Heart failure module 5: surgical management and palliative care of HF

Released 24 May 2024     Expires: 24 May 2026      Programme:

Sponsorship Statement: Novartis Pharmaceuticals UK Ltd has provided OmniaMed Communications Ltd with an arm’s length sponsorship towards the update of the BJC e-learning programme for heart failure.


Although left ventricular (LV) systolic function recovers in around 15% of patients with heart failure due to a reduced ejection fraction (HFrEF) within three years with optimal medical treatment (OMT),1 the same proportion will progress to end-stage disease and surgical intervention is sometimes necessary.2

Surgical treatment for heart failure (HF) includes:

  • mechanical circulatory support
    • LV assist devices (LVAD)
  • cardiac transplantation
  • coronary revascularisation
  • surgical ventricular restoration
  • valve surgery.

As many as one-quarter of patients with end-stage HF may have an unrecognised need for advanced therapies.3

While identifying the need for mechanical circulatory support in a patient with cardiogenic shock may be easy enough, identifying ambulatory patients with chronic HF who require advanced therapy (such as LVAD or transplantation) is more difficult.

Donor organ shortage is a frequently cited reason for the low rate of heart transplantation in the UK – according to Eurotransplant (a non-profit organisation that co-ordinates organ transplantation across continental Europe) there are approximately twice as many patients awaiting heart transplant per year than those who receive one.4

Mechanical circulatory support


Figure 1. HeartMate II® (Thoratec Corporation)
Figure 1. An example of a left ventricular assist device

Mechanical circulatory support (MCS) was developed as a rescue therapy for patients in intractable cardiogenic shock. The first devices were conceived as a continuation for patients who were unable to come off cardiopulmonary bypass (CPB) and have progressed to separate, implantable LVADs (figure 1).

Historically, LVADs were only indicated as a holding measure until an organ became available or until a decision was made regarding cardiac transplantation; so-called ‘bridge-to-transplantation’ (BTT) or ‘bridge-to-decision’ (BTD).

However, in 2015, the National Institute for Health and Clinical Excellence (NICE) published guidelines also recommending LVADs as long-term therapy for patients ineligible for transplantation, so-called ‘destination therapy’ (DT).5

In America, LVADs are licenced for a third indication known as ‘bridge-to-candidacy’, whereby the LVAD is implanted in a patient ineligible for heart transplantation with the hope that the improvement in haemodynamics may enable the patient to become eligible for transplant at a later date.

LVADs are used as DT more commonly than other indications worldwide (figure 2).6 In a minority of patients, the haemodynamic relief provided by the LVAD can allow recovery of myocardial function and explant of the device, though the majority will require continued support.

Heart failure module 5 - Figure 2. Contemporary indications for left ventricular assist device (LVAD) implantation
Figure 2. Contemporary indications for left ventricular assist device implantation

Adapted from the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS)6

The standard LVAD circuit pumps blood from the LV cavity through the device into the ascending aorta, creating a mechanical bypass of the LV outflow. The left ventricle is thus off-loaded (and the aortic valve may remain closed). Cardiac output is thus increased.7

Beneficial effects of LVAD include:

  • increased systemic blood pressure
  • improved organ perfusion and subsequent beneficial neuro-hormonal changes
  • reduced cardiac chamber size
  • reduced left atrial and pulmonary pressures.
Development of LVADs8

The first generation of LVADs (e.g. HeartMate® I) were large, pulsatile displacement pumps. The haemodynamic benefits were offset by significant morbidity from extensive surgical dissection required for a large device, high rates of infection due to the high calibre driveline, and limited durability necessitating reoperation.

The second-generation pumps (e.g. HeartMate® II, Jarvik 2000®) are smaller devices with impeller pumps that provide continuous flow compared to biphasic flow of first-generation devices. In head-to-head trials with first-generation technology, the HeartMate® II device was associated with higher survival rates at two years free of disabling stroke or reoperation to replace the device (46% vs. 11%; p<0.001; HR, 0.38; 95% CI, 0.27–0.54) possibly due to the smaller size.9

Various third-generation devices are now in use or undergoing further evaluation. An example is the HeartMate® III, which has a miniaturised centrifugal pump that uses magnetic and hydrodynamic forces to levitate and rotate the impeller, theoretically avoiding wear on bearings. The smaller device size allows for quick and less-invasive implantation, though the adverse event rate remains stubbornly high – see ‘Evidence‘ below.

Complications of LVAD therapy10

Despite developments in design, the morbidity associated with LVAD therapy continues to impede progress in the field; 70% of patients with either continuous or pulsatile LVAD suffer a first episode of infection, bleeding, device malfunction, stroke or death within one year.10

The most frequent problems encountered during LVAD therapy are:

