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CLINICAL UPDATES

Non-acute heart failure management in primary care

Rachel Roskvist,

1

Kyle Eggleton,

1

Bruce Arroll,

1

Ralph Stewart

2

What you need to know

• Heart failure should be considered in any patient presenting with breathlessness in primary care

• B-type natriuretic peptide (BNP) is an important initial test for heart failure, with a negative result usefully ruling out the condition

• Heart failure encompasses various causes, many of which have specific treatment options

Heart failure is prevalent worldwide, impacts quality of life, and is associated with high morbidity and mortality. Global prevalence estimates indicate that 1-2% of adults in the developed world have known heart failure.1 2In the UK alone, almost one million people have diagnosed heart failure, placing a substantial demand on specialist cardiology services.3 Heart failure often presents in primary care, where many patients have risk factors and long term treatments are usually indicated even after symptoms have improved. This update focuses on recent evidence and changes to heart failure clinical practice guidelines, emphasising aspects most relevant to primary care.

Stages and classes of heart failure

A universal definition and novel classification system for heart failure was proposed in 2021 by the Heart Failure Society of America (HFSA), Heart Failure Association of the European Society of Cardiology (HFA-ESC), and Japanese Heart Failure Society (JHFS), and the system has been included in the recent American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Failure Society of America (HFSA) guidelines.4 5This four-stage classification system recognises two pre-heart failure stages without symptoms (stages A “at risk” and B

“pre-heart failure”) and two symptomatic stages encompassing the clinical syndrome of heart failure (stages C “symptomatic” and D “advanced”) (box 1).4 5Most guideline-directed pharmacological treatments target stages C and D, but they may also be indicated in asymptomatic patients to reduce the risk of progression to symptomatic heart failure. The New York Heart Association (NYHA) functional classification system complements this staging system and is applied to stages C and D, where the severity of symptoms can be assessed using this functional classification.

In addition, the ESC (European Society of Cardiology) and AHA/ACC/HFSA guidelines for heart failure5 6 and the universal definition proposed by the HFSA/HFA-ESC/JHFS4distinguish between patients with reduced left ventricular ejection fraction (HFrEF), those with mildly reduced (previously called

mid-range) ejection fraction (HFmrEF), and those with preserved ejection fraction (HFpEF) (box 1).

Many of the treatments discussed improve cardiac function and outcomes for heart failure with reduced left ventricular ejection fraction but have less benefit and evidence for patients with preserved ejection fraction.

Box 1: Definition and classification of heart failure Definition*

• Heart failure is

‐ A clinical syndrome with symptoms and/or signs caused by a structural and/or functional cardiac abnormality and

‐ Corroborated by elevated B-type natriuretic peptide (BNP) levels and/or objective evidence of pulmonary or systemic congestion

Stages†

Stage A: At risk—Risk factors such as coronary artery disease, diabetes, hypertension, atrial fibrillation, valvular heart disease

Stage B: Pre-heart failure—Raised BNP levels, reduced ejection fraction

Stage C: Symptomatic—Symptoms such as dyspnoea, ankle swelling, fatigue

Stage D: Advanced

New York Heart Association (NYHA) functional classification system (applied to stages C and D)

Class 1: No limitation

Class 2: Slight limitation

Class 3: Marked limitation

Class 4: Symptoms at rest

Classes by left ventricular ejection fraction

HFrEF—Heart failure with reduced ejection fraction (≤40%)

HFmrEF—Heart failure with mildly reduced ejection fraction (41-49%)

HFpEF—Heart failure with preserved ejection fraction (≥50%)

HFimpEF—Heart failure with improved ejection fraction (≤40% before treatment, >40% at follow-up)

* Universal definition proposed by the Heart Failure Society of America (HFSA), Heart Failure Association of the European Society of Cardiology (HFA-ESC), and Japanese Heart Failure Society (JHFS)4

† Stages included in guidelines from American Heart Association (AHA), American College of Cardiology (ACC), and Heart Failure Society of America (HFSA)5

