Approach
Goals of treatment of chronic heart failure (HF) are to:
Alleviate symptoms
Delay progression
Reduce mortality
The following recommendations cover management of chronic HF with reduced ejection fraction (EF<40%) or mildly reduced ejection fraction (EF 41% to 49%).
For details of management of acute exacerbation of HF, please see Acute heart failure.
For details of management of patients with preserved ejection fraction (EF ≥50%), please see Heart failure with preserved ejection fraction.
General principles of therapy
Recommended initial therapies include:[7][9][122]
Renin-angiotensin system inhibitors (angiotensin receptor-neprilysin inhibitor [ARNi], ACE inhibitor, or angiotensin-II receptor antagonist)
Beta-blockers
Aldosterone antagonists
Sodium-glucose cotransporter-2 (SGLT2) inhibitors
For most patients with HF with reduced ejection fraction (HFrEF), a combination of drugs from all four of these medication classes should be started and continued long term.[7][9][122] Medications may be started simultaneously or sequentially. Patients who have signs of congestion and volume overload will need diuretics.
Additional therapies, including implantable devices, may be considered in selected patients.
Lifestyle changes
The success of pharmacological therapy is strongly related to, and greatly enhanced by, encouraging the patient and his/her family to participate in various complementary non-pharmacological management strategies. These mainly include lifestyle changes, dietary and nutritional modifications, exercise training, and health maintenance.[123]
In patients with HF, cardiac rehabilitation and exercise training improves functional status, exercise tolerance, and quality of life, with decreased morbidity and mortality.[124][125][126][127][128][129][130][131][132] Patients with stable HF who are able to participate are therefore encouraged to do regular exercise and enrol in a cardiac rehabilitation programme.[7][9]
[ 
]
There is developing evidence to support home-based cardiac rehabilitation alternatives to centre-based programmes.[133][134][135]
Dietary sodium intake is an easily modifiable factor that complements pharmacological therapy for HF. There is limited evidence for restriction of sodium in patients with HF; however, guidelines recommend that excessive sodium intake should be avoided.[7][9][122][136]
Management of comorbidities
Screening and treatment of common comorbidities, such as chronic kidney disease (CKD), atrial fibrillation (AF), iron deficiency, hypertension, sleep disorders, diabetes, and coronary artery disease (CAD) is an important factor in the management of patients with HF.[7][9] Consult your local drug information source for details of cautions, contraindications, and dose adjustments that may be required in the presence of comorbid conditions.
See below for more information on management of HF with specific comorbidities.
Drugs that may be harmful and should be avoided in patients with HFrEF include: non-dihydropyridine calcium-channel blockers (e.g., diltiazem, verapamil); class IC antiarrhythmics (e.g., propafenone, flecainide) and dronedarone; thiazolidinediones (e.g., rosiglitazone, pioglitazone); dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g., alogliptin, linagliptin, saxagliptin, sitagliptin); and non-steroidal anti-inflammatory drugs (NSAIDs).[7]
Initial drug treatments
Diuretics
All patients with symptoms and signs of congestion should receive diuretics, irrespective of the left ventricular ejection fraction (LVEF). In patients with reduced LVEF, diuretics should always be used in combination with other guideline-directed medical therapy (e.g., ARNi or ACE inhibitor or angiotensin-II receptor antagonist, beta-blocker, aldosterone antagonist, and SGLT2 inhibitor [see below for details on use]).[7][9]
Loop diuretics used for the treatment of HF and congestion include furosemide, bumetanide, and torasemide. The most commonly used agent appears to be furosemide, but some patients may respond more favourably to another loop diuretic.[137] In resistant cases, loop diuretics should be combined with a thiazide diuretic (e.g., hydrochlorothiazide) or a thiazide-like diuretic (e.g., metolazone, indapamide).
