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W2181350280 abstract "Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians and other healthcare providers in selecting the best management strategies for a typical patient, suffering from a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines are no substitutes for textbooks. The legal implications of medical guidelines have been discussed previously. A great number of Guidelines and Expert Consensus Documents have been issued in recent years by the European Society of Cardiology (ESC) as well as by other societies and organizations. Because of the impact on clinical practice, quality criteria for development of guidelines have been established in order to make all decisions transparent to the user. The recommendations for formulating and issuing ESC Guidelines and Expert Consensus Documents can be found on the ESC Web Site in the guidelines section (www.escardio.org). In brief, experts in the field are selected and undertake a comprehensive review of the published evidence for management and/or prevention of a given condition. A critical evaluation of diagnostic and therapeutic procedures is performed, including assessment of the risk–benefit ratio. Estimates of expected health outcomes for larger societies are included, where data exist. The level of evidence and the strength of recommendation of particular treatment options are weighed and graded according to pre-defined scales, as outlined in Tables 1 and 2. The experts of the writing panels have provided disclosure statements of all relationships they may have which might be perceived as real or potential sources of conflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. Any changes in conflict of interest that arise during the writing period must be notified to the ESC. The Task Force report was entirely supported financially by the ESC and was developed without any involvement of the industry. The ESC Committee for Practice Guidelines (CPG) supervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces, expert groups, or consensus panels. The Committee is also responsible for the endorsement process of these Guidelines and Expert Consensus Documents or statements. Once the document has been finalized and approved by all the experts involved in the Task Force, it is submitted to outside specialists for review. The document is revised, and finally approved by the CPG and subsequently published. After publication, dissemination of the message is of paramount importance. Pocket-sized versions and personal digital assistant (PDA)-downloadable versions are useful at the point of care. Some surveys have shown that the intended end-users are sometimes not aware of the existence of guidelines, or simply do not translate them into practice, so this is why implementation programmes for new guidelines form an important component of the dissemination of knowledge. Meetings are organized by the ESC, and directed towards its member National Societies and key opinion leaders in Europe. Implementation meetings can also be undertaken at national levels, once the guidelines have been endorsed by the ESC member societies, and translated into the national language. Implementation programmes are needed because it has been shown that the outcome of disease may be favourably influenced by the thorough application of clinical recommendations. Thus, the task of writing Guidelines or Expert Consensus documents covers not only the integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations. The loop between clinical research, writing of guidelines, and implementing them into clinical practice can then only be completed if surveys and registries are performed to verify that real-life daily practice is in keeping with what is recommended in the guidelines. Such surveys and registries also make it possible to evaluate the impact of implementation of the guidelines on patient outcomes. Guidelines and recommendations should help physicians and other healthcare providers to make decisions in their daily practice. However, the ultimate judgement regarding the care of an individual patient must be made by the physician in charge of his/her care. The aim of this document is to provide practical guidelines for the diagnosis, assessment, and treatment of acute and chronic heart failure (HF). These guidelines are a development and revision of guidelines published in 1995,1 1997,2 2001,3 and 2005.4,5 Much new information relating to the treatment of HF has emerged. This has necessitated a revision of some previous recommendations. The recommendations are relevant to clinical practice, epidemiological surveys, observational studies, and clinical trials. Particular attention in this revision has been given to the simplification and clarity of recommendations, and to the problems associated with implementation. The intention has been to merge and modify previous documents relating to HF. The guidelines are intended as a support for practising physicians and other healthcare professionals providing advice on how to manage these patients, including recommendations for referral. Documented and published evidence on diagnosis, efficacy, and safety of therapeutic interventions is