause the troublesome cough seen in about 10% of patients on ACE inhibitors.

In 2003 the CHARM group of studies – looking at the use of candesartan in HF – found it reduced both CV mortality and hospital admissions in a broad spectrum of patients. These benefits were achieved on top of ‘best treatment' with other effective concomitant therapies, including ß-blockers and/or ACE inhibitors5.

Specifically, in patients intolerant of ACE inhibitors, the ARB reduced the risk of CV death or hospitalisation by 23% compared with placebo.

Current advice should be that ARBs might be considered as a replacement for patients with LVSD intolerant of ACE inhibitors. But CHARM also suggested a combination of ACE inhibitor and candesatran may be considered in certain groups of patients still symptomatic on optimal conventional therapies.

Candesartan and valsartan are the only ARBs licensed for use in HF in the UK.

7. What ACE inhibitor dose should we aim for in heart failure patients, and what should we do if creatinine rises during treatment?

The ATLAS study aimed to evaluate the differences in morbidity and mortality between high-dose lisinopril – 32.5-35mg once daily – and low dose – 2.5mg-5mg once daily – over four years6.

Both dose regimens were similarly well tolerated but there was a significant 12% additional reduction in the combined end point of all-cause mortality plus all-cause hospitalisation in the high-dose group.

There was also a significant 15% reduction in the combined end point of all-cause mortality and hospitalisation for heart failure.

These studies suggest that we should be aiming for high-dose ACE inhibitors as target doses – for example, 40mg lisinopril, 10mg ramipril or 8mg perindopril.

Following introduction of an ACE inhibitor, urea and electrolytes should be checked one to two weeks later and also after each dose increase. An increase of creatinine level of up to 50% over baseline or to 200mmol/l (whichever is smaller) is acceptable. Reducing diuretic doses may be helpful in minimising creatinine changes. A rise in serum potassium level up to 5.9 is acceptable.

I'd suggest halving the ACE inhibitor dose and rechecking U&Es within a week. If under 200mmol/l or less than 50%, stay on that dose. Otherwise keep halving until it is – or stop altogether.

8. We are now encouraged to start ß-blockers in primary care. How should we initiate treatment, and what is the optimal dose to aim for? If symptoms deteriorate, should we stop or reduce the ß-blocker?

There is now overwhelming evidence that ß-blockers are beneficial in all grades of heart failure. But there is still some reluctance to use them.

ß-blockers should be introduced at the lowest dose once the patient is stable and oedema-free on an ACE inhibitor.

The dose should be slowly increased to target doses if possible – 10mg od bisoprolol, 25-50mg twice daily carvedilol or 5mg od nebivolol.

We should aim for a resting pulse of about 60/min. Patients should be advised that it may take three to six months for symptoms to improve. If troublesome symptoms occur, try halving the dose rather than stopping the ß-blocker.

Asymptomatic hypotension – an SBP below 90mmHg – should be monitored. If pulse falls below 50/min, halve the dose of ß-blocker or, if severe deterioration or if significantly symptomatic, stop and consult a specialist.

Consider other drugs that may slow the heart rate, such as digoxin, amiodarone, verapamil or diltiazem, and stop if possible.

Recently some of the traditional contraindications and cautions to ß-blockers have been questioned.

Various Cochrane reviews have suggested that evidence-based ß-blockers – bisoprolol, carvedilol, nebivolol and metoprolol – are safe to use in chronic obstructive pulmonary disease (COPD), peripheral arterial disease, diabetes mellitus and the elderly.

It's important to address these areas so as not to deny patients with these comorbid conditions and HF the opportunity to benefit from ß-blocker therapy.

9. When are ACE inhibitors, ß-blockers and spironolactone contraindicated?

ß-blockers are contraindicated in patients with acute heart failure, second- or third-degree heart block, hypotension (BP lower than 100mmHg systolic) and asthma.

ACE inhibitor, ARB and spironolactone initiation should be under specialist supervision if creatinine is more than 200mmol/l, urea more than 12mmol/l, sodium less than 130mmol/l, diuretic dose more than furosemide 80mg or equivalent, or if there is known or suspected renovascular disease such as peripheral arterial disease or frail elderly patients.

10. How often should patients have electrolytes, creatinine and eGFR monitored once stable on treatment?

All patients with CHF caused by LVSD need regular monitoring, as many of the agents used in its treatment can lead to electrolyte imbalance, renal dysfunction and cardiac rhythm abnormalities.

The frequency of monitoring depends on the stage of disease, severity and drug therapy. Monitoring intervals should be short if clinical status or treatment changes have been made – such as an increase in ACE inhibitor dose – and is suggested six-monthly for stable patients with LVSD.

