Heart failure learning module 2: diagnosis

Introduction

Heart failure (HF) is a syndrome and not a diagnosis. Once a patient has been identified as having the HF syndrome, a cause must be sought. For example, in the majority of patients with HF and a reduced ejection fraction (HFrEF), the underlying cause will be ischaemic heart disease (IHD).

The signs and symptoms of HF are common and non-specific; misdiagnosis and under-diagnosis are common (figure 1–3).

Key: JVP = jugular venous pressure

Figure 3. Jugular venous pressure (Click arrow below to play, or bottom-right for full screen)

Clinical presentation

A patient can be said to have the HF syndrome if they meet all of the following criteria:

1. Typical symptoms and signs (figure 1)
2. Evidence of cardiac dysfunction – raised serum natriuretic peptide (NP) concentration
3. Structural and / or functional abnormalities of the heart detected on imaging

This module will cover the common investigations and tests used to diagnose and monitor patients with HF with specific focus on the National Institute of Health and Care Excellence (NICE) guidelines and the European Society of Cardiology (ESC) 2021 guidelines and the 2023 update.^5–7

Symptom severity assessment

Assessing functional and exercise capacity is an important part of the clinical assessment of patients with HF. The New York Heart Association (NYHA) classification is a widely used tool to grade the severity of a patient’s symptoms (table 1). However, reproducibility of NYHA class is low, with low validity and reproducibility.^8–10

Modes of presentation (table 2)

Acute or decompensated HF

If a patient with chronic HF deteriorates, either suddenly or slowly, the episode may be described as ‘decompensated’ HF which can be divided in to two modes of presentation. Additionally, a patient can also present acutely in cardiogenic shock, with or without a previous diagnosis of HF.

• Acute pulmonary oedema
  A medical emergency usually triggered by an acute event, such as ischaemia or arrhythmia.
• Anasarca
  Anasarca refers to patients presenting with worsening symptoms or signs of fluid retention. Such patients are often presenting for the first time, but may be patients having an exacerbation of their previously stable HF.
• Cardiogenic shock
  Cardiogenic shock is multi-organ dysfunction due to hypoperfusion caused by a sudden fall in cardiac output. It is typically seen following a large (acute) myocardial infarction. It is a distinct clinical entity not further covered here.

Chronic HF

Patients with chronic HF have been treated medically and will usually have few, if any, symptoms or signs at rest. The term ‘congestive’ HF, often used to describe patients in this condition (particularly in North America), is inappropriate – patients with treated HF should not be congested.^3,11

Investigations

Blood tests

NPs

• NP release and actions
  NPs are secreted by the myocardium in response to stretch caused by volume and/or pressure overload. In health, they are part of the homeostatic system which maintains blood volume. They counter-act many of the pathophysiological processes of HF (figure 4).



Table 3. Cardiac and non-cardiac causes of raised and reduced BNP and NT-proBNP

Causes of raised NP levels
Cardiac
Right ventricular strain
Acute coronary syndrome
Heart muscle disease including LVH
Valvular heart disease
Pericardial disease
Atrial fibrillation
Myocarditis
Cardiac surgery
Cardioversion
Non-cardiac
Advancing age (>70)
Anemia
Renal failure
Pulmonary: OSA, pneumonia, pulmonary hypertension, PE, hypoxia, COPD
Sepsis
Burns
Liver failure
Diabetes
Causes of reduced NP levels
BMI >35 kg/m2
Drugs, including diuretics, ACE inhibitors, ARBs, beta blockers, MRAs
African-Caribbean family origin
Key: ACE = angiotensin-converting enzyme; ARBs = angiotensin receptor blockers; BMI = body mass index; BNP = B-type natriuretic peptide; COPD = chronic obstructive pulmonary disease; LVH = left ventricular hypertrophy; MRA = mineralocorticoid receptor antagonist; NP = natriuretic peptide; NT-proBNP = N-terminal fragment of the prohormone BNP; OSA = obstructive sleep apnoea; PE = pulmonary embolism

• Measuring NPs in practice¹²
  Low serum NP concentration has a high negative predictive value (94%) for the presence of HF. Serum NP concentration gives useful prognostic information: the higher the level, the worse the prognosis, regardless of underlying pathology.

  However, raised NP concentrations are not synonymous with HF. There are many causes of raised NPs (table 3). Very high NP levels ought to prompt investigations for other serious illness such as malignancy or bacteraemia. As with any test, the results of NP testing must be interpreted in the clinical context.