the main basis for these guidelines. Where evidence is lacking or does not resolve a clinical issue, a consensus opinion is presented. ESC Guidelines are relevant to 51 member states with diverse economies and, therefore, recommendations based on cost-effectiveness have, in general, been avoided. National health policy as well as clinical judgement may dictate the order of priorities in implementation. The recommendations in these guidelines should always be considered in the light of national policies and local regulatory guidance on the use of any diagnostic procedure, medicine, or device. This report was drafted by a Writing Group of the Task Force (see title page) appointed by the CPG of the ESC. Within this Task Force, statements of conflicts of interests were collected, which are available at the ESC Office. The draft was sent to the CPG and the document reviewers (see title page). After consideration of their input, the document was updated, reviewed, and then approved for publication by the entire Task Force. An evidence-based approach has been used to generate the grade of any recommendation in the guidelines, with an additional assessment of the quality of the evidence. For the diagnosis of HF, evidence is incomplete. Where that is so, recommendations and statements are based on a consensus of expert opinions. Many definitions of HF have been put forward over the last 50 years.6 These highlight one or several features of this complex syndrome such as haemodynamics, oxygen consumption, or exercise capacity. In recent years, most definitions have emphasized the need for both the presence of symptoms of HF and physical signs of fluid retention.5,7–9 HF is a syndrome in which the patients should have the following features: symptoms of HF, typically shortness of breath at rest or during exertion, and/or fatigue; signs of fluid retention such as pulmonary congestion or ankle swelling; and objective evidence of an abnormality of the structure or function of the heart at rest (Table 3). A clinical response to treatment directed at HF alone is not sufficient for the diagnosis, but is helpful when the diagnosis remains unclear after appropriate diagnostic investigations. Patients with HF would usually be expected to show some improvement in symptoms and signs in response to those treatments from which a relatively fast symptomatic improvement could be anticipated (e.g. diuretic or vasodilator administration). The major and common clinical manifestations of HF are shown in Table 4. Asymptomatic structural or functional abnormalities of the heart are considered as precursors of symptomatic HF and are associated with a high mortality.10,11 Treatment is available for these conditions, when diagnosed, and for that reason these conditions are included in these guidelines. An advantage of the definition of HF used here is that it is practical and allows a more precise approach both in clinical practice and when undertaking observational surveys, epidemiological studies, or clinical trials. HF should never be a sole diagnosis. The cause should always be sought. Many additional words or phrases are used to characterize patients with HF. These terms can overlap, and physicians do sometimes use words with a slightly different meaning. The word ‘acute’ in the context of acute HF has become confusing because some clinicians use the word to indicate severity (the medical emergency of life-threatening pulmonary oedema) and others use the word to indicate decompensated, recent-onset, or even new-onset HF.4 The word is then an indicator of time rather than severity. The words acute, advanced, and decompensated should not be used interchangeably when applied to HF. A useful classification of HF based on the nature of the clinical presentation is shown in Table 5. A distinction is made between new-onset HF, transient HF, and chronic HF. New-onset HF is self-explanatory and refers to the first presentation. Transient HF refers to symptomatic HF over a limited time period, although long-term treatment may be indicated. Examples would be patients with mild myocarditis from which recovery is near complete, patients with a myocardial infarction (MI) who need diuretics in the coronary care unit but in whom long-term treatment is not necessary, or transient HF caused by ischaemia and resolved by revascularization. Worsening HF on a background of chronic HF (decompensation) is by far the most common form of HF leading to hospital admission, accounting for 80% of cases. Treatment should be based on the clinical presentation for which specific therapy is indicated (e.g. pulmonary oedema, hypertension emergency, acute MI). A distinction is frequently made between systolic and diastolic HF.12,13 The distinction is somewhat arbitrary.14–16 Patients with diastolic HF have symptoms and/or signs of HF and a preserved left ventricular ejection fraction (LVEF) >40–50%.17 There is no consensus concerning the cut-off for preserved EF. The EF is the stroke volume divided by the end-diastolic volume for the relevant ventricular chamber of the heart and is therefore largely determined by the end-diastolic volume of the ventricular chamber (i.e. a dilated heart). An EF below or above 40%, distinguishes