Clinical Medicine 2016 Vol 16, No 1: 25–33 REVIEW

Heart failure – what the general physician needs to know

Authors: Eleanor C WicksA and Lewis C DaviesB

The British Society of Heart Failure (BSH) meetings highlight muscle damage, coronary artery disease (CAD), hypertension,
diabetes, valvular heart disease or arrhythmias (including atrial
ABSTRACT

the latest advancements within the field of heart failure

(HF) and provide education for training and revalidation fibrillation).1,4 Epidemiological studies suggest that genetics
for cardiologists and general physicians. This article reviews predispose individuals to HF through maladaptive modulation
take-home messages from the 7th BSH HF revalidation and of responses to common pathophysiological stressors (such
training meeting. It emphasises what every physician needs to as CAD) or maladaptive responses to pharmacotherapy.
know about the latest acute HF guidelines, diagnostics in HF, Other causes of HF include inflammatory cardiomyopathies
management strategies (including pharmacotherapeutics and and genetic disorders (‘inherited cardiomyopathies’, such as
device therapy), and when to consider referring to a transplant dilated cardiomyopathy) which are complex, rare and clinically
centre for mechanical circulatory support or transplantation. heterogeneous heart muscle diseases predominantly inherited
It describes the practical challenges faced and provides as autosomal dominant disorders that require family screening,
clinicians with a framework to assist with service development risk stratification and early institution of disease modifying or
and commissioning of resources to deliver optimal, integrated device therapy.5
services that meet the ever-advancing needs of our HF Survival and quality of life remains poor in HF with a
communities. reported four-year survival following diagnosis of only 50%.1
Admission to hospital is common and is often associated
KEYWORDS: Heart failure, guidelines, diagnosis, transplant, with significant length of stay. Acute HF accounts for over
ventricular assist device, commissioning, service development 67,000 admissions per year in England and Wales and is the
leading cause of hospitalisation in those aged over 65 years.6
Early discharges are often counter-productive and contribute
significantly to re-hospitalisation rates, particularly within the
Introduction
post-discharge ‘vulnerable period’. These place considerable
Heart failure (HF) is defined, clinically, as a syndrome in pressures on resources. Radical improvements in the delivery
which patients have typical symptoms (eg breathlessness, ankle of HF services to ensure early and effective diagnoses and
swelling and fatigue) and signs (eg elevated jugular venous management of patients, careful optimisation prior to discharge
pressure, fluid retention, pulmonary congestion and a displaced and targeted planning pre- and early discharge to tackle
apex beat) resulting from an abnormality of cardiac structure ‘vulnerable periods’ are warranted to minimise high post-
or function (either left ventricular systolic dysfunction (LVSD) discharge morbidity, mortality and re-hospitalisation rates.
or diastolic dysfunction (termed HF with preserved ejection Advances in research provide a clear evidence base for
fraction (HF-PEF)) which fails to deliver oxygen to meet the treatments to reduce morbidity and mortality. These underpin
requirements of metabolising tissues.1–3 It is a common acute the development of practice guidelines and quality standards in
and chronic medical problem with an estimated prevalence of HF. However, there remain diverse unmet needs, and delivering
2–4% in Europe.1 This figure continues to grow as a result of the burgeoning demand for comprehensive HF care within
an ageing population, an increasing prevalence of diabetes and the ever-increasing socioeconomic restraints requires major
hypertension, and better survival from cardiovascular disease. service redesign beyond the use of pharmaceuticals alone. This
Acute heart failure (AHF) can present as new-onset HF, or as review summarises key HF guidelines and describes strategies
an acute decompensation of chronic HF (CHF). Most cases of for the future to deliver an engaged, collaborative and ‘seamless’
HF are acquired and caused by dysfunction of the heart due to system of HF care to enable the optimal management of each
and every patient along their healthcare journey.