Minimum requirements are for assessment of fluid status, cardiac rhythm and BP, laboratory assessment of renal function and ideally assessment of functional capacity.

Patients should be asked about potential drug side-effects and the development of anxiety or depression, a common occurrence in CHF. Appropriate education of patients and carers about self-monitoring is desirable.

Patients on diuretics, ACE inhibitors, ARBs, spironolactone or ß-blockers should be advised that if they have diarrhoea or vomiting – or if they are not drinking enough – they should stop taking these medications for one to two days until they recover. This is to avoid dehydration, hypotension and acute renal failure.

It may be justified to halve ß-blocker dose if concerned about precipitating angina.

If symptoms persist beyond two days they should see a GP and have bloods checked. Brief withdrawal of these drugs is unlikely to cause sudden deterioration in HF.

11. What is the role of spironolactone in heart failure, what is the optimal dose, and should we be initiating it in primary care?

Spironolactone is a competitive aldosterone antagonist. The RALES Study demonstrated that Spironolactone improved all cause mortality (a 27% risk reduction), reduced hospitalisations for all cardiac causes (30% RR) and for worsening heart failure (35% RR).

Patients with moderate to severe LVSD should be considered for treatment with low dose spironolactone (25-50mg) if they remain symptomatic on an ACE inhibitor and a ß-blocker.

Close monitoring and judicious use of spironolactone is necessary when prescribing in real life practice. Some specialists have called for mandatory, close monitoring of blood chemistry after starting spironolactone, and advised that spironolactone should be stopped immediately if diarrhoea develops7.

Eplerenone is a newer aldosterone antagonist with potentially fewer side effects. In the EPHESUS study adding of 25-50mg of eplerenone to optimal therapy reduced morbidity and mortality among patients with acute MI8 complicated by LVSD and HF. The rate of serious hyperkalaemia was 5.5% in the eplerenone group and 3.9% in the placebo group. Incidence of gynaecomastia and impotence in the eplerenone group was no greater than in the placebo group. As these are common problems with spironolactone, eplerenone should be a suitable alternative in management of HF due to LVSD.

12. What can we do to reduce our patients' future risk of developing heart failure?

Despite growing public awareness of the risk factors for heart failure, chronic heart failure (CHF) as a result of coronary heart disease continues to inflict a terrible toll on the people of this country. The current estimate that 900,000 people in the UK have CHF is predicted to increase by about 10% each year.

GPs have a vital role to play in early detection and treatment of the main risk factors for HF, which may help to prevent progression to HF. CHD clinics in primary care can be used to address post MI care, lifestyle modification, the treatment of hypertension, IHD and diabetes, smoking cessation and hyperlipidaemia. Identifying patients at risk of developing HF and initiation of ACE inhibitors, in particular may help prevent development of HF.

Dr Ahmet Fuat is a GP and GP specialist in cardiology in Darlington, honorary secretary of the Primary Care Cardiovascular Society and senior clinical lecturer at Durham University

Competing interests: Dr Fuat has received honoraria for lecturing and advisory boards from AstraZeneca, Pfizer, Servier, GSK, Takeda, Novartis, Daiichi-Sankyo, Sanofi-Aventis and Bristol-Myers Squibb. He has received educational grants from: MSD, Boehringer, Roche, Merck and research grants from Sanofi-Aventis, Roche Diagnostics, NHSE, the Workforce Development Fund, the Patient Benefit Program and Heart Research UK

What I will do now What I will do now

Dr Pam Brown considers the responses to her questions

We're lucky to have open access to echo locally, and I always carry out an ECG prior to referral. But we don't have access to BNP. So until this becomes available, I'll continue to refer those who have a history suggestive of HF but normal ECG.

I'll consider heart failure as a differential in patients presenting with fatigue who have previous MI, DM or AF.

It's useful to know about the improved absorption of bumetanide when there is gut oedema, and now I understand why some of our patients are coming out of hospital on torasemide.

It's reassuring to read that candesartan has similar mortality reduction benefit to ACE inhibitors as many patients do suffer from troublesome cough and require switching.

Most of our heart failure patients are on lower-dose ACE inhibitors than recommended here so I'll make an effort to slowly increase the dose with careful biochemistry monitoring.

I will be more likely to encourage patients to stop their ACE inhibitors, diuretics, spironolactone or ß-blockers if they develop severe diarrhoea or vomiting. Previously I would have been reluctant to advise this, believing this carried a risk of rapid deterioration of their heart failure.

I will be more proactive in identifying those with risk factors for heart failure and using ACE inhibitors in their management plans in preference to other agents, such as when treating hypertension.

Dr Pam Brown is a GP in Swansea

thps Identifying LVSD is the key to treating heart failure Identifying LVSD is the key to treating heart failure

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