Patients with heart failure, whether with preserved or reduced left ventricular ejection fraction, face high mortality and morbidity.2The differences in prognosis

1 Department of General Practice and Primary Health Care, School of Population Health, University of Auckland, New Zealand 2 Department of Medicine, School of

Medicine, University of Auckland, New Zealand

Correspondence to: B Arroll [email protected] Cite this as:BMJ 2024;384:e077057 http://dx.doi.org/10.1136/bmj-2023-077057

on 8 April 2024 at University of Auckland. Protected by copyright.http://www.bmj.com/

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between patients with preserved ejection fraction and those with reduced ejection fraction are uncertain, with conflicting evidence suggesting that preserved ejection fraction confers a lower mortality risk.2 6The prognosis for patients with mildly reduced ejection fraction is better than for those with reduced ejection fraction, provided ejection fraction does not deteriorate.6In patients with reduced ejection fraction, this may improve with medications or by treating underlying causes, and this subgroup is referred to as heart failure with improved ejection fraction (HFimpEF) (box 1). Disease modifying medications typically need to be continued for these patients, even with improved ejection fraction.4 5 7

What helps to diagnose heart failure?

Heart failure should be considered in any patient with breathlessness, which can be acute or develop slowly. Other symptoms include lower limb swelling, fatigue, abdominal discomfort, and loss of appetite. Clinical signs include an elevated jugular venous pressure, pulmonary crackles or wheeze, peripheral oedema, and a displaced cardiac apex. Cardiac auscultation may reveal a gallop rhythm or heart murmur. Signs may not manifest in patients with early stage heart failure or those undergoing treatment.6Missed diagnoses are common, particularly in those with pre-existing respiratory diseases.

Initial key investigations in primary care include an

electrocardiogram, a chest radiograph, and measurement of B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptide (box 2).5 6Other investigations to assess potential causes or comorbid diseases that may affect management include a full blood count, creatinine, urea and electrolytes, thyroid function tests, liver function tests, haemoglobin A1c, ferritin, and iron studies.6 8 9

Box 2: Key initial investigations in primary care

B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP)—A low or normal plasma BNP or NT-proBNP concentration makes heart failure unlikely.6However, BNP can be normal in some patients with heart failure with preserved ejection fraction,4 10 11and those who are obese.4 11The cut-off value for natriuretic peptide levels varies between guidelines: the National Institute for Health and Care Excellence (NICE) 2018 guidelines require higher levels than those in the ESC 2021 guidelines and may potentially miss one in five cases.12

Electrocardiogram—This is often abnormal in patients with heart failure.13It is important for determining the underlying cardiac rhythm and may provide clues to the underlying pathology.6 14

Chest x ray—This may confirm pulmonary congestion or identify other reasons for dyspnoea. However, a normal chest x ray does not rule out heart failure.13 -15

The key diagnostic investigation is an echocardiograph to determine left ventricular ejection fraction (LVEF), which represents the proportion of left ventricular volume ejected per heartbeat and guides pharmacological treatment and indications for cardiac devices.5 6 14Echocardiography, or other cardiac imaging modalities, can also evaluate cardiac structure and function and identify potential causes of heart failure. Diagnosis of heart failure with reduced or improved ejection fraction in symptomatic patients rests on the echocardiographic determination of LVEF.

The diagnosis of heart failure with preserved ejection fraction is made when there is clinical evidence (symptoms, signs) of heart failure and the LVEF is >50%. Diagnosis is supported by increased left ventricular filling pressures at rest or during exercise, structural

abnormalities such as left atrial enlargement, decreased longitudinal strain, or left ventricular hypertrophy on echocardiography or other cardiac imaging. No one feature is diagnostic, and the probability increases as the number of objective non-invasive markers (including cardiac imaging and natriuretic peptide levels) of raised left ventricular filling pressures increases.6Invasive testing provides certainty, but this has risks and is not commonly done.