AHF guidelines
Authors: Aconsultant cardiologist, Department of Cardiology,
Bart’s Heart Centre, St Bartholomew's Hospital, London, UK, The AHF National Institute for Health and Care Excellence
and PhD, University College London, London, UK; Bconsultant (NICE) guidelines highlight key priorities for organising the
cardiologist, Department of Cardiology, and honorary senior totality of acute HF care (diagnosis, assessment, monitoring,
lecturer, Cardiovascular Biomedical Research Unit, Bart’s Heart management and stabilisation) for patients aged over 18 years
Centre, St Bartholomew's Hospital, London, UK who are admitted with a new diagnosis of HF or decompensation

© Royal College of Physicians 2016. All rights reserved. 25

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 Eleanor C Wicks and Lewis C Davies

guide the use of echocardiography to determine aetiology. It

Box 1. Key priorities for the implementation of the
signposts clinicians to presentation-guided management and
NICE acute HF guidance. Adapted with permission.7 to the instigation and up-titration to maximum tolerated doses
Organisation of care of disease-modifying pharmacological therapies according to
> Hospitals admitting people with suspected AHF should symptomatic hypotension, renal function and potassium levels
provide specialist HF services based on a cardiology ward and (Fig 3). It also considers advanced therapies (including devices)
additional outreach services. as disease severity escalates and New York Heart Association
(NYHA) class worsens.
> All patients admitted to hospital with suspected AHF should
receive early and continuing input from dedicated specialist
HF teams. HF discharge planning
Diagnosis, assessment and monitoring Hospitalised patients should be discharged once stable for
48 hours on optimal medical therapy. All pertinent clinical
> Use a single measurement of serum natriuretic peptides
information, including aetiology and echocardiographic
(BNP or NT-proBNP) to rule out the diagnosis of HF in people
evidence for HF, major comorbidities, electrocardiography
presenting with new suspected AHF.
parameters (rhythm, QRS duration, morphology or paced),
> Where natriuretic peptide level is raised, perform transthoracic peptide level, discharge parameters (dry weight, blood
Doppler 2D echocardiography to establish the presence or pressure, heart rate, haematology and biochemistry values)
absence of cardiac abnormalities within 48 h of admission to and medications (including limitations and advice for up-
enable early specialist management. titration) should be communicated to the community HF team.
Treatment after stabilisation Documentation should specify contact details and the date
of follow-up by the HF team within two weeks of discharge,
> In a person presenting with AHF who is already taking beta-
alongside the future care plan (detailing device, rehabilitation,
blockers, continue the beta-blocker treatment unless they have
palliative needs) to ensure continuity of care, early review and
a heart rate <50 bpm, second- or third-degree atrioventricular
the delivery of ongoing holistic and meaningful care within the
block, or shock.
community.
> Start (or restart) beta-blocker treatment during the hospital
admission for LVSD once condition has stabilised (ie once iv
Traditional drug therapies for CHF and recent
diuretics are no longer required).
updates
> Offer an ACEi and MRA to patients with AHF and LVSD during
their hospital admission. The evidence base for treating HF primarily relates to LVSD.3,8
Neurohormonal activation underpins the pathophysiological
> Ensure that the person's condition is stable for 48 h before basis of LVSD (Fig 4). Thus neurohormonal inhibition using
discharging from hospital and/or after starting or restarting pharmacotherapy (beta-blockers, angiotensin-converting
beta-blockers. enzyme inhibitors (ACEi) and mineralocorticoid receptor
> Plan a person's discharge from hospital after the acute antagonists (MRAs)), provides the bedrock for all treatments
phase. Communicate information about a person's condition, (Fig 3).
treatment, prognosis and subsequent management plan to Drugs that block the sympathetic nervous system (beta-
primary and secondary care (including HF MDT). blockers) reduce morbidity and mortality. MERIT-HF,
> Ensure that a follow-up appointment is made with the COPERNICUS and CIBIS-2 have demonstrated significant
specialist HF team within two weeks of discharge from reductions in mortality with the use of metoprolol CR/XL
hospital. (relative risk reduction (RRR) 34%), carvediolol (RRR
35%) and bisoprolol (RRR 34%), respectively.9–11 SENIORS
ACEi = angiotensin-converting enzyme inhibitor; AHF = acute heart failure;
BNP = B-type natriuretic peptide; HF = heart failure; MDT = multidisciplinary
demonstrated a 12% RRR in event rate with the use of
team; MRA = mineralocorticoid receptor antagonist; NICE = National institute nebevilol.12
for Health and Care Excellence; LVSD = left ventricular systolic dysfunction; Beyond beta-blockers, two trials, CONSENSUS and SOLVD,
NT-proBNP = N-terminal pro-B-type natriuretic peptide. underpin the guidance for using renin–angiotensin system
(RAS) blockers (ACEi) in HF, demonstrating that ACEi
(namely enalapril) improve survival.13,14 Where ACEi cannot
of previously stable HF (Box 1).7 They promote that any hospital be instituted due to cough or other reason (eg angioedema),
admitting patients with suspected AHF should provide an angiotensin receptor blockers (ARB) offer an alternative
integrated and engaged specialist multidisciplinary HF service block within the RAS for most. Cautious commencement
led by a specialist HF lead to provide early and continuing should be adopted in cases of prior angioedema with
hospital-wide outreach services and liaison with the community ACEi to ensure the absence of cross-reactivity with ARB
(Fig 1) to ensure that local needs are met, that services are use in up to 10% of cases. The CHARM-Alternative trial
accessible and regulated and that education is safeguarded. used candesartan to a target dose of 32 mg per day and
demonstrated a significant 20% RRR for death or HF
hospitalisation when compared with placebo.15 Importantly,
AHF diagnostic pathway and management
there is no evidence to suggest that an ARB is any less likely
The diagnostic and management pathway for AHF is described to cause hypotension, renal dysfunction or hyperkalaemia
in Fig 2. It utilises natriuretic peptides to ‘rule out’ HF and than an ACEi. Renin inhibitors also offer neurohormonal

