Heart failure learning module 2: diagnosis

Released7 May 2020     Expires: 07 May 2022      Programme:

Sponsorship Statement: Vifor Pharma UK has provided an unrestricted educational grant to fund this activity and has not had any input into any aspect of this learning resource.

Introduction

The signs and symptoms of heart failure are common and notoriously non-specific (module 1); misdiagnosis and underdiagnosis are common.

  • 10–20% of patients who are eventually diagnosed as having acute heart failure following admission to hospital may have initial treatment for an alternative diagnosis such as chronic obstructive airway disease.1,2
  • The estimated prevalence of heart failure in the UK is 1–2% but the prevalence of systolic dysfunction (left ventricular ejection fraction [LVEF] <50%) in patients over 45 years of age may be as high as 6%.3 As many as 16% of patients over the age of 65 presenting with breathlessness to their general practitioner (GP) may have undiagnosed heart failure as the cause.4

The heart failure syndrome is a broad spectrum ranging from those presenting in extremis to the emergency department to patients presenting to either primary or secondary care with symptoms for many months.

  • Acute heart failure generally refers to patients presenting as emergencies to hospital, usually with either pulmonary oedema or with gross fluid retention. Such patients are often presenting for the first time, but may be patients having an exacerbation of their previously stable heart failure; sometimes described as ‘decompensated’ heart failure. They have acutely abnormal haemodynamics.
  • In contrast, most patients with chronic heart failure have been treated medically and will usually have few, if any, symptoms or signs at rest. The term ‘congestive’ heart failure, often used to describe patients in this condition (particularly in North America), is inappropriate: patients with treated heart failure should not be congested.3,4

The diagnosis of heart failure requires the combination of symptoms suggestive of the condition, appropriate abnormalities on imaging and raised serum natriuretic peptides (see below).

Natriuretic peptides (NP)

NP release and actions

Natriuretic peptides (NPs) are secreted by the myocardium in response to stretch. In health, they are part of the homeostatic systems maintaining blood volume. They counteract many of the pathophysiological processes of heart failure. There are four different natriuretic peptides: A-type natriuretic peptide (ANP), B-type natriuretic peptide (BNP), C-type natriuretic peptide (CNP) and urodilatin.

Actions of NPs (figure 1):

  • natriuresis/diuresis
  • vasodilatation
  • inhibition of the sympathetic nervous system
  • inhibition of the renin–angiotensin–aldosterone system (RAAS).
Figure 1. Actions of B-type natriuretic peptide (BNP)
Figure 1. Actions of B-type natriuretic peptide (BNP)

Serum NP levels can be measured using immunoassay testing which is quick, easy and cheap. The major role for natriuretic peptide testing is in excluding the diagnosis of heart failure in a breathless patient: those patients with levels below defined cut-offs do not have heart failure, and an alternative diagnosis for the symptoms should be sought. Natriuretic peptide testing may prove to be useful for screening, and gives prognostic information about patients with heart failure.5

NPs and diagnosis

Table 1. Cardiac and non-cardiac causes of raised BNP and NTproBNP

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
Key: BNP = B-type natriuretic peptide; COPD = chronic obstructive pulmonary disease; LVH = left ventricular hypertrophy; NT-proBNP = N-terminal fragment of the prohormone BNP; OSA = obstructive sleep apnoea; PE = Pulmonary embolism

The signs and symptoms of heart failure can be misinterpreted in the absence of further investigation. NPs can exclude heart failure as a cause of breathlessness in patients presenting either acutely or with a more gradual onset of symptoms.

Low serum NPs have a high negative predictive value and very high levels of NPs have a high positive predictive value for the diagnosis of heart failure. However, there are several non-cardiac causes for elevated levels that should be considered in the clinical context (table 1).

BNP and the N-terminal fragment of the prohormone (NT-proBNP) are the most frequently measured NPs: 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 natriuretic peptide system). The emergence of neprilysin inhibitors, which prevent the breakdown of BNP (thus increasing levels), means that NT-proBNP is now the standard test in clinical practice.

NPs and prognosis

Serum NPs are, at present, the best single prognostic test for heart failure.