Should delays in access to investigations such as echocardiography occur, a clinical diagnosis of heart failure can be made and treatment initiated (such as diuretics and potentially, as some advocate, sodium-glucose cotransporter 2 inhibitors, given their benefit across the spectrum of heart failure) before a definitive diagnosis.13Point-of-care testing of troponins and natriuretic peptides,16as well as point-of-care ultrasound scanning of the lungs8and heart17may be helpful in rural and remote prehospital settings. However, confirming the diagnosis and ascertaining LVEF are critically important to ensure longer term treatment is appropriate.5

How is heart failure managed in primary care?

Treatment of congestion

Loop diuretics are used across all subtypes of heart failure to decrease pulmonary and peripheral congestion, in both acute and chronic settings, as well as for prevention of congestion in high risk patients.8These drugs effectively alleviate congestion related symptoms, with dosing targeted to achieve euvolaemia.5However, additional management is needed to treat the cause of heart failure (where possible) or to improve cardiac function over time.5For this reason, long term heart failure management should not rely on diuretics alone.

Use of diuretics may result in electrolyte disturbances, particularly hypokalaemia. Without careful monitoring and patient education, there is a risk of over-diuresis, which might precipitate symptomatic hypotension or pre-renal acute kidney injury. Polyuria is a common and expected effect and can reduce patients’ quality of life, leading to non-adherence to therapy. Lowering the dose may be helpful, but if dose reduction is not possible the timing of administration can be adjusted, in discussion with patients, to best fit their schedule.5 14With effective, guideline-directed management, diuretic requirements may decrease, necessitating adjustments to avoid hypovolaemia. Regular review of diuretic needs and self management strategies can further optimise therapy.

What medications to consider for heart failure with reduced LVEF?

Current clinical practice guidelines agree in recommending that foundational pharmacological therapy for heart failure with reduced ejection fraction should, when possible, include a combination of drugs from four distinct classes: renin-angiotensin-aldosterone system inhibitors (RAASi), β blockers, mineralocorticoid receptor antagonists (MRA), and sodium-glucose co-transporter 2 inhibitors (SGLT2i).5 6 18 -20Each of these drug classes has been shown to reduce mortality and hospitalisations for heart failure,5 6and combination therapy provides additive benefits in improving outcomes.21Titration to target or the maximal tolerated dose is recommended. However, benefits are seen even if maximal (target) doses are not reached.22

In a network meta-analysis the most favourable combination of SGLT2i, β blockers, angiotensin receptor-neprilysin inhibitors (ARNi), and MRA greatly decreased all-cause mortality (hazard ratio 0.39 (95% confidence interval (CI) 0.31 to 0.49)) and the composite measure of cardiovascular death or first hospitalisation for heart

on 8 April 2024 at University of Auckland. Protected by copyright.http://www.bmj.com/

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failure (hazard ratio 0.36 (95% CI 0.29 to 0.46)).21Typically, these medications need to be continued long term, even if symptoms resolve and left ventricular function improves.4 5 7

Polypharmacy is often a concern in primary care, and the suggestion of combination therapy may raise alarm. However, this concern needs to be balanced against the evidence for the additive benefits described. Emerging evidence suggests that more novel agents (SGLT2i and ARNi) “work together” to improve tolerance and persistence of other medication classes, such as MRA.22 -26 Renin angiotensin system inhibitors

Patients should be offered one of the following: an

angiotensin-converting enzyme inhibitor (ACEi), an angiotensin receptor blocker (ARB), or an ARNi (a combination medication containing valsartan, an angiotensin receptor blocker, and sacubitril, a neprilysin inhibitor). These medications improve symptoms (over a few weeks to months) and exercise capacity, reduce the risk of hospitalisation for heart failure, and increase survival.27Guidelines offer mixed recommendations on which RAASi to start treatment with. The AHA/ACC/HFSA guidelines recommend ARNi as first line therapy, as do the Canadian Cardiovascular Society (CCS) guidelines.5 20The ESC guidelines recommend ARNi when symptoms persist despite optimal ACEi or ARB treatment, but suggest it can also be considered as first line therapy.6Pre-existing ACEi or ARB treatment must be stopped (with a washout period of 36 hours for ACEi) before initiating ARNi. Once commenced, withdrawal of ARNi can lead to clinical deterioration.27

