This year’s 24th British Society for Heart Failure annual meeting successfully brought together experts in heart failure from all over the UK as well as keynote speaker and the Philip Poole-Wilson Memorial lecturer, Professor Milton Packer from the USA. This hybrid meeting, held in London in December 2021 at Queen Elizabeth II Exhibition Centre, welcomed a hugely diverse faculty including prominent figures in heart failure as well as key opinion leaders from the multidisciplinary heart failure team including nurses, cardiologists, pharmacists, elderly care physicians and patients living with heart failure. In contrast to many cardiovascular meetings, 44% of the British Society for Heart Failure (BSH) faculty were women. Dr Sarah Maria Birkhoelzer reports its highlights.
Heart failure as a neurohormonal disorder
Professor Milton Packer (Baylor University Medical Center, Dallas, Texas, USA) highlighted in the Philip Poole Wilson Memorial lecture the journey through heart failure (HF) research and how common, important and serious it is with more deaths from HF than all cancers combined.
The foundation of HF research is based on the view that it is a haemodynamic disease and, until 1970, diuretics were the prime focus of drug development. In the 1970s, vasodilator and inotropic drugs were developed to keep haemodynamic variables in the normal range and to stimulate cardiac contractility, which markedly improved cardiac performance. The fundamental holdback in the development of ground-breaking, disease-modifying drugs in HF was the paradigm that downregulation of activated renin-angiotensin system and sympathetic nervous system was contraindicated in HF.
The first landmark trials published in 1987 recognised HF as a neurohormonal disorder and demonstrated a reduction in hospitalisation and mortality with angiotensin-converting enzyme (ACE) inhibitors.1,2 From the late 1990s, beta blockers3–5 and mineral corticoid receptor antagonists6,7 were added to HF treatment. The spotlight subsequently moved to neprilysin inhibitors8 and sodium-dependent glucose cotransporters 2 (SGLT2) inhibitors, with combined SGLT 1 and 2 inhibitors now on the horizon.9 Table 1 summarises this journey.
Table 1. Pathophysiology of heart failure
Focus of heart failure care | ||
---|---|---|
Haemodynamic disease | 1960s | Diuretics |
1970s | Vasodilators and inotropes | |
Neurohormonal disease | 1980s | Angiotensin-converting enzyme (ACE) inhibitors |
1990s | Beta blockers | |
2000 | Mineralocorticoid receptor anatagonists (MRAs) | |
2010 | Angiotensin receptor-neprilysin Inhibitor (ARNI) sodium-dependent glucose cotransporters 2 (SGLT2) inhibitors |
|
2020 | Combined SGLT1 and 2 inhibitors |
Professor Packer highlighted the marked discrepancy between clinical trial results with advances in the outcomes of patients with HF and real-life settings in the community, highlighting regional changes and health inequalities. He pledges us to first translate these ground-breaking results into clinical practice before we aim to discover more treatment options.
New ESC guidelines: parallel instead of sequential initiation for four pillars of HF care
The sequential treatment therapy approach in HF guidelines originated from the order of clinical trial evidence delivered over the last 40 years (as highlighted by Professor Packer). Now the paradigm has shifted towards the initiation of all four HF drugs in parallel. Professor Teresa McDonagh (Kings College Hospital, London) presented the new European Society of Cardiology (ESC) guidelines on heart failure at the meeting, highlighting how as all four drugs are independently beneficial of each other within the first months of treatment, reaching the target dose of each individual medication now becomes secondary.
There is some concern that the discrepancy of National Institute for Health and Care Excellence (NICE) guidance in comparison to the new ESC guidance will impact, particularly for non-medical prescribers who take a huge role in optimising medical treatment in the community. Professor McDonagh drew attention to the fact that the new guidelines do not cover prevention or asymptomatic patients with left ventricular systolic dysfunction (LVSD) but focus on symptomatic HF with reduced ejection fraction (New York Heart Association [NYHA] II-IV). It is important to realise that patients with asymptomatic LVSD were not included in the trials examining SGLT2 inhibitors or angiotensin receptor-neprilysin Inhibitors (ARNIs). The question, however, remains, as to how asymptomatic HF is defined and what the role might be, for example, for cardio-pulmonary exercise testing or NT-proBNP, in this patient group (table 2).