26 © Royal College of Physicians 2016. All rights reserved.

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 Heart failure

General cardiology
HF MDT Primary care
clinics
Hospital HF ‘team’ acvies
Integrate HF service > daily review of HF paents
General medical > HF cardiologist and named HF lead Open access echo
clinics > hospital-wide ward rounds
> HF specialist nurses
> echocardiography MDT
> consultant cardiologists (intervenon, EP)
> HP, GPwSIs geriatrician, medical speciales > MDT for hospitalised
Inpaent > physiologist, pharmacist, diecian, psychologist, paents
decompensated occupaonal therapist, physiotherapist, social care > MDT for community
CHF HF team
Paent referred for > MDT at terary centre for
Post-MI paents complex HF paents
device treatment
> deliver rapid access,
one-stop HF diagnosc
Diagnosis
clinics
Planning of Fig 1. Elements of an inte-
management HF clinic follow-up > responsibility for HF audit
Primary care grated and multidisciplinary
(periodic review) ± specialist nurse to drive change
HF service. CHF = chronic heart
> lead must revalidate in HF
as subspecialty failure; HF = heart failure;
MDT = multidisciplinary team
Primary care HF Palliave care
Advanced HF service MI = myocardial infarction.
Adapted with permission.48

Clinical suspicion of acute

heart failure

Serum natriurec
pepde
Persisng Hypertension/
hypoxaemia despite Peripheral or
Cardiogenic shock myocardial
oxygen therapy or pulmonary oedema
ischaemia
acidaemia

BNP <100 ng/L or NT BNP >100 ng/L or NT

proBNP <300 ng/L proBNP >300 ng/L
Consider non-
Offer iv diurec Consider iv nitrate
invasive venlaon Consider iv inotropes
Perform ± vasopressors.
transthoracic ECG Discuss with
Pursue alternave
with 48 h of transplant centre
diagnosis
admission Consider regarding mechanical
ultrafiltraon circulatory support

Acute severe mitral Crical aorc Le ventricular Other cardiac

regurgitaon stenosis systolic dysfuncon abnormality

Consider mitral Offer surgical valve

valve replacement replacement Start ACEi/ARB early
and uptrate; add
MRA and uptrate; Specific treatment/
start beta-blockers seek specialist
Consider early following advice
transcatheter stabilisaon and only
aorc valve discharge following
replacement 48 h of stability

Fig 2. Diagnostic and management algorithm for acute HF.7 ACEi = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker;
BNP = brain natriuretic peptide; ECG = electrocardiogram; HF = heart failure; MRA = mineralocorticoid receptor antagonist; NT proBNP = N-terminal pro-B-type
natriuretic peptide.

© Royal College of Physicians 2016. All rights reserved. 27

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 Eleanor C Wicks and Lewis C Davies