  • Bleeding and thrombosis
    • All patients require anticoagulation, with the specific regime varying between devices
    • All patients also develop acquired von Willebrand factor deficiency
    • The tiny pulse pressure with continuous flow pumps is associated with gastrointestinal bleeding due to the development of angiodysplasia (much like in severe aortic stenosis)
    • Device thrombosis is a difficult problem manifested by increased power consumption, clinical or laboratory signs of haemolysis (e.g. elevated bilirubin, plasma haemoglobin and lactate dehydrogenase levels) or device stoppage. It can be treated with intravenous heparin, fibrinolytics or surgery (pump exchange or urgent transplant).
  • Infection
    • The risk of infection is high; the artificial surfaces of the pump itself create sites for colonisation and the percutaneous driveline that delivers power is an extremely common site of infection
    • Severity of infection can vary from asymptomatic driveline site colonisation to deep abscesses or device-related endocarditis. Wound care requires specialist nursing oversight.
  • Right ventricular failure
    • This is precipitated by failure of the right ventricle (RV) to handle the volume returned to it by the assisted LV (particularly because the right ventricle can be involved in the underlying disease process)
    • This can be manifested by distended neck veins, liver congestion and increasing oedema, accompanied by a deterioration in exercise capacity and increasing natriuretic peptides
    • Treatment is with diuretics, adjustment of the LVAD speed, or insertion of a right-sided ventricular assist device (VAD) in extreme cases.
  • Stroke
    • Both types of stroke – ischaemic due to embolism or haemorrhagic due to bleeding – are often catastrophic, if they occur
    • Haemorrhagic stroke is especially feared; anticoagulation cannot be stopped due to the high likelihood of device thrombosis and failure.
  • Acquired aortic regurgitation
    • LVAD therapy creates a large pressure gradient from the aorta to the LV, transmitted across the aortic valve; this can lead to aortic regurgitation, which decreases the efficacy of support and longevity of the device
    • Up to 50% will have moderate to severe aortic regurgitation at 18 months, which is difficult to treat. Options include open or transcatheter valve replacement or cardiac transplantation.
  • Arrhythmia
    • Both atrial and ventricular arrhythmia are common in patients with LVAD. Patients with LVADs are unique in regard to ventricular arrhythmia in that an episode of VF does not lead to death as peripheral blood flow is maintained by the pump. Cardioversion is still required!

High adverse event rates are inevitable in severely unwell and unstable patients, such as those suitable for LVAD therapy. Trials of LVADs in patients with less severe disease have had mixed results.

REVIVE-IT (Randomised Evaluation of VAD Intervention Before Inotropic Therapy), a randomised controlled trial of LVADs in patients who were less ill than patients currently eligible for destination therapy (New York Heart Association [NYHA] class II–IV with ‘advanced HF’ defined by markers such as hyponatraemia or high natriuretic peptide), was discontinued because of the high adverse event rate.11

In the ROADMAP (Risk Assessment and Comparative Effectiveness of Left Ventricular Assist Device and Medical Management in Ambulatory Heart Failure Patients) study, investigators enrolled 200 patients (average age, 64 years; median B-type natriuretic peptide [BNP], 547 pg/ml in the LVAD arm) who were eligible for LVAD therapy with a second-generation device (HeartMate® II).12 Treatment was assigned per patient wishes to either LVAD implantation or OMT. The primary end point was survival on original therapy with >75 metre improvement in six-minute walk distance at one year. More patients in the LVAD group met the primary end point, with the difference increasing at two-years’ follow up (30% vs. 12%; p=0.012).12,13 In an as-treated analysis, LVAD implantation was associated with a better one-year survival (80% vs. 63%; p=0.02), but because 30% of patients in the OMT group had LVAD implantation over two years, there was no significant difference in intention-to-treat analysis.12,13 However, while the results are promising, it is essential to bear in mind treatment with an LVAD in the ROADMAP study was not randomised; almost a third of patients in the ‘control’ arm changed their mind and opted for an LVAD during the two-year study period. As a result, the data are compromised.

In the ENDURANCE trial (Intrapericardial Left Ventricular Assist Device for Advanced Heart Failure), investigators enrolled 446 patients (average age, 64 years; NYHA III–IV; average left ventricular ejection fraction (LVEF), 17%), all of whom were eligible for LVAD therapy but ineligible for heart transplantation (i.e. the LVAD was a ‘destination therapy’ or ‘bridge to candidacy’ – common indications for implantation in America but not in the UK).14 Patients were randomised to either the commonly used HeartMate® II device with an axial rotating pump implanted in the abdominal cavity, or the HeartWare™ HVAD™ with a smaller, magnetically levitated pump implanted in the pericardium.14 The absence of bearings in the magnetically levitated pump was hypothesised to reduce the risk of device failure, thrombus formation and stroke.

The primary end point was a composite of survival free from disabling stroke, urgent transplantation or device explant or replacement due to complications two years after implantation.14 The primary end point was similar between the two devices, suggesting non-inferiority of the HeartWare™ HVAD™ compared to the HeartMate® II device.14 However, adverse event rates were high in both arms. While patients with the HeartMate® II device were more likely to require device replacement, explantation or urgent transplantation (16% vs. 9%; p=0.03), they were less likely to have a stroke (12% vs. 30%; p<0.001), right HF (27% vs. 39%; p=0.02) or sepsis (15% vs. 24%; p=0.05) compared to the HeartWare™ HVAD™.15

In the very similar MOMENTUM 3 trial (Multicenter Study of MagLev™ Technology in Patients Undergoing Left Ventricular Assist Device Therapy with HeartMate 3™), investigators enrolled 294 patients with end-stage HF who were randomised to either the HeartMate® II device or the HeartMate® III device (similar to the HeartWare™ HVAD™ device with a magnetically levitated centrifugal pump that is implanted in the pericardial space).15 More patients in the HeartMate® III arm met the primary end point of survival free of disabling stroke or device explant or replacement due to complications six months after implantation (86% vs. 77%; p<0.001), suggesting non-inferiority (p<0.001).15 Although the study was not powered to detect superiority, the HeartMate® III did appear to be the better device (p=0.04).15 Adverse event rates were again high but similar in the two groups.15

A retrospective cohort analysis comparing outcomes amongst patients in the UK implanted with the HeartMate® II device or the HeartWare™ HVAD™ device found no significant difference in outcome or adverse event rates between the devices.16