Loop diuretics and thiazide diuretics differ in their pharmacological actions. Loop diuretics increase excretion of up to 20% to 25% of the filtered load of sodium, enhance free-water clearance, and maintain their efficacy unless renal function is severely impaired. In contrast, thiazide diuretics increase the fractional excretion of sodium to only 5% to 10% of the filtered load, tend to decrease free-water clearance, and lose their effectiveness in patients with impaired renal function (i.e., creatinine clearance less than 40 mL/minute).
Careful monitoring of renal function and electrolytes is essential. The minimum dose of diuretic should be used to relieve congestion, keep the patient asymptomatic, and maintain a dry weight. Some patients may be able to come off the diuretics completely, but they need very close long-term follow-up.
ARNi
In the PARADIGM-HF trial, in patients with HFrEF (New York Heart Association [NYHA] class II to IV) and ejection fraction of 40% or less (which was later changed to an ejection fraction of 35% or less), sacubitril/valsartan (a combination of a neprilysin inhibitor and an angiotensin-II receptor antagonist, or ARNi) was superior to enalapril in reducing mortality and HF hospitalisation.[138] In this study, the ejection fraction was 29 ± 6.1% in the sacubitril/valsartan group and 29.4 ± 6.3% in the enalapril group.[138] Meta-analyses have found that sacubitril/valsartan significantly reduces clinical outcomes such as all-cause mortality, cardiovascular mortality, and hospitalisations for heart failure, especially among patients with reduced EF.[139][140][141] Sacubitril/valsartan has also been found to improve a patient's physical and social activities compared with enalapril.[142]
The American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Failure Society of America (HFSA) guidelines recommend sacubitril/valsartan for all patients with HFrEF and NYHA class II to III symptoms, in preference to an ACE inhibitor or angiotensin-II receptor antagonist, because of improvement in morbidity and mortality.[7]
European guidelines recommend sacubitril/valsartan as a replacement for an ACE inhibitor in patients with HFrEF who remain symptomatic despite optimal treatment with an ACE inhibitor, a beta-blocker, an aldosterone antagonist, and a sodium-glucose cotransporter-2 (SGLT2) inhibitor, to reduce the risk of hospitalisation and death.[9]
Guidelines advise that use of an ARNi may be considered in patients with mildly reduced ejection fraction (HFmrEF) to reduce risk of HF hospitalisation and cardiovascular mortality.[7][9]
Concomitant administration of an ARNi with an ACE inhibitor, or within 36 hours of the last dose of an ACE inhibitor, is not recommended.[7]
ACE inhibitors
ACE inhibitors have been shown to decrease the morbidity and mortality associated with HFrEF. US guidelines recommend the use of ACE inhibitors when use of ARNi is not feasible in patients with HFrEF.[7] European and UK guidelines recommend ACE inhibitors in all patients with HFrEF unless contraindicated or not tolerated.[9][122]
Guidelines advise that use of an ACE inhibitor may be considered in patients with HFmrEF to reduce risk of HF hospitalisation and cardiovascular mortality.[7][9][143]
When using an ACE inhibitor and beta-blocker for HF, in practice most physicians start an ACE inhibitor first and then add a beta-blocker; the origin of this practice is historical, as the benefits of ACE inhibitors were demonstrated 10 years before those of beta-blockers. Also, most large-scale studies of beta-blockers were conducted using ACE-inhibitor therapy as comparator or standard. If a patient cannot tolerate target doses of both an ACE inhibitor and a beta-blocker when these drugs are co-administered, it is preferable to co-administer lower doses of both drugs than to reach the target dose in one class and not be able to initiate the other.
Beta-blockers
Beta-blockers have also been shown to decrease the morbidity and mortality associated with HF.[7][9][122] All patients with HFrEF receive a beta-blocker, unless there is a contraindication based on bradycardia, reactive airway disease, and unstable or low-output HF.[7][9][122] They are initiated at low doses and titrated to target dosages.[7][9][122][144]
Patients with sinus rhythm: one meta-analysis found that, irrespective of pre-treatment heart rate, beta-blockers reduced mortality in patients with HFrEF in sinus rhythm.[145] Achieving a lower heart rate is associated with better prognosis for patients in sinus rhythm. Mortality was lower for patients in sinus rhythm randomised to beta-blockers (hazard ratio: 0.73 vs. placebo; 95% confidence interval [CI] 0.67 to 0.79; P <0.001), regardless of baseline heart rate (interaction P = 0.35).