Common issues include symptomatic postural hypotension, which should prompt dose reduction,22 27but this may improve with time.27 Diuretic dose adjustment may be necessary as ARNi may reduce diuretic requirements.20ACEi can cause a troublesome cough, necessitating a medication change, typically to an ARB. Other causes for cough should also be considered, particularly ongoing congestion, if the cough is nocturnal. Angioedema, a rare but serious side effect of ACEi, poses an increased risk when ACEi are used in combination with an ARNi, so their co-prescription is

contraindicated.

Mineralocorticoid receptor antagonists

Mineralocorticoid receptor antagonists (MRAs) improve symptoms over several weeks to months, reduce the risk of heart failure hospitalisation, and increase survival.27These favourable effects are probably mediated predominantly by the non-diuretic effects of aldosterone receptor blockade, which include decreasing adverse myocardial remodelling and fibrosis.28Common issues with MRAs include painful gynaecomastia with spironolactone (patients should be warned about this), often necessitating a change to eplerenone, which has a greatly reduced incidence. Hyperkalaemia is also a concern, necessitating careful monitoring of renal function and potassium levels.27 29Recommendations for monitoring suggest checking renal function and electrolytes one week after initiating or increasing the dose, then monthly for the first three months, quarterly for a year, and then every six months.30Use of MRAs should be avoided in patients with an estimated glomerular filtration rate (eGFR) of <30 mL/min/1.73 m2.20 30During an intercurrent, volume-depleting illness (such as gastroenteritis), MRAs should be withheld to prevent hyperkalaemia.

Β blockers

The β blockers metoprolol succinate, bisoprolol (β1-selective, cardioselective), or carvedilol (a non-selective β blocker with additional selective α1 receptor blockade) should be considered in all patients with reduced LVEF without contraindications.5

Importantly, the β1-selective β blockers can be safely used in most patients with chronic obstructive pulmonary disease.31These medications improve symptoms, but this may take several months.20 27They also reduce the risk of heart failure hospitalisation and increase survival.27Initiation usually requires low doses and slow up-titration, particularly after recent decompensation or with severe cardiac impairment.20A deterioration in symptoms can occur with initiation and up-titration despite long term positive benefits.

Hypotension and bradycardia are potential adverse events, and the dose should be reduced with symptomatic postural hypotension or a heart rate of less than 50 beats per minute.22

Sodium-glucose co-transporter 2 inhibitors

Sodium-glucose co-transporter 2 inhibitors (SGLT2i) improve quality of life (within weeks to a few months), reduce the risk of heart failure hospitalisation, and increase survival.27They should be considered for all patients with reduced LVEF who do not have

contraindications. This recommendation is a recent addition to ACC/AHA/HFSA (2022), ESC (2021), CCS (2021), and Australian (2022) guidance.5 6 19 20Adverse effects include urinary infections, fungal and yeast infections, and a mild lowering of blood pressure. In people with type 2 diabetes, other glucose lowering medications may need adjustment, and SGLT2i are presently not routinely recommended for patients with type 1 diabetes. Adjustment and down-titration of diuretics may be required as diuresis can be intensified.5 6 29Even though SGLT2i may worsen measured renal function in the short term, they slow the decline in renal function in the long term as well as improve other clinical outcomes.20 29 Titration is unnecessary as a single dose is recommended.

When and how are medications started for heart failure with reduced LVEF?