between large or normal left end-diastolic ventricular volumes. The distinction has arisen largely because in the past most patients admitted to hospitals for investigation or entered into clinical trials have had dilated hearts with a reduced EF <35 or 40%. Most patients with HF have evidence of both systolic and diastolic dysfunction at rest or on exercise. Diastolic and systolic HFs should not be considered as separate entities.18 Other phrases have been used to describe diastolic HF, such as HF with preserved ejection fraction (HFPEF), HF with normal ejection fraction (HFNEF), or HF with preserved systolic function (HFPSF). We have elected to use the abbreviation HFPEF in this document. Many other phrases have been used in describing patients with HF that do not have aetiological significance. Forward and backward HF are old terms used to express the concept that perfusion of tissue and an increase in the left atrial pressure can under some circumstance such as acute HF and cardiogenic shock contribute to the pathophysiology.19,20 Preload and afterload are terms linked to the left and/or right atrial pressures (often reflecting volume overload) and the work of the myocardium (often reflecting pressure overload or high impedance). However, measures of these parameters are often imprecise. Right and left HF refer to syndromes presenting predominantly with congestion of the systemic or pulmonary veins, leading to signs of fluid retention with ankle swelling or pulmonary oedema, respectively. The most common cause of right ventricular failure is a raised pulmonary artery pressure due to failure of the LV leading to poor perfusion of the kidney, retention of salt and water, and accumulation of fluid in the systemic circulation. High and low output HF refer to the observation that a number of specific medical conditions lead to a clinical picture which mimics the signs and symptoms of HF. Common causes of high output states mimicking HF are anaemia, thyrotoxicosis, septicaemia, liver failure, arteriovenous shunts, Paget's disease, and beri-beri. In these conditions, the primary abnormality is not disease of the heart and the conditions are reversible with treatment. The conditions are better labelled as HF secondary to circulatory high output conditions and are important because they are treatable and should be excluded when diagnosing HF. Mild, moderate, or severe HF is used as a clinical symptomatic description, where mild is used for patients who can move around with no important limitations of dyspnoea or fatigue, severe for patients who are markedly symptomatic and need frequent medical attention, and moderate for the remaining patient cohort. Two classifications (Table 6) of the severity of HF are commonly employed. One is based on symptoms and exercise capacity [the New York Heart Association (NYHA) functional classification21,22]. The NYHA functional classification has proved to be clinically useful and it is employed routinely in most randomized clinical trials. The other describes HF in stages based on structural changes and symptoms. All patients with overt HF are in stages C and D.7 Much is now known about the epidemiology of HF.23–27 The ESC represents countries with a population of >900 million, and there are at least 15 million patients with HF in those 51 countries. The prevalence of asymptomatic ventricular dysfunction is similar, so that HF or asymptomatic ventricular dysfunction is evident in ~4% of the population. The prevalence of HF is between 2 and 3% and rises sharply at ~75 years of age, so the prevalence in 70- to 80-year-old people is between 10 and 20%. In younger age groups HF is more common in men because the most common cause, coronary heart disease, occurs in earlier decades. In the elderly, the prevalence is equal between the sexes. The overall prevalence of HF is increasing because of the ageing of the population, the success in prolonging survival in patients suffering coronary events, and the success in postponing coronary events by effective prevention in those at high risk or those who have already survived a first event (secondary prevention).28,29 In some countries the age-adjusted mortality from HF is falling at least in part due to modern treatment.28,30–32 The mean age of patients with HF in the community in developed countries is 75 years. HFPEF is more common in the elderly, women, and those with hypertension or diabetes. HF is the cause of 5% of acute hospital admissions, is present in 10% of patients in hospital beds, and accounts for ~2% of national expenditure on health, mostly due to the cost of hospital admissions.33 Substantial under-reporting is probably due to clinicians' preference for aetiological diagnoses (e.g. aortic stenosis) or the diagnosis of a major co-morbidity (e.g. diabetes). The outlook is, in general, gloomy, although some patients can live for many years.23,29,34,35 Overall 50% of patients are dead at 4 years. Forty per cent of patients admitted to hospital with HF are dead or readmitted within 1 year. Studies show that the accuracy of diagnosis of HF by clinical means alone is often inadequate, particularly in women, the elderly, and the obese.36,37 HFPEF (EF >45–50%) is present in half the