Patients with atrial fibrillation: the same meta-analysis found that beta-blockers had no effect on mortality in patients with atrial fibrillation (hazard ratio: 0.96; 95% CI 0.81 to 1.12; P = 0.58) at any heart rate (interaction P = 0.48).[145] However, this was a retrospective analysis and authors commented that background therapy, including devices, may have changed since these trials were conducted and that the heart rate was not measured in a standardised fashion across the trials. In a randomised trial of patients with atrial fibrillation and HFrEF, during a median follow-up of 37 months, beta-blockers were associated with significantly lower all-cause mortality (hazard ratio: 0.721; 95% CI 0.549 to 0.945; P = 0.0180) but not hospitalisation (hazard ratio: 0.886; 95% CI 0.715 to 1.100; P = 0.2232).[146] The result of this study supports the evidence-based recommendations for beta-blockers in patients with HFrEF, whether or not they have associated atrial fibrillation.
Although adverse effects can include bradycardia, worsening of reactive airway disease, and worsening HF, these can often be avoided by careful patient selection, dose titration, and close monitoring. [
]
Clinical improvement may be delayed and may take 2-3 months to become apparent. However, long-term treatment with beta-blockers can lessen the symptoms of HF and improve clinical status.Guidelines advise that evidence-based beta-blockers for HFrEF may be considered in patients with HFmrEF to reduce risk of HF hospitalisation and cardiovascular mortality.[7][9][143]
Angiotensin-II receptor antagonists
Angiotensin-II receptor antagonists are considered a reasonable alternative to an ARNi or an ACE inhibitor in patients with HFrEF who are intolerant of ACE inhibitors because of cough or angio-oedema and when use of ARNi is not feasible.[7][9][122][147] Experience with these drugs in controlled clinical trials of patients with HF is considerably less than that with ACE inhibitors. Nevertheless, valsartan and candesartan have demonstrated benefit by reducing hospitalisations and mortality.[7][148]
Guidelines advise that use of an angiotensin-II receptor antagonist may be considered in patients with HFmrEF to reduce risk of HF hospitalisation and cardiovascular mortality.[7][9][143]
The addition of an angiotensin-II receptor antagonist to the combination of an ACE inhibitor and an aldosterone antagonist is not recommended in patients with HF, because of the increased risk of renal dysfunction and hyperkalaemia.[9]
Aldosterone antagonists
Aldosterone antagonists (sometimes known as mineralocorticoid receptor antagonists) such as spironolactone and eplerenone are recommended in patients with HFrEF to reduce mortality and morbidity.[7][9]
Guidelines advise that use of an aldosterone antagonist may be considered in patients with HFmrEF to reduce risk of HF hospitalisation and cardiovascular mortality.[7][9][143]
Spironolactone and eplerenone can both cause hyperkalaemia, and precautions should be taken to minimise the risk; regular monitoring of serum potassium and renal function is recommended.[7][9] In the EPHESUS trial, the addition of eplerenone to standard care did not increase the risk of hyperkalaemia when potassium was regularly monitored.[149]
SGLT2 inhibitors
An SGLT2 inhibitor (e.g., dapagliflozin, empagliflozin) is recommended, in addition to optimal medical therapy with a renin-angiotensin system inhibitor, a beta-blocker, and an aldosterone antagonist, for patients with HFrEF regardless of diabetes status.[7][9][150][151][152]
SGLT2 inhibitors are also recommended for patients with HFmrEF, to reduce HF hospitalisations and cardiovascular mortality.[7][143][153][154]
Two key randomised controlled trials, DAPA-HF and EMPEROR-Reduced, compared dapagliflozin and empagliflozin, respectively, with placebo in patients with NYHA class II, III, or IV HF, LVEF ≤40%, and on guideline-directed medical therapy (GDMT).[155][156] In both trials, the risk of worsening HF or death from cardiovascular causes was lower among those who received an SGLT2 inhibitor than among those who received placebo, regardless of the presence or absence of diabetes.[150][157][158][159][160][161][162][163] SGLT2 inhibitors also slowed the rate of renal function decline in patients with and without diabetes and reduced levels of uric acid.[156][164][165][166][167] In the EMPEROR-Reduced trial, the benefit of empagliflozin on major heart failure events was seen in patients across the spectrum of baseline kidney function.[168] Effects were sustained for 1-3 years of treatment and reversed after withdrawal.[169]