Initiation and titration

ACEi, ARB, ARNI and MRA act within the

renin-angiotensin-aldosterone system. Disturbances to renal function and electrolytes are possible, and monitoring of these when commencing or up-titrating medications is important. A baseline minimum eGFR of >30 mL/min/1.73 m2and blood potassium level

<5.4 mmol/L are recommended as necessary for initiation.22Some disturbances may be tolerable; for instance, the ESC guidelines suggest a creatinine rise of up to 50% above baseline, or 266 µmol/L (3 mg/dL) or an eGFR <25 mL/min/1.73 m2, whichever is the smaller, and an increased potassium level to 5.5 mmol/L are tolerable when initiating ACEi.27Elsewhere it is proposed that a 30% rise in creatinine above baseline may be tolerated, after which the drug dose must be reduced, or stopped if the rise is greater than 50%.22 30 32Strategies such as temporary discontinuation of medication can be used, but re-initiation trials when renal function improves are important.32 33

A systolic blood pressure of >100 mm Hg is recommended before starting drugs that may lower blood pressure. If such a drug is tolerated, lower blood pressure or mild symptomatic hypotension should not automatically lead to medication cessation but may warrant dose reduction. Symptomatic postural hypotension should prompt dose reduction.22In discussion with patients, strategies such as staggering medication administration or reducing other drugs without cardiovascular benefit (such as calcium channel blockers) and reviewing diuretic dose may allow continuation of these medications, which are critically important for optimal management and for the benefits of combination therapy.22 33

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Sequencing of drug initiation

Traditional guidance for initiation of these disease modifying medicines followed a sequential approach in which a drug from each class is introduced singly at low dose, with achievement of its target or maximal tolerated dose before the next drug is added (fig 1).22However, more rapid initiation of a low dose of each of the four classes of disease modifying medications is currently recommended to more rapidly achieve additive benefits with combination therapy.22Simultaneous commencement of all classes at low dose

has been suggested,34 35and other protocols have been proposed though evidence based randomised trial data is not yet available to support these (seefig 1for examples).18 35 -37The ACC/AHA/HFSA guidelines suggest the introduction and increase in dose of medications should be individualised to the patient and does not necessarily need to follow that of trial publications (the traditional sequential approach).5There is presently a gap in evidence for sequencing strategies in primary care, but both the ESC and ACC/AHA/HFSA guidelines suggest initiation and up-titration of these drugs are possible in the community in stable patients.5 6

Fig 1 | Proposed protocols for initiation and sequencing of pharmacological therapy for heart failure with reduced ejection fraction. In the traditional approach based on the major clinical trial sequences,22each drug is initiated (1) and then up-titrated to its to maximal dose or maximal tolerated dose (2) before the next drug is introduced (3), etc. In a rapid sequential approach (such as that proposed by Kittleson37) each drug is initiated at low dose stepwise every 1-2 weeks (steps 1 to 4) before the ARNi and β blocker are up-titrated (5, 6). In a rapid initiation approach (proposed Straw et al18; see also McMurray and Packer36) low dose SGLT2i and ARNi are introduced simultaneously (1) and then, a few days later, the β blocker and MRA are added (2), and the four drugs are up-titrated together (3)

Cost considerations

Β blockers, ACEi, ARB, and MRA are widely available with generic options, and provide high economic value.5ARNi and SGLT2i may be less widely available in resource-constrained health systems, and the economic value of these medications may be lower.5 However, some analyses have suggested there are cost savings to healthcare systems with ARNi,38particularly in early initiation.39 What treatments to consider for heart failure with mildly reduced LVEF?

The medications described above for heart failure with reduced LVEF should also be considered cases with mildly reduced LVEF, but the evidence base is less robust.6An exception to this is the SGLT2i. Recent trial evidence and a meta-analysis have resulted in an endorsement for this medication for management of mildly reduced LVEF in the 2023 focused update of the ESC guidelines, to reduce the risk of hospitalisation for heart failure or cardiovascular death.40

What drug management is recommended for heart failure with preserved LVEF?