In the UK, data on LVAD implantation is collected by the NHS Organ Donation and Transplant Service which releases annual activity reports. In 2021/22, there were 334 LVAD implantations for long-term bridging.17 The median time on an LVAD was 1,101 days.17 The majority of patients were listed for a heart transplant within a year of LVAD implantation but only 5% of patients underwent transplantation within that time frame. While outcome has improved, it remains poor – more patients die on support (31%) than are transplanted (13%) or have the device explanted due to recovery (5%).17

The future of LVADs lies not only in developing technology to reduce the morbidity and cost of long-term therapy, but also in their appropriate deployment. Many patients are referred too late in the natural history of HF (or when there is serious co-morbidity) and thus outcomes are poor and the only viable long-term treatment – transplantation – is often contraindicated. The timing of LVAD insertion remains critical. The economic argument will only carry weight when the up-front cost is a great deal lower. No publicly funded health care system can afford the present costs of a device in even larger numbers of patients than at the moment.

Cardiac transplantation

Cardiac transplantation has evolved significantly since its inception in the 1960s and remains the best long-term therapy for advanced HF, despite its risks and complications (figure 3).18

Heart failure module 5 - Figure 3. Long-term survival for adult recipients after cardiac transplantation
Figure 3. Long-term survival for adult recipients after cardiac transplantation by transplant era in the UK

Data obtained from NHS BTCAG-H, 202218

Clinically, the key challenges are management of patient selection, donor organ selection, the peri-operative period and long-term follow up, in addition to availability of donor organs. Practically, the key challenge is shortage of available donor organs, which limits the expansion of the transplant population.19

By the end of March 2023 in the UK, there were 254 adult patients on the heart transplant waiting list.17 Between 2018 and 2020 amongst 302 patients on the non-urgent transplant list, 20% had been transplanted within three years of listing, whilst 27% were still waiting, 29% had progressed to the urgent list and 10% had died while waiting.17

Patient selection19

The aim is to identify those patients with a sufficiently poor prognosis to justify the increased early mortality risk with better long-term survival being the reward.

Good cardiac transplant candidates have advanced and severely symptomatic HF, but do not have other end-organ complications or co-morbidities associated with high peri-operative risk or which adversely affect long-term outcome. In-patient referral may be considered for patients admitted with acute HF with intractable inotrope dependence or cardiogenic shock.19,20

Box 1. Clinical features that should prompt consideration for transplant

>2 admissions with acute HF in the last 12 months
Persistent signs and symptoms of HF despite maximal therapy
Evidence of right ventricular dysfunction or increasing pulmonary arterial pressure
(aim to refer before mean pulmonary artery pressure is >50 mmHg)
End-organ damage that is attributable to HF and may be correctable with transplant:

  • weight loss
  • liver dysfunction
  • anaemia
  • hyponatraemia
  • renal dysfunction preventing increasing dose of diuretics sufficient to treat congestion.

(Aim to refer before estimated glomerular filtration rate <40 ml/min/1.73 m2)

Key: HF = heart failure

Box 2. Criteria for heart transplantation

Left ventricular systolic dysfunction not due to a correctable cause, such as valve disease
NYHA class III or IV
Optimal medical and device therapy (if indicated)
Evidence of a poor prognosis:

  • reduced peak oxygen consumption (VO2) on cardiopulmonary exercise testing
  • significantly raised natriuretic peptides
  • high risk on established prognostic scoring systems such as HF survival score (HFSS).
Key: HF = heart failure; NYHA = New York Heart Association

Box 3. Criteria for urgent in-patient referral

Persistent cardiogenic shock due to primary cardiovascular cause
Continuous intravenous inotropic support
Mechanical circulatory support
Ongoing coronary ischaemia with no revascularisation treatment options
No contraindication to transplantation.

Box 4. Absolute contraindications to heart transplantation

Primary end-organ damage not secondary to advanced HF:

  • renal dysfunction
  • liver dysfunction
Pulmonary hypertension:

  • pulmonary vascular resistance >5 Wood units
  • transpulmonary gradient >15 mmHg
  • pulmonary arterial systolic pressure >60 mmHg
Active infection or sepsis (other than in the case of an infected LVAD21)
Recent pulmonary embolism
Microvascular complications of diabetes other than non-proliferative retinopathy
Primary end-organ damage not secondary to advanced HF
Key: HF = heart failure; LVAD = left ventricular assist device

Box 5. Relative contra-indications to heart transplantation


  • Body mass index >32 kg/m2
Active malignancy other than localised non-melanoma skin cancer
Symptomatic peripheral or cerebrovascular disease
Auto-immune disease
Infiltrative cardiac disease:

  • sarcoidosis
  • amyloidosis
Severe skeletal myopathy with associated cardiomyopathy
Excessive alcohol use
History of non-adherence to treatments

Transplant assessment is summarised in table 1.20,22

Patients who undergo transplantation require life-long follow up, monitoring and treatment – a stable home life with adequate social support and psychological evaluation are also important aspects of patient selection.11

