Addressing heart failure in primary care:
Part 2 – Initiating and optimising treatment for heart failure

Key practice points:

• Following clinical diagnosis, pharmacological treatment for patients with heart failure should immediately proceed under the assumption they have reduced left ventricular ejection fraction (HFrEF)
• Rather than sequential treatment escalation in response to symptoms, patients with heart failure should be promptly established on four guideline-directed medical therapy (GDMT) medicines and up-titrated to the highest tolerated or target dose, unless contraindicated. GDMT maximises prognostic outcomes (e.g. risk of hospitalisation and mortality) and limits disease progression. This includes:
  • An angiotensin receptor-neprilysin inhibitor (ARNI; preferred) or an ACE inhibitor/ARB if this is not possible; and
  • A beta blocker (either bisoprolol, metoprolol succinate or carvedilol); and
  • A mineralocorticoid receptor antagonist (MRA); and
  • A sodium-glucose co-transporter-2 (SGLT-2) inhibitor
• Special Authority restrictions may influence the introduction of GDMT. For example, the ARNI and SGLT-2 inhibitor cannot be initiated (funded) without patients first being established on “concomitant optimal standard chronic heart failure treatments” (among other criteria).
  • When an ARNI is introduced, stop the ACE inhibitor (or ARB) before initiating treatment due to the risk of angioedema
  • SGLT-2 inhibitors have been funded with Special Authority approval for patients with HFrEF (regardless of diabetes status) since 1^st December, 2024
• In addition to GDMT, assertive treatment with a loop diuretic is required if the patient has fluid overload. Withhold beta blocker initiation until the patient is euvolemic.
• For patients initially diagnosed in primary care, aim to achieve optimal dosing of all four GDMT medicines within three months where practically possible. If a patient is already taking a GDMT medicine, or is hospitalised for heart failure, aim for optimisation within a shorter timeframe, e.g. within six weeks.
• Regular monitoring is essential in patients with heart failure. Key short-term considerations include medicine adverse effects, clinical/symptomatic status, blood pressure, renal function and serum potassium.
  • Further BNP testing (preferably NT-proBNP) can be considered, but only if it will influence management decisions
  • Repeat echocardiography is helpful to monitor disease progression in the long-term, including consideration for further treatments, e.g. implantable cardioverter defibrillator (ICD), cardiac resynchronisation therapy (CRT) or CRT-defibrillation
• If heart failure with preserved ejection fraction (HFpEF) is confirmed based on echocardiography at any point, a cardiologist should generally be involved to refine treatment
  • HFpEF management focuses mainly on controlling fluid balance using diuretics at the lowest possible dose, in addition to managing associated co-morbidities, especially hypertension and atrial fibrillation
  • SGLT-2 inhibitors are effective in patients with HFpEF, but those with echocardiography-confirmed HFpEF are not currently eligible for Special Authority approval

The general principles of management

Once heart failure has been diagnosed, initiate pharmacological treatment as soon as practically possible:¹

Patients with acute onset of significant heart failure symptoms may require immediate hospital admission where initial treatment decisions will be made.² However, in patients with a more gradual onset of symptoms, the process can begin in primary care. In this scenario, it is unlikely that echocardiography will have been performed yet, and therefore it will not be known whether the patient has heart failure with reduced ejection fraction (HFrEF; i.e. left ventricular ejection fraction [LVEF] of ≤ 40%), mildly reduced ejection fraction (HFmrEF; i.e. LVEF 41 – 49%) or preserved ejection fraction (HFpEF; i.e. LVEF ≥ 50%).

For further information on the terminology associated with heart failure, see: Part 1 – Identifying and diagnosing heart failure

Proceed assuming the patient has HFrEF. Given that most evidence regarding effective management relates to patients with HFrEF, it is practical to initiate treatment in primary care assuming they have this subtype (see: “Guideline-directed medical therapy (GDMT): The four pillars of heart failure treatment”), and then modify the approach later on if echocardiography proves otherwise (see: “Treatment of patients with heart failure with preserved ejection fraction (HFpEF)”). The medicines used in GDMT are still likely beneficial if the patient is subsequently found to have HFpEF, and are unlikely to cause harm. For example, sodium-glucose co-transporter-2 (SGLT-2) inhibitors are recommended across international guidelines for all patients with heart failure, regardless of their associated LVEF.

