Heart failure: grasping the reins
Last month (October) saw the start of the first phase of the cardiovascular disease direct enhanced service (CVD DES) which aims to improve the diagnosis and management of heart failure and other CVDs. GPNs will have a key role in the detection and treatment of this condition
The pandemic has meant that there have been unavoidable missed opportunities to find people who have atrial fibrillation, hypertension, dyslipidaemia and heart failure, and this is likely to result in increased morbidity and mortality in the months and years to come. General practice nurses (GPNs) have a key role to play in identifying people with heart failure, ensuring appropriate referrals and tests have been completed and perhaps most importantly, in reviewing people living with heart failure and ensuring that care is optimised. This whole approach aligns with the ‘Detect, protect, perfect’ ethos that surrounds the CVD DES.
In this article, we discuss the risk factors for heart failure and consider the tests that should be carried out to ensure that the diagnosis is made competently and confidently. We also discuss the importance of optimising the lifestyle and pharmacological interventions that will have the most impact on symptoms and survival.
By the end of this article, you should be able to:
- Determine the pathophysiology that drives heart failure
- Recognise the risk factors for heart failure
- Consider how the diagnosis of heart failure is made
- Evaluate the pharmacological and lifestyle interventions which should be implemented
- Identify the role of the annual review in optimising care and quality of life
THE PATHOPHYSIOLOGY OF HEART FAILURE
Heart failure is a term that describes the failure of the heart to meet the circulatory needs of the body.1 Heart failure is usually categorised based on the ejection fraction, measure on echocardiogram. The ejection fraction reflects the amount of blood being pumped out from the left ventricle in the systolic phase of the heart’s cycle.2 In the UK, a normal left ventricular ejection fraction (LVEF) is defined as one of 55% or above.3 The European Society of Cardiology (ESC) guidelines state that an LVEF value of 50% or more is normal.4 ESC recommends that heart failure with reduced ejection fraction (HFrEF) should be diagnosed if the individual has symptoms of heart failure and an LVEF of less than 40%.
Depending on the mechanism that has led to heart failure and the findings on the echocardiogram, the diagnosis may be either heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF).5 There is also another category, known as heart failure with mid-range ejection (HFmrEF) which may progress to either HFrEF or HFpEF.4
In HFrEF the heart fails to pump out an adequate supply of blood to the body because the left ventricle, the main pumping chamber, is underperforming. Baroreceptors around the body, along with the kidneys, recognise that the circulation pressure is low and interpret this as a blood loss, and so instigate a rescue plan to keep fluid volumes and salt levels up in order to increase and maintain the circulation. These rescue mechanisms are based within the renin angiotensin aldosterone system (RAAS) and the sympathetic nervous system (SNS).5 What the body has failed to recognise, however, is that the reduced circulatory pressure is not the result of a blood loss but the result of the heart’s failure to push blood around the body. As a consequence of this misinterpretation, the inappropriate activation of the RAAS and the SNS, and the subsequent vasoconstriction and fluid overload, puts extra pressure on the failing heart. Much of heart failure management, then, focuses on downregulating these systems in order to take pressure off the heart. As well as addressing the impact of the RAAS and SNS, the role of neprilysin in heart failure has been recognised and modified through the use of neprilysin inhibition. Neprilysin limits the effects of natriuretic peptides (NPs), which are secreted from the atria and ventricles in increased quantities in heart failure. The benefits of NPs include reduction of volume and load through their vasodilatory and diuretic properties. Inhibition of neprilysin results in improvements in both the symptoms and mortality of heart failure.6 Sacubitril is a neprilysin inhibitor and is discussed later in this article.
In the past few years, the role of sodium glucose co-transporter (SGLT) receptors in cardiorenal metabolic disease has also been recognised. SGLT2 inhibition has been shown to have a positive impact on the endothelial layer of blood vessels as well as regulating sodium/hydrogen exchange within the heart and kidney, all of which leads to increased cardiovascular and renal protection. Inhibition of SGLT2 receptors has been shown to confer benefit in both HFrEF and HFpEF.7
HFpEF is, as its name suggests, when the individual has symptoms of heart failure but the LVEF is normal. However, on echocardiogram, the diastolic phase of the cycle is impaired and the left ventricular filling pressure (LVFP) is increased.8 The LVFP measures the pressure that builds up in the ventricle in diastole, when the heart relaxes and blood enters, ready to be pumped out during systole. Elevated filling pressure results from diastolic dysfunction. If diastolic function is impaired, the heart will not fill adequately and, even though the LVEF is normal, the amount of blood available to be ejected is reduced.