B-type NP (BNP) or N-terminal pro-BNP (NT-proBNP)
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There are four different NPs:

• A-type NP (ANP)
• B-type NP (BNP)
• C-type NP (CNP) and
• urodilatin.

BNP is produced by cleavage of a precursor molecule, proBNP, into an inactive fragment (amino-terminal proBNP, NT-proBNP), and BNP itself. Both can potentially be measured (as can many other elements of the NP system). NT-proBNP is more stable and has a longer half-life than BNP and as a consequence, is the test recommended by NICE.



If the patient has symptoms and signs of HF with a raised NT-proBNP, the next step is specialist referral for cardiac imaging.⁵ NICE guidance for chronic HF gives detailed guidance on thresholds of NT-proBNP concentrations to guide referral.⁵

All patients with suspected HF should have NT-proBNP tested:⁵

• A level greater than 2,000 ng/L should lead to referral for urgent specialist assessment with echocardiography within two weeks
• A level between 400–2,000 ng/L should lead to referral for specialist assessment with echocardiography within six weeks
• A level less than 400 ng/L makes HF unlikely and another cause for any symptoms should be sought.

The ESC HF guidelines 2021 have lower serum NP thresholds for referral for echocardiography: BNP >35 pg/ml and NT-proBNP >125 pg/ml.⁶

• NP testing for patients admitted to hospital with HF
  The NICE guidelines for acute HF recommend an NT-proBNP cut-off of <300 ng/L to rule out a diagnosis of HF in patients admitted to hospital.¹³ This is an unhelpful recommendation. Many conditions that may present as an emergency and mimic HF, including respiratory tract infections, anaemia, arrhythmia, old age and frailty, are also associated with raised NPs. It would be highly unusual for a patient presenting with pneumonia or atrial fibrillation (AF) with a fast ventricular rate to have a serum NT-proBNP concentration <300 ng/L.

  The likelihood of HF should always be based on the history and examination, and not on blood tests considered in isolation.

  The cut off of 300 ng/L in acute HF is lower than that used for patients presenting in the community. The distinction leads to odd conclusions. For example, a patient presenting to their GP with signs and symptoms of HF and an NT-proBNP concentration of 350 ng/L has HF ruled out as a cause of their symptoms. However, if that same patient had presented to Accident and Emergency, HF would still be a possible diagnosis.

• NP testing for monitoring patients with confirmed HF
  • Serum NPs are, at present, the best single prognostic test for patients with confirmed HF but serial measurements are not recommended for monitoring⁵
  • NP concentrations are more closely related to outcome than left ventricular ejection fraction (LVEF) or other neurohormones in patients with advanced HF
  • High serum NP concentrations are associated with an increased risk of sudden death in patients with chronic HF
  • High NP concentrations are associated with an increased risk of in-hospital mortality, regardless of ejection fraction (EF)
  • High NP concentrations at discharge are associated with increased risk of re-admission or death for at least six months post-admission
  • An increase in NP concentration during admission is associated with increased risk of adverse events, whereas a decrease in serum NP is associated with lower risk.

Other tests

Following diagnosis, other laboratory investigations should be performed for a patient with incident HF, including full blood count, urea and electrolytes, thyroid function, fasting glucose and glycosylated haemaglobin (HbA_1c), lipids, and iron status.^5,6 The aim is to detect common co-morbidities or treatable precipitants of decompensated HF. Baseline measurements of renal function and serum electrolytes also guide treatment. Upon an initial presentation of HF, one may wish to consider investigating for underlying amyloidosis, which includes urine and serum protein electrophoresis. (See figure 18 and tables 4 and 5 below)

The electrocardiogram

All patients with suspected HF or decompensated HF should have a 12-lead electrocardiogram (ECG) as part of their investigations. It may be diagnostic and guide future management. It is also helpful to compare the latest ECG to older ones to detect any changes. For example:

• Q-waves may indicate an established area of infarcted myocardium giving a clue to the aetiology;
• increased voltages in the leads over the left ventricle (LV) (V3–V6) suggest LV hypertrophy, perhaps due to hypertensive or genetic cardiomyopathy;
• approximately a quarter of patients with HF have AF at presentation, which should be managed with anticoagulation and appropriate rate or rhythm control:
  • in some patients, AF with an abnormally fast (or slow) ventricular rate may be the cause of HF;
• high degrees of atrioventricular (AV) block causing bradycardia is a curable cause of HF.