A 2022 Australian study found that patients with heart failure attend general practice over 14 times each year on average (New Zealand data not available, but is reported to be similar); this indicates there is ample opportunity to not only monitor disease progression and medicine tolerance, but to further optimise treatment and improve clinical outcomes.³

Guideline-directed medical therapy (GDMT): The four pillars of heart failure treatment

Among cardiovascular conditions commonly encountered in primary care, the approach to heart failure management has perhaps undergone the most substantial changes over recent times (Figure 1A). International guidelines increasingly recommend that most patients with heart failure should be established on guideline-directed medical therapy (GDMT) – also referred to as the “four pillars” of heart failure treatment – as early as practically possible.^{4, 5} This includes optimised use of:

• An angiotensin receptor-neprilysin inhibitor (ARNI; preferred) or an ACE inhibitor/ARB if this is not possible; and
• A beta blocker (either bisoprolol, metoprolol succinate or carvedilol); and
• A mineralocorticoid receptor antagonist (MRA); and
• A sodium-glucose co-transporter-2 (SGLT-2) inhibitor

Combined use of these four medicines in patients with HFrEF reduces the relative risk of all-cause mortality by 61%, and cardiovascular mortality or heart failure hospitalisation by 64% (Figure 1B). Compared with standard ACE inhibitor/ARB and beta blocker treatment, GDMT is estimated to confer more than six additional years of life (on average) for a patient aged 55 years, or 1.4 additional years for a patient aged 80 years.⁶ Despite these benefits, and the otherwise poor prognostic outlook for patients with heart failure, GDMT is significantly underutilised in daily practice (see: “Most patients with heart failure are undertreated”).

A closer look at the treatments for patients with heart failure with reduced ejection fraction (HFrEF)

Immediately prescribe a loop diuretic if the patient has fluid overload

Patients with symptomatic heart failure often have presenting features such as shortness of breath, elevated jugular venous pressure, bibasilar crackles or peripheral oedema – all of which are caused by hypervolaemia (fluid overload).¹⁹ Persisting hypervolaemia is a marker for poor prognosis in patients with heart failure.¹⁹ Many patients hospitalised for acute heart failure are discharged while still congested.

Immediate and assertive treatment with a loop diuretic such as furosemide is a first priority for managing patients with heart failure and fluid overload:^{19, 20}

• Initially 20 – 40 mg daily
• For resistant fluid overload, up-titrate in 20 – 40 mg increments to the minimum dose that improves symptoms and achieves weight loss of approximately 1 kg/day with a return to dry body weight
• The frequency of up-titration will depend on patient response and the severity of fluid overload (weekly is common)
• The usual dose range is 40 – 240 mg daily (patients with renal impairment may require higher doses within this range, but prolonged use may further compromise renal function)

Diuretics have not been shown to improve survival in patients with heart failure and are therefore not considered one of the “pillars of heart failure treatment”. However, they significantly improve quality of life by alleviating fluid overload, which can be particularly important in severely congested patients.

Patients should initially be weighed and a “dry weight” target* established to progressively evaluate diuresis. Measure blood pressure, serum potassium and renal function throughout treatment, and ask patients about urine output.² Taper diuretic dosing over time as control is achieved to the lowest effective dose that maintains euvolemia; avoid long-term continuous treatment where possible unless patients are symptomatic.¹ Diuretics can be re-started in response to re-emerging symptoms/signs of fluid overload. Some patients may be able to self-manage diuretic dosing.

* Dry weight is the patient’s recorded/reported average weight before they began experiencing symptoms/signs of fluid overload

Other medicines for promoting diuresis

Supress the renin-angiotensin-aldosterone system (RAAS)

The RAAS regulates blood volume, electrolyte balance and systemic vascular resistance, and comprises three main components: renin, angiotensin II (derived from angiotensin I) and aldosterone.²² In a normal physiological context, these factors help maintain blood pressure and fluid balance.²² However, in heart failure, the RAAS is often overactivated as a compensatory mechanism that drives excessive vasoconstriction, sodium retention and fluid overload, contributing to increased blood pressure, worsening oedema and adverse cardiac effects, e.g. hypertrophy, fibrosis (Figure 2A).