RISK FACTORS
Commonly recognised risk factors for heart failure include a history of myocardial infarction, hypertension, atrial fibrillation and thyroid disorders.1 However, heart failure has been noted to be one of the earliest and most deadly complications of type 2 diabetes.9 Risk factors for HFpEF are age, being female, and having comorbidities such as hypertension, coronary artery disease, diabetes, obesity, chronic kidney disease, atrial fibrillation, and chronic obstructive pulmonary disease.10 HFpEF has been recognised as being responsible for half of admissions for decompensated heart failure.11
THE DIAGNOSIS OF HEART FAILURE
The symptoms of heart failure are often non-specific, with breathlessness, oedema and fatigue being most common.1 As with most consultations, then, the focus should be on careful history taking in order to identify symptoms and risk factors. Examination can also identify any signs that might support the possibility of a heart failure diagnosis, including lung crackles, raised jugular pressure or third heart sounds. Although echocardiogram is the only diagnostic test which confirms the diagnosis of heart failure, other tests can be useful and can be carried out in primary care. These include blood tests for anaemia, diabetes, renal function, thyroid disorders and more specifically for NT-pro-BNP. This blood test is an important ‘rule out’ investigation for heart failure, in that if it is normal (<400 pg/mL) a diagnosis of heart failure can usually (but not always) be discounted. In someone with heart failure symptoms, any increase in NT-pro-BNP above 400 pg/mL would indicate the need for specialist assessment, including echocardiogram.1
Other tests that may be carried out in primary care include electrocardiogram (ECG). This is to identify any underlying abnormalities such as those associated with ischaemia, left ventricular hypertrophy or arrhythmias.1 A chest X-ray may show an abnormal cardiothoracic ratio and/or evidence of lung disease, and lung function tests may also help to identify undiagnosed lung problems, which may simulate or co-exist with heart failure.1 Ultimately, however, echocardiography is the gold standard test for heart failure as it can measure the ejection fraction and left ventricular filling pressure, which may help to identify the type of heart failure, as well as assessing the heart’s structure.1
THE MANAGEMENT OF HEART FAILURE
The management of heart failure should include lifestyle interventions and pharmacological therapies including for any correctable causes such as thyroid disorders, and for comorbidities such as chronic obstructive pulmonary disease (COPD), hypertension or diabetes.
Loop diuretics such as furosemide, bumetanide and metolazone are given to relieve symptoms of fluid overload, such as breathlessness and oedema but have no impact on mortality. In symptomatic patients who are awaiting specialist assessment and diagnosis, loop diuretics can be initiated prior to the assessment. The dose should be titrated to the symptoms and the individual. Inappropriate use of diuretic therapy is associated with adverse effects and hospital admissions so dose titration needs to be managed with care.12
With respect to the management of heart failure beyond symptom control, the focus will be on modifying the impact of the RAAS (including the use of angiotensin converting enzyme inhibitors [ACEi] or angiotensin receptor blockers [ARBs] and aldosterone blockers). Concurrent use of medication to reduce the negative effects of the SNS should be implemented, along with consideration of the place for neprilysin and SGLT2 inhibition. The evidence for RAAS inhibition is well recognised, through studies such as CONSENSUS and SOLVD which showed ACEi-related improvements in morbidity and mortality.13,14 ARBs such as candesartan, have also been shown to offer these benefits.15 Dose optimisation will achieve the best outcomes. Recently, there has been an increased focus on using ARB therapy in combination with a neprilysin inhibitor. The NICE guidelines on heart failure support the use of the ARB/neprilysin inhibitor (ARNI [sacubitril/valsartan]), Entresto®.1,16 The PARADIGM-HF trial of sacubitril/ valsartan demonstrated early mortality benefit which was sustained throughout treatment, and the trial was stopped early as a result.17 Local guidelines and pathways will differ with respect to where this drug combination should be used but increasingly, in my experience, it is being initiated early on in the medication algorithm. NICE recommends that it should be a specialist-only-initiated drug, ‘most likely to be a cardiology consultant’, although the phrase is open to interpretation.1 Closer working between primary and secondary care may help to facilitate the earlier initiation of sacubitril/valsartan in appropriate patients.
The activity of the SNS can be modified through the use of beta blockers, such as bisoprolol, carvedilol, metoprolol and nebivolol. Studies have confirmed that using beta blockers alongside drugs which act on the RAAS, also improves morbidity and mortality.18 The advice to ‘start low, go slow’ should be heeded when initiating and uptitrating beta blockers as around one in three people will find their symptoms deteriorate after starting or increasing the dose of a beta blocker.1 Mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone have also shown evidence of benefit in people with heart failure, irrespective of symptoms, although NICE reserves these drugs for people who remain symptomatic on ACE inhibitors and beta blockers.1
A previously mentioned, SGLT2 inhibitors have shown evidence of benefit in both HFrEF and HFpEF. Cardiovascular outcome trials (CVOTs) carried out in people with diabetes demonstrated unexpected benefits in terms of reductions in hospitalisations for heart failure (HHF). These findings led to further trials being carried out, aimed specifically at heart failure outcomes. The first of these, DAPA-HF, looked at cardiovascular death rates and worsening heart failure in people with a LVEF of 40% or less, in people taking dapagliflozin in addition to usual standard of care and showed benefits in both HHF, cardiovascular death and all cause mortality.19 Furthermore, treatment with dapagliflozin improved symptoms, physical function, health status and quality of life in patients with HFrEF, on top of the benefits offered by standard heart failure management.