A normal ECG has a high negative predictive value (93%) for excluding LV systolic dysfunction.¹⁵

In chronic HF, serial ECGs may detect incident AF or incident left bundle branch block (~10% per year),^16,17 which might change management, for example, with cardiac resynchronisation therapy (module 4).

Functional capacity assessment

Objective measures of functional and exercise capacity, such as the six-minute walk test (6MWT) or incremental exercise test, give more reliable information regarding a patient’s exercise capacity and may be useful to diagnose and assess the severity of HF. However, both are susceptible to a ‘learning effect’ and can be difficult to use routinely in a busy clinic.

They include the following:

The 6MWT
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The 6MWT measures the distance walked during six minutes on a hard, flat surface. The patient goes at their own pace and rests as needed. It can be performed in the corridor of a ward or outpatient clinic without the need for equipment; the recommended corridor length is 30 metres.¹⁸

In healthy adults, the normal 6MWT distance is between 400–700 metres. In patients with HF, a 6MWT distance less than 300 metres is associated with worse cardiovascular outcomes.^19,20

Incremental exercise capacity tests²¹
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While the 6MWT is a test of aerobic endurance, incremental exercise tests, such as the Bruce treadmill test or incremental shuttle walk test, are a better indicator of maximal aerobic performance. In patients without significant limitation, incremental exercise tests may be preferable to the 6MWT for assessing the exercise capacity of patients with HF.

Gas exchange analysis using the peak oxygen consumption (peak VO₂)
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An incremental protocol can be coupled to the measurement of metabolic gas exchange to derive objective measures of exercise capacity, such as the anaerobic threshold, peak VO₂ and the ventilatory response to exercise. Such tests can be helpful in differentiating dyspnoea of cardiac or respiratory origin, and are often used as part of the assessment for heart transplantation.

Imaging

Chest radiograph/X-ray

The most important role of a CXR in patients with chronic HF is to exclude other potential causes of breathlessness, and not to assess the HF.

© Nevit Dilman (via http://commons.wikimedia.org/wiki/File:Radiology_1300577_Nevit.jpg)

A chest X-ray (CXR) (figure 5) is an essential investigation for anyone presenting with breathlessness, regardless of whether the patient is known to have HF or lung disease. In patients with acute HF, it may show:⁵

• alveolar shadowing indicative of frank pulmonary oedema – fluffy opacities throughout the lung fields
• upper lobe blood diversion in the pulmonary vasculature – as blood is diverted to the upper lobes to compensate for the ventilation-perfusion mismatch caused by pulmonary oedema
• Kerley B lines – interstitial oedema appearing as short horizontal lines in the peripheries of the lung field
• pleural effusion
• cardiomegaly – may be the only abnormality in patients with chronic HF.*

* Cardiothoracic ratio is an unreliable finding to suggest the presence of HF; poor inspiratory effort and fat pads around the heart may give misleading results.²⁶

Lung ultrasound

Lung ultrasound may be used to confirm a diagnosis of acute HF, especially when NP testing is not available.⁶ However, it is over 40 years since pulmonary congestion on ultrasound – so-called ‘lung comets’ due to the typical ultrasound appearances – was first described,²⁷ and it is not in routine clinical practice. Many patients without HF have lung comets on lung ultrasound,²⁸ and it is unclear whether ultrasound is any better than a stethoscope for diagnosing pulmonary congestion.

Cardiac imaging

Cardiac imaging is essential for demonstrating abnormal cardiac structure and/or function, and thus, for making a diagnosis of HF. Imaging can also detect complications of HF, such as a LV thrombus or valve disease.

• Transthoracic echocardiography

  Echocardiography is the most commonly used imaging investigation. It is widely available, portable and relatively cheap. The combination of M-mode, 2D, spectral Doppler and colour Doppler echocardiography can provide a wealth of information on cardiac structure and function. However, almost all variables that are measured using ultrasound are prone to inter- and intra-observer error.