  • NP concentrations predict outcome more accurately than LVEF or other neurohormones in patients with advanced heart failure
  • high serum NP concentrations are associated with an increased risk of sudden death in patients with chronic heart failure
  • high NP concentrations are associated with an increased risk of in-hospital mortality, regardless of ejection fraction
  • 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 levels are associated with lower risk.

NPs and guidelines for specialist referral

Ambulatory ECG being fitted

The diagnosis of heart failure can only be fully established by specialist assessment coupled with appropriate imaging, most commonly echocardiography.

The National Institute for Health and Care Excellence (NICE) guidance for chronic heart failure gives detailed guidance on thresholds of NP concentration to guide referral.6 All patients with suspected heart failure should have NTproBNP tested:

  • a level greater than 2,000 ng/L warrants urgent referral for specialist assessment with echocardiography within two weeks
  • a level between 400–2,000 ng/L warrants referral for specialist assessment with echocardiography within six weeks
  • a level less than 400 ng/L makes heart failure unlikely and another cause for any symptoms should be sought
  • the requirement to refer all patients with suspected heart failure and history of myocardial infarction (MI) for specialist assessment within two weeks without testing NP levels is not included in the 2018 NICE guidelines.

The 2016 European Society of Cardiology (ESC) heart failure guidelines  have lower serum NP thresholds for referral for echocardiography: BNP >35 pg/mL and NTproBNP >125 pg/mL.7

A normal NT-proBNP excludes the diagnosis of heart failure without the need for an echocardiogram. Essential initial investigations include a 12-lead electrocardiogram (ECG) and laboratory tests (see below). Other diagnostic tests are generally only required if the diagnosis remains unclear.

Heart failure module 2 - Figure 2. NICE diagnostic algorithm for chronic heart failure
Figure 2. NICE diagnostic algorithm for chronic heart failure

HeFNEF versus HeFREF

Screen shot 2014-01-28 at 17.58.57

Although NP levels tend to be lower amongst patients with heart failure with a normal ejection fraction (HeFNEF) compared to patients with heart failure with a reduced ejection fraction (HeFREF) with similar symptoms of congestion,8 they cannot be used to distinguish between the two phenotypes. The distinction at diagnosis is important as it changes management.

While there are several evidence-based drug and device treatments for HeFREF, no treatment for patients with HeFNEF has shown convincing outcome benefit in randomised controlled trials. Symptomatic relief with diuretics and treatment of co-morbidities are the best treatment strategies for these patients.

Chronic heart failure

Table 2. New York Heart Association (NYHA) classification

Class I Patients with cardiac disease but with no limitation during ordinary physical activity
Class II Slight limitations caused by cardiac disease. Activity such as walking causes dyspnoea
Class III Marked limitation. Symptoms are provoked easily, for example, by walking on flat ground
Class IV Breathlessness at rest

The vast majority of patients with heart failure receive active treatment so that following a presentation with an acute episode of heart failure (either to the emergency department or GP), venous congestion is treated.

The chronic heart failure syndrome is what affects patients with heart failure once they are taking appropriate combination therapy.9 Most patients with chronic heart failure complain of varying degrees of dyspnoea, fatigue and exercise intolerance although some may be asymptomatic. The New York Heart Association (NYHA) is the most widely used symptom classification (table 2).

Acute heart failure – new onset or acute decompensation of heart failure

In acute or decompensated heart failure, the majority of patients present with fluid in the wrong place (table 3). The fluid can be in the lungs (pulmonary oedema), in the tissues (peripheral oedema) but usually in both to varying degrees.

Table 3. Clinical features of the different modes of presentation with acute heart failure

Fluid retention Pulmonary oedema
Comfortable at rest but breathless on minimal exertion Pale and clammy. Unable to lie flat or talk in full sentences
Tachycardia – sinus or atrial fibrillation Tachypnoea, hypoxia, respiratory failure
Low systemic blood pressure Tachycardia
Pitting oedema † – see figure 3 Pink, frothy sputum – oedema
Pleural effusion Hypertension due to sympathetic activation
Ascites
Raised jugular venous pulse (JVP) – see figure 4 Signs and symptoms of precipitating cause such as myocardial ischaemia or arrhythmia
Bibasal lung crackles
Hepatic congestion
† Oedema accumulates with gravity; in an ambulatory patient the ankles are affected first rising to the kness, thighs and then sacrum sequentially. In bedbound patients the sacrum is often affected first. Extreme fluid retention causes pleural effusions, ascites, pericardial effusions and abdominal or thoracic wall oedema.
Pedal oedema during and after the application of pressure to the skin
Figure 3. Pedal oedema during and after the application of pressure to the skin