Table 1. Summary of transplant assessment

Assessment Key findings
Heart failure aetiology and current therapy ● Standard heart failure assessment with history, clinical examination and targeted investigations ● Establish aetiology of heart failure and correct precipitants where possible
● Ensure medical and device therapy are optimised
Heart function and prognosis ● NYHA functional class
● Serum levels of natriuretic peptides
● Echocardiogram +/- cardiac MRI
● 6 minute walk test
● Cardiopulmonary exercise test
● Cardiac catheterisation including coronary angiogram and right heart study
● Meeting criteria for transplantation
– Severe symptoms despite maximal medical/device
– Indicators of poor prognonsis, for example low maximal oxygen uptake on exercise testing, or significantly elevated natriuretic peptides
Complications of heart failure, particularly renal impairment, liver congestion, anaemia, and pulmonary hypertension ● Serum electrolytes and renal function
● 24 hour urine for protein and creatinine clearance
● Liver enzymes
● Full blood count and coagulation screen
● Potential contraindications to transplantation
– Irreversible pulmonary hypertension
– Irreversible renal failure
– Liver dysfunction
Other co-morbidities or risk factors with implications for long-term outcome ● Smoking status
● Chest radiograph and lung function tests
● Autoimmune screen
● Targeted screens for malignancy based on symptoms
● Psychological assessment
● Potential contraindications to transplantation
– Active malignancy
– Substance use e.g. smoking or excess alcohol
– Respiratory failure
– Autoimmune disorders
– Inadequate social support
Consideration of allograph immunology ● Blood group
● HLA screen
● Serology screen (includes hepatitis B and C viruses, human immunodeficiency disease, varicella zoster virus, cytomegalovirus, toxoplasma and syphilis
● Screen for other infection (e.g. blood cultures, urine cultures, skin swabs, dental assessment, MRSA screen)
● Planning organ selection to minimise risk of immune incompatibility
● Potential contraindications to transplantation
– Ongoing acute or chronic infection
– High levels of HLA sensitisation
Key: HLA = human leukocyte antigen; MRI = magnetic resonance imaging; MRSA = methicillin-resistant Staphylococcus aureus; NYHA = New York Heart Association

The Organ Donation (Deemed Consent) Act 2019 became law from 15th March 2020 in England, Wales and Northern Ireland, meaning that all adults are presumed to have given consent for organ donation, unless there is a documented decision otherwise. The act may increase the availability of organs for heart transplantation.

Donor organ selection and peri-operative management19

Specialised teams based at cardiac transplant centres carry out organ retrieval. Techniques for selecting suitable organs are complex and usually involve clinical examination, electrocardiography (ECG), haemodynamic studies using a pulmonary artery catheter, and direct visual inspection (figure 4). This is complemented by data from echocardiography or cardiac catheterisation, if available. The organ is transferred to the centre in cold storage or in an organ care system that maintains a warm, perfused state, where available.

Heart failure module 5 - Figure 4. Key aspects of donor organ selection for cardiac transplantation
Figure 4. Key aspects of donor organ selection for cardiac transplantation

Key: ECG = electrocardiography; Echo = echocardiography; PA = pulmonary artery

Performing a heart transplant

The surgical transplant operation has evolved over time.22 The bi-atrial technique left some recipient right atrium in situ and required long, sometimes fallible atrial anastomoses (figure 5a). The total orthotopic technique involved separate anastomoses for each pulmonary vein and the great vessels (not pictured). The bicaval technique involved the insertion of the recipient’s pulmonary veins into the left atrium remains in situ, with the donor left atrium anastamosed to the remnant and the donor right atrium is anastamosed to the great veins (figure 5b).

Heart failure module 5 - Figure 5. Evolving surgical technique, with the donor organ in red, recipient structures in blue, and surgical instruments in grey. Panel A shows the biatrial technique where the recipient right atrium remains in situ necessitating a long atrial anastamosis but retaining more normal haemodynamics with native structures. Panel B shows the bicaval technique, where the recipient right atrium is removed and great veins anastamosed to the donor atrium
Figure 5. Evolving surgical technique, with the donor organ in red, recipient structures in blue, and surgical instruments in grey. Panel A shows the biatrial technique where the recipient right atrium remains in situ necessitating a long atrial anastamosis but retaining more normal haemodynamics with native structures. Panel B shows the bicaval technique, where the recipient right atrium is removed and great veins anastamosed to the donor atrium

Reproduced with kind permission from Hunt22

The operation and post-operative recovery can vary from the routine (such as in a stable patient with a first sternotomy) to extremely high-risk (such as in patients with several previous sternotomies, a VAD in situ, or in patients who are critically ill). Specific early problems that should be anticipated are summarised in table 2.

Table 2. Problems to anticipate following cardiac transplantation19

Right ventricular failure
Right ventricular function is particularly susceptible to ischaemia and this becomes aparent after ceasing CPB. This can be compounded by high recipient pulmonary vascular resistance and multiple blood transfusion
Usually sinus bradycardia or sinus arrest. Most centres use expectant temporary atrial pacing or isoprenaline to maintain an early relative tachycardia. This overcomes the initially low stroke volume that normalises with improving ventricular compliance
Systemic inflammatory response
This particularly occurs with prolonged CPB or pre-existing infection (e.g. chronic LVAD infection), often requiring high-dose vasopressors
Frequently this is due to coagulopathy rather than a surgical cause. Pericardial bleeding can be exacerbated by the presence of potential space after removal of the enlarged heart, or by size mismatch of the donor organ
Biventricular failure
In the early phase, this raises concern for primary graft failure and hyperacute rejection
Key: CPB = cardiopulmonary bypass; LVAD = left ventricular assist device

Long-term management

Cardiac transplant dramatically improves survival and quality of life (QoL) in the right patient. Based on the NHS’ annual report on heart transplantation in the UK published in 2023, the national rate of patient survival following adult heart transplant at one and five years is 85.9% and 71.4% respectively.17

However, morbidity rates are high.23 The crux of follow-up lies in careful management of immunosuppression, finding the balance between avoidance of rejection and avoidance of side effects of therapy.

