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Notably, once a person diagnosed with HIV and has started treatment they should not be retested. Testing and diagnosis of HIV-exposed infants has been a challenge. For infants and children less than 18 months of age, serological testing is not sufficient to identify HIV infection — virological testing must be provided at 6 weeks of age, or as early as birth to detect the presence of the virus in infants born to mothers living with HIV.

However, new technologies are now becoming available to perform the test at the point of care and enable return of the result on the same day to accelerate appropriate linkage and treatment initiation. HIV testing should be voluntary and the right to decline testing should be recognized. Mandatory or coerced testing by a health care provider, authority, or by a partner or family member is not acceptable as it undermines good public health practice and infringes on human rights. New technologies to help people test themselves are being introduced, with many countries implementing self-testing as an additional option to encourage HIV diagnosis.

HIV self-testing is a process whereby a person who wants to know his or her HIV status collects a specimen, performs a test and interprets the test results in private or with someone they trust. HIV self-testing does not provide a definitive HIV-positive diagnosis — instead, it is an initial test which requires further testing by a health worker. The sexual partners and drug injecting partners of people diagnosed with HIV infection have an increased probability of also being HIV-positive. WHO recommends assisted HIV partner notification services as a simple and effective way to reach these partners, many of whom are undiagnosed and unaware of their HIV exposure, and may welcome support and an opportunity to test for HIV.

Individuals can reduce the risk of HIV infection by limiting exposure to risk factors. Key approaches for HIV prevention, which are often used in combination, are listed below. Correct and consistent use of male and female condoms during vaginal or anal penetration can protect against the spread of sexually transmitted infections, including HIV. This way people learn of their own infection status and access necessary prevention and treatment services without delay.

WHO also recommends offering testing for partners or couples. Additionally, WHO is recommending assisted partner notification approaches so that people with HIV receive support to inform their partners either on their own, or with the help of health care providers. It is fatal if undetected or untreated and is the leading cause of death among people with HIV, responsible for more than 1 of 3 HIV-associated deaths.

VMMC is also regarded as a good approach to reach men and adolescent boys who do not often seek health care services.

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More than 10 randomized controlled studies have demonstrated the effectiveness of PrEP in reducing HIV transmission among a range of populations including serodiscordant heterosexual couples where one partner is infected and the other is not , men who have sex with men, transgender women, high-risk heterosexual couples, and people who inject drugs. WHO recommends PEP use for both occupational and non-occupational exposures and for adults and children. People who inject drugs can take precautions against becoming infected with HIV by using sterile injecting equipment, including needles and syringes, for each injection and not sharing drug using equipment and drug solutions.

An abnormal electrocardiogram ECG increases the likelihood of the diagnosis of HF, but has low specificity. Echocardiography is the most useful, widely available test in patients with suspected HF to establish the diagnosis. It provides immediate information on chamber volumes, ventricular systolic and diastolic function, wall thickness, valve function and pulmonary hypertension.

The information provided by careful clinical evaluation and the above mentioned tests will permit an initial working diagnosis and treatment plan in most patients. Other tests are generally required only if the diagnosis remains uncertain e. The diagnosis of HF in the acute setting is discussed in Section If all elements are normal, HF is highly unlikely and other diagnoses need to be considered. If at least one element is abnormal, plasma NPs should be measured, if available, to identify those who need echocardiography an echocardiogram is indicated if the NP level is above the exclusion threshold or if circulating NP levels cannot be assessed.

The diagnosis of HFpEF remains challenging. This section summarizes practical recommendations necessary for proper diagnosis of this clinical entity in clinical practice.

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The diagnosis of chronic HFpEF, especially in the typical elderly patient with co-morbidities and no obvious signs of central fluid overload, is cumbersome and a validated gold standard is missing. To improve the specificity of diagnosing HFpEF, the clinical diagnosis needs to be supported by objective measures of cardiac dysfunction at rest or during exercise. Objective evidence of other cardiac functional and structural alterations underlying HF for details, see below. In case of uncertainty, a stress test or invasively measured elevated LV filling pressure may be needed to confirm the diagnosis for details, see below.