The lack of comparison with optimal medical therapy limited

TX the value of this study.20 Nevertheless, subgroup analysis
Digoxin
VAD
Ivabradine within those with severe functional limitation (NYHA III/
IV), a very low ejection function (<25%) or with an increased
Surgery H-ISDN cardiothoracic ratio on chest radiograph, showed striking
CRT
improvements in HF hospitalisation and mortality with digoxin
ICD therapy, suggesting that digoxin does provide some benefit in
HF.
Beta-blocker ACEi ± ARB MRA For patients in sinus rhythm, the SHIFT trial demonstrated
reductions in the primary composite end point of
Fig 3. The building blocks of pharmacological and advanced therapies cardiovascular death and HF hospitalisation in those with
in HF with LVSD (HF-REF). ACEi = angiotensin-converting enzyme inhibitor; a persistently high heart rate when ivabradine was added
ARB = angiotensin receptor blocker; CRT = cardiac resynchronisation therapy; alongside conventional HF therapy.21 In contrast, the V-HeFT
HF-REF = heart failure reduced ejection fraction; H-ISDN = hydralazine- trial failed to show a significant benefit with the use of
isosorbide dinitrate; ICD = implantable cardioverter defibrillator; LVSD = left hydralazine and isosorbide dinitrate.22 However, a possible
ventricular systolic dysfunction; MRA = mineralocorticoid receptor antagonist;
benefit was demonstrated in sub-selected African Americans
Tx = transplantation; VAD = ventricular assist device.
in the A-HeFT trial, although the mechanistic basis of this
remains uncertain.23
HF management not only blocks the destructive RAS
blockade. The ATMOSPHERE trial of 7,063 patients is pathways as described above, but also aims to simultaneously
underway to compare the use of enalapril (10 mg twice daily) augment beneficial neuro-humoral systems to restore
versus the direct renin inhibitor, aliskiren (separately and in imbalance through ‘neuro-humoral modulation.’ The
combination), in HF.16 angiotensin receptor neprilysin inhibitor, LCZ696, is a novel
Other RAS inhibitors that are used in combination with therapy examined in PARADIGM-HF that has demonstrated
disease-modifying agents are MRAs. RALES and EMPHASIS- a marked independent reduction in hospitalisation and
HF are the two pivotal trials that demonstrated reduced mortality benefit 16% over and above that achieved with the
morbidity and mortality with spironolactone or eplerenone, use of enalapril alone.24 LCZ696 further lessened symptomatic
respectively.17,18 Heightened interest in combining MRAs with deterioration, admissions to hospital and the need for
potassium-combining resins which bind potassium in the colon intensification of oral HF therapy versus enalapril. LCZ696
to avoid hyperkalaemia (such as sodium zirconium cyclosilicate therefore has the potential to slow the progression of LVSD and
examined in the HARMONIZE trial), may enable the wider use thus lends itself as a novel therapy in the management of HF.
of MRAs in clinical practice.19 Finally, PEP-CHF, I-PRESERVE, CHARM-Preserved
Additional therapies in HF are occasionally considered in and TOPCAT are major trials that have been conducted in
addition to beta-blockers, ACEi and MRAs. The DIG study patients with HF-PEF.25–28 Each of these studies have failed
compared the use of digoxin alongside ACEi versus placebo. to demonstrate significant reductions in event rates in those
administered with perindopril, irbesartan, candesartan and
spironolactone, respectively.

MI Intravenous therapies in AHF

The treatment goals in AHF are to achieve decongestion,
LVSD preserve renal function and avoid harm. Beyond the instigation
and up-titration of disease-modifying therapies, intravenous
Received reducon (iv) therapies are utilised. To alleviate decongestion, the DOSE
in circulaon volume trial examined the administration of bolus versus infusion
and pressure iv diuretic therapy and found no significant differences with
respect to weight loss or symptomatology.29 Unsurprisingly,
Systemic higher doses of diuretics promoted an enhanced fluid loss
vasconstricon, and improved symptoms. Clinicians are guided to cautiously
renal sodium and water Neurohumoral acvaon
retenon > RAAS increase the dose of diuretics in AHF for those already taking
> SNS diuretics, unless there has been recent non-adherence with
> ET, AVP etc diuretic therapy. Renal function, weight and urine output
> (natriurec pepdes)
should be monitored to avoid over-diuresis.
Fig 4. The pathophysiological basis of therapy in HF. Myocardial injury Beyond diuretics, NICE guidance suggests that the routine
leads to LVSD which invokes a perceived reduction in circulating volume and use of opiates, nitrates, sodium nitroprusside, inotropes or
pressure. This promotes neuro-hormonal activation of the RAAS, the SNS, ET,
vasopressors in people with acute HF should be avoided unless
AVP, natriuretic and other systems. These invoke systemic vasoconstriction
and renal sodium and water retention which worsen LVSD and promote the
there is evidence of concurrent myocardial ischaemia, severe
downward cyclical process in HF. AVP = arginine vasopressin; ET = endothe- hypertension, valvular, or diseases other pathology which
lial; HF = heart failure; MI = myocardial infarction; LVSD = left ventricular warrant their institution within an advanced care setting.
systolic dysfunction; RAAS = renin angiotensin aldosterone system; SNS = Small studies suggest that the use of low-dose dopamine (<3
sympathetic nervous system. µg/kg/min) and nesiritide (a recombinant brain natriuretic