RAAS inhibition is therefore an important early objective in patients with heart failure.²³ For decades this was achieved using ACE inhibitors or ARBs, but the development of ARNIs has since provided an alternative and more effective option (see: “Angiotensin receptor-neprilysin inhibitor (ARNI)”).²³ Special Authority funding restrictions in New Zealand for ARNIs mean that ACE inhibitors/ARBs are still often the first step for RAAS inhibition due to the requirement that patients are receiving “concomitant optimal standard chronic heart failure treatments”.¹³

ACE inhibitor and ARB treatment

ACE inhibitors reduce symptom severity and mortality in patients with HFrEF, and any option is suitable as beneficial effects are class-wide (Table 1).⁴ ARBs, such as losartan or candesartan, are an alternative if an ACE inhibitor is not tolerated (e.g. due to cough or angioedema).² Preference for an ACE inhibitor first is largely based on their wider use in clinical trials, but some guidelines do not prioritise ACE inhibitors over ARBs.⁴ If a patient is already taking an ARB (e.g. for pre-existing hypertension) there is no need for them to switch to an ACE inhibitor following a diagnosis of heart failure. Furthermore, changing from an ARB to an ARNI is more straightforward than from an ACE inhibitor to ARNI, due to the requirement for a wash out period (see next section).

Following diagnosis, ACE inhibitor/ARB treatment should be initiated at a low dose as soon as practically possible unless contraindicated (Table 1), including when symptoms of fluid overload are still present.^{1, 4, 24} A conservative approach to up-titration was previously recommended (doubling doses every two to four weeks), however, recent guidelines advocate for more assertive treatment escalation (increasing doses every one to two weeks under close supervision).⁴ In primary care, this schedule will be dictated by the capacity for regular patient review (i.e. whether appropriate monitoring can still occur with each dose change) and in many cases, fortnightly up-titration remains a reasonable strategy. Minor increases in serum creatinine and asymptomatic decreases in blood pressure are to be expected following initiation of the ACE inhibitor/ARB; if these exceed acceptable limits (Table 1), delaying up-titration (until resolution) or dose decreases may be needed.²

Angiotensin receptor-neprilysin inhibitor (ARNI)

Sacubitril + valsartan (Entresto) is the only available example in a medicine class combining an ARB with a neprilysin inhibitor (ARNI), providing a dual mechanism of action (Figure 2B). ARNI treatment is superior to ACE inhibitor/ARB use across a range of key outcomes in patients with HFrEF, including all-cause and cardiovascular death, major adverse cardiac events and hospitalisation.²⁵ ARNIs also improve markers of cardiac function such as left ventricular function (systolic and diastolic), BNP concentrations, burden of ventricular arrhythmias, as well as other clinical endpoints, e.g. quality of life, duration of hospitalisation required.⁴ As such, there is a growing consensus that immediate or early ARNI use should be prioritised for RAAS inhibition where possible, including in patients already stabilised on an ACE inhibitor/ARB.⁴

Read the evidence

Funded with Special Authority approval. Special Authority applications for sacubitril + valsartan can be made by any relevant practitioner for patients who have NYHA class II – IV symptoms and who are receiving concomitant optimal standard chronic heart failure treatments.²⁰ The criteria state that patients should either have a confirmed LVEF ≤ 35%, or if echocardiography is not practically possible, the medicine can be initiated if the clinician believes they are “likely to benefit from treatment”.²⁰

Dosing recommendations. Sacubitril + valsartan should not be initiated until at least 36 hours after the last dose of ACE inhibitor (a “wash out” period) due to the risk of angioedema.^{1, 4} A wash out period is not required for patients switching from an ARB; the ARNI can be initiated 24 hours after the last ARB dose, i.e. when the next ARB dose would have been due. There are three strengths of sacubitril + valsartan available, each prescribed twice daily (Table 1):²⁰

• 24.3 mg sacubitril/25.7 mg valsartan (rounded to 24 mg/26 mg)
• 48.6 mg sacubitril /51.4 mg valsartan (rounded to 49 mg/51 mg)
• 97.2 mg sacubitril /102.8 mg valsartan (rounded to 97 mg/103 mg)

In general, patients can be initiated on the “medium” 49 mg/51 mg dose, and up-titrated to the “high” 97 mg/103 mg dose if tolerated. The “low” 24 mg/26 mg starting dose is reserved for high risk patient groups, e.g. those with hypotension, older or frail patients, severe renal or hepatic impairment.²⁰