Patients presenting with acute heart failure thus fall into one of two broad categories, although there is often some overlap:

  • those with gross fluid retention who are breathless on modest exertion but are comfortable at rest (the most common mode of presentation)
  • those with sudden onset breathlessness due to pulmonary oedema.

Acute cardiogenic shock is sometimes considered to be a form of acute heart failure and usually complicates some catastrophic mechanical problem, such as a large myocardial infarct or papillary muscle rupture. The patient is hypotensive and oliguric, and often agitated and confused. The prognosis is extremely bleak.

Jugular venous pressure
Figure 4. Jugular venous pressure (Click arrow below to play, or bottom-right for full screen)

Laboratory investigations

Following diagnosis, laboratory investigations should be undertaken in the initial assessment of a patient with incident heart failure.6,7 Investigations aim to detect common co-morbidites or treatable precipitants of acute heart failure. Baseline measurements of full blood count and renal function also guide treatment.

Investigations include:

  • full blood count (haematocrit, haemoglobin, leucocyte count and platelets)
    • anaemia is common in patients with heart failure and is associated with an increased risk of mortality
    • anaemia can exacerbate underlying cardiac disease and severe anaemia may even present as heart failure
    • iron deficiency is common in heart failure, and may be a target for treatment
  • renal function and electrolytes
    • almost all drugs used to treat heart failure may have an adverse impact on renal function or electrolyte balance
    • renal dysfunction itself can cause heart failure
    • hyponatraemia, hypochloraemia and renal impairment are all associated with an increased risk of mortality in heart failure
  • liver function including serum albumin
    • liver function tests may be deranged due to congestion or underlying aetiology such as haemochromatosis
    • albumin should be measured to ensure that any oedema is not due to nephrotic syndrome or other hypoalbuminaemic states such as chronic liver disease
  • thyroid function tests (usually thyroid-stimulating hormone)
    • both hypo and hyperthyroidism are treatable precipitants of heart failure and hypothyroidism can mimic heart failure
  • fasting plasma glucose
    • diabetes is a risk factor for developing heart failure and is common among patients with the disease. Although treating a high blood sugar may not improve cardiovascular outcome, it remains the cornerstone of diabetic treatment
  • iron studies and serum ferritin to exclude haemachromatosis
  • serum and urine protein electrophoresis to exclude AL amyloidosis
  • creatine kinase, particularly in younger patients, to exclude possible generalised myopathy.

The electrocardiogram

Ambulatory ECG being fitted

All patients with suspected heart failure should have a 12-lead electrocardiogram (ECG) as part of their initial investigations. It may be diagnostic and guide future management.6,7

  • Q-waves may indicate infarcted or non-viable myocardium
  • increased voltages in the left-sided leads suggest left ventricular hypertrophy, perhaps due to hypertensive or genetic cardiomyopathy
  • approximately one quarter of patients with heart failure have atrial fibrillation at presentation which should be managed with anticoagulation and appropriate rate or rhythm control: in some patients, atrial fibrillation may be the cause of heart failure
  • high degrees of atrioventricular block are a treatable cause of heart failure – approximately one third of patients have left bundle branch block at diagnosis.

In chronic heart failure, serial ECGs may detect incident atrial fibrillation or left bundle branch block (~10% per year) which might change management, for example, with cardiac resynchronisation therapy (module 4).

Chest radiograph/X-ray

800px-Radiology_1300577_Nevit
Figure 5. X-ray of a patient with pulmonary congestion due to heart failure (click to enlarge)

A chest X-ray (CXR) (see figure 5) is an essential investigation for anyone presenting with breathlessness. In patients with acute heart failure it may show:7

  • alveolar shadowing indicative of frank pulmonary oedema – fluffy opacities throughout the lung fields
  • upper lobe blood diversion of 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 heart failure.*

* Cardiothoracic ratio is an unreliable finding to suggest the presence of heart failure; poor inspiratory effort and fat pads around the heart may give misleading results.10

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

The basic investigations needed in a patient presenting with heart failure for the first time are shown in table 4.