Table 2. Outstanding questions
– How is asymptomatic heart failure defined? – How should we treat asymptomatic patients with heart failure with reduced ejection raction (HFrEF)? – How should we treat the elderly with HFrEF? – Is NTproBNP under-utilised in the assessment of disease control? – Does remote monitoring in heart failure reduce costs and improve outcomes? |
Devices in heart failure
Professor Roy Gardner (Golden Jubilee Hospital, Clydebank) emphasised the importance of optimal medical therapy (OMT). Cardiac resynchronisation therapy (CRT) is recommended for symptomatic patients with HF of ischaemic aetiology: in sinus rhythm with a QRS duration ≥150 ms, a left bundle branch block (LBBB) QRS morphology, and a left ventricular ejection fraction (LVEF) of ≤35%, despite OMT, in order to improve symptoms and reduce morbidity and mortality (Class I, A recommendation, ESC HF guideline 2021). In non-ischaemic cardiomyopathy, he particularly encourages a wait beyond the recommended three months to allow potential recovery of the ejection fraction (EF) before considering a device. CRT does not reduce mortality or hospitalisation for HF in patients with HF and a QRS <130 ms10 (table 3).
Table 3. Univariate predictors of patient-reported severe pain
Downgraded to IIa recommendation | Primary prevention implantable cardioverter defibrillators (ICDs) in patients with non-ischaemic cardiomyopathy |
Level IIb, B | Cardiac resynchronisation therapy (CRT) may be considered in non-left bundle branch block QRS |
Class III, A | ICD not recommended – within 40 days of a myocardial infarction – in New York Heart Association class IV heart failure with severe symptoms refractory to pharmacological therapy unless patients are candidates for CRT, a ventricular assist device (VAD), or cardiac transplantation |
With the changing patient demographics in HF, as people live longer and the prevalence of HF increases in the elderly, the question arises of which age cut off should be considered for the primary prevention of implantable cardioverter defibrillators (ICDs), particularly when the average age of patients with non-ischaemic cardiomyopathy was 64 years in the landmark trial examining ICDs.11 It is important to highlight that older patients are at higher risk of mortality from other causes, hence the need for individualised decision making and risk assessment. Results from the ongoing RHYTHM-HF study are awaited to understand the role of arrhythmia in HF mortality.
Phenotyping in heart failure
Table 4. Phenotyping in heart failure
HF with reduced EF (HFrEF) | HF with mildly reduced EF (HFmrEF) | HF with preserved EF (HFpEF) | Is there heart failure with supra-normal LVEF? (12) |
---|---|---|---|
LVEF 40% or less | LVEF 41-49% | LVEF 50% or more | LVEF 65% |
Professor Andrew Clark (Hull York Medical School) refers to HF as a condition that responds to HF treatment. The reason why HF phenotyping and subsequent treatment is affixed to LVEF is due to the wealth of evidence for patients with HFrEF (LVEF 40% or less). LVEF is a potent predictor of outcome with hospitalisation, cardiovascular death and all-cause death being significantly higher the lower the EF.12 The new ESC guidelines highlight the Level I evidence for HFrEF with limited evidence for patients with HF with mildly reduced EF (HFmrEF) (LVEF 41–49%) and no evidence for those patients with HF with preserved EF (HFpEF) (LVEF of 50% or more) or normal EF. However, what is normal ejection fraction,13 how do we measure it and what does it mean? It is not surprising that there is a degree of confusion when guidelines across the world have different ranges and nomenclature of EF (see table 5).
Table 5. Nomenclature used in guidelines
Nomenclature | Range |
---|---|
Normal | Ejection fraction (EF) of 50% and above |
Moderately impaired/moderately abnormal/preserved | EF range between 30-50% |
Severely impaired/abnormal/reduced | EF less than 40% |
So how can we phenotype patients with HF better in the future? Should we use artificial intelligence14 and analysis of big data15 to guide the diagnosis of HF? Should a new phenotype characterised by supra-normal LVEF be considered as deviation of LVEF from 60% to 65% as it is associated with poorer survival?16
How can we co-create the digital future of heart failure?