Monitoring considerations. Blood pressure, renal function and serum potassium should be reviewed at initiation, with each dose increase, and every three to six months once the patient is stable (in the absence of relevant risk factors; Table 1).¹ If a patient’s systolic blood pressure is < 100 mmHg at initiation, delay use until this is resolved.²⁰ Using BNP as a biomarker for treatment efficacy is not routinely recommended, but NT-proBNP (N-terminal proBNP) monitoring can be considered if necessary if this specific test is available at the local community laboratory (see: “Long-term monitoring”).

Select a beta blocker with evidence of effectiveness in heart failure

Like RAAS inhibitors, beta blockers also reduce symptom severity and mortality in patients with HFrEF.¹ These medicines help to counteract the effects of prolonged sympathetic stimulation (Figure 2A), reversing adverse left ventricular remodelling, improving the ejection fraction, in addition to their rate controlling and anti-arrhythmic properties.^{9, 27}

Bisoprolol, metoprolol succinate or carvedilol are recommended for patients with HFrEF.^{1, 4} In general, bisoprolol and carvedilol are better tolerated, and generally safe in patients with asthma/COPD. Only these beta blockers with evidence of effectiveness in heart failure should be used in patients with HFrEF,⁴ so switching is appropriate if a patient is already taking a different beta blocker for a co-morbidity.

Beta blockers should be initiated at a low dose as soon as practically possible (Table 1), but only once symptoms of acute fluid overload have resolved, if present (to improve tolerance).^{1, 4, 24} Up-titration every two weeks until the target or maximum tolerated dose is reached is usually recommended in a community setting;²⁴ general resting heart rate targets are 50 – 60 bpm for patients in sinus rhythm or < 80 bpm for those with atrial fibrillation (although international guidelines differ in their recommendations for this target).²⁸ Blood pressure, serum potassium and creatinine should also be monitored at each dose increase (Table 1). For some patients, up-titration needs to be more gradual to reduce the risk of adverse effects, and it can take longer to observe a change in symptoms.²⁴ Once beta blocker treatment is established, dose reduction or discontinuation is not needed during episodes of acute deterioration (see: “Decompensation in previously stable patients”) or fluid overload, unless there are obvious signs of hypoperfusion.^{1, 4}

Mineralocorticoid receptor antagonists (MRAs) recommended for most patients regardless of symptom severity

Aldosterone levels are frequently elevated in patients with heart failure, contributing to sodium retention (and potassium loss), sympathetic activation and myocardial fibrosis.⁹ MRAs block these effects in patients with heart failure (Figure 2A), and when added to a background of RAAS inhibition and beta blocker treatment, significantly bolster reductions in hospitalisation/cardiovascular mortality risk (Figure 1B).⁸

Given these benefits, there has been a shift from the conventional sequence of starting treatment with an ACE inhibitor/ARB and a beta blocker, and only adding a MRA if the patient remains symptomatic, to early MRA introduction regardless of heart failure severity.^{4, 5} Spironolactone is the first MRA option used (Table 1).^{1, 2} This medicine should be prescribed with caution in patients with impaired renal function and may cause hyperkalaemia; creatinine and electrolytes should therefore be monitored regularly, and patients should be advised to avoid over the counter NSAIDs.²

If spironolactone is not tolerated or the patient experiences significant anti-androgenic adverse effects, an alternative dose-equivalent MRA, eplerenone, can be prescribed with Special Authority approval, provided that the patient has a LVEF < 40%.^{20, 29} Both MRAs act on the same biological receptor, but eplerenone is more selective, and is associated with lower rates of gynaecomastia or breast tenderness which are common reasons for treatment discontinuation in males taking spironolactone.²⁹ A 2024 meta-analysis demonstrated that eplerenone is superior to spironolactone in reducing all-cause (HR = 0.78) and cardiovascular (HR = 0.54) mortality events.²⁹

Sodium-glucose co-transporter-2 (SGLT-2) inhibitors address the cardiovascular-kidney connection

There is substantial interconnectedness between the cardiovascular system and the kidneys. SGLT-2 inhibitors (e.g. empagliflozin) were initially developed for the treatment of diabetes, but are also highly effective for improving prognostic outcomes in patients with heart failure (regardless of LVEF) and protect against the progression of proteinuric renal dysfunction in patients with chronic kidney disease (which is common in this setting; Figure 2C).