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 Heart failure

peptide (BNP)) may promote renal vasodilation and enhance

diuresis. However, the ROSE AHF trial conferred no benefit Table 1. NICE Guidance for device therapy according
with their use.30,31 Therefore, NICE corroborates American to NYHA class and QRS duration. Reproduced with
and European guidelines suggesting that such therapies are permission.37
best avoided and only considered in end-stage disease or
cardiogenic shock. NYHA Class
Finally, RELAX-AHF a placebo-controlled study using QRS Interval I II III IV
serelaxin, a novel recombinant human hormone with known
renal protective properties and systemic vasodilator effects, <120 msec ICD if there is a high risk ICD and CRT not
demonstrated significant improvements in symptomatology of sudden cardiac death clinically indicated
(dyspnoea and congestion) and was associated with 120–149 msec ICD ICD ICD CRT-P
significantly fewer cardiovascular deaths at 180 days following without LBBB
acute treatment.32 120–149 msec ICD CRT-D CRT-P or CRT-P
with LBBB CRT-D
Differentiating the aetiology of HF is important >150 msec with CRT-D CRT-D CRT-P or CRT- P
Felker et al (2000) demonstrated that the underlying cause or without LBBB CRT-D
of HF has prognostic value in patients with unexplained CRT = cardiac resynchronisation therapy; CRT-D = defibrillator; CRT-P =
cardiomyopathy.33 They detailed that patients with peripartum pacemaker; ICD = implanted cardioverter defibrillator; LBBB = left bundle
branch block; NYHA = New York Heart Association.
cardiomyopathy have improved outcomes when compared
with those suffering from other cardiomyopathies. They
noted that the prognosis in idiopathic cardiomyopathy was
better when compared with cardiac sarcoidosis, amyloid or which demonstrated a superior response in those with
haemochromatosis and that the prognosis within each of a broad QRS irrespective of bundle branch morphology
these conditions becomes sequentially worse. Those with versus narrow QRS, CRT-D can now be utilised.39,40 Since
cardiomyopathy related to infiltrative myocardial diseases, the PROSPECT trial there is no longer evidence that
HIV infection or doxorubicin therapy have an especially poor dyssynchrony echocardiography improves patient selection for
prognosis. CRT.41 Therefore dyssynchrony echocardiography is no longer
The clinical history, electrocardiography, echocardiography warranted in the device selection process. Finally, the use of
(including strain imaging) and cardiac magnetic resonance ventricular tachycardia stimulation to guide device suitability
imaging (CMR) tissue characterisation and nuclear imaging has been excluded.
techniques help differentiate between underlying aetiologies. Clinicians must remain mindful of the impact of an ICD and
While HF is treated along the same algorithm irrespective ensure its appropriate use, particularly in those with NYHA
of cause, establishment of the aetiology enables the targeted class IV symptoms. Consideration of the cost versus benefit
allocation of specific therapies to disease processes. In of device implantation, and awareness that ICD implantation
thalassaemia, CMR T2* imaging has enabled diagnoses, does not improve symptoms, LV function or the mode of death,
monitoring and instigation of chelating therapies, resulting and can be associated with inappropriate shocks, psychological
in a dramatic reduction in mortality by 80%.34,35 Similarly, burden and implications for driving, is vital.
differentiation between amyloid light chain (AL) versus Finally, the advantages of devices in atrial fibrillation,
transthyretin (ATTR) amyloid is key for delivering specific bradycardia, HF-PEF, or in those with paced cardiac
chemotherapy and in guiding prognosis.36 Furthermore, rhythms who are considered for ‘upgrading’ to CRT, remain
establishment of aetiology can guide risk stratification and unknown. Nevertheless, advancements in device technology
the need for device therapy or family screening, such as in the and ‘tele-monitoring’ capabilities (including leadless
presence of a lamin (LMNA) variant in a patient with dilated technology, subcutaneous extra-cardiac devices, quadripolar
cardiomyopathy.