The DELIVER trial found that dapagliflozin reduced the combined risk of worsening HF or cardiovascular death among patients with HF and a mildly reduced or preserved ejection fraction, both in those with and without history of recent HF hospitalisation, across the spectrum of baseline kidney function and glycaemic range, and regardless of the duration of heart failure.[170][171][172][173][174][175][176][177][178][179] The effects were also similar regardless of background diuretic use, and dapagliflozin was also associated with a reduced likelihood of diuretic initiation.[180] Overall health status, as reported by KCCQ, was improved with dapagliflozin.[181][182] Improvements in symptoms, physical function, and quality of life were larger in patients with the greatest level of frailty.[183] In a pooled analysis of DELIVER and DAPA-HF trials, the response to dapagliflozin was similar between men and women across the range of EF.[184] Another pooled analysis found that the benefit of dapagliflozin was consistent irrespective of gout, and dapagliflozin use was associated with a reduction in the initiation of new treatments for hyperuricaemia and gout.[185] Pooled analysis from the DEFINE-HF and PRESERVED-HF trials found that dapagliflozin produced significant improvements in symptoms and physical limitations across the full range of EF.[186]
Meta-analyses have shown that SGLT2 inhibitors reduce the risk of cardiovascular death and hospitalisations for HF in a broad range of patients with HF.[187][188][189][190][191][192][193][194][195][196] In one meta-analysis of 15 randomised trials involving 20,241 patients with HF, SGLT2 inhibitors significantly reduced all-cause and cardiovascular mortality compared with placebo, and the composite of cardiovascular mortality or hospitalisations/urgent visits for HF was reduced with SGLT2 inhibitors across subgroups of sex, age, race, eGFR, functional class, and ejection fraction.[188] Another meta-analysis found that in HFpEF and HFmrEF, SGLT2 inhibitors, ARNi, and aldosterone antagonists were associated with a significant decrease in the risk of heart failure hospitalisation compared with placebo, with SGLT2 inhibitors the optimal drug class in terms of reducing the risk for heart failure hospitalisation. Combining data from three randomised controlled trials (PRESERVED-HF, DEFINE-HF [Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure], and CHIEF-HF [A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure]) found that treatment with an SGLT2 inhibitor resulted in health status improvements for both black and white patients with heart failure.[197] One meta-analysis looking at adverse events found that SGLT2 inhibitor use was not associated with a clinically relevant risk of hypotension and volume depletion, and the risk of acute kidney injury was reduced.[198]
Additional treatments
Hydralazine and nitrates
The addition of a combination of hydralazine and a nitrate is reasonable for patients with reduced LVEF who have persistent symptoms despite receiving optimal medical therapy, and it has demonstrated benefit in black patients with HF.[199][200]
Guidelines recommend considering the combination of hydralazine and isosorbide dinitrate for black patients with NYHA class III to IV HFrEF receiving optimal medical therapy to improve symptoms and reduce morbidity and mortality.[7][9][122]
The combined use of hydralazine and isosorbide dinitrate may also be considered as a therapeutic option in symptomatic patients who cannot receive renin-angiotensin system inhibitors because of intolerance or contraindications; consultation with a specialist is advised.[7][9]
Ivabradine
Ivabradine can be considered for patients with stable, symptomatic chronic HF with LVEF ≤35%, who are in sinus rhythm with a resting heart rate ≥70 beats per minute (UK National Institute for Health and Care Excellence guidelines advise ≥75 beats per minute) and are either on a maximum dose of a beta-blocker or have a contraindication to beta-blockers.[7][9][122]
One meta-analysis found that addition of ivabradine to standard HF therapy was associated with cardiac function improvement, reduction on worsening HF readmission, greater HR reduction, and better exercise capacity in chronic HFrEF patients, but it was not associated with a reduction in cardiovascular mortality or improvement in quality of life.[201] One Cochrane review concluded that long‐term treatment with ivabradine in patients with HFrEF does not reduce cardiovascular mortality or rate of serious adverse events compared with placebo/usual care/no treatment.[202]