Read the evidence

SGLT-2 inhibitors are taken at one specified dose in patients with heart failure, without the need for up-titration (Table 1).²⁰ Empagliflozin is the only SGLT-2 inhibitor available in New Zealand, funded with Special Authority approval. As of 1^st December, 2024, the empagliflozin Special Authority criteria has been widened to include patients with symptomatic HFrEF regardless of their diabetes status.³² These changes now facilitate funded delivery of the final GDMT component for patients with HFrEF in New Zealand.

Table 1. Recommendations for medicine use in patients with HFrEF or an undifferentiated clinical diagnosis of heart failure. See Figure 1 for further information. N.B. If the target dose cannot be achieved, aim for the highest tolerated dose.^{1, 4, 20}

Monitoring the effectiveness of treatment

Monitoring patients with newly diagnosed heart failure is influenced by multiple factors, including their baseline clinical status and co-morbidities, the presentation setting (i.e. community versus hospital) and profile of medicines introduced. In some cases, patients may already be taking some GDMT medicines, whereas others may require the introduction of several within a short timeframe. A unifying principle is that assessment should be more intensive initially, and then gradually relaxed as clinical improvements and treatment optimisation occurs.

Short-term monitoring

Patients with newly diagnosed heart failure who do not require hospitalisation should initially be reviewed at least weekly.^{4, 11} Key monitoring requirements include:^{1, 4}

• Medicine-specific adverse effects (see Table 1 and NZF)
• Changes in symptoms and signs (particularly congestion), exercise tolerance and the associated impact on daily activities
• Blood pressure
• Routine laboratory tests, e.g. electrolytes, renal function. There is some evidence from the STRONG-HF trial that NT-proBNP testing may assist decision-making when undertaking assertive GDMT up-titration (i.e. at one week post-initiation), but this is not routinely recommended in primary care.³⁷

Review can progress to every two weeks once the clinical situation improves and initial progress with GDMT has been made. In patients who required hospitalisation, close follow up is particularly important during the first six weeks post-discharge to reduce the risk of re-hospitalisation and death.^{4, 11}

Adverse effects should be expected with GDMT, and occur in 75 – 80% of patients.³⁸ However, a meta-analysis suggests that overall reported rates across RCTs are not substantially different between intervention and placebo arms;³⁸ this may reflect the significant impact heart failure has on general health, rather than effects solely attributable to specific medicines.³⁸ Renal impairment and/or hyperkalaemia are common barriers to the initiation and up-titration of GDMT.⁴ In patients with hyperkalaemia, educate about the importance of a low potassium diet and prioritise introducing a SGLT-2 inhibitor (alleviates high potassium).⁴

The cumulative blood pressure lowering effects of GDMT medicines may be a limiting factor when trying to achieve target doses, particularly in older frail patients.⁴ However, unless blood pressure is < 90 – 100/60 mmHg (or there is evidence of orthostatic hypotension, hypoperfusion or low output) and all other potential causes have been excluded, low blood pressure alone should not be a reason to withhold GDMT.⁷ In addition, a potentially paradoxical effect for ARNIs, beta blockers and MRAs on blood pressure has been noted in clinical trials depending on the patients initial blood pressure, where:^40–42

• Blood pressure reduces in patients who at the start of treatment have systolic measurements > 135 – 140 mmHg
• Blood pressure gradually increases in patients who at the start of treatment have systolic measurements < 105 – 110 mmHg

Long-term monitoring

Most patients with stable heart failure on optimised GDMT dosing can be reviewed every three to six months in primary care.⁴ However, certain patients may require more frequent follow up, e.g. those who are frail or at increased risk of decompensation.

Repeat echocardiography is recommended to assess structural and functional cardiac changes in the long-term for patients receiving treatment, e.g. three to six months after medicine titration has been completed.⁴ Many patients diagnosed with HFrEF who are treated using GDMT can achieve a LVEF > 40%.⁴ This approach allows for further decisions regarding the use of advanced treatments (see: “Beyond primary care”), and further imaging may be considered based on the patient-specific symptoms and characteristics. N.B. While the frequency of echocardiography should depend on clinical indication, the timing of access may be influenced by region-specific resource availability.