The use of devices in HF

COMPANION CONTAK-CD 3M
CRT-P CRT-D
Unified and pragmatic device therapy guidance based on the CARE-HF CONTAK-CD 6M
COMPANION MADIT-CRT
best available evidence, have recently been updated to include MIRACLE MIRACLE ICD
primary prevention device therapy in non-ischaemic LVSD MUSTIC-SR Piccirillo 2006
RESPOND Pinter 2009
and expanding indications for cardiac resynchronisation REVERSE CRT-P Eu COMPANION
RAFT
REVERSE CRT-P US RETHINQ
therapy (CRT) or defibrillator (ICD) therapy (Table 1 and VECTOR REVERSE CRT-D Eu
Fig 5).37 These include data from the SCD-HeFT primary OMT ICD REVERSE CRT-D US
RYTHMN-ICD
prevention study which demonstrated a 23% reduction in AMIOVIRT
CAT
mortality following the implantation of an ICD in those with DEFINITE
severe LVSD (ischaemic and non-ischaemic cardiomyopathy) MADIT
MADIT II
and NYHA II-III symptoms.38 ICD implantation can now SCD HeFT
also be considered in patients with a narrow QRS complex Fig 5. Diagrammatic summary of device trials in heart failure. CRT =
providing there is a high risk of sudden cardiac death. cardiac resynchronisation therapy; CRT-D = defibrillator; CRT-P = pacemaker;
Furthermore, since the advent of MADIT-CRT and RAFT, ICD = implanted cardioverter defibrillator; OMT = oral medical therapy.

© Royal College of Physicians 2016. All rights reserved. 29

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 Eleanor C Wicks and Lewis C Davies

Box 2. Conventional criteria for HTx and clinical indicators that should prompt consideration for referral to a
transplant centre. Adapted with permission.42
Conventional criteria for HTx:
> impaired left ventricle systolic dysfunction
> NYHA III or IV symptoms
> receiving optimal medical treatment (target or maximum tolerated doses of beta-blockers, ACEi, MRA)
> CRT, ICD or CRTD (if indicated)
> evidence of poor prognosis:
– cardiorespiratory exercise testing (VO2 max <12 mL/kg/min if on beta-blockade, <14 mL/kg/min if not on beta-blockade, ensuring
respiratory quotient ≥1.05)
– markedly elevated BNP (or NT-proBNP) serum levels despite full medical treatment
– using established composite prognostic scoring system (eg HFSS or SHFM).
Clinical indicators that should prompt consideration for referral:
> two or more admissions for treatment of decompensated HF within the last 12 months
> persistent overt HF despite optimal medical treatment
> SHFM score indicating ≥20% 1-year mortality
> echocardiographic evidence of right ventricular dysfunction or increasing PA pressure on optimal medical therapy
> anaemia, involuntary weight loss, liver dysfunction or hyponatraemia attributable to HF
> deteriorating renal function attributable to HF or inability to tolerate diuretic dosages sufficient to clear congestion without change in
renal function (refer before creatinine clearance falls below 50 mL/min or the eGFR drops below 40 mL/min/1.73 m2)
> significant episodes of ventricular arrhythmia despite full pharmacological and device treatment
> increasing plasma BNP or NT-proBNP levels despite adequate HF treatment
> refractory angina where debilitating, significant and recurrent myocardial ischaemia is evident and is not amenable to
revascularisation or full anti-anginal treatment
> restrictive or hypertrophic cardiomyopathy with persisting NYHA III/IV symptoms refractory to conventional treatment ± recurrent
admissions with decompensated HF.
Clinical indicators that should prompt urgent inpatient referral for HTx:
> the need for continuous inotrope infusion (± IABP to prevent multiorgan failure
> persistent circulatory shock due to a primary cardiac disorder
> no scope for revascularisation in the setting of persistent coronary ischaemia.
Relative (R) and absolute (A) contraindications for transplantation:
> microvascular complications of diabetes (excluding non-proliferative retinopathy) (A)
> active malignancy other than localised non-melanoma skin cancer (A)
> extracardiac vascular disease (peripheral or cerebrovascular) (R)
> sepsis and active infection (A); chronic viral infections (R)
> recent pulmonary embolism (A) due to the risks of RV failure post-operatively
> autoimmune disorders (R)
> aggressive skeletal myopathies (A)
> substance misuse (tobacco or excessive alcohol consumption) (R)
> a history of non-adherence to treatment or follow-up (R)
> those with a BMI >32 kg/m2 are advised to loose weight (R)
> age is not a contraindication, but age <75 years is associated with lower risk
> multiple prior sternotomies increases the risk, but is not a contraindication.
ACEi = angiotensin-converting enzyme inhibitor; BNP = B-type natriuretic peptide; CRT = cardiac resynchronisation treatment; CRTD = cardiac resynchronization
therapy defibrillator; eGFR = estimated glomerular filtration rate; HF = heart failure; HFSS = heart failure survival score; HTx = heart transplantation; IABP = intra-aortic
balloon pump; ICD = implantable cardioverter defibrillator; MRA = mineralocorticoid receptor antagonist; NT-proBNP = N-terminal pro-B-type natriuretic peptide;
NYHA = New York Heart Association; PA = pulmonary artery; SHFM = Seattle heart failure model.