patients with HF. The prognosis in more recent studies has been shown to be essentially similar to that of systolic HF.38,39 There are only a limited number of ways in which the function of the heart can be affected. The most common causes of functional deterioration of the heart are damage or loss of heart muscle, acute or chronic ischaemia, increased vascular resistance with hypertension, or the development of a tachyarrhythmia such as atrial fibrillation (AF). Coronary heart disease is by far the most common cause of myocardial disease, being the initiating cause in ~70% of patients with HF.28,40 Valve disease accounts for 10% and cardiomyopathies for another 10% (Table 7). A cardiomyopathy is a myocardial disorder in which the heart muscle is structurally and functionally abnormal [in the absence of coronary artery disease (CAD), hypertension, valvular disease, or congenital heart disease] sufficient to cause the observed myocardial abnormality.41 A classification of the cardiomyopathies has been published recently by the Working Group on Myocardial and Pericardial Diseases of the ESC.41 The American Heart Association has issued a scientific statement.42 Both take into account the great advances made recently in understanding the genetic origins and the biology of the cardiomyopathies. The European proposal was guided by the relevance of the new classification to everyday clinical practice and maintains the previously defined morpho-functional phenotypes which are further subdivided into familial/genetic and non-familial/non-genetic forms. The European classification abandoned the older distinction between ‘primary’ and ‘secondary’ cardiomyopathies, and does not include ion channelopathies among cardiomyopathies. In 1933 Sir Thomas Lewis wrote in his textbook on heart disease that ‘The very essence of cardiovascular medicine is the recognition of early heart failure’.43 The symptoms and signs of HF are the key to early detection because that is what causes patients to seek medical attention. Taking a good history and careful physical examination are skills, which are essential to master (Table 8). Breathlessness, tiredness, and fatigue are the characteristic symptoms, but eliciting and assessing these symptoms particularly in the elderly requires experience and skill.44–46 The clinical signs of HF (Table 9) should be assessed in a careful clinical examination, including observation, palpation, and auscultation.47–51 Like symptoms, the signs of early HF can be difficult to interpret, not only in elderly patients, but also in the obese. The clinical suspicion of HF must then be confirmed by more objective tests particularly targeting assessment of cardiac function. The origins of the symptoms of HF are not fully understood.52–55 Increased pulmonary capillary pressure is undoubtedly responsible for pulmonary oedema and shortness of breath in the context of acute HF with evidence of fluid overload. In contrast, studies conducted during exercise in patients with chronic HF demonstrate only a weak relationship between capillary pressure and exercise performance. HF is a condition which eventually results in pathology in almost all body organs. Tiredness and fatigue are frequently reported symptoms, but are non-specific with multiple causes. Loss of skeletal muscle mass and strength is a late manifestation.55,56 Signals from skeletal muscle are often interpreted by the brain as breathlessness or as fatigue. This may explain why the response to treatment may be slow in patients with HF because the quality of skeletal muscle must be restored. Variation in the degree of mitral regurgitation or transitory dysrhythmia, common in HF, will also exacerbate breathlessness. There is a poor relationship between symptoms and the severity of cardiac dysfunction. Symptoms do relate more closely to prognosis if persistent after therapy and can then be used to classify the severity of HF and to monitor the effects of therapy. However, symptoms alone should not guide the optimal titration of neurohormonal inhibitors such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, or aldosterone antagonists, because these drugs impact on mortality in a manner that is not closely related to symptoms. Patients should be titrated to the optimal, tolerated dose. The severity of heart failure is most often classified using the NYHA functional classification. A more recent classification is based on both the structure of the heart and symptoms. In the context of MI, two other classifications of the severity of HF, the Killip57 and Forrester58 classifications, are used (Table 10). An algorithm for the diagnosis of HF or LV dysfunction is shown in Figure 1. The diagnosis of HF is not sufficient alone. Appropriate investigations are required to establish the cause of the HF, because although the general treatment of HF is common to most patients, some causes require specific treatments and may be correctable. Several diagnostic tests are employed routinely to confirm or rule out the diagnosis of HF (Table 11). Diagnostic tests are usually most sensitive for the detection of patients with HF and reduced EF. Diagnostic findings are often less pronounced in patients with HFPEF. Echocardiography is the