Digoxin
Digoxin can be beneficial in patients with current or prior symptoms of HF or reduced LVEF, especially those with atrial fibrillation. When added to ACE inhibitors, beta-blockers, and diuretics, digoxin can reduce symptoms, prevent hospitalisation, control rhythm, and enhance exercise tolerance.[203] Digoxin reduces the composite end point of mortality or hospitalisations in ambulatory patients with chronic HF with NYHA class III or IV symptoms, LVEF <25%, or cardiothoracic ratio of >55% and should be considered in these patients.[204]
Digoxin reduces the composite end point of mortality or hospitalisations, but does not reduce all-cause mortality.[204] Digoxin should be used cautiously with plasma level monitoring. One meta-analysis suggests that digoxin use in patients with HF is associated with a higher risk of all-cause mortality.[205]
One systematic review and meta-analysis of observational and controlled trial data showed that digoxin has a neutral effect on mortality in randomised trials and reduces hospital admissions.[206]
Vericiguat
Vericiguat, an oral soluble guanylate cyclase stimulator, may be considered in selected high-risk patients with HFrEF and NYHA class II-IV symptoms, who have had worsening HF despite treatment with an ACE inhibitor or ARNi, a beta-blocker, and an aldosterone antagonist, to reduce the risk of cardiovascular mortality or HF hospitalisation.[7][9]
Omega-3 polyunsaturated fatty acid (PUFA)
In patients with NYHA class II to IV symptoms and HF who are already on GDMT and other evidence-based therapies, omega-3 PUFA supplementation may be reasonable to use as adjunctive therapy to reduce mortality and cardiovascular hospitalisations.[7]
Vasopressin antagonists
Use of vasopressin antagonists such as tolvaptan can be considered for patients with symptomatic or severe hyponatraemia (<130 mmol/L) and persistent congestion despite standard therapy, to correct hyponatraemia and related symptoms.[7][9]
Cardiac implantable devices
Device therapy with implantable cardioverter-defibrillator (ICD) or cardiac re-synchronisation therapy (CRT) should be considered in selected patients to reduce mortality and morbidity.
ICDs have been shown to decrease mortality in patients with HF, both ischaemic and non-ischaemic, by reducing risk of sudden cardiac death. The SCD-Heft trial enrolled patients who had left ventricular dysfunction and no prior history of syncope or sustained ventricular tachycardia, and included patients with a prior myocardial infarction and no prior coronary artery disease. Use of ICDs led to a 23% relative mortality risk reduction at 5 years.[207]
It has been estimated that one quarter to one third of patients with HF have left bundle-branch block (LBBB): that is, manifest a QRS duration greater than 120 milliseconds (ms).[208] Patients with HFrEF who have LBBB, known as ventricular dyssynchrony, have a poorer prognosis than those without LBBB.[209] Studies have shown that, in these patients, CRT decreases hospitalisation and, when combined with an ICD, significantly reduces mortality.[210][211][212][213][214][215] In patients who have conduction delay and left ventricular dysfunction, biventricular pacemakers have been shown to improve exercise tolerance and quality of life while decreasing morbidity and mortality.[210][211][212][213][215][216][217][218] The CARE-HF study randomised patients with a widened QRS, LVEF of 35% or less, and persistent moderate or severe symptoms of HF despite pharmacological therapy, to implantation of a CRT device or not.[219] The main study observed substantial benefits on morbidity and mortality that persisted or increased with longer follow-up.[220][221][222][223][224][225][226][227][228][229][230] Reduction in mortality was due to fewer deaths from HF and from reduced sudden death.[220] Long-term data from the REVERSE study suggest that improvements in left ventricular function and remodelling can be sustained for over 5 years.[231][232]
ICDs are recommended to reduce sudden cardiac death and mortality in selected patients when there is a reasonable expectation of meaningful survival for at least 1 year, LVEF is ≤35% (NYHA class II-III) or ≤30% (NYHA class I) despite GDMT, and the patient is at least 40 days post-myocardial infarction.[7][9] Specific indications vary in different countries, and guidelines should be consulted for full details.