Table 6. Outstanding questions in digital health
Will the use of digital health data… |
– increase health care utilisation? |
– add value to standard care? |
– improve hard outcomes? |
– increase health inequalities? |
Table 7. Benefits of the using the Luscii app
– ongoing care of heart failure (HF) patients during the pandemic |
– telephone consultations for up-titration of HF medication |
– HF team to intervene if vital signs fall outside acceptable ranges |
– increase clinic capacity by decreasing review time for each patient |
– audit tool to assess HF team performance |
– education of patients via app education modules |
In the Journal of the American College of Cardiology Heart failure (JACC-HF) lecture, Professor Martin Cowie (National Heart and Lung Institute, Imperial College London) reminds us that the reason why we embrace digital technology in almost all aspects of life is because it is easier, more convenient and shows obvious benefit. Digital health should augment the work of healthcare professionals and help patients to live with their comorbidities in a more convenient way and support them in day-to-day life. The COVID-19 pandemic evolved into a ‘techcelleration’ (https://www.sciencedirect.com/science/article/pii/S2213177921005540) with a huge market of wearable technology available to deliver the digital future. One success story of digital medicine in HF, even before the pandemic, was the use of pulmonary artery pressure-guided therapy in ambulatory patients with HF (NYHA Class III) which was associated with fewer HF hospitalisations and improved quality of life.17 Early data suggest that digital medicine does not increase admission or mortality in patients with heart failure.18 Future work needs to be done to ensure health technology is more accessible and vulnerable and deprived groups won’t be disadvantaged (table 6).19
Dr Carla Plymen is leading the heart failure team at Imperial College Healthcare NHS Trust and is at the forefront of digital advances in HF care. Her team uses an app called Luscii which is a novel remote monitoring and education tool. It monitors patient’s vital signs, weight, quality of life and symptoms with Bluetooth connected blood pressure machine and scales. This allows the HF team to review vital signs and quality of life remotely. Results to demonstrate beneficial outcomes for patients are eagerly awaited (table 7).
The Cardiovascular disease prevention pathway (CPIP) and what does it mean for you
Dr Raj Thakkar (National Primary Care Cardiac Pathways Lead, NHS England) presented a multidisciplinary breathlessness pathway across primary and secondary care with the focus on the whole patient pathway. Evidence suggests that patients with breathlessness have repeated interactions with healthcare professionals with delayed diagnosis and management (table 8). The breathless pathway has been produced by ‘NHS RightCare’ to reduce variation and inequalities in practice and improve outcomes. It makes sure that the right person has the right care, in the right place, at the right time, making the best use of available resources. Initial investigations – beyond history and examination – should include an electrocardiogram/NT-proBNP, full blood count/thyroid function test/biochemistry, patient health questionnaire (PHQ4), GP physical activity questionnaire (GPPAQ), spirometry, and fractional exhaled nitric oxide. The overall aim of the new breathlessness pathway is to provide a comprehensive management plan within six months of presentation to the health service.
Table 8. Outcomes of the ‘breathless’ patient
– 50% of breathlessness in adults over 40 years of age is caused by heart failure (HF), chronic obstructive pulmonary disease (COPD), anaemia, anxiety or depression |
COPD – 58% of patients with COPD presented with respiratory symptoms for over five years prior to diagnosis20 |
HF – 41% presented with HF symptoms in the five years prior to diagnosis. – 79% were diagnosed during an acute admission to hospital21 |
Interstitial lung disease/ fibrosis – 55% experienced misdiagnosis before the correct diagnosis was made22 |
Long COVID: STIMULATE CP Study
Dr Ami Banerjee (University College Hospital London) made us reconsider COVID-19 as a syndemic, a convergence of an infectious disease, under-treated non-communicable diseases and social determinants of health.23 With his background in epidemiology and big data he built a framework of a learning health system which is relevant to COVID-19 and HF. It aims to join up thinking between the silos of science, care and evidence to support the two million people in the UK that are estimated to have persistent symptoms for more than 12 weeks following COVID infection. As a result, 80 long COVID clinics have been established.
Dr Banerjee is co-principal investigator of the STIMULATE CP (Symptoms, Trajectory, Inequalities and Management: Understanding Long-COVID to Address and Transform Existing Integrated Care Pathway) study. To reduce the impact on patients, healthcare and economy, this study is trying to establish how to diagnose long COVID as well as aiming to understand how to manage Long COVID, including assessment of the outcomes of current clinical practice.