Table 4. Summary of basic investigations in a patient presenting with heart failure for the first time

Test Rationale
Full blood count Anaemia; evidence of active infection; blood dyscrasias
Renal function and electrolytes Baseline renal function before initiating treatment; electrolyte abnormalities that may influence prognosis or guide treatment
Liver function and serum albumin Evidence of heart failure aetiology such as haemochromatosis or other causes of presentation such as hypoalbuminaemia
Thyroid function Abnormal thyroid function is a treatable precipitant of heart failure
Glucose Diabetes is common in patients with heart failure and may be undiagnosed
Iron studies / ferritin, transferrin saturation Investigation for haemochromatosis and aetiology of anaemia if present
Serum and urine electrophoresis Investigation for amyloidosis
Creatinine kinase Investigation for myopathy, particularly in younger patients presenting with heart failure
Electrocardiogram Investigation for aetiology of heart failure: ischaemia, cardiomyopathy, arrhythmia
Chest X ray Investigation for alternative causes of breathlessness; to establish the extent of pulmonary oedema.

Exercise capacity testing

Assessing functional and exercise capacity is an important part of the clinical assessment of patients with heart failure.

The NYHA classification is a widely used tool to grade the severity of a patient’s symptoms. However, reproducibility of NYHA class is low, with low validity and reproducibility.11,12 Objective measures such as the six-minute walk test (6MWT) give more reliable information regarding a patients’ exercise capacity, although are susceptible to a ‘learning effect’.

The 6MWT

6-minute walk test

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 is easy to perform in the corridor of a ward or outpatient clinic without the need for equipment: the recommended corridor length is 30 metres.13

In healthy adults, the normal 6MWT distance is between 400-700m. In patients with heart failure, 6MWT distance <300m is associated with worse cardiovascular outcomes.14

Incremental ETTs

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 heart failure.

Gas exchange analysis using the peak oxygen consumption (peak VO2)

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 oxygen consumption 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 assessment for heart transplant.

Normal exercise capacity in a patient not receiving treatment effectively excludes the diagnosis of symptomatic heart failure. However, there is a poor correlation between exercise capacity and resting haemodynamic measures, including ejection fraction.

Haemodynamic studies

Haemodynamic assessments of patients with heart failure can give information on a patient’s fluid status. They are usually invasive, and continuous monitoring techniques in ambulatory patients are not routinely available.

Click here to read more

Implantable devices for continuous measurement of pulmonary artery pressure (and even of left atrial pressure) have been developed. Pulmonary artery pressure increases in patients with chronic stable heart failure as they decompensate before the onset of symptoms. Some studies have shown that an implantable device that measures pulmonary artery pressure results in patients receiving more aggressive medical therapy and reduces hospital admissions with heart failure.15,16

Measuring cardiac output with thermodilution together with direct measurement of intra-cardiac pressures can occasionally be useful in patients hospitalised with severe or refractory heart failure.

Cardiac imaging

Cardiac imaging is essential for demonstrating abnormal cardiac function and thus, making a diagnosis of heart failure. Imaging can detect complications of heart failure, such as left ventricular thrombus, and provides an objective measure of deterioration which may influence treatment.

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.

Cardiac structure

Echocardiography allows accurate measurement of:

  • LV end-diastolic and end-systolic dimensions – often increased in heart failure (figure 6)
  • LV end-diastolic and end-systolic volumes – for estimation of ejection fraction
  • left atrial (LA) size/volume – often increased in heart failure: LA size indexed for body surface area is a diagnostic criterion for heart failure with a normal ejection fraction (HeFNEF)
  • mitral valve structure – often systolic tenting or restricted posterior leaflet in ischaemic cardiomyopathy (figure 7)
  • aortic, pulmonary and tricuspid valve structure
  • size of pleural +/- pericardial effusions
  • size and collapsibility of the inferior vena cava (IVC) – rarely entirely normal in heart failure; this gives a useful non-invasive indication of right atrial pressures (figure 8)
  • complications of cardiac dysfunction – e.g. intra-cardiac thrombus (figure 9).