The immunosuppressant therapies all target T-cells, which drive cellular rejection. Induction immunosuppression given pre-operatively is sometimes included. The calcineurin inhibitors, tacrolimus and ciclosporin, are the mainstay of therapy and are often combined with corticosteroids and a cell-cycle agent, such as mycophenolate, for long-term maintenance. The drugs have many side effects, many of which are dose-dependent making monitoring of drug levels mandatory.24

Cardiac allograft vasculopathy (CAV) is the most common late complication (weeks to months from transplantation). It is an accelerated form of coronary artery disease in a transplanted heart. As only around 10–30% of patients regain any innervation to the heart post-transplant, angina symptoms are uncommon and patients often present with breathlessness following silent myocardial infarction, or with HF, or as sudden death.25 CAV is often diffuse and therefore not amenable to revascularisation. Careful symptomatic (anti-anginals) and preventative (statins) medical therapy is a priority; most patients are started on low-dose atorvastatin (10 mg once daily) due to the lower incidence of myositis compared with other statins.26

Box 6. Key factors to consider in long-term follow up

Anticipation and early treatment of allograft rejection:

  • Frequent studies of LV dimensions and wall thickness by echocardiography, accompanied usually by endomyocardial biopsy for histological assessment, are required early after the transplant
  • If rejection is identified, treatment depends on the underlying mechanism:24
    • Cellular rejection (most common) responds to high-dose corticosteroids
    • Antibody-mediated rejection (e.g. due to pre-existing or de novo human leukocyte antigen [HLA] sensitisation) can require inhibition of B-cells and antibody removal, for example by plasmapheresis.
Monitoring for evidence of chronic allograft dysfunction with surveillance echocardiography
Stringent monitoring of drug levels and renal function is essential to prevent nephropathy. Kidney disease can be exacerbated by other factors such as pre- or peri- transplant renal injury, coexistent diabetes and hypertension
Careful management of hypertension and hyperlipidaemia; both common pre-morbid diagnoses that can be caused or exacerbated by immunosuppressive drugs. Cardiac denervation may also contribute to hypertension. Together, these can increase the risk of CAV
Prompt treatment of infection, due to ongoing susceptibility with immunosuppression, and the possibility of superadded bone marrow suppression due to the drugs
Monitoring for immunosuppression-associated malignancy, particularly non-melanoma skin tumours and B-cell lymphomas
Key: CAV = cardiac allograft vasculopathy; HLA = human leukocyte antigen; LV = left ventricular

Revascularisation, ventricular restoration and valve surgery

Patients with HF are commonly considered for coronary revascularisation and valve surgery. Surgical ventricular restoration (SVR) involves exclusion of scar on the ventricular wall from previous myocardial infarction and is not commonly performed. Such decisions are difficult, not least because patients with HF often have multiple co-morbidities, including frailty, which makes the long-term benefit of invasive treatment less certain. However, there may be a subset of patients who benefit from certain treatments. As ever, patient selection and shared decision-making is key.27


Inadequate myocardial perfusion can cause impaired contractility; this can be either fixed (infarction leading to scar) or reversible (hibernation). Differentiating hibernating myocardium from infarcted tissue can be done, for example with dobutamine stress echocardiography or thallium scintigraphy. Coronary revascularisation in HF aims to improve myocardial function by restoring perfusion to hibernating myocardium, so reducing LV volumes and improving LV function (figures 6a and 6b).

Figure 6a. Echocardiogram before coronary artery bypass grafting (CABG) in the setting of hibernating myocardium (Click arrow below to play, or bottom-right for full screen)

Figure 6b. Echocardiogram after CABG in the setting of hibernating myocardium. On the postoperative scan, the left ventricular (LV) volumes have reduced and there is improved LV function (Click arrow below to play, or bottom-right for full screen)


Until publication of the STICH (Surgical Treatment for Ischaemic Heart Failure) trial results in 2011, the practice of revascularising hibernating myocardium was common but based on anecdotal evidence.

The STICH trial (n=1,212; median age, 59 years; NYHA I–IV; median LVEF, 27% in the treatment arm) was designed to test whether revascularisation improved outcomes in patients with HF and underlying coronary disease without angina severe enough to warrant revascularisation on its own merits.28 There was no significant difference in all-cause mortality between patients treated by revascularisation with coronary artery bypass grafting (CABG) plus OMT and those treated with OMT alone.28 There was no requirement for patients to undergo functional testing before entering the trial and thus the investigators were unable to differentiate between hibernating or infarcted myocardium.28

The STICH extension (STICHES) was published in 2016.29 The original patient cohort from STICH was followed for almost 10 years and at that point, there was a small, but definite, survival advantage for the surgically treated group.29 It is important to note that the patients in STICH had a mean age just short of 60 years and that it took a very long time for the survival advantage to appear.29

The HEART trial (Heart Failure Revascularisation Trial) (n=138; average age, 65 years, two-thirds of whom were NYHA I–II; median wall motion index 0.8 [equivalent to LVEF of 24%]) was a randomised trial of OMT versus OMT plus angiography with the intent to revascularise either via percutaneous coronary intervention (PCI) or CABG.30 Unlike STICH, all eligible patients underwent perfusion testing and the presence of myocardial viability was an inclusion criterion.30 However, like STICH, there was no difference in mortality between the OMT group and the revascularisation group.30 The study was closed early due to slow recruitment, sponsor withdrawal and the start of the STICH study – the results are underpowered as a result.30