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Not all of the recommended values are identical to those published in previous guidelines, because of the inclusion of new data published in recent reports, in particular by Cabarello et al. AF higher cut-offs. LAVI is increased by AF, and functional parameters of diastolic dysfunction are less well established in AF, and other cut-off values probably apply. Patients with HFpEF are a heterogeneous group with various underlying aetiologies and pathophysiological abnormalities. Cardiac imaging plays a central role in the diagnosis of HF and in guiding treatment.

Of several imaging modalities available, echocardiography is the method of choice in patients with suspected HF, for reasons of accuracy, availability including portability , safety and cost. In general, imaging tests should only be performed when they have a meaningful clinical consequence. The reliability of the outcomes is highly dependent on the imaging modality, the operator and centre experience and imaging quality.

Normal values may vary with age, sex and imaging modality. A chest X-ray is of limited use in the diagnostic work-up of patients with suspected HF. It is probably most useful in identifying an alternative, pulmonary explanation for a patient's symptoms and signs, i.

For the diagnosis of asthma or chronic obstructive pulmonary disease COPD , pulmonary function testing with spirometry is needed. The chest X-ray may, however, show pulmonary venous congestion or oedema in a patient with HF, and is more helpful in the acute setting than in the non-acute setting. Transthoracic echocardiography TTE is the method of choice for assessment of myocardial systolic and diastolic function of both left and right ventricles.

This method relies on accurate tracing of endocardial borders. In case of poor image quality, contrast agents should be used to improve endocardial delineation. Three-dimensional echocardiography of adequate quality improves the quantification of LV volumes and LVEF and has the best accuracy compared with values obtained through CMR. Doppler techniques allow the calculation of haemodynamic variables, such as stroke volume index and cardiac output, based on the velocity time integral at the LV outflow tract area. In recent years, tissue Doppler parameters S wave and deformation imaging techniques strain and strain rate have been shown to be reproducible and feasible for clinical use, especially in detecting subtle abnormalities in systolic function in the preclinical stage; however, measurements may vary among vendors and software versions.

LV diastolic dysfunction is thought to be the underlying pathophysiological abnormality in patients with HFpEF and perhaps HFmrEF, and thus its assessment plays an important role in diagnosis. Although echocardiography is at present the only imaging technique that can allow for the diagnosis of diastolic dysfunction, no single echocardiography variable is sufficiently accurate to be used in isolation to make a diagnosis of LV diastolic dysfunction. Therefore, a comprehensive echocardiography examination incorporating all relevant two-dimensional and Doppler data is recommended see Section 4.

An obligatory element of echocardiography examination is the assessment of right ventricle RV structure and function, including RV and right atrial RA dimensions, an estimation of RV systolic function and pulmonary arterial pressure.

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In laboratories with experience in three-dimensional echocardiography, when knowledge of RV volumes may be clinically important, three-dimensional measurement of RV volumes is recommended. Transoesophageal echocardiography TOE is not needed in the routine diagnostic assessment of HF; however, it may be valuable in some clinical scenarios of patients with valve disease, suspected aortic dissection, suspected endocarditis or congenital heart disease and for ruling out intracavitary thrombi in AF patients requiring cardioversion.

When the severity of mitral or aortic valve disease does not match the patient's symptoms using TTE alone, a TOE examination should be performed. CMR is acknowledged as the gold standard for the measurements of volumes, mass and EF of both the left and right ventricles. It is the best alternative cardiac imaging modality for patients with non-diagnostic echocardiographic studies particularly for imaging of the right heart and is the method of choice in patients with complex congenital heart diseases.

CMR is the preferred imaging method to assess myocardial fibrosis using late gadolinium enhancement LGE along with T1 mapping and can be useful for establishing HF aetiology. In addition, CMR allows the characterization of myocardial tissue of myocarditis, amyloidosis, sarcoidosis, Chagas disease, Fabry disease non-compaction cardiomyopathy and haemochromatosis. CMR may also be used for the assessment of myocardial ischaemia and viability in patients with HF and CAD considered suitable for coronary revascularization.

However, limited evidence from RCTs has failed to show that viability assessed by CMR or other means identified patients who obtained clinical benefit from revascularization. Clinical limitations of CMR include local expertise, lower availability and higher costs compared with echocardiography, uncertainty about safety in patients with metallic implants including cardiac devices and less reliable measurements in patients with tachyarrhythmias. Claustrophobia is an important limitation for CMR. Positron emission tomography PET alone or with CT may be used to assess ischaemia and viability, but the flow tracers N ammonia or O water require an on-site cyclotron.