Figure 6. Echocardiogram showing dilated left ventricular end-diastolic and end-systolic dimensions in a patient with heart failure

Figure 7. Echocardiogram showing mitral valve structure in ischaemic cardiomyopathy (Click arrow below to play, or bottom-right for full screen)

Echocardiogram showing inferior vena cava in a patient with heart failure
Figure 8. Echocardiogram showing inferior vena cava in a patient with heart failure (Click arrow below to play, or bottom-right for full screen)

Figure 9. Echocardiogram showing intra-cardiac thrombus
Figure 9. Echocardiogram showing intra-cardiac thrombus
Cardiac function

Echocardiography also gives an assessment of:

  • global systolic function – can be measured in various ways
    • stroke volume (LV outflow tract area x left ventricular outflow tract velocity time integral [VTI]),
    • cardiac output (stroke volume x heart rate)
    • ejection fraction (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 heart failure
    • tricuspid regurgitation (figure 10) also allows estimation of right ventricular systolic pressures (figure 11). In combination with IVC appearances, this 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 and to determine whether non-contracting myocardium is viable.

Echocardiogram showing tricuspid regurgitation
Figure 10. Echocardiogram showing tricuspid regurgitation (Click arrow below to play, or bottom-right for full screen)

Figure 11. Echocardiogram showing estimated right ventricular systolic pressures
Figure 11. Echocardiogram showing estimated right ventricular systolic pressures
Transoesophageal echocardiography (TOE)

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, TOE can give more detailed information to guide diagnosis and management.

Cardiovascular magnetic resonance

Cardiac magnetic resonance (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 heart failure. CMR is recommended by the ESC as the best alternative imaging modality in patients with non-diagnostic echocardiographic studies as recommended in the ESC heart failure guidelines. For a more detailed discussion with examples, please click below.

Click here to read more

In the last 10 years there has been an exponential growth in the use and availability of CMR in the UK, with the most common reason for referral being the assessment of heart failure and cardiomyopathy.17 ESC guidelines recommend CMR in patients with inconclusive echocardiographic imaging and suspected inflammatory or infiltrative conditions.6 European registry data suggest that CMR changes patient management in around two-thirds of cases and is diagnostic in up to 16%.18 A typical CMR study involves the following steps:

Anatomical thoraco-abdominal imaging

This can be done in any plane, but typically involves a transverse stack. Figure 12 shows a patient presenting with acute pulmonary oedema in the week before the CMR study. A white blood transverse stack is shown. There is a large abdominal aortic aneurysm with intramural thrombus. A number of renal cysts are seen. In the thorax, sternal wires are present and the left ventricle and atrium are dilated. The aorta follows a tortuous course.

A white blood transverse stack is shown on the CMR in a patient presenting with acute pulmonary oedema
Figure 12. A white blood transverse stack is shown on the CMR in a patient presenting with acute pulmonary oedema (Click arrow below to play, or bottom-right for full screen)

Cardiac anatomy and ventricular volumes, function and mass assessment

Cine imaging can be taken in any tissue plane, typically the long axis and short axis views. Figure 13 shows the long and short axis cine images from the same patient. The left ventricle is dilated with an indexed end diastolic volume of 182 ml/m2 (normal: 60–95) and has an ejection fraction of 47%. Note the regional wall motion abnormalities and the small apical microaneurysm. The indexed LV mass is raised at 206 g/m2 (57–90). The views of the aortic valve in figure 14a show significant aortic regurgitation (AR). A short axis cut through the valve (figure 15) shows it to be functionally bicuspid with an early aneurysm of the right sinus of Valsalva. Flow imaging found a large regurgitation fraction (51%) through the valve, confirming severe AR.