The REVIVED-BCIS-2 trial (Revascularization for Ischemic Ventricular Dysfunction- British Cardiovascular Intervention Society-2) (n=700; average age, 70 years; 77% NYHA class I/II, 66% of whom had no angina; mean LVEF, 27%; median NT-proBNP, 1,376 ng/L) tested the hypothesis that PCI in patients with HFrEF due to ischaemic cardiomyopathy may improve outcomes.31 Although superficially similar to the STICH study, patients had to have extensive coronary artery disease and demonstrable myocardial viability in segments supplied by vessels that were amenable to PCI.28,31 The primary end point was hospitalisation for HF or all-cause mortality.31 After a median follow up of 41 months, PCI had no effect on the primary end point (37% vs. 38%) or any of its component parts, regardless of the extent of viability, nor did PCI have any effect on LVEF measured in a sub-set of participants at six and 12 months.31

There is a reasonable argument that selected younger patients with HF (in whom angina is not a prominent symptom) should be offered coronary angiography with a view to surgical revascularisation. There is no role for PCI for the treatment of LV systolic dysfunction, even in the presence of so-called viable myocardium.

Surgical ventricular restoration27

The aims of surgical ventricular restoration (SVR) are to:

  • normalise ventricular geometry
  • improve myocardial perfusion
  • reduce LV work
  • improve LV contraction.

The early procedures were similar to partial left ventriculectomy for aneurysm, while the contemporary SVR involves resection of the non-functional myocardium before placement of an endoventricular Dacron patch to exclude the scar (figures 7a–d). It is usually done during CABG for patients with ischaemic HF and anterior wall akinesia or severe dyskinesia. It adds about 20 minutes to the procedure time without increasing operative risk.

Figure 7a. Surgical ventricular restoration by the Dor procedure. First the area of scar is identified and partially excised
Figure 7a. Surgical ventricular restoration by the Dor procedure. First the area of scar is identified and partially excised

With kind permission from Gemma Price
Figure 7b. Surgical ventricular restoration by the Dor procedure. An interventricular stitch is placed to create a neoventricle
Figure 7b. Surgical ventricular restoration by the Dor procedure. An interventricular stitch is placed to create a neoventricle

With kind permission from Gemma Price
Figure 7c. Surgical ventricular restoration by the Dor procedure. A Dacron patch is placed to create a neoventricle
Figure 7c. Surgical ventricular restoration by the Dor procedure. A Dacron patch is placed to create a neoventricle

With kind permission from Gemma Price
Figure 7d. Surgical ventricular restoration by the Dor procedure. Finally the remaining scar is used to cover the patch or excised, and the defect is closed
Figure 7d. Surgical ventricular restoration by the Dor procedure. Finally the remaining scar is used to cover the patch or excised, and the defect is closed

With kind permission from Gemma Price

In non-randomised studies, SVR improves LVEF and other haemodynamic variables.27 However, hypothesis 2 of the STICH trial compared outcomes of patients randomised to CABG plus SVR to CABG alone and found no significant difference in the composite end point of all-cause mortality or cardiovascular hospitalisation.

Percutaneous ventricular restoration has also been investigated: the Parachute device, a percutaneously delivered device that partitions the LV as a means of ventricular restoration, appears safe and feasible in patients with HF and LV dilatation.33 However, a phase III trial was terminated in June 2017.34

There may yet be sub-groups who do benefit from surgical or percutaneous ventricular restoration and, similar to revascularisation, this book is not yet closed.

Valve surgery

An important cause of the HF syndrome is valvular heart disease. Every patient presenting with HF should be assessed for valvular disease; aortic stenosis is a particularly common cause. Appropriate patients should be offered aortic valve replacement as a potentially curative procedure. Many patients, however, may be too frail for surgical valve replacement by the time they present with HF.

In these cases, transcatheter aortic valve implantation (TAVI) should be considered as being a lower-risk alternative.35 TAVI is certainly superior to medical therapy in inoperable patients and is increasingly being shown in trials to be as effective as surgical valve replacement in lower-risk patients.35

A more difficult problem is that of mitral valve surgery. Functional mitral regurgitation (MR) is very common in HF as a consequence of valve ring dilation, together with tethering of the posterior leaflet of the valve.36


There are two randomised controlled trials of the MitraClip® device in patients with HFrEF and MR with conflicting results.

In the COAPT study (Cardiovascular Outcomes Assessment of the MitraClip® Percutaneous Therapy for Heart Failure Patients with Functional Mitral Regurgitation), investigators enrolled 614 patients with LVEF <50% and moderate–severe or severe functional MR (average age, 72 years; ~90% NYHA II–III; average NT-proBNP, 5,174 ng/L; average LVEF, 31%; 51% severe MR) who were randomised to either transcatheter mitral valve repair with the MitraClip® device or OMT.37 The primary end point was HF hospitalisations with 24 months follow up. Of the 302 patients in the treatment group, 287 successfully underwent device implantation.37 Treatment with the device was associated with a lower risk of hospitalisation with HF (36% per patient-year vs. 68%; p<0.001) and lower mortality (a non-powered secondary end point; 18% vs. 22%, p<0.001) compared to medical treatment alone.37

In the MITRA-FR study (Percutaneous Repair with the MitraClip® Device for Severe Functional/Secondary Mitral Regurgitation), investigators enrolled 304 patients with LVEF <40% and severe functional MR (average age, 70 years; 91% NYHA II–III, median NT-proBNP, 3,407 ng/L; average LVEF, 33%) who were randomised to mitral valve repair with the MitraClip® device or OMT.38 The primary outcome was all-cause mortality or hospitalisation with HF. Of the 152 patients in the treatment group, 138 had the device successfully implanted.38 There was no difference in the primary end point between the groups after 12 months (55% vs. 51%; p=0.51).38