Subsequently the EMPEROR-Reduced trial showed that patients treated with empagliflozin had a lower risk of cardiovascular death or hospitalisation for heart failure than those in the placebo group.20 These two trails showed that the benefits of these SGLT2 inhibitors extended to people with and without diabetes, leading to them being licensed for the treatment of HFrEF in people without diabetes as well as those with. There are various mechanisms which are thought to lead to the improvements seen in people with (and at risk of) heart failure who take SGLT2 inhibitors. These include stimulation of natriuresis and diuresis, effects on the cardiac myocytes, improvements in diastolic and systolic function, improved endothelial function and inhibition of cardiac fibrosis.21
As a result of the trial evidence from DAPA-HF and EMPEROR-Reduced, local guidelines are being updated to reflect the importance of using dapagliflozin or empagliflozin in people diagnosed with HFrEF and GPNs should be aware of this when carrying out heart failure reviews. This is important, whether the GPN is a prescriber or not. As a non-prescriber, a GPN may work to a practice protocol and alongside a qualified prescriber to optimise heart failure management.
So what about HFpEF? Sowden et al described HFpEF as the Cinderella of heart failure syndromes, in spite of the number of people being diagnosed with it and the high number of admissions associated with decompensated HFpEF.22 Until recently, the only real option for people with HFpEF was cardiac rehabilitation.23 However, the recent publication of the EMPEROR-Preserved trail caused much excitement in the cardiology community when it was revealed that empagliflozin reduced the rate of CV death and HHF in people with HFpEF and that the effect was seen in people with and without diabetes.24 This was the first time a drug had been shown to improve outcomes for people with HFpEF. At this stage, however, empagliflozin is not licensed for use in HFpEF.
LIFESTYLE INTERVENTIONS
As well as pharmacological therapies, lifestyle interventions can have a positive effect on heart failure outcomes.1 People with a diagnosis of heart failure should be advised to eat healthily, stop smoking, keep alcohol intake within government recommendations and to remain physically active. Breathing exercises may help with functional capacity, and improve symptoms such as breathlessness and quality of life,25 and cardiac rehabilitation may be offered, based on evidence that showed that cardiac rehabilitation for people with heart failure can extend and improve quality of life.26 As a result of the disease process and the drugs used to manage heart failure, sodium reduction should be encouraged, and advice should be given about the importance of avoiding hidden salts in foods, as well as the risks of adding salt when cooking or at the table.1 Fluid restriction is rarely required in heart failure patients.
THE ANNUAL REVIEW IN PRIMARY CARE
When reviewing an individual with heart failure, consideration should be given to their signs and symptoms, optimisation of medication, lifestyle interventions and the role of the multidisciplinary team. The New York Heart Association classification system relates to how symptomatic the patient is. As symptoms can vary over a period of time, so can the person’s classification score. Poor functional status (i.e. the ability to perform activities of daily living (ADL)) is associated with poor outcomes including the likelihood of needing hospitalisation and increased risk of dying.27 Heart rate and rhythm should be recorded along with blood pressure, recognising that the medication being used to manage heart failure may also lower BP and pulse. Regular weighing, in surgery or at home, along with assessment of leg swelling, can help to identify fluid retention and the need to uptitrate diuretics. A management plan should be agreed and put in place and this should include discussion on end of life care.1 However, in people with intractable symptoms which might suggest end-stage heart failure, it is worth considering a referral for consideration of device therapy. Cardiac resynchronisation therapy (CRT) and implantable cardiac devices (ICDs) can have a significant impact on people with heart failure and ICDs can help to correct and restore arrhythmias if they are detected.28,29
IN SUMMARY
Heart failure is the result of the inability of the heart to meet the circulatory needs of the body. Heart failure with reduced ejection fraction results from a failure of the left ventricle to pump out enough blood and the ejection fraction will normally be below 40%. Heart failure with preserved ejection fraction is associated with structural abnormalities of the heart, raised NT-pro-BNP levels, raised left ventricular filling pressure and a normal ejection fraction. When making the diagnosis of heart failure it is important to take a full history to identify symptoms and risk factors, and an examination can then reveal signs which may be associated with heart failure. An NT-pro-BNP blood test will help to identify at-risk individuals so that specialist assessment and echocardiography can be carried out in a timely fashion. The management of HFrEF is based around optimised doses of ACE inhibitors (or an ARNI, i.e., Entresto) and a beta blocker, with an appropriately licensed SGLT2 inhibitor and an MRA, i.e., spironolactone or eplerenone.
Close collaboration with the local heart failure specialist nurse and community heart failure team will ensure GPNs are supported in all aspects of heart failure management.
REFERENCES
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