Long and short axis cine images from the same patient. Panel A shows the aortic valve to be diseased, and that significant aortic regurgitation is present
Figure 13. Long and short axis cine images from the same patient. Panel A shows the aortic valve to be diseased, and that significant aortic regurgitation is present (Click arrow below to play, or bottom-right for full screen)

Long and short axis cine images from the same patient
Figure 14. Long and short axis cine images from the same patient. Panel B (Click arrow below to play, or bottom-right for full screen)

A short axis cut through the valve, showing it to be functionally bicuspid with an early aneurysm of the right sinus of Valsalva
Figure 15. A short axis cut through the valve, showing it to be functionally bicuspid with an early aneurysm of the right sinus of Valsalva (Click arrow below to play, or bottom-right for full screen)

Late gadolinium enhancement

Gadolinium is an extracellular contrast agent. Following intravenous administration, it will accumulate in areas of the myocardium where there is expansion of the extracellular space. Expansion can occur as a result of fibrosis, infarction, oedema and infiltration. Areas of focal expansion can then be shown using CMR sequences which are particularly affected by the presence of gadolinium. These areas of abnormality appear white and are known as late gadolinium enhancement (LGE). The pattern of LGE can suggest the cause for heart failure and give prognostic information.

CMR in the dilated LV: differential diagnosis

In patients with global LV dysfunction, LGE-CMR accurately differentiates ischaemic from non-ischaemic cardiomyopathy and hence can be used as a ‘gatekeeper’ for coronary angiography.19 Areas of infarction will involve the sub-endocardium, a pattern very rarely seen in non-ischaemic cardiomyopathy. In figures 16 and 17, patients with global LV impairment are shown. Figure 16a shows that the patient has transmural LGE in the septum and anterior walls, and was found to have three-vessel disease on angiography. Figure 16b shows the patient has mid-wall and epicardial LGE. He had a family history of dilated cardiomyopathy and was found to have a desmosomal mutation.

Figure 16. Panel A shows that the patient has transmural late gadolinium enhancement (LGE) in the septum and anterior walls, and was found to have three vessel disease on angiography. Panel B shows that the patient has mid-wall and epicardial LGE
Figure 16. Panel A shows that the patient has transmural late gadolinium enhancement (LGE) in the septum and anterior walls, and was found to have three vessel disease on angiography. Panel B shows that the patient has mid-wall and epicardial LGE (Click arrow below to play, or bottom-right for full screen)
Figure 17a. A coronal image from a patient presenting with severe heart failure
Figure 17a. A coronal image from a patient presenting with severe heart failure (Click arrow below to play, or bottom-right for full screen)

CMR can also identify other causes of a dilated LV. Figure 17a shows a coronal image from a patient presenting with severe heart failure, and figure 17b shows his severe biventricular dilatation and dysfunction. Bilateral large pleural effusions are seen and the liver appears more “black” than usual. This is 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).

Severe biventricular dilatation and dysfunction in the same patient. Bilateral large pleural effusions are visible
Figure 17b. Severe biventricular dilatation and dysfunction in the same patient. Bilateral large pleural effusions are visible (Click arrow below to play, or bottom-right for full screen)

Following a diagnosis of haemochromatosis and iron chelation therapy, cardiac function is shown to recover
Figure 17c. Following a diagnosis of haemochromatosis and iron chelation therapy, cardiac function is shown to recover (Click arrow below to play, or bottom-right for full screen)

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.

Cine imaging of a patient presenting with a two month history of increasing breathlessness, showing severe biventricular failure
Figure 18a. Cine imaging of a patient presenting with a two month history of increasing breathlessness, showing severe biventricular failure (Click arrow below to play, or bottom-right for full screen)

Late gadolinium enhancement imaging in the same patient
Figure 18b. Late gadolinium enhancement imaging in the same patient (Click arrow below to play, or bottom-right for full screen)

Figure 18c. Areas of lymphadenopathy are arrowed. A diagnosis of sarcoidosis was confirmed on lymph node biopsy (Click arrow below to play, or bottom-right for full screen)
Figure 18c. Areas of lymphadenopathy are arrowed. A diagnosis of sarcoidosis was confirmed on lymph node biopsy

Myocardial viability and coronary revascularisation

For over two decades, cardiologists worldwide have used the results of non-invasive imaging tests to help determine the need for revascularisation in patients with ischaemic LV dysfunction. This dogma was challenged by the results of the STICH (Surgical Treatment for Ischemic Heart Failure) trial which suggested that there was no role for revascularisation in patients without angina.20 However, the STICH extension study suggests that there may be a small benefit from revascularisation in carefully selected patients,21 and so imaging is still used to assess viability. Techniques used include:

  • dobutamine stress echocardiography
  • myocardial contrast echocardiography
  • myocardial perfusion scintigraphy
  • positron emission tomography
  • LGE-CMR
  • dobutamine-CMR

Other imaging modalities

Other imaging techniques can be helpful.1,21

Cardiac catheterisation and coronary angiography

This is indicated in the following clinical scenarios:

  • heart failure caused by systolic dysfunction in association with angina with regional wall motion abnormalities and/or scintigraphic evidence of reversible myocardial ischaemia when revascularisation is being considered
  • ‘work-up’ for cardiac transplantation
  • heart failure secondary to complications of MI such as ventricular aneurysm.
Nuclear imaging

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

Cardiac computed tomography (CT) scanning of the heart is not usually required in the routine diagnosis and management of heart failure. Multidetector CT (MDCT) 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 (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.

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, transthyretin amyloidosis (ATTR) is increasingly recognised as a common cause of heart failure in those with heart failure and left ventricular hypertrophy. DPD scanning is a straightforward, sensitive and specific (and relatively cheap) way to detect it (figure 19).

Heart failure Module 2 - Figure 19. Amyloid deposits can be detected by a DPD scan
Figure 19. Amyloid deposits can be detected by a DPD scan

Imaging summary statement

Appropriate and timely imaging is crucial in a patient with suspected heart failure; it can make a diagnosis, reveal an underlying cause, guide therapy and predict outcome.