Limited availability, radiation exposure and cost are the main limitations. Indications for coronary angiography in patients with HF are in concordance with the recommendations of other relevant ESC guidelines. Coronary angiography is also recommended in patients with a history of symptomatic ventricular arrhythmia or aborted cardiac arrest. Coronary angiography should be considered in patients with HF and intermediate to high pre-test probability of CAD and the presence of ischaemia in non-invasive stress tests in order to establish the ischaemic aetiology and CAD severity.

The main use of cardiac CT in patients with HF is as a non-invasive means to visualize the coronary anatomy in patients with HF with low intermediate pre-test probability of CAD or those with equivocal non-invasive stress tests in order to exclude the diagnosis of CAD, in the absence of relative contraindications.

However, the test is only required when its results might affect a therapeutic decision. The most important clinical indications for the applicability of certain imaging methods in patients with suspected or confirmed HF are shown in the recommendations table. Comprehensive assessment of patients with HF comprises, besides medical history and physical examination, including adequate imaging techniques, a set of additional diagnostic tests, i.

The major typical indications are summarized in the recommendations table for diagnostic tests in patients with HF. Although there is extensive research on biomarkers in HF e. ST2, galectin 3, copeptin, adrenomedullin , there is no definite evidence to recommend them for clinical practice. Molecular genetic analysis in patients with cardiomyopathies is recommended when the prevalence of detectable mutations is sufficiently high and consistent to justify routine targeted genetic screening.

Restrictive cardiomyopathy and isolated non-compaction cardiomyopathies are of a possible genetic origin and should also be considered for genetic testing. HCM is mostly inherited as an autosomal dominant disease with variable expressivity and age-related penetrance. There are already more than 50 genes identified that are associated with DCM.

Many genes are related to the cytoskeleton. ARVC is hereditary in most cases and is caused by gene mutations that encode elements of the desmosome. Counselling should be performed by someone with sufficient knowledge of the specific psychological, social and medical implications of a diagnosis. Determination of the genotype is important, since some forms [e. DNA analysis could also be of help to establish the diagnosis of rare forms, such as mitochondrial cardiomyopathies.

Screening of first-degree relatives for early detection is recommended from early adolescence onwards, although earlier screening may be considered depending on the age of disease onset in other family members. There is considerable evidence that the onset of HF may be delayed or prevented through interventions aimed at modifying risk factors for HF or treating asymptomatic LV systolic dysfunction see recommendations table. Many trials show that control of hypertension will delay the onset of HF and some also show that it will prolong life.

Recently, empaglifozin an inhibitor of sodium-glucose cotransporter 2 , has been shown to improve outcomes including the reduction of mortality and HF hospitalizations in patients with type 2 diabetes. Intensification of hypoglycaemic therapy to drive down glycated haemoglobin HbA1c with agents other than empagliflozin does not reduce the risk of developing HF for details see Section Although smoking cessation has not been shown to reduce the risk of developing HF, the epidemiological associations with the development of cardiovascular disease suggest that such advice, if followed, would be beneficial.

An inverse relationship between physical activity and the risk of HF has been reported. A recent meta-analysis found that doses of physical activity in excess of the guideline recommended minimal levels may be required for more substantial reductions in HF risk. Statins reduce the rate of cardiovascular events and mortality; there is also reasonable evidence that they prevent or delay the onset of HF. Obesity is also a risk factor for HF, but the impact of treatments of obesity on the development of HF is unknown. In patients with CAD, without LV systolic dysfunction or HF, ACEIs prevent or delay the onset of HF and reduce cardiovascular and all-cause mortality, although the benefit may be small in the contemporary setting, especially in patients receiving aspirin.

Recommendations to prevent or delay the development of overt heart failure or prevent death before the onset of symptoms. The goals of treatment in patients with HF are to improve their clinical status, functional capacity and quality of life, prevent hospital admission and reduce mortality.