CRT is recommended in selected patients to reduce morbidity and mortality and improve symptoms. It can be used as a pacemaker alone (CRT-P) or combined with an ICD (CRT-D). Broadly, CRT is recommended in patients with LVEF ≤35% despite GDMT, who are in sinus rhythm, with a LBBB and QRS ≥150 ms.[7][9][233] CRT should also be considered in those with LBBB and QRS ≥120-149 ms or those with a non-LBBB pattern and QRS ≥150 ms. Again, specific indications vary in different countries, and guidelines should be consulted for full details.
Advanced heart failure
Patients with indicators of advanced HF require timely referral to specialist care to assess suitability for management options that may include cardiac transplantation, mechanical circulatory support, and palliative care.[7][9][234]
Early referral is important so options may be offered before development of end-organ dysfunction. US guidelines note that the acronym I-Need-Help can help in identifying patients for referral:[7][235]
I: intravenous inotropes
N: New York Heart Association (NYHA) class IIIB/IV or persistently elevated natriuretic peptides
E: end-organ dysfunction
E: ejection fraction ≤35%
D: defibrillator shocks
H: hospitalisations >1
E: oedema despite escalating diuretics
L: low systolic blood pressure ≤90, high heart rate
P: prognostic medication; progressive intolerance or down-titration of GDMT.
Inotropic support:
Intravenous inotropic support may improve haemodynamic compromise, increasing cardiac output, and maintaining perfusion. In patients with advanced HF refractory to optimal medical and device therapy, prolonged inotropic support may be used as a bridge to long-term mechanical circulatory support or cardiac transplant.[7]
Continuous intravenous inotropic support may also be considered as palliative therapy for the relief of symptoms in patients without other treatment options.[7][9]
Mechanical circulatory support (MCS):
MCS helps to maintain sufficient end organ perfusion by unloading the heart. Temporary MCS, such as percutaneous and extracorporeal ventricular assist devices, may be used in patients with advanced HF and haemodynamic compromise or shock as a bridge to recovery or bridge to decision about future care.[7][9] Long-term MCS, such as a durable left ventricular assist device (LVAD), is considered in carefully selected patients who have end-stage HF despite optimal medical and device therapy, or dependence on intravenous inotropes or temporary MCS, either as a bridge to transplantation or as destination therapy (permanent pump implantation in patients not eligible for cardiac transplantation).[7][9][236][237]
Some of the absolute contraindications for providing durable mechanical support include irreversible hepatic, renal, and neurological disease, medical non-adherence, and severe psychosocial limitations.[238]
Cardiac transplantation:
Cardiac transplantation significantly improves quality of life and functional status and is the established treatment for eligible patients with advanced HF refractory to optimal medical and device therapy.[7][9]
Palliative and supportive care:
Palliative and supportive care should be provided to all patients with HF to improve quality of life, and this care intensifies as disease progresses to advanced and end-of-life stages.[7][9]
Palliative and supportive care is a multidisciplinary approach that includes high-quality communication, discussion of prognosis, shared decision-making, advance care planning, relief from pain and other distressing symptoms, attention to emotional, psychological, and spiritual aspects of care, and support for families and carers during illness and bereavement.[7][9]
Considerations for management of specific comorbidities
Anaemia/iron-deficiency:
In patients with HFrEF or HFmrEF and iron deficiency (ferritin level <100 nanograms/mL or 100 to 300 nanograms/mL, with transferrin saturation <20%) with or without anaemia, intravenous iron supplementation is recommended to improve symptoms and quality of life.[7][9][143] European guidelines also recommend considering intravenous iron supplementation to reduce risk of HF hospitalisation.[143]