  • Cardiac structural measurements on echocardiography

    Echocardiography allows accurate measurement of:

    • LV end-diastolic and end-systolic dimensions – often increased in HF (figure 6)
    • LV end-diastolic and end-systolic volumes – used to calculate LVEF using Simpson’s biplane method

    LVEF =	End diastolic volume (ml) – End systoltic volume (ml)
    	End diastolic volume (ml)

    • left atrial (LA) size/volume – often increased in HF: LA size indexed for body surface area is a diagnostic criterion for heart failure with preserved ejection fraction (HFpEF)
    • mitral valve structure – often systolic tenting or restricted posterior leaflet in ischaemic cardiomyopathy (figure 7)
    • aortic, pulmonary and tricuspid valve structure
    • presence and size of pleural/pericardial effusions
    • size and collapsibility of the inferior vena cava (IVC) – rarely entirely normal in HF; the IVC gives a useful non-invasive indication of right atrial pressure (figure 8)
    • complications of cardiac dysfunction – e.g. intracardiac thrombus (figure 9).

    

    

    
    

    

    
    

    

  • Cardiac function measurements on echocardiography

    Echocardiography also gives an assessment of:

    • global systolic function – can be measured in various ways
      • stroke volume (LV outflow tract area × LV outflow tract velocity time integral [VTI])
      • cardiac output (stroke volume × heart rate)
      • EF (biplane Simpson’s method)
    • diastolic function (LV filling pressures)
      • restrictive filling pattern on transmitral, spectral Doppler is associated with worse outcome
      • longitudinal systolic and diastolic function by tissue Doppler imaging
      • the ratio of the early mitral peak velocity to early diastolic mitral annular velocity is used to estimate LV filling pressure
    • valvular regurgitation
      • can be secondary to ventricular dilatation in HF
      • the velocity of any tricuspid regurgitation (TR) (figure 10) allows estimation of right ventricular systolic pressure (figure 11). In combination with the IVC appearance, TR can be used to estimate pulmonary artery systolic pressure.

Exercise or pharmacological stress echocardiography may be used to identify the presence and extent of inducible ischaemia (evidence of myocardial ischaemia not seen at rest) and to clarify the severity of aortic stenosis.²⁹

• Transoesophageal echocardiography

Transoesophageal echocardiography (TOE) is usually not needed in routine diagnostic assessment, unless the transthoracic ultrasound window is inadequate (e.g. because of obesity or chronic lung disease, or in ventilated patients) and an alternative modality (e.g. cardiac magnetic resonance [CMR] imaging) is not available or appropriate. In special cases, such as endocarditis or complex valve disease, TOE can give more detailed information to guide diagnosis and management.

• Cardiovascular magnetic resonance scanning

CMR scanning is becoming more widely available and can provide a range of information on different aspects of cardiac function, as well as suggest the underlying cause of HF.³⁰ It is recommended by the ESC as the best alternative imaging modality in patients with non-diagnostic echocardiographic studies.⁶ For a more detailed discussion with examples, please click below.

CMR can also identify other causes of a dilated LV. Figure 17a shows a coronal image from a patient presenting with severe HF, and figure 17b shows his severe biventricular dilation and dysfunction. There are bilateral large pleural effusions and the liver appears more ‘black’ than usual. These features are seen in patients with iron overload. A specific sequence, T2*, was therefore performed, which allows myocardial and liver iron quantification. There was severe iron overload in both organs. Following genotyping, a diagnosis of haemochromatosis was made and cardiac function recovered after iron chelation therapy (figure 17c).

The cine imaging of a patient presenting with a two-month history of increasing breathlessness is shown in figure 18a. There is severe biventricular failure. The LGE imaging is shown in figure 18b. There is a large amount of LGE which does not correspond with coronary artery territories, although it is transmural in places. In figure 18c, areas of lymphadenopathy are arrowed. A diagnosis of sarcoidosis was subsequently confirmed on lymph node biopsy.

CMR also has a limited role in identifying cardiac pathology in patients with normal LV function. There are two forms of cardiac amyloidosis – AL amyloid (deposition of abnormal light chains within the myocardium) and ATTR amyloid (deposition of transthyretin – a protein responsible for transporting thyroxine and retinol) – both of which may cause HF. LGE is ubiquitous in patients with cardiac amyloidosis; the majority have transmural LGE not related to coronary artery territories.³⁴ Other features of cardiac amyloid, such as poor longitudinal systolic function, dilated atria and LV hypertrophy are also seen on CMR. However, CMR is unable to differentiate between AL and ATTR amyloid³⁵; further imaging is almost always needed to confirm the diagnosis (see Nuclear imaging section below).