It is not clear why two very similar trials have yielded two very different results. One explanation may be that medical supervision of the control group was far more strict and the number and changes in medication were greater in the MITRA-FR trial than the COAPT study.39 For example, despite the high number of hospitalisations with HF in the COAPT study, there were no significant changes in HF medications (including diuretics) during the study period; it may be that mitral valve repair in patients with HFrEF is beneficial only when compared to inadequate medical management.39 Another favoured explanation is that the patients in COAPT had smaller LV volumes for a given severity of MR, implying that they had MR out of proportion to their LV impairment. They were, therefore, more likely to respond to mitral intervention.39

The benefit of the MitraClip® in COAPT was maintained at five-year follow up,40 but perhaps the most important finding of the COAPT trial is just how unwell patients were. More than 90% of patients in the control arm had been hospitalised with HF or died after five-year follow up, and despite the benefit of the MitraClip®, 73% of patients in the treatment arm met the primary end point. Mortality rates were 67% and 57% in the control and treatment arms respectively after five years.40 The presence of severe MR in patients with HF should prompt discussion about prognosis, and the goals of treatment, including MitraClip®.

How transcatheter mitral valve repair will fit into future guidelines is not clear, but it is certain that, as with all surgical treatment options for HF, appropriate and timely patient selection will be key to effective use.


Revascularisation, either by CABG or PCI, is commonly performed with patients with LV systolic dysfunction. However, there is little evidence that it influences prognosis outside of an acute coronary syndrome. If HF is thought to be due primarily to valve disease, then treatment of the valve is likely to benefit the patient only if they are fit for the intervention; patient selection for surgical or transcatheter valve interventions is difficult, but key to success.

Palliative care in HF

Palliative care is an approach that improves the QoL of patients and their families

“Palliative care is an approach that improves the quality of life of patients and their families”

At any stage of the disease, patients with HF have poorer QoL than the general population,41,42 largely due to the significant symptom burden which worsens as the disease progresses.43 In those patients where surgical intervention is not appropriate, or in end-stage disease, end-of-life and palliative care should be implemented.

There is very little data on the benefits of palliative care in patients with HF. A recent meta-analysis of all randomised controlled trial data involving 921 patients with HF found that palliative care interventions were associated with an improvement in QoL and symptom burden, and reduced hospitalisations compared to usual care. The European Society of Cardiology (ESC) and NICE HF guidelines recognise the need for supportive and palliative care services for patients with end-stage HF.44–46

Integrated working between primary care, HF services and specialist palliative care is essential but a palliative approach to care and access to palliative care is patchy, both nationally and internationally.47

Barriers to effective palliative care in patients with HF include:

  • unpredictable disease trajectory
  • poor communication between members of the multidisciplinary team (MDT) – for example, a lack of clarity about the appropriate ceiling of medical therapy
  • reluctance of clinical staff to have the difficult conversations around the end of life due to concerns about destroying hope
  • healthcare services are poorly set up for timely and effective palliative interventions.

What is palliative care?

Table 3. World Health Organisation definition of palliative care47

Palliative care
Provides relief from pain and other distressing symptoms
Affirms life and regards dying as a normal process
Intends neither to hasten or postpone death
Integrates the psychological and spiritual aspects of patient care
Offers a support system to help patients live as actively possible until death
Offers a support system to help the family cope during the patient’s illness and in their own bereavement
Uses a team approach to address the needs of patients and their families, including bereavement counselling, if needed
Will enhance quality of life, and may also positively influence the course of illness
Is applicable early in the course of illness, in conjunction with other therapies that are intended to prolong life, such as chemotherapy or radiation therapy, and includes those investigations needed to better understand and manage distressing clinical complications

A palliative care approach should run in parallel with conventional HF management. A holistic approach is required, taking into consideration the patient’s symptoms, plans and expectations for the future, as well as the needs and expectations of carers.

Palliative care (table 3) aims to improve the QoL of patients with chronic or terminal illness and help their families face the problems associated with life-threatening illness. The primary goal is the prevention and relief of suffering by early identification, assessment and treatment of pain and/or psychological distress, as well as addressing spiritual needs.

Palliative care for patients with HF is provided by an MDT led by a palliative care specialist, in conjunction with a HF specialist, with access to other relevant services for persistent or complex needs. It involves a problem-based integrated approach to advanced care planning, communication and symptom control. In order to explore the palliative care of patients with HF, each aspect will be addressed in turn.

There are several common misunderstandings about palliative care. These include:

  • a belief that palliative care is only applicable to patients for whom there is clearly apparent irreversible deterioration with death expected within days to months
  • requires a handover of the patient to the palliative care team
  • only relates to physical symptom control in the dying patient and can only be provided once all other therapeutic options are exhausted.
Problem-based integrated approach

Educating the patient, carers and families about the condition allows for informed joint decision-making. This should be an ongoing process across multiple clinical encounters; the unpredictable trajectory of HF means constant reassessment of a patients’ risk of adverse outcomes and, therefore, potential need for palliative care services is essential.

The level of palliative care intervention at different stages in a patient’s disease process will vary from patient-to-patient, dependent on their needs. Most patients can be cared for in primary care and by their usual secondary care teams, but some require access to specialist palliative care services. This integrated approach allows patients to receive palliative care depending upon need rather than prognosis.48,49

Discussions about the appropriate ‘ceiling of care’ are essential to avoid unnecessary hospital admissions or futile treatment – both of which ultimately may cause harm to the patient.