Meta-analyses have shown an association between intravenous iron supplementation and lower rates of recurrent cardiovascular hospitalisations and mortality.[239][240][241] One prospective randomised trial in the UK (IRONMAN) found that in patients with HFrEF and iron deficiency, intravenous iron supplementation was associated with a lower risk of hospitalisation and cardiovascular death.[242] Another randomised trial (HEART-FID) found no significant difference between intravenous iron supplementation and placebo for the composite endpoint of death, hospitalisations for heart failure, or 6-minute walk distance.[243]
Oral iron is not recommended. The IRONOUT HF trial found that oral iron does not adequately treat iron deficiency anaemia in patients with HFrEF.[244]
Due to a lack of benefit and an increased risk of adverse events such as stroke, erythropoietin-stimulating agents are not recommended for the treatment of anaemia in patients with HF.[7]
For more details on management, see Iron-deficiency anaemia (Management approach).
AF:
AF and HF may cause or exacerbate each other and the relationship is complex. HF therapies should be optimised. Beta-blockers may be used in HFrEF whether or not the patient has associated AF.[145][146] Treatment of AF involves correction of the abnormal rate/rhythm, along with anticoagulation. Options for rate and rhythm control are determined by the presence of HF and extent of LV dysfunction.[7][9]
For details of management of patients with AF and HF, see Established atrial fibrillation (Management approach).
Hypertension:
Treatment of HFrEF is similar in patients with and without hypertension.[9] Recommended medicines for HF also lower BP; however, HF guidelines note that clinical trials assessing the impact of BP reduction on outcomes in patients with hypertension and HF are lacking and that the optimal BP goal and antihypertensive regimen are not known.[7][9]
The 2022 AHA/ACC/HFSA guidelines suggest that in patients with HFrEF and hypertension, guideline-directed medical therapy (GDMT) for HF can be uptitrated to the maximally tolerated target dose, to achieve blood pressure targets.[7]
In people with HF, hypertension and mild fluid retention, thiazide diuretics may be preferred over loop diuretics as they confer more persistent antihypertensive effects.
For more details on management of hypertension, see Essential hypertension (Management approach).
CKD:
The effectiveness of GDMT for HF in patients with concomitant CKD is uncertain.[245] Some drugs should be used with caution in patients with renal impairment and a dose adjustment may be required. Some drugs may also be contraindicated in patients with renal impairment. Check your local drug information source for more information.
Most patients will tolerate mild-to-moderate degrees of functional renal impairment without difficulty. Initiation of GDMT for HF with an ACE inhibitor, angiotensin-II receptor antagonist, ARNi, or SGLT2 inhibitor may result in an initial rise in serum creatinine and a drop in estimated glomerular filtration rate (eGFR), but this change is generally transient and should not necessarily be a reason for discontinuation.[9][246]
An increase in serum creatinine of <50% above baseline, up to 265 micromols/L (3 mg/dL), or a decrease in eGFR of <10% from baseline, as long as eGFR is >25 mL/minute/1.73 m², may be considered as acceptable
If the serum creatinine increases to >265 micromols/L (>3 mg/dL), the renal insufficiency can severely limit the efficacy and enhance the toxicity of established treatments.[247][248]
Aldosterone antagonists should be used with caution in patients with CKD and hyperkalaemia. US guidelines advise that they are only initiated in patients with eGFR >30 mL/minute/1.73 m² and serum potassium <5.0 mEq/L.[7]
Consultation with a nephrology specialist should be considered.