Other imaging modalities⁶

Other imaging techniques can be helpful, but are not mandatory for diagnosis or monitoring of HF.^1,32

Cardiac catheterisation and coronary angiography
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NICE recommends against the use of routine coronary angiography in patients with HF.⁵ In patients with HF and angina, other diagnostic imaging modalities are preferred – CT coronary angiogram or non-invasive functional imaging such myocardial perfusion imaging.³⁶

However, right heart catheterisation can provide useful haemodynamic information for patients being considered for advanced therapies (LV assist devices and transplant) and can help clarify a diagnosis of pulmonary arterial hypertension, which may mimic HF.²²

Nuclear imaging
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Nuclear imaging, including ECG-gated myocardial perfusion imaging, can be used to assess heart function and damage in HF. ECG-gated single-photon emission computer tomography (SPECT) can be used to assess global LVEF, regional wall motion abnormalities and regional wall thickening. If coronary artery disease is suspected, SPECT can also assess ischaemia and myocardial viability.

Cardiac computed tomography
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Cardiac computed tomography (CT) scanning of the heart is not usually required in the routine diagnosis and management of HF. Multidetector CT scanning is useful in delineating congenital and valvular abnormalities; however, echocardiography and CMR may provide similar information without exposing the patient to ionising radiation.

Positron emission tomography
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Positron emission tomography (PET) (alone or with CT) may also be used to assess ischaemia and viability, but lack of availability, radiation exposure, and wide availability of cheaper alternatives limit its use.

DPD scanning
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Tracers used in bone scanning, such as ^99mTc-labelled 3,3-diphosphono-1,2-propanodicarboxylic acid (DPD), are avidly taken up by transthyretin amyloid deposits in the heart. Cardiac amyloidosis caused by accumulation of immunoglobulin light chains (AL amyloid) is not common and DPD scanning is not a sensitive way to detect it; however, ATTR is increasingly recognised as a common cause of HF in those with HF and LV hypertrophy. DPD scanning is a straightforward, sensitive and specific (and relatively cheap) way to detect it (figure 19).

Whether surgical revascularisation may lead to outcome benefit in the era of modern quadruple therapy is unknown. While viability assessment may still be performed in patients with HF, its role in decision making is diminished.

Diagnosis in the acute setting

Initial investigations should be guided by the clinical condition of the patient. Table 4 provides and overview of the pertinent tests and some examples of their findings and interpretations in the diagnostic workup of a suspected case of acute HF, based on the history, symptoms and signs. Specific investigations will be discussed in more detail later in this module.

Immediate/emergency echocardiography is recommended in patients with haemodynamic instability/cardiogenic shock and in suspected life-threatening structural/functional cardiac disease (i.e. mechanical complications of acute myocardial infarction, acute valve disease, aortic dissection). Where comprehensive echocardiography is not available, point-of-care or focused cardiac ultrasound (PoCUS/FoCUS) may be used in the first instance⁴⁴ with comprehensive echocardiography being performed later, though as early as possible. NICE recommends that people presenting to hospital with new suspected HF should have echocardiography within 48 hours of admission to guide early specialist treatment.¹³

Diagnosis in the chronic setting

The diagnosis of chronic HF requires the presence of signs and/or symptoms of HF, in conjunction with objective evidence of cardiac structural and/or functional abnormalities. The priorities for the diagnostic workup in chronic HF are illustrated in figure 20. In the chronic setting, additional focus is placed on determining the underlying aetiology and comorbidities which will also further impact management (table 5).

Key: ECG = electrocardiogram; ESC = The European Society of Cardiology; HF = heart failure; NICE = The National Institute for Health and Care Excellence; NT-proBNP = N-terminal pro B-type natriuretic peptide

Classification of HF according to LVEF (phenotypic classification)⁶

Heart failure with a reduced ejection fraction (HFrEF)

HFrEF is due to impaired systolic, contractile function of the LV. However, impaired systolic function does not happen in isolation – patients with HFrEF invariably also have abnormal diastolic function.

Heart failure with preserved ejection fraction (HFpEF)

Some patients have signs and symptoms of HF but have a normal EF on echocardiography (figure 21).⁴⁶ Such patients are variously labelled as having normal (HFnEF) or preserved ejection fraction (HFpEF) or ‘diastolic HF’ (figure 21).