Management of heart failure with preserved LVEF has until recently focused on symptom management with diuretics and managing comorbid disease, particularly hypertension (aiming for blood pressure <130/80 mm Hg, with medication choice guided by other comorbidities5), atrial fibrillation, and obesity, as well as other risk factors.5 33 41

There is now an established role for SGLT2i in the treatment of heart failure with preserved LVEF. Two recent randomised controlled trials of SGLT2i have established a benefit with reductions in a composite outcome of hospitalisations or cardiovascular mortality,42 43and a recent meta-analysis has reinforced these findings (hazard ratio 0.80 (95% CI 0.73 to 0.87)).44

The 2022 ACC/AHA/HFSA guidelines and an Australian consensus statement give a moderate strength recommendation to the use of SGLT2i in patients with heart failure with preserved LVEF, and the 2023 focused update of the ESC guidelines also endorses their use.5 19 40

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ACEi, ARB, ARNi, MRA, and β blockers have less benefit heart failure with preserved LVEF. MRA and ARB or ARNi may have a role in reducing hospitalisations, but the evidence base is limited and weak.5 45 -48Reflecting this, the strength of recommendation in the ACC/AHA/HFSA guidelines for these interventions is “weak” for patients with preserved LVEF.5

Non-pharmacological management of heart failure Psychosocial support and education for patients and family are important to improve understanding of heart failure. This includes recognising the importance of medication adherence, learning when to take action for symptoms or signs of decompensation, and addressing barriers to care.6

Exercise

Many patients with heart failure reduce physical activity, which adds to deconditioning and loss of fitness. Regular exercise improves quality of life and exercise capacity.14 49 50Supervised exercise programmes or formal cardiac rehabilitation have evidence of benefit, and, ideally, all patients should be referred for this where available.51 52

Diet

Loss of lean body mass is common in heart failure. Appetite may be poor because of gut congestion or reduced cardiac output, but it often improves with effective heart failure therapy. Patients are encouraged to consume tolerated foods to maintain body weight.6 Strict fluid restriction is no longer generally recommended for patients with stable heart failure, though avoidance of excessive

fluid intake is suggested.53This recommendation is based on limited evidence showing no significant difference in outcomes with and without fluid restriction.53The exceptions are for acute

exacerbations of heart failure, patients with hyponatraemia, or advanced heart failure; in these settings, fluid restriction should be guided by heart failure specialists.6 53

Similarly, sodium restriction is falling out of favour. A recent meta-analysis found that sodium restriction did not reduce the risk of all-cause death, hospitalisation, or a composite measure of death and hospitalisation in patients with heart failure.54Low sodium table salt alternatives should be avoided because of the potential for clinically important hyperkalaemia. Alcohol intake should not exceed general guideline recommendations and should be avoided when heart failure or comorbid diseases related to alcohol are present.6 55 56

Evidence for vitamin or other supplements (without indication) is weak and not presently recommended.56

Immunisation

Influenza vaccine is recommended, with evidence from a

meta-analysis suggesting that it leads to reduced all-cause mortality in patients with heart failure (though the evidence quality is noted to be low).57Vaccination against pneumococcal disease6and covid-1958are also recommended.

Addressing causes and contributors

Heart failure stems from diverse pathways and causes (table 1), most requiring specific treatments.5

Table 1 | Common causes of heart failure and specific treatments

Examples of specific treatments Examples

Cause*

Reduce and/or treat risk factors Coronary revascularisation with stents or surgery Previous myocardial infarction

Coronary artery disease

Control blood pressure Essential hypertension

Hypertension

Treat specific cause Secondary hypertension:

• Phaeochromocytoma

• 1° aldosteronism

Valve repair or replacement as appropriate Aortic stenosis

Mitral regurgitation Valvular disease

Rate control medication Cardioversion to sinus rhythm

Ablation Treat reversible causes Atrial origin (such as atrial fibrillation)

Arrhythmia

Medication Ablation Implantable cardiac defibrillator Ventricular origin

Cardiac resynchronisation therapy Left bundle branch block

Disease modifying therapies Septal surgery

Ablation

Treat specific cause (such as amyloidosis) Dilated

Hypertrophic Infiltrative conditions Cardiomyopathies

Avoid toxic substance Adapt cancer drugs Alcohol, methamphetamine, cancer drugs

Toxins

* This is not a comprehensive list of all causes.