Diabetes:
Treatment of HFrEF is similar in patients with and without diabetes. SGLT2 inhibitors are recommended as first-line treatment of hyperglycaemia in patients with type 2 diabetes and HF to reduce HF-related morbidity and mortality.[7][9] See information above on SGLT2 inhibitors.
Finerenone, a non-steroidal mineralocorticoid receptor antagonist, is recommended for the prevention of HF hospitalisation in patients with CKD and type 2 diabetes.[143]
See Overview of diabetes.
Obesity:
Treatment of obesity in patients with HFrEF may improve symptoms, functional status, quality of life, and comorbidities.[38] In advanced HF, weight loss in patients with obesity may allow the option of heart transplantation (obesity may be a contraindication).
Obesity has a stronger association with HF with preserved EF, and in those patients treatment of obesity with a glucagon-like peptide-1 (GLP-1) receptor agonist have shown symptomatic benefit. More studies are needed for HFrEF.
See Obesity in adults.
Chronic coronary disease:
Patients with HF should be assessed for presence of CAD. In selected patients with CAD and HF with LVEF ≤35% and suitable coronary anatomy, surgical revascularisation in addition to GDMT may improve symptoms, cardiovascular hospitalisations, and long-term all-cause mortality.[7][9]
For more details, see Chronic coronary disease (Management approach).
Valvular heart disease (VHD):
Aortic stenosis, aortic regurgitation, mitral regurgitation, and tricuspid regurgitation are associated with adverse outcomes in patients with HF and timely management (by a multidisciplinary team with expertise in HF and VHD) is important to prevent worsening of HF.[7][9]
For more details, see Aortic stenosis (Management approach), Aortic regurgitation (Management approach), Mitral regurgitation (Management approach), Tricuspid regurgitation (Management approach).
Hyperlipidaemia:
All patients with HFrEF and hyperlipidaemia will need lifestyle modifications and most will also require treatment with a statin possibly with additional non-statin lipid-lowering therapy.
For details of management of HF with hypercholesterolaemia, see Hypercholesterolaemia (Management approach).
Thyroid disorders:
Both hypo- and hyperthyroidism are associated with HF and assessment of thyroid function is recommended.
Thyroid disorders are treated as per endocrinology guidelines; referral to endocrinologist should be considered.
Sleep disorders:
Patients with HF and daytime sleepiness may have sleep studies to assess for obstructive sleep apnoea and central sleep apnoea.[7][9]
In patients with HF and obstructive sleep apnoea, continuous positive airway pressure is recommended to improve sleep quality and reduce daytime sleepiness; however, it does not seem to reduce mortality.[7][9]
Adaptive servo-ventilation has been associated with increased mortality and is not recommended for the treatment of central sleep apnoea in patients with HFrEF.[7][9]
See Obstructive sleep apnoea in adults and Central sleep apnoea.
Depression:
Depression is common in patients with HF and is associated with a reduced quality of life and increased mortality. Treatment with conventional therapies (e.g., antidepressants) does not seem to directly improve these outcomes. However, interventions that focus on improving HF self-care (e.g., psychotherapy, nurse-led support) may reduce hospitalisation and mortality in patients with moderate or severe depression.[7][9]
See Depression in adults.
Cancer:
Patients who develop HF and/or depressed LV systolic function secondary to cancer therapy should be treated with GDMT. Generally, GDMT should not be discontinued unless there are specific and compelling reasons to hold these medicines and this should be managed by a multidisciplinary team. Before starting any cardiotoxic cancer therapy, baseline cardiac function should be measured and ongoing monitoring after completion of a course of chemotherapy may be helpful for risk stratification.[7][9]
Special consideration: amyloidosis
HF GDMT may be poorly tolerated in patients with amyloid cardiomyopathy. Tafamidis (a transthyretin stabiliser) may be considered in select patients to reduce cardiovascular morbidity and mortality.[7][9]
See Amyloidosis.
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