With kind permission from Han Bin Xiao46 Key: LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle

The EuroHeart Failure survey among women (n = 2,048; 41% of total enrolled) and men (n = 3,249; 57% of total enrolled) found that a reduced LVEF was more prevalent in men compared to women with HF (51% and 28%, respectively).⁴⁷ Around half of all patients with the HF syndrome have a normal or preserved LV systolic function.^47,48 When compared to patients with HFrEF, those with normal or preserved EF are usually:^49,50

• older
• more likely to be female
• less likely to have coronary artery disease
• more likely to have hypertension
• more likely to have valvular heart disease
• more likely to have AF
• more likely to have diabetes or COPD
• more likely to have muscle wasting (or sarcopaenia)
• more likely to be anaemic
• more likely to have renal dysfunction
• often given different pharmacotherapy
• less likely to be admitted for HF
• less likely to respond to treatment directed at HF
• less likely to die of HF
• have a lower mortality rate.⁴⁸

HFnEF remains a controversial entity; many believe that there is a significant risk of inappropriate diagnosis. The label applied can also be provocative. Many prefer the term ‘preserved’ to describe a normal EF, but this is surely a misnomer – although LVEF might be in the normal range, it might have fallen to reach that point, and cannot be known to be ‘preserved’. The ESC discussed changing HFpEF to HFnEF in its 2023 update to the 2021 ESC HF guidance but decided that any changes in its terminology would be considered in its next HF guidelines.⁷ Therefore, HFnEF will be referred to as HFpEF in these modules.

Heart failure with mildly reduced ejection fraction (HFmrEF)

To complicate things further, a third HF phenotype has been proposed that lies in the ‘grey area’ between HFrEF and HFpEF: HFmrEF with LVEF 41–49%.⁷

The prevalence of HFmrEF is between 14% and 18% of patients with HF.^52–55 Patients with HFmrEF are older and more likely to be female with greater burden of co-morbidities than patients with HFrEF, but with a similar prevalence of IHD.⁵⁶ Patients with HFmrEF are thus similar to patients with HFpEF. However, their prognosis is similar to that of HFrEF and their causes of death are closer to those seen in patients with HFrEF than HFpEF.^57,58

The clinical and laboratory characteristics of patients with HFmrEF are intermediate between HFpEF and HFrEF.⁵⁹ It is possible that those with HFmrEF are in transition from HFpEF to HFrEF or vice versa.^60–63 Although HFmrEF has become ingrained in clinical trials since it was first described in 2016, a diagnosis of HFmrEF acknowledges that the patient has HF symptoms and that the ventricular function is neither obviously normal nor obviously impaired; the utility of such a diagnosis is questionable.

Identifying the HF phenotype is essential for management

Despite much debate surrounding the value of LVEF as a measure of cardiac function, there is no doubt that it is helpful in identifying patients who are likely to respond to specific therapies. Clinical trials have unequivocally demonstrated the benefit of medical and device therapy for patients with HF, but only previously amongst those with reduced EF, whichever way that is defined.

It is important to remember that signs may not be present in the early stages of HF (especially in HFpEF) and in optimally treated patients. Therefore, in addition to symptoms, physical signs and risk factors for HF, it would be pertinent to obtain objective evidence to support the diagnosis of HF. This would include echocardiography findings (table 6)⁶⁴ and NT-proBNP levels.

Although NP levels tend to be lower amongst patients with HFpEF compared to patients with HFrEF with similar symptoms of congestion,⁵⁵ they cannot be used to distinguish between the two phenotypes.

Key: HFmrEF = heart failure with mildly reduced ejection fraction; HFpEF = heart failure with preserved ejection fraction; HFrEF = heart failure with reduced ejection fraction; LVEF = left ventricular ejection fraction

Additionally, there has been a lack of clarity on how to treat patients with HFmrEF. Following the results of more recent trials, the latest ESC 2023 focused update has made some recommendations (see module 3).^6,7

Summary

NP testing is key to making a diagnosis of HF but is a ‘rule-out’ test. The probability that a patient has the HF syndrome should be determined mainly by history and examination. Appropriate and timely imaging is crucial in a patient with suspected HF; it can make a diagnosis, reveal an underlying cause, guide therapy and predict outcome. However, access to diagnostic services in a timely fashion is patchy nationally and long waiting times are commonplace.

Echocardiography is the primary imaging investigation due to its widespread availability, low cost and wealth of clinical experience. CMR, however, is also a powerful imaging modality in HF which may give more information as to its aetiology.

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References

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