Specialist cardiology assessment is usually indicated in patients with arrhythmias such as atrial fibrillation or flutter, left bundle branch block causing left ventricular dyssynchrony, or valve disease contributing to heart failure. In these patients, arrhythmia ablation, resynchronisation by pacing, or heart valve replacement or repair

respectively may be indicated. Deterioration should also prompt a review to identify new conditions or causes. Additionally, some causes have implications regarding the screening of family members (such as cardiomyopathy).

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Comorbidities such as hypertension, diabetes, atrial fibrillation, coronary artery disease, and chronic obstructive pulmonary disease may contribute to heart failure, be a part of the underlying cause, and/or make the diagnosis more difficult.2 4 59 60Optimal treatment of these is an important part of heart failure management.5 14For patients with heart failure and atrial fibrillation, oral anticoagulation is usually indicated to decrease stroke risk. Direct oral

anticoagulants are usually preferred, with dose reduction if renal function is impaired.6

Medications commonly prescribed in primary care can worsen heart failure, including non-steroidal anti-inflammatory medications, corticosteroids, tricyclic antidepressants, and α blockers. These should be avoided.5 41Medications known to decrease

cardiovascular mortality or heart failure hospitalisation should be used in preference to non-dihydropyridine calcium antagonists unless there is another specific indication.

Iron deficiency is common in chronic heart failure29and can be treated with intravenous ferric carboxymaltose. Treatment improves quality of life61and reduced a composite measure of cardiovascular mortality and hospitalisation (relative risk 0.85 (95% CI 0.77 to 0.95)) in patients with heart failure with reduced LVEF.62The benefits for patients with preserved LVEF are not yet established but are under investigation.62Notably, the definition of iron deficiency commonly used in clinical trials (serum ferritin <100 μg/L) likely differs from commonly reported cut-off values used in primary care. Oral iron therapy benefits are limited due to variable absorption and intolerance.29

Monitoring

Monitoring is important to guide treatment and detect deterioration.

Stable patients on optimal therapy should be reviewed regularly,14 including clinical evaluation of jugular venous pressure, chest and cardiac auscultation, heart rate and rhythm, and blood pressure.

Little evidence exists for the frequency of review, but some guidelines recommend a review every six months,6and this review can be undertaken in primary care.63Regular laboratory

investigations include full blood count, electrolytes, and renal function.6B-type natriuretic peptide is not recommended for routine monitoring of stable patients.6An annual electrocardiograph is recommended.5A new finding of a QRS duration over 140 milliseconds in a patient with reduced ejection fraction should prompt a referral for consideration of cardiac resynchronisation therapy.64 65

Patients can self monitor symptoms such as dyspnoea, fatigue, and pedal oedema, as well as changes in daily weight, which may reflect fluid accumulation or dehydration from excessive diuresis. Patients can be taught how to self adjust their diuretic doses and when to contact their care team.6For instance, increasing their diuretic dose if their weight increases persistently (for >48 hours) by more than 1.5-2.0 kg/day.

Covid-19 has highlighted the value of telemedicine, particularly as it provides opportunities to increase access to care without the risk of exposure to other illnesses.6Telemedicine can be useful particularly when optimising treatment, allowing for more frequent review and adjustment of medications.6A systematic review and meta-analysis of mobile health technology found interventions incorporating remote monitoring and clinical support reduced mortality and heart failure hospitalisations.66

We think that simple devices which allow patients to measure heart rate, rhythm, and blood pressure are, combined with telemedicine, useful. Healthcare systems will need to adapt to use these

technologies to fulfil their potential and manage any associated burden, particularly for primary care.

End of life considerations

The disease trajectory of heart failure patients can be difficult to predict. Death may be from progressive heart failure or occur suddenly and unexpectedly.

Many of the elements that contribute to effective care of patients with heart failure at the end of life can be initiated early on in primary care alongside other heart failure management.14 67This is particularly crucial when deterioration becomes apparent, such as following progression to advanced kidney disease, worsening hypotension requiring withdrawal or down-titration of the four pillars of medical therapy, frequent hospital admissions in the absence of clear precipitants, or diuretic resistance.