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 Heart failure

leads, multi-point pacing, vagal nerve stimulation and

Box 3. Future training opportunities offered by the
sensors to measure pulmonary pressures), are postulated to
reduce HF admissions and are likely to become increasingly BSH.
accessible. > 8th BSH Heart Failure Day for Revalidation and Training,
3 March 2016, Golden Jubilee Hotel, Glasgow
When to refer for transplantation and mechanical > 6th BSH Heart Failure Nurse Study Day, 4 March 2016, Golden
circulatory support Jubilee Hotel, Glasgow
Patients with advanced HF have a poor quality of life and > 19th BSH Annual Autumn Meeting, 24–25 November 2016,
dismal prognosis. Heart transplantation (HTx) provides an QE II Centre, London.
effective lifeline for selective patients and an HF specialist E-mail: info@bsh.org.uk
plays a vital role in the timely identification and referral of www.bsh.org.uk
potential candidates prior to the development of irreversible @BSHeartFailure
complications (pulmonary arterial hypertension or cardiorenal
syndrome). Banner et al (2011) summarise the pertinent aspects flow VAD placement, infection (particularly drive-line related),
in deciding when and whom to refer for transplantation and thromboembolic events, VAD thrombosis and the potential for
the role of left ventricular assist devices (VADs) as a ‘bridge worsening aortic valve insufficiency), must be discussed with
to transplantation’.42 The International Society for Heart patients. It is therefore imperative to seek early involvement
and Lung Transplantation (ISHLT) guidelines and policy from transplantation centres to access advanced HF expertise.
standards provide corroborative guidance.43 Recent NICE
guidance (2015) has extended funding for VADS as a ‘bridge to
The future of HF and service development
transplantation’ to include ‘destination therapy’ for those who
are ineligible for HTx.44 HF is a young, albeit growing, cardiac subspecialty. Over the
Conventional criteria for referral for HTx are described in last ten years, multidisciplinary engagement from the BSH
Box 2. Those with LVSD are more commonly referred, however have driven the development of NICE guidelines and quality
HF-PEF is not excluded. Triggers for referral include poor standards for delivering optimal HF care. The National HF
prognostic markers – worsening HF symptoms, a significantly Audit, introduced in 2007 to monitor the care and treatment
raised or increasing BNP, renal or liver dysfunction, rising of patients with AHF in England and Wales, has documented
diuretic requirements, the need for dose reduction of disease improved clinical standards in HF. The Care Quality
modifying medications, ventricular arrhythmias, or the need Commission recognises the delivery of HF care within a trust
for inotropic or balloon pump support. Composite risk scoring as a key discerning determinant of acute hospital care. HF care
systems, such as the Seattle HF Model, Heart Failure Survival should be delivered in a multi-professional manner, adhere to
Score or Meta-Analysis Global Group in HF Calculator help common guidelines and should function across all sectors of
derive a one-year mortality risk greater than 20%.45–47 care. Multidisciplinary strategies, lifestyle recommendations
Contraindications for transplantation are also noteworthy. and rehabilitation programs should be incorporated to
Advanced age >75 years, body mass index >30, active smoking improve functional capacity, reduce symptoms, improve
and excessive alcohol intake infer a worsened outcome adherence with therapy and reduce hospitalisation. Clinicians
and are relative contraindications. There are few absolute must focus on improving communication, consistency and
contraindications but these comprise neoplasia (unless in continuity of care for HF patients throughout their patient
remission for five years), recent pulmonary embolism, marked journey.
pulmonary artery hypertension (with a transpulmonary Structurally, it is suggested that hospitals ensure that 25%
gradient >15 mmHg or pulmonary vascular resistance (>5 of their cardiologists have a remit in HF and that larger trusts
Woods units)), and the presence of microvasular complications have a specific HF cardiologist.49 Services should aim to have
of diabetes. one HF nurse per 100,000 of population to enable home visits,
Recommending HTx requires specific expertise and telephone contact, facilitation of telemonitoring, conducting of
evaluation of the risks, benefits, alternative options and scarce nurse-led clinics and provision of education, patient self-care
availability of donor hearts to optimise receiver suitability and optimisation of medical therapy, particularly in the early
and the potential for functional recovery, survival and discharge stages. Diagnostic services must be collaboratively
improved quality of life. Early referral is therefore key. Patient developed between primary and secondary care to enable
selection is based on clinical need, the capacity to benefit efficient and effective evaluation of patients. Therapeutic
from transplantation, biological matching (blood group pathways must enable the timely delivery of evidence-based
compatibility, donor versus recipient size and HLA status) therapy with referral pathways in place for surgical and
and logistical factors that influence the cardiac ischaemia device input alongside palliative care. Structured follow-up
time and fairness. There are significant potential risks with of stable patients, with more frequent review of those recently
HTx and mechanical circulatory support, as described within discharged or with deteriorating symptoms, must be available
the ISHLT and the Interagency Registry for Mechanically to all to enable the provision of complex care. Furthermore,
Assisted Circulatory Support (INTERMACS Registry).43,48 careful evaluation of services using audit, quality improvement,
Perioperative, early postoperative and long-terms risks to quality indicators and monitoring through registries are key to
transplantation (including risks of antibody and cell-mediated ensuring continuous service refinement.
rejection, among others) and risks with VADs (bleeding, the Commissioning drivers, forthcoming acute HF quality
acquisition of von Willebrand syndrome following continuous- standards and the development of the best practice tariff are a