Culturally appropriate cardiac rehab and health care inequalities
Table 9. Coronary risk factors
Biological factors | Genetic components |
Psychosocial factors | Social class and personality type |
Behavioural factors | Levels of physical activity and behaviours |
Coronary risk factors can be divided into three groups: biological, psychological, and behavioural (table 9). Nikki Gardiner, Clinical Lead for Cardiac and Pulmonary Rehabilitation at University Hospital Leicester NHS Trust, presented the culturally tailored rehab programme, which is being carried out in Leicester, one of the most culturally and ethnically diverse cities in the UK. The programme was designed to challenge health inequalities and to reach ethnic minorities, particularly those from the South Asian community and women, to participate in cardiac rehab. As part of this programme, multilingual cardiac rehab assistants are being employed, who can interpret three different South Asian languages. Volunteer posts have been offered to past participants of the programme to assist with exercise classes. This more bespoke South Asian rehabilitation programme resulted in a 116% uptake for South Asian people attending cardiac rehab with a significant increase in women attending six months after the programme had started. Interestingly, this programme resulted in a higher proportion of women from Asian backgrounds participating than women from British backgrounds participating in the English-speaking classes.
Are cardiologists ageist: frailty and the heart
In the National Institute for Cardiovascular Outcomes Research (NICOR) 2019/2020 National Cardiac Audit Programme, there was a significant decline in the prescription of disease-modifying drugs for patients with HFrEF with a marked reduction in patients above the age of 85 years. But even in patients over 55 years, there was an age-marked reduction in access to diagnostics, drugs and specialist care. How can we improve the care and outcomes of the elderly population?
Dr Patricia Cantley (Midlothian Frailty Project, Edinburgh) presented her work with hospital at home and end of life care for patients with HF. Hospital at home is a new concept to deal with the increased demand for bed-based hospital care (table 10). First trials suggest that acute care at home led by hospital specialists might be an alternative to hospitalisation for selected older persons.24
Table 10. Hospital at home
What is hospital at home? | What is it not? |
---|---|
Medical care is led by hospital specialist | Not early supportive discharge |
Urgent access to hospital level diagnostics | Not a virtual ward for chronic disease management |
Acute complex conditions managed at home | Early supported discharge |
Short time limited acute episodes of care | Outpatient anti-microbial team |
New BSH board appointments 2021–2023
Chair | Professor Roy Gardner |
Past Chair | Professor Simon Williams |
Chair Elect | Dr Lisa Anderson |
Deputy Chair | Ms Carys Barton |
Treasurer | Dr Sue Piper |
Councillor | Dr Patricia Campbell |
Councillor | Ms Margaret Simpson |
Councillor | Professor Zaheer Zousef |
Nurse Forum Chair | Ms Poppy Brooks |
Future of heart failure research: Early Investigator Award
In the heart failure research workshops, the BSH is aiming to put a bigger emphasis on mentoring research in this area. The aim is to diversify the research community and promote novel ideas from outside the established research centres. It was therefore welcome that the Early Investigator Award – an opportunity open to BSH members (physicians in training, nurses and other professionals allied to medicine) to showcase their work – was, for the first time in history, awarded to all three finalists (table 11).
Table 11. The three finalists for the Early Investigator Award
BSH Member | Location | Topic |
---|---|---|
Dr Simon Beggs | University of Glasgow | A novel method to characterise cardiac rhythm at the time of death in patients with heart failure (RHYTHM-HF) |
Rosalyn Austin | Portsmouth Hospitals University NHS Trust | Chronic heart failure SYMptoms imPACT on burden of treatment (SYMPACT): a mixed method observational study |
Dr Amrit S Lota | Royal Brompton Hospital, London; National Heart & Lung Institute, Imperial College London |
Genetic architecture of acute myocarditis and the overlap with inherited cardiomyopathy |
Sarah Birkhoelzer
Cardiology Registrar
Queen Alexandra Hospital, Portsmouth Hospitals University NHS Trust
References
1. Group CTS. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987;316:1429–35.
2. Investigators S. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991;325:293–302.
3. Group M-HS. Effect of metoprolol CR/XL in chronic heart failure: metoprolol CR/XL randomised intervention trial in-congestive heart failure (MERIT-HF). The Lancet 1999;353:2001–7.
4. Krum H RE, Mohacsi P, Rouleau JL, et al. Effects of initiating carvedilol in patients with severe chronic heart failure: results from the COPERNICUS Study. JAMA 2003;289:712–8.
5. Poole-Wilson PA SK, Cleland JG, Di Lenarda A, et al. Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial. Lancet 2003;362:7–13.