If BNP levels were substantially elevated at diagnosis, monitoring for decreases can be considered as a further marker of treatment efficacy. However, serial measurements are not routinely recommended in the setting of chronic heart failure and decreases may not occur in all patients.⁴ BNP monitoring is likely only suitable if it will influence management decisions, particularly if there is uncertainty about the cause of a change in symptoms, e.g. whether improvement in shortness of breath is due to the changing status of COPD or heart failure. If serial BNP testing is done for any reason, do not repeat tests within two weeks, and ideally request no more than four tests per year.⁴³

Additional medicines to consider based on patient co-morbidities

Digoxin. Consider digoxin if patients have heart failure associated with atrial fibrillation and symptoms cannot be adequately controlled with a beta blocker.^{1, 2} There is some evidence digoxin may improve symptoms and reduce the rate of hospitalisation, however, it does not improve survival.¹ If digoxin is used, lower doses (e.g. 62.5 – 125 micrograms once daily) are generally recommended;^{2, 21} there is evidence that mortality is significantly higher in patients with serum levels ≥ 1.2 ng/ml.²¹ Monitoring of digoxin serum levels is not routinely required and treatment effect is assessed based on the patient’s heart rate. If serum digoxin needs to be investigated to rule out high or toxic levels (e.g. significant adverse effects), consider assessment after four weeks, aiming for levels of 0.5 – 0.9 ng/mL.²

Anticoagulants. An anticoagulant should be considered in patients with heart failure associated with atrial fibrillation who are at risk of stroke.¹ The CHA₂DS₂-VASc is a recommended tool to assess stroke risk.

Intravenous iron. Anaemia is common in patients with heart failure and often occurs as a result of iron deficiency; other potential causes include vitamin B12 and folate deficiency or chronic kidney disease.¹ Iron deficiency can also occur without anaemia.¹ After addressing any reversible causes, e.g. blood loss, consider iron replacement for patients with heart failure who have serum ferritin levels < 100 micrograms/L, or serum ferritin levels 100 – 300 micrograms/L and transferrin saturation (TSAT) < 20%.^{1, 2} Conventional thresholds for diagnosing iron deficiency (usually serum ferritin ≤ 20 micrograms/L) are not reliable in patients with heart failure as this condition involves a systemic inflammatory state and ferritin levels become elevated in response to inflammation.⁴⁴ Oral iron supplementation has minimal benefit in such patients.¹ Instead, administering intravenous iron is often preferred in patients with heart failure who are iron deficient and correction can improve symptoms, exercise tolerance and reduce the risk of hospitalisation, as well as improve quality of life outcomes.^{1, 2}

N.B. Ferric carboxymaltose (Ferinject) is suitable for administration in primary care and is funded with Special Authority approval for patients with anaemia or iron deficiency anaemia who meet specific criteria. As of January, 2025, patients with iron deficiency alone are not eligible for funded treatment in primary care but some PHOs may offer funding for select patients. See the Special Authority form for the most recent criteria as this may change over time.

Treatment of patients with heart failure with a preserved ejection fraction (HFpEF)

The prognosis for patients with HFpEF is less well defined compared with HFrEF. Evidence suggests morbidity outcomes (e.g. hospitalisation rates, symptom severity) are similar between the two groups.⁴⁵ Patients with HFpEF have an increased risk of all-cause mortality (potentially reflecting the higher burden of co‐morbidities among this group), whereas those with HFrEF have higher rates of cardiovascular mortality.⁴⁶

Unlike HFrEF, there is minimal evidence for the effective treatment of patients with HFpEF. With the exception of SGLT-2 inhibitor treatment, trials investigating GDMT in these patients have not demonstrated the same level of efficacy.¹³ If at any point echocardiography results demonstrate that the patient has HFpEF, seek cardiology advice which will guide further treatment decisions (if not already detailed on the echocardiography report).