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

close window and return to take test

References

  1. Remes J, Miettinen H, Reunanen A, Pyorala K. Validity of clinical diagnosis of heart failure in primary health care. Eur Heart J 1991;12:315–21. https://doi.org/10.1093/oxfordjournals.eurheartj.a059896
  2. Collins SP, Lindsell CJ, Peacock WF, Eckert DC, Askew J, Storrow AB. Clinical characteristics of emergency department heart failure patients initially diagnosed as non-heart failure. BMC Emerg Med 2006;6:11 http://dx.doi.org/10.1186/1471-227X-6-11
  3. Redfield MM, Jacobsen SJ, Burnett JC Jr, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA 2003;289(2):194–202 http://dx.doi.org/10.1001/jama.289.2.194
  4. van Riet EE, Hoes AW, Limburg A, Landman MA, van der Hoeven H, Rutten FH. Prevalence of unrecognized heart failure in older persons with shortness of breath on exertion. Eur J Heart Fail 2014;16(7):772–7 http://dx.doi.org/10.1002/ejhf.110
  5. Singh JSS, Burrell LM, Cherif M, Squire IB, Clark AL, Lang CC. Sacubitril/valsartan: beyond natriuretic peptides. Heart 2017;103(20):1569–77. http://dx.doi.org/10.1136/heartjnl-2017-311295
  6. National Institute for Health and Care Excellence. Chronic heart failure in adults: diagnosis and management [NG106]. London: NICE, 2018. Available from http://www.nice.org.uk/cg106 (last accessed 30th January 2020)
  7. Ponikowski P, Voors AA, Anker SD et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur J Heart Fail 2016;18:891–975. http://dx.doi.org/10.1002/ejhf.592
  8. Fonarow GC, Stough WG, Abraham WT, et al. Characteristics, treatments, and outcomes of patients with preserved systolic function hospitalized for heart failure: a report from the OPTIMIZE-HF Registry. J Am Col. Cardiol 2007;50:768–77 https://doi.org/10.1016/j.jacc.2007.04.064
  9. McDonagh TA, Gardner RS, Clark AL, Dargie H (eds). Oxford Textbook of Heart Failure. Oxford University Press. July 2011. http://dx.doi.org/10.1093/med/9780199577729.001.0001
  10. Clark AL, Coats AJS. Unreliability of cardiothoracic ratio as a marker of left ventricular impairment: comparison with radionuclide ventriculography and echocardiography. Postgrad Med J 2000;76:289–91 http://dx.doi.org/10.1136/pmj.76.895.289
  11. Raphael C, Briscoe C, Davies J et al. Limitations of the New York Heart Association functional classification system and self-reported walking distances in chronic heart failure. Heart 2007;93:476–82 http://dx.doi.org/10.1136/hrt.2006.089656
  12. Goldman L, Hashimoto B, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing cardiovascular functional class: advantages of a new specific activity scale. Circulation 1981;64:1227–34 https://doi.org/10.1161/01.CIR.64.6.1227
  13. American Thoracic Society Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories. ATS statement: Guidelines for the six-minute walk test. Am J Respir Crit Care Med 2002;166:111–7 https://doi.org/10.1164/ajrccm.166.1.at1102
  14. Roul G, Germain P, Bareiss P, et al. Does the 6-minute walk test predict the prognosis in patients with NYHA class II or III chronic heart failure? Am Heart J 1998;136:449–57 http://dx.doi.org/10.1016/S0002-8703(98)70219-4
  15. Abraham WT, Adamson PB, Bourge RC, et al. Wireless pulmonary artery haemodynamic monitoring in chronic heart failure: a randomised controlled trial. Lancet 2011;377:658–66. http://dx.doi.org/10.1016/S0140-6736(11)60101-3
  16. Bourge RC, Abraham WT, Adamson PB, et al. Randomized controlled trial of an implantable continuous hemodynamic monitor in patients with advanced heart failure: the COMPASS-HF study. J Am Coll Cardiol 2008;51:1073–9. http://dx.doi.org/10.1016/j.jacc.2007.10.061
  17. Antony R, Daghem M, McCann GP, et al. Cardiovascular magnetic resonance activity in the United Kingdom: a survey on behalf of the British Society of Cardiovascular Magnetic Resonance. J Cardiovasc Magn Reson 2011;13:57. http://dx.doi.org/10.1186/1532-429X-13-57
  18. Bruder O, Schneider S, Nothnagel D, et al. EuroCMR (European Cardiovascular Magnetic Resonance) registry: results of the German pilot phase. J Am Coll Cardiol 2009;54:1457–66. http://dx.doi.org/10.1016/j.jacc.2009.07.003
  19. Assomull RG, Shakespeare C, Kalra PR, et al. Role of cardiovascular magnetic resonance as a gatekeeper to invasive coronary angiography in patients presenting with heart failure of unknown etiology. Circulation 2011;124:1351–60. http://dx.doi.org/10.1161/CIRCULATIONAHA.110.011346
  20. Carson P, Wertheimer J, Miller A, et al.The STICH Trial (Surgical Treatment for Ischemic Heart Failure). JCHF 2013;1:400–8. http://dx.doi.org/10.1016/j.jchf.2013.04.012
  21. Velazquez EJ, Lee KL, Jones RH et al. Coronary-Artery Bypass Surgery in Patients with Ischemic Cardiomyopathy. N Engl J Med 2016;374(16):1511-20 http://dx.doi.org/10.1056/NEJMoa1602001

Further reading

Yu CM, Sanderson JE, Gorcsan J. Echocardiography, dyssynchrony and the response to cardiac resynchronization therapy. Eur Heart J 2010;19:2326–37. http://dx.doi.org/10.1093/eurheartj/ehq263

Shah BN, Khattar RS, Senior R. The hibernating myocardium: current concepts, diagnostic dilemmas and clinical challenges in the post-STICH era. Eur Heart J 2013:34:1323–36. http://dx.doi.org/10.1093/eurheartj/eht018

close window and return to take test

THERE ARE CURRENTLY NO COMMENTS FOR THIS ARTICLE - LEAVE A COMMENT

All rights reserved. No part of this programme may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the publishers, Medinews (Cardiology) Limited.

It shall not, by way of trade or otherwise, be lent, re-sold, hired or otherwise circulated without the publisher’s prior consent.

Medical knowledge is constantly changing. As new information becomes available, changes in treatment, procedures, equipment and the use of drugs becomes necessary. The editors/authors/contributors and the publishers have taken care to ensure that the information given in this text is accurate and up to date. Readers are strongly advised to confirm that the information, especially with regard to drug usage, complies with the latest legislation and standards of practice.

Healthcare professionals should consult up-to-date Prescribing Information and the full Summary of Product Characteristics available from the manufacturers before prescribing any product. Medinews (Cardiology) Limited cannot accept responsibility for any errors in prescribing which may occur.