Important considerations in patients with HF receiving palliative care include:

  • Frailty and malnutrition
  • Regardless of how they are defined, frailty and malnutrition are common in HF, affecting over 50% of patients.50,51 Patients with frailty and/or malnutrition have more severe disease; are less likely to be treated with disease-modifying drugs; and are at greater risk of hospitalisation or death.51–54 The majority of hospitalisations or deaths occurring in frail patients are due to non-cardiovascular causes.52 Indeed, in all patients with chronic HF – whether frail or not – non-cardiovascular causes account for the majority of morbidity and mortality in the last year of life.55

    All disease-modifying therapies for HFrEF are given on the basis that they reduce HF hospitalisation and cardiovascular mortality.46 Thus, the presence of frailty or malnutrition (or the suspicion that the patient may be in or near the last year of life – see below) should prompt discussions about discontinuing HF therapies, especially if the patient is experiencing side effects.

  • Advance care planning
  • 14300490-active-retirement-two-old-male-friends-talking-and-shaking-hands-on-bench-in-public-park

    Advance care planning is defined by the General Medical Council as “the process of discussing the type of treatment and care that a patient would or would not wish to receive in the event that they lose capacity to decide or are unable to express a preference.”50

    Advance care planning is important to many patients; it increases the likelihood of end-of-life wishes being carried out and improves the quality of care for both patients and their carers.51–54

    One aspect of advance care planning is decision-making about preferred place of care. In the UK, there is a gross disparity between preferred place of care for cancer patients and HF patients.56 Palliative care services tend to be structured to meet the needs of patients with cancer, many of whom have a predictable disease trajectory; as a consequence, most patients will die at home or in a hospice. In contrast, patients dying from cardiovascular diseases, including HF, are much more likely to die in hospital (59%) with fewer than 1% dying in a hospice.55,57

    For example, decisions regarding deactivation of an implantable cardioverter-defibrillator (ICD) in a patient predicted to be in the last few weeks of life can be particularly difficult but are an essential aspect of care; if an ICD is not re-programmed to pacemaker mode only, dying may be complicated by repeated shocks.58

  • Communication
  • Guidance and training have been developed to help physicians and the many patients with HF who want to discuss end-of-life issues.59,60 Patients are involved in decisions about their future care, despite uncertain disease trajectories by “hoping for the best, and preparing for the worst.”61–66 Such discussions should be ongoing through the natural history of disease and not reserved for when a patient displays clear signs of end-stage disease. Regarding ICDs, it is good practice to inform the patient that the time may come at which treatment with an ICD is no longer appropriate as part of counselling before implantation.

  • Symptom control
  • Breathlessness (figure 8) is the predominant symptom of end-stage HF. Decisions on investigations and treatment must be taken in the context of the patient’s wishes and stage of the disease.67

    For example, intravenous (IV) diuretics, vasodilators and inotropes are not appropriate for someone in the last few days of life whose primary wish is to be kept comfortable in whom less aggressive treatments are essential.

Box 7. Palliative management of breathlessness68

Assessment and treatment of reversible causes, dependent upon the patient’s wishes and stage of illness
SC furosemide infusion, which may be as effective as IV treatment for venous congestion and may prevent admission to hospital in patients with advanced HF69,70
Cardiac exercise programmes, which also address patient education and psycho-social support are available, even for severely limited patients64
Handheld fans may ease the sensation of dyspnoea71
Low-dose opioids may improve symptoms of breathlessness in patients with HF.72 However, as the largest trial to date was closed early due to poor recruitment, the data in support of long-term opiate use for breathlessness in patients with HF remain scant73
Benzodiazepines may be helpful. However, there is very little evidence to support their use; they should only be used as second-line agents.74
Key: HF = heart failure; IV = intravenous; SC = subcutaneous
Heart failure learning module 5 - Figure 8. Breathlessness is a particularly distressing symptom for patients with heart failure and their carers
Figure 8. Breathlessness is a particularly distressing symptom for patients with heart failure and their carers

Courtesy of the British Heart Foundation

Despite its widespread use, there is no evidence to support the use of home-based oxygen as a treatment for breathlessness.75 Home oxygen therapy for patients with NYHA III or IV class symptoms has no impact on QoL measures or survival.76

Pragmatic approach to HF treatment

Many medications used to treat HF lower blood pressure or heart rate, yet confer prognostic benefit. Postural hypotension is common among elderly patients77 and is associated with an increased risk of falls and injury.78 In patients with HF who are approaching the end of their lives who often require high-dose oral diuretics, continuing high-dose medications such as beta blockers, ACE inhibitors and mineralocorticoid receptor antagonists may cause more harm than long-term benefit.

How do we know a patient with HF is nearing the end of their life?

The natural history of HF is defined by periods of relative stability punctuated by periods of unpredictable and often sudden decline from which the patient may, or may not, recover. Thus, distinguishing patients whose conditions are salvageable from those who are entering the last few weeks of life is difficult. The ESC list five criteria, the presence of one or more of which ought to prompt consideration of end-of-life care for patients in whom advanced treatment, such as with heart transplantation or LVADs, has been deemed futile44:

  • Progressive functional decline and increasing dependence with activities of daily living
  • Severe symptoms and poor QoL, despite optimal HF management
  • Frequent hospital admissions or other severe decompensation episodes, despite OMT
  • Cardiac cachexia
  • Clinically judged to be end-of-life for another reason, such as severe infection or advanced cancer.


Incorporation of a palliative care approach in response to patient need rather than estimated prognosis will result in better care for patients with advanced HF. Interventions to support the patient and family with symptom control with the aim of improving QoL should be used alongside optimal HF management. Palliative care should be provided by the usual clinical teams in primary and secondary care, with access to specialist palliative care services when needed for persistent or complex problems.

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