6. Zannad F MJ, Krum H, van Veldhuisen DJ, et al. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011;364:11–21. https://doi.org/10.1056/NEJMoa1009492
7. Pitt B ZF, Remme WJ, Cody R, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 1999;341:709–17.
8. McMurray JJ, Milton P, Desai AS, Gong J, et al. Angiotensin–neprilysin inhibition versus enalapril in heart failure. N Engl J Med 2014;11:993–1004. https://doi.org/10.1056/NEJMoa1409077
9. Bhatt DL SM, Steg PG, Cannon CP, et al. Sotagliflozin in patients with diabetes and recent worsening heart failure. N Engl J Med 2021;384:117–28. https://doi.org/10.1056/NEJMoa2030183
10. Ruschitzka F AW, Singh JP, Bax JJ et al. Cardiac-resynchronization therapy in heart failure with a narrow QRS complex. N Engl J Med 2013;369:1395–405. https://doi.org/10.1056/NEJMoa1306687
11. Køber L TJ, Nielsen JC, Haarbo J, et al. Defibrillator implantation in patients with nonischemic systolic heart failure. N Engl J Med 2016;375:1121–30. https://doi.org/10.1056/NEJMoa1608029
12. Lund LH, Claggett B, Liu J, Lam CS, et al. Heart failure with mid-range ejection fraction in CHARM: characteristics, outcomes and effect of candesartan across the entire ejection fraction spectrum. Eur J Heart Fail 2018(20):1230–9. https://doi.org/10.1002/ejhf.1149
13. Hudson S PS. What is ‘normal’ left ventricular ejection fraction? Heart 2020;106:1445–6. http://doi.org/10.1136/heartjnl-2020-317604
14. Woolley RJ CD, Ouwerkerk W, Tromp J, et al. Machine learning based on biomarker profiles identifies distinct subgroups of heart failure with preserved ejection fraction. Eur J Heart Fail 2021;23:983–91. https://doi.org/10.1002/ejhf.2144
15. Uijl A SG, Vaartjes I, Dahlström U, et al. Identification of distinct phenotypic clusters in heart failure with preserved ejection fraction. Eur J Heart Fail 2021;23:973–82. https://doi.org/10.1002/ejhf.2169
16. Wehner GJ JL, Haggerty CM, Suever JD, et al. Routinely reported ejection fraction and mortality in clinical practice: where does the nadir of risk lie? Eur Heart J 2020;41:1249–57. https://doi.org/10.1093/eurheartj/ehz550
17. Angermann CE AB, Anker SD, Asselbergs FW, et al. Pulmonary artery pressure-guided therapy in ambulatory patients with symptomatic heart failure: the CardioMEMS European Monitoring Study for Heart Failure (MEMS-HF). Eur J Heart Fail 2020;22:1891–901. https://doi.org/10.1002/ejhf.1943
18. Sammour Y SJ, Austin A, Magalski A, et al. Outpatient management of heart failure during the COVID-19 pandemic after adoption of a telehealth model. JACC: Heart Failure 2021;9:916–24. https://doi.org/10.1016/j.jchf.2021.07.003
19. Reed M.E. HJ, Graetz I, et al. Patient characteristics associated with choosing a telemedicine visit vs office visit with the same primary care clinicians. JAMA Netw Open 2020(e205873). https://doi.org/10.1001/jamanetworkopen.2020.5873
20. Jones RC PD, Ryan D, Sims EJ, et al. Opportunities to diagnose chronic obstructive pulmonary disease in routine care in the UK: a retrospective study of a clinical cohort. Lancet Respir Med 2014;2:267–76. https://doi.org/10.1016/S2213-2600(14)70008-6
21. Bottle A KD, Aylin P, et al. Routes to diagnosis of heart failure: observational study using linked data in England. Heart 2018;104:600–5. http://doi.org/10.1136/openhrt-2018-000935
22. Cosgrove GP BP, Danese S, Lederer DJ. Barriers to timely diagnosis of interstitial lung disease in the real world: the INTENSITY survey. BMC Pulm Med 2018;18:9. https://doi.org/10.1186/s12890-017-0560-x
23. Horton R. Offline: COVID-19 is not a pandemic. Lancet 2020;396:874. https://doi.org/10.1016/S0140-6736(20)32000-6
24. Shepperd S BC, Cradduck-Bamford A, Ellis G, et al. Is comprehensive geriatric assessment admission avoidance hospital at home an alternative to hospital admission for older persons? Ann Intern Med 2021;174:889–98. https://doi.org/10.7326/M20-5688