Timely conversations regarding expectations of treatment, advance care planning, assessing and relieving emotional distress and burden to patient and family, and consideration of involvement of specialist palliative care services are important roles for primary care practitioners.68 69

Sources and selection criteria

We conducted a literature search of Medline and EMBASE databases using the terms “heart failure,” “preserved ejection fraction,” “reduced ejection fraction,” and “epidemiology.” We sought further items from the reference lists of relevant articles. We also consulted the latest National Institute for Health Care Excellence (NICE) guidelines and, particularly, the recently released European Society of Cardiology and American Heart Association/American College of Cardiology/Heart Failure Society America guidelines. Further references as suggested by reviewers were also included where relevant.

Additional educational resources

• European Society of Cardiology (https://www.escardio.org/Guide- lines/Clinical-Practice-Guidelines/Acute-and-Chronic-Heart-Failure).

2021 guidelines and associated resources. The supplementary tables are particularly helpful for troubleshooting medication issues.

• BMJ best practice (https://www.bmj.com/company/bmj-re- sources/bmj-best-practice/)

• Patient Info. Articles for professionals on heart failure management and diagnosis and investigation. (https://patient.info/doctor/heart- failure-management,https://patient.info/doctor/heart-failure-diag- nosis-and-investigation)

• Heart Foundation of Australia. Articles for professionals on heart failure clinical guidelines (https://www.heartfoundation.org.au/for- professionals/clinical-guidelines-position-statements,

https://www.heartfoundation.org.au/for-professionals/heart-failure- tools-and-resources)

Information resources for patients

• Patient Info. Congestive heart failure. (https://patient.info/heart- health/heart-failure-leaflet)

• American Heart Association. Heart failure tools and resources.

(https://www.heart.org/en/health-topics/heart-failure/heart-failure- tools-resources)

• Health Navigator. Heart failure. (https://healthify.nz/health-a- z/h/heart-failure)

• British Heart Foundation. Heart failure. (https://www.bhf.org.uk/in- formationsupport/conditions/heart-failure)

• Heart Failure Matters. (https://www.heartfailurematters.org/)

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Education into practice

• Consider an audit of your current patients with heart failure with reduced ejection fraction. Are these patients receiving all four disease-modifying treatments with dosing to target or tolerance?

How were patients involved in the creation of this article?

One of our team asked a primary care patient with heart failure (preserved ejection fraction) to review a draft of the paper. He commented that clinicians should be aware that, as a patient, he had questions about management, particularly medication, and wanted information that was meaningful to him in terms of impact on his day-to-day life such as: “What symptoms (in patient friendly terminology) will it affect?” “What are the likely effects and expected onset of these (such as furosemide and its associated inconvenience of diuresis)?” This led us to revise sections related to pharmacological management and psychosocial support. In addition, one of the first reviewers was a carer of a patient with heart failure, and we incorporated their suggestions into the final version.

Contributors: BA conceived the original idea. All authors were involved in the development and planning of the manuscript. BA and RR conducted the literature search. RR oversaw the creation of the article.

All authors contributed to writing the manuscript and will act as guarantors.

Competing interests: TheBMJ has judged that there were no disqualifying financial ties to commercial companies at the time of commissioning and writing the article (https://www.bmj.com/sites/de- fault/files/attachments/resources/2016/03/16-current-bmj-education-coi-form.pdf). The authors declare the following other interests two years after commissioning and submission of the first draft: RS is a co-investigator for phase 3 randomised clinical trials on treatment of atrial fibrillation, acute coronary syndromes, and LDL cholesterol lowering (Librexis-ACS, Librexia-AF, and Victorion trials).

Provenance and peer review: Commissioned; externally peer reviewed.

1 Norhammar A, Bodegard J, Vanderheyden M, etal. Prevalence, outcomes and costs of a contemporary, multinational population with heart failure.Heart 2023;109:-56.

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