© Royal College of Physicians 2016. All rights reserved. 31

CMJv16n1-Wicks.indd 31 18/01/16 6:05 PM

 Eleanor C Wicks and Lewis C Davies

reality for HF services, and will stimulate future improvements XL Randomized Intervention Trial in congestive heart failure
in the delivery of HF care. HF is increasing in prevalence, (MERIT-HF). MERIT-HF Study Group. JAMA 2000;283:1295–302.
is high in morbidity and mortality and has an increasingly 10 Packer M, Coats A J, Fowler M B et al. Effect of carvedilol on sur-
complex management. We must get the basics right and ensure vival in severe chronic heart failure. N Engl J Med 2001;344:1651–8.
11 The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a ran-
that the evidence-based disease-modifying treatments are
domised trial. Lancet 1999;353:9–13.
initiated and up-titrated. Each and every clinician must also 12 Flather MD, Shibata MC, Coayts AJ et al. Randomized trial to
play a proactive role in developing services and driving clinical determine the effect of nebivolol on mortality and cardiovas-
standards to ensure the optimal delivery of acute and chronic cular hospital admission in elderly patients with heart failure
HF services. ■ (SENIORS). Eur Heart J 2005;26:215–25.
13 listed No authors. Effects of enalapril on mortality in severe con-
Acknowledgements gestive heart failure. Results of the Cooperative North Scandinavian
Enalapril Survival Study (CONSENSUS). The CONSENSUS Trial
This work forms part of the research areas contributing to translational Study Group. N Engl J Med 1987;316:1429–35.
research portfolio of the Cardiovascular Biomedical Research Unit 14 No authors listed. Effect of enalapril on survival in patients with
at St Bartholomew's Hospital, which is supported and funded by reduced left ventricular ejection fractions and congestive heart
the National Institute for Health Research (from which LCD is failure. The SOLVD Investigators. N Engl J Med 1991;325:293–302.
directly funded). We also gratefully acknowledge the BSH who have 15 Granger CB, McMurray JJ, Yusuf S et al. Effects of candesartan in
supported this review as part of the 7th BSH HF Day for Training patients with chronic heart failure and reduced left-ventricular sys-
and Revalidation (2015) and the Friends of BSH: Bayer HealthCare, tolic function intolerant to angiotensin-converting-enzyme inhibi-
Medtronic, Novartis, Pfizer, ResMed, Servier Laboratories and Vifor tors: the CHARM-Alternative trial. Lancet 2003;362:772–6.
Pharma. 16 McMurray JJ, Abraham WT, Dickstein K et al. Aliskiren,
ALTITUDE, and the implications for ATMOSPHERE. Eur J Heart
Fail 2012;14:341–3.
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