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However, it is now recognized that preventing HF hospitalization and improving functional capacity are important benefits to be considered if a mortality excess is ruled out. The recommendations for each treatment are summarized below. Therapeutic algorithm for a patient with symptomatic heart failure with reduced ejection fraction. Green indicates a class I recommendation; yellow indicates a class IIa recommendation. For further details, see Sections 7 and 8 and corresponding web pages.

Ivabradine reduces the elevated heart rate often seen in HFrEF and has also been shown to improve outcomes, and should be considered when appropriate. The use of diuretics should be modulated according to the patient's clinical status. The recommendations given in Sections 7. Evidence-based doses of disease-modifying drugs in key randomized trials in heart failure with reduced ejection fraction or after myocardial infarction. ACEIs have been shown to reduce mortality and morbidity in patients with HFrEF 2 , 5 , — and are recommended unless contraindicated or not tolerated in all symptomatic patients.

ACEIs should be up-titrated to the maximum tolerated dose in order to achieve adequate inhibition of the renin—angiotensin—aldosterone system RAAS. There is evidence that in clinical practice the majority of patients receive suboptimal doses of ACEI. Beta-blockers reduce mortality and morbidity in symptomatic patients with HFrEF, despite treatment with an ACEI and, in most cases, a diuretic, , , , , but have not been tested in congested or decompensated patients. There is no evidence favouring the initiation of treatment with a beta-blocker before an ACEI has been started.

In patients admitted due to acute HF AHF beta-blockers should be cautiously initiated in hospital, once the patient is stabilized.

1. Preamble

An individual patient data meta-analysis of all the major beta-blocker trials in HFrEF has shown no benefit on hospital admissions and mortality in the subgroup of patients with HFrEF who are in AF. Beta-blockers should be considered for rate control in patients with HFrEF and AF, especially in those with high heart rate see Section Beta-blockers are recommended in patients with a history of myocardial infarction and asymptomatic LV systolic dysfunction to reduce the risk of death see Section 6.

MRAs spironolactone and eplerenone block receptors that bind aldosterone and, with different degrees of affinity, other steroid hormone e. Regular checks of serum potassium levels and renal function should be performed according to clinical status. Diuretics are recommended to reduce the signs and symptoms of congestion in patients with HFrEF, but their effects on mortality and morbidity have not been studied in RCTs. A Cochrane meta-analysis has shown that in patients with chronic HF, loop and thiazide diuretics appear to reduce the risk of death and worsening HF compared with placebo, and compared with an active control, diuretics appear to improve exercise capacity.

Loop diuretics produce a more intense and shorter diuresis than thiazides, although they act synergistically and the combination may be used to treat resistant oedema. However, adverse effects are more likely and these combinations should only be used with care. The aim of diuretic therapy is to achieve and maintain euvolaemia with the lowest achievable dose.

The dose of the diuretic must be adjusted according to the individual needs over time. Amiloride and triamterene should not be combined with an MRA. A new therapeutic class of agents acting on the RAAS and the neutral endopeptidase system has been developed [angiotensin receptor neprilysin inhibitor ARNI ]. The first in class is LCZ, which is a molecule that combines the moieties of valsartan and sacubitril neprilysin inhibitor in a single substance.

By inhibiting neprilysin, the degradation of NPs, bradykinin and other peptides is slowed. High circulating A-type natriuretic peptide ANP and BNP exert physiologic effects through binding to NP receptors and the augmented generation of cGMP, thereby enhancing diuresis, natriuresis and myocardial relaxation and anti-remodelling. Selective AT1-receptor blockade reduces vasoconstriction, sodium and water retention and myocardial hypertrophy.

Also, the number of African American patients, who are at a higher risk of angioedema, was relatively small in this study. There are additional concerns about its effects on the degradation of beta-amyloid peptide in the brain, which could theoretically accelerate amyloid deposition. Ivabradine slows the heart rate through inhibition of the I f channel in the sinus node and therefore should only be used for patients in sinus rhythm. There is no clear evidence to suggest the use of this fixed-dose combination therapy in all patients with HFrEF.

Evidence on the clinical utility of this combination is scanty and comes from one relatively small RCT conducted exclusively in men and before ACEIs or beta-blockers were used to treat HF. Additionally, a combination of hydralazine and isosorbide dinitrate may be considered in symptomatic patients with HFrEF who can tolerate neither ACEI nor ARB or they are contraindicated to reduce mortality.