General principles of management for patients with HFpEF includes:^{2, 5}

• Loop diuretic at the lowest possible dose if the patient has fluid overload
• Management of co-morbidities, e.g. atrial fibrillation, ischaemic heart disease, hypertension, diabetes
• Non-pharmacological management strategies (see: “Non-pharmacological changes to support treatment success”)
• ARB (rather than ACE inhibitor) and/or beta blocker as required without the need to maximise the dose. Diltiazem and verapamil can be considered as an alternative to beta blockers for rate control (these are contraindicated in patients with HFrEF). ARNIs are a possible alternative to ARBs, however, patients may not be eligible for funded treatment (see: “Angiotensin receptor-neprilysin inhibitor (ARNI)”)
• MRA can be considered to reduce the risk of hospitalisation
• SGLT-2 inhibitor, but Special Authority restrictions may limit access (see below, and: “Sodium-glucose co-transporter-2 (SGLT-2) inhibitors address the cardiovascular-kidney connection”)

Medicine selection depends on underlying co-morbidities (and optimisation should be directed by a cardiologist), but ideally should include a SGLT-2 inhibitor; international guidelines strongly advocate for their use in all patients with HFpEF without contraindications.^{5, 11, 13} However, despite demonstrated benefits, patients with HFpEF (i.e. LVEF ≥ 50%) are not eligible for initial SGLT-2 inhibitor (empagliflozin) Special Authority approval unless the application is submitted prior to imaging confirmation (i.e. an echocardiogram is “not reasonably practical, and in the opinion of the treating practitioner the patient would benefit from treatment”). Patients with echocardiography-confirmed HFpEF not already established on a SGLT-2 inhibitor may wish to consider self-funding treatment, but this will be a barrier to access for some patients.

Non-pharmacological changes to support treatment success

Lifestyle advice and education are important to improve the outcomes of pharmacological treatment in all patients with heart failure, regardless of the subtype.²

This includes:^{1, 2, 4}

• Understanding appropriate action(s) to take if symptoms worsen
• Regular exercise as appropriate/tolerated
• Reducing daily sodium intake (preferably < 3 g daily; no more than 5 g daily)

Read the evidence

The SODIUM-HF trial demonstrated that a strict low sodium diet of < 1.5 g daily did not reduce the risk of a composite endpoint including cardiovascular-related admission to hospital, cardiovascular-related emergency department visit, or all-cause death in patients with heart failure compared with those receiving “general advice to restrict dietary sodium” (N.B. This comparator group is therefore still sodium restricted).⁴⁷ However, modest improvements in patient-reported quality of life and clinician-assessed NYHA functional class were identified in the low sodium group.⁴⁷

• Weight loss if the patient is overweight
• Consuming an adequate but not excessive amount of fluid, e.g. 1.5 – 2 L daily
• Reducing alcohol intake and smoking cessation, if relevant
• Encouraging influenza, pneumococcal and COVID-19 vaccination (these infections can be a significant cause of decompensation); people with congestive heart failure are eligible for funded annual influenza vaccination

Beyond primary care

The journey for patients with heart failure can vary substantially. For patients who remain symptomatic despite optimal medicine use, or who require frequent secondary care involvement, additional options to improve survival include surgery or device management, e.g. with an implantable cardioverter defibrillator, cardiac resynchronisation therapy (CRT) or CRT-defibrillation.²

Consider referral to a cardiologist to discuss these advanced procedures for patients with:²

• LVEF persistently < 40% or high symptom burden even with GDMT
• Valvular heart disease, or other forms of confirmed underlying cardiac pathology
• Heart failure and syncope – insertion of a pacemaker may be required
• Heart failure and left bundle branch block, with a wide QRS complex on ECG associated with ventricular dyssynchrony – CRT may be indicated
• A history of cardiac arrest or ventricular tachycardia – defibrillator therapy may be indicated

Despite advances in pharmacological, surgical and device interventions over time, fewer than one in five patients hospitalised for heart failure are alive ten years later (mean survival following first hospitalisation for those aged 75 – 84 years = 2.87 years).⁴⁸ If patients with advanced heart failure continue to experience deteriorating and distressing symptoms when treated, the focus may need to shift from prevention of disease progression to improving quality of life outcomes in a palliative care setting. Given that this can be a confronting topic, it is important to introduce the concept as early as possible during a shared discussion between the patient, family/whānau or carer, cardiologist and primary care team.² Through this approach, patients can progressively evaluate and convey when they feel the time is right to make this transition.

For further information on advance care planning, see: www.hqsc.govt.nz/our-programmes/advance-care-planning/