However, this recommendation is based on the results of the Veterans Administration Cooperative Study, which recruited symptomatic HFrEF patients who received only digoxin and diuretics. This section describes treatments that have shown benefits in terms of symptomatic improvement, reduction in HF hospitalizations or both, and are useful additional treatments in patients with HFrEF.

Digoxin may be considered in patients in sinus rhythm with symptomatic HFrEF to reduce the risk of hospitalization both all-cause and HF hospitalizations , although its effect on top of beta-blockers has never been tested. In patients with symptomatic HF and AF, digoxin may be useful to slow a rapid ventricular rate, but it is only recommended for the treatment of patients with HFrEF and AF with rapid ventricular rate when other therapeutic options cannot be pursued.

A resting ventricular rate in the range of 70—90 bpm is recommended based on current opinion, although one trial suggested that a resting ventricular rate of up to bpm might still be acceptable. Digitalis should always be prescribed under specialist supervision. Given its distribution and clearance, caution should be exerted in females, in the elderly and in patients with reduced renal function.

In the latter patients, digitoxin should be preferred. Although statins reduce mortality and morbidity in patients with atherosclerotic disease, statins are not effective in improving the prognosis in patients with HFrEF. Most statin trials excluded patients with HF because it was uncertain that they would benefit. Patients with HFrEF receiving oral anticoagulation because of concurrent AF or risk of venous thromboembolism should continue anticoagulation.

Detailed information is provided in Section Similarly, there is no evidence on the benefits of antiplatelet drugs including acetylsalicylic acid in patients with HF without accompanying CAD, whereas there is a substantial risk of gastrointestinal bleeding, particularly in elderly subjects, related with this treatment. Aliskiren direct renin inhibitor failed to improve outcomes for patients hospitalized for HF at 6 months or 12 months in one study and is not presently recommended as an alternative to an ACEI or ARB.

Diltiazem and verapamil have been shown to be unsafe in patients with HFrEF. There is a variety of dihydropyridine CCBs; some are known to increase sympathetic tone and they may have a negative safety profile in HFrEF. There is only evidence on safety for amlodipine and felodipine in patients with HFrEF, and they can be used only if there is a compelling indication in patients with HFrEF. Currently, the evidence is considered insufficient to support specific guideline recommendations for other therapeutic technologies, including baroreflex activation therapy, vagal stimulation, diaphragmatic pacing , and cardiac contractility modulation; , further research is required.

Implantable devices to monitor arrhythmias or haemodynamics are discussed elsewhere in these guidelines. A high proportion of deaths among patients with HF, especially those with milder symptoms, occur suddenly and unexpectedly. Many of these are due to electrical disturbances, including ventricular arrhythmias, bradycardia and asystole, although some are due to coronary, cerebral or aortic vascular events. Treatments that improve or delay the progression of cardiovascular disease will reduce the annual rate of sudden death, but they may have little effect on lifetime risk and will not treat arrhythmic events when they occur.

ICDs are effective in preventing bradycardia and correcting potentially lethal ventricular arrhythmias. Some antiarrhythmic drugs might reduce the rate of tachyarrhythmias and sudden death, but they do not reduce overall mortality and may increase it. Compared with amiodarone treatment, ICDs reduce mortality in survivors of cardiac arrest and in patients who have experienced sustained symptomatic ventricular arrhythmias.

Although amiodarone may have reduced mortality in older trials of HF, , contemporary studies conducted since the widespread introduction of beta-blockers suggest that it does not reduce mortality in patients with HFrEF. Accordingly, an ICD is contraindicated in this time period. A wearable defibrillator may be considered if the patient is deemed to be at high risk of ventricular fibrillation, although evidence from randomized trials is lacking. Conservative programming with long delays between detection and the ICD delivering therapy dramatically reduces the risk of both inappropriate due to artefacts or AF and appropriate but unnecessary [due to self-terminating ventricular tachycardia VT ] shocks.

See the guideline on CRT for further details Section 8. ICD therapy is not recommended in patients in NYHA Class IV with severe symptoms refractory to pharmacological therapy who are not candidates for CRT, a ventricular assist device or cardiac transplantation, because such patients have a very limited life expectancy and are likely to die from pump failure.

Patients with serious co-morbidities who are unlikely to survive substantially more than 1 year are unlikely to obtain substantial benefit from an ICD. Patients should be counselled as to the purpose of an ICD, complications related to implantation and device activation predominantly inappropriate shocks and under what circumstances it might be deactivated terminal disease or explanted infection, recovery of LV function. If HF deteriorates, deactivation of a patient's ICD may be considered after appropriate discussion with the patient and caregiver s. If the ICD generator reaches its end of life or requires explantation, it should not automatically be replaced.

Treatment goals may have changed and the risk of fatal arrhythmia may be lower or the risk of non-arrhythmic death higher. It is a matter of some controversy whether patients whose LVEF has greatly improved and who have not required device therapy during the lifetime of the ICD should have another device implanted. Subcutaneous defibrillators may be as effective as conventional ICDs with a lower risk from the implantation procedure. Patients must be carefully selected, as they have limited capacity to treat serious bradyarrhythmia and can deliver neither antitachycardia pacing nor CRT.

Substantial RCTs with these devices and more data on safety and efficacy are awaited. Recommendations for cardiac resynchronization therapy implantation in patients with heart failure. CRT improves cardiac performance in appropriately selected patients and improves symptoms and well-being and reduces morbidity and mortality. The prevention of lethal bradycardia might be an important mechanism of benefit shared by all pacing devices.

Not all patients respond favourably to CRT. Patients with ischaemic aetiology will have less improvement in LV function due to myocardial scar tissue, which is less likely to undergo favourable remodelling. Several studies have shown that patients with left bundle branch block LBBB morphology are more likely to respond favourably to CRT, whereas there is less certainty about patients with non-LBBB morphology. Evidence from two IPD meta-analyses indicates that after accounting for QRS duration, there is little evidence to suggest that QRS morphology or aetiology of disease influence the effect of CRT on morbidity or mortality.

Clinical practice varies widely among countries. It is unclear whether CRT reduces the need for an ICD by reducing the arrhythmia burden or increases the benefit from an ICD by reducing mortality rates from worsening HF, leading to longer exposure to the risk of arrhythmia. This can be prevented by CRT, which might improve patient outcomes. Only two small trials have compared pharmacological therapy alone vs. CRT in patients with AF, with conflicting results.

This observation has not been confirmed in a randomized trial. Imaging tests for dyssynchrony have not yet been shown to be of value in selecting patients for CRT. The reader is directed to guidelines on pacing and CRT for recommendations on device implantation procedures.

John A. Palumbo

The value of trying to optimize AV or VV intervals after implantation using echo- or electrocardiographic criteria or blood pressure response is uncertain, but may be considered for patients who have had a disappointing response to CRT. For patients with HFrEF who remain symptomatic despite OMT and do not have an indication for CRT, new device therapies have been proposed and in some cases are approved for clinical use in several European Union EU countries but remain under trial evaluation.

Cardiac contractility modulation CCM is similar in its mode of insertion to CRT, but it involves non-excitatory electrical stimulation of the ventricle during the absolute refractory period to enhance contractile performance without activating extra systolic contractions.

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  • Most other devices under evaluation involve some modification of the activity of the autonomic nervous system ANS by targeted electrical stimulation. As new data and analyses become available, it might be possible to make recommendations for each phenotype separately. The pathophysiology underlying HFpEF and HFmrEF is heterogeneous, and they are associated with different phenotypes including diverse concomitant cardiovascular diseases e.

    However, since these patients are often elderly and highly symptomatic, and often have a poor quality of life, an important aim of therapy may be to alleviate symptoms and improve well-being. Diuretics will usually improve congestion, if present, thereby improving symptoms and signs of HF. The evidence that diuretics improve symptoms is similar across the spectrum of LVEF. Evidence that beta-blockers and MRAs improve symptoms in these patients is lacking.

    For patients in sinus rhythm, there is some evidence that nebivolol, , , digoxin, spironolactone and candesartan might reduce HF hospitalizations. For patients in AF, beta-blockers do not appear to be effective and digoxin has not been studied. Patients in AF should receive an anticoagulant to reduce the risk of thromboembolic events for details, see the ESC guidelines of AF ].

    Antiplatelet agents are ineffective for this purpose. Renal dysfunction, which is common in this population, may contraindicate or increase the risk of haemorrhage with NOACs. Whether digoxin, beta-blockers or rate-limiting CCBs, or a combination of these, should be preferred is unknown. Verapamil or diltiazem should not be combined with a beta-blocker.

    Recently, a trial of empagliflozin showed a reduction in blood pressure and body weight, probably by inducing glycosuria and osmotic diuresis. Its use was associated with a reduction in hospitalization for HF and in cardiovascular mortality. Myocardial ischaemia may contribute to symptoms, morbidity and mortality and should be considered when assessing patients. However, there is only anecdotal evidence that revascularization improves symptoms or outcome.

    Patients with angina should follow the same management route as patients with HFrEF. Patients with HFpEF and HFmrEF have impaired exercise tolerance, commonly accompanied by an augmented blood pressure response to exercise and chronotropic incompetence. Recommendations for treatment of patients with heart failure with preserved ejection fraction and heart failure with mid-range ejection fraction.

    Ambulatory electrocardiographic monitoring can be used to investigate symptoms that may be due to arrhythmias, — but evidence is lacking to support routine, systematic monitoring for all patients with HF to identify tachy- and bradyarrhythmias. There is no evidence that clinical decisions based on routine ambulatory electrocardiographic monitoring improve outcomes for patients with HF. Ambulatory electrocardiographic recording detects premature ventricular complexes in virtually all patients with HF.

    Episodes of asymptomatic, non-sustained VT are common, increasing in frequency with the severity of HF and ventricular dysfunction and indicating a poor prognosis in patients with HF, but provide little discrimination between sudden death or death due to progressive HF. AF is the most common arrhythmia in HF irrespective of concomitant LVEF; it increases the risk of thromboembolic complications particularly stroke and may impair cardiac function, leading to worsening symptoms of HF.

    Amiodarone will reduce the incidence of AF, induce pharmacological cardioversion, maintain more patients in sinus rhythm after cardioversion and may be used to control symptoms in patients with paroxysmal AF if beta-blockers fail to do so. Dronedarone is contraindicated in patients with HF and AF. If the patient has no distressing symptoms of HF, then treatment with oral beta-blockers may be initiated to provide ventricular rate control. For patients with marked congestion who nonetheless have few symptoms at rest, initial treatment with oral or intravenous i.

    For patients in haemodynamic instability, an i. Longer-term infusion of amiodarone should be given only by central or long-line venous access to avoid peripheral vein phlebitis. In patients with haemodynamic collapse, emergency electrical cardioversion is recommended see also Section A resting ventricular rate in the range of 60— bpm may be considered based on the current opinion of this Task Force, , although one trial suggested that a resting ventricular rate of up to bpm might still be acceptable, and this is currently recommended by the ESC guidelines on AF.

    Assessment of ventricular rate control from the radial pulse is not ideal, especially in patients with HF, as ventricular activation may not always generate a palpable pulse. Rate control should be documented electrocardiographically. A wearable device enables ventricular rate to be assessed during rest, exercise and sleep, but the value of routine monitoring has not yet been established. The optimal resting ventricular rate in patients with AF and HF is uncertain but may be between 60— bpm. Beta-blockers reduce ventricular rate during periods of activity, while digoxin exerts a greater effect at night.

    Rarely, ventricular rate cannot be reduced below — bpm by pharmacological means alone and AV node ablation with ventricular pacing may be considered; in this situation, for patients with HFrEF, CRT should be considered instead of conventional RV pacing. Also, if the patient is indicated for an ICD, AV node ablation with implantation of CRT-D may be a preferred option, especially if the patient has moderate to severe symptoms.

    In patients with chronic HF, a rhythm control strategy including pharmacological or electrical cardioversion has not been shown to be superior to a rate control strategy in reducing mortality or morbidity. A rhythm control strategy is probably best reserved for patients with a reversible secondary cause of AF e. The use of class I antiarrhythmic agents and dronedarone increases morbidity and mortality in patients with HF and AF and should be avoided.

    The safety and efficacy of catheter ablation in the atria and pulmonary veins PV as a rhythm control strategy in HF is at present uncertain except for tachycardia induced cardiomyopathy. Two small studies of AF ablation compared with rate control met with mixed success in terms of procedural complications and success in improving symptoms. Recommendations for a rhythm control management strategy in patients with atrial fibrillation, symptomatic heart failure NYHA Class II—IV and left ventricular systolic dysfunction and no evidence of acute decompensation. NOACs are preferred for patients with HF with non-valvular AF, as NOACs compared with vitamin K antagonists seem to be at least similarly effective and even safer less intracranial haemorrhage in patients with HF than in subjects without HF, , , although concerns exist about their safety in older patients with HF and poor renal function , [for a detailed description of the interaction between NOAC and renal function, see Heidbuchel et al.

    In patients with HF and AF who have mechanical heart valves or at least moderate mitral stenosis, only oral vitamin K antagonists should be used for prevention of thromboembolic stroke. The dabigatran dose should be reduced to mg b. A left atrial occlusion device could be considered in a patient with AF as an alternative to an oral anticoagulant who is at high-risk both of thromboembolism and of bleeding in order to avoid the risk of haemorrhage due to anticoagulation risk.

    The clinical relevance of myocardial ischaemia for the provocation of ventricular arrhythmias is uncertain, although anecdotal cases of ischaemia-induced arrhythmias exist. Randomized trials of revascularization for patients with HFrEF have not reduced overall mortality, , even in subgroups of patients with angina or myocardial ischaemia, , but further analysis did suggest a reduction in sudden deaths.

    Amiodarone often in combination with a beta-blocker may be used to suppress symptomatic ventricular arrhythmias, but it may adversely affect prognosis, especially in patients with more severe HF. Seeking the advice of the members of the HF Team with expertise in electrophysiology is recommended in patients with recalcitrant ventricular arrhythmias. For patients in AF, a reduction in the dose of beta-blockers allowing the daytime resting ventricular rate to rise to 70—90 bpm may be considered, since evidence that beta-blockers improve outcome in patients with AF is lacking.

    However, evidence is lacking to support a strategy of pacing solely to permit initiation or titration of beta-blocker therapy in the absence of a conventional pacing indication; this strategy is not recommended. When the cause of bradycardia or pauses is sinus node disease with intact AV conduction, then therapeutic strategies that avoid inducing ventricular dyssynchrony are preferred, although clinical trial evidence to support this expert opinion for patients with HF is sparse.

    The drugs used to treat co-morbidities may cause worsening of HF e. Management of co-morbidities is a key component of the holistic care of patients with HF see Section Many co-morbidities are actively managed by specialists in the field of the co-morbidity, and these physicians will follow their own specialist guidelines.

    The current guidelines will identify where the presence of HF should change the way a co-morbidity would normally be treated. This may be because either safety or efficacy may be different in the presence of HF or may simply be unknown or because of evidence of particular effects in an HF population, either beneficial or detrimental.

    HFpEF has an even higher prevalence of co-morbidities compared with HFrEF, and many of these may be instrumental in the progression of this syndrome. Beta-blockers, and in selected patients ivabradine, are effective agents for angina control, as well as an essential component of HFrEF therapy. In HFpEF patients, they may also be used for angina relief, although this has never been formally tested.

    Trimetazidine has been shown to exert some beneficial effect as an add-on to beta-blockers in patients with HF and angina. For indications for invasive coronary angiography in patients with HF, please refer to Section 5. Percutaneous and surgical revascularization are complementary approaches for symptomatic relief of angina in HFpEF, but whether these interventions improve outcomes is not entirely clear. Recent ESC guidelines on myocardial revascularization recommended coronary artery bypass grafting CABG for patients with significant left main stenosis and left main equivalent proximal stenosis of both the left anterior descending and left circumflex arteries to improve prognosis.

    Post hoc analyses from the STICH trial revealed that the presence of inducible myocardial ischaemia either on radionuclide stress test or dobutamine stress echocardiogram or angina does not identify those with worse prognosis and greater benefit from CABG over OMT. The choice between CABG and PCI should be made by the Heart Team after careful evaluation of the patient's clinical status and coronary anatomy, expected completeness of revascularization, coexisting valvular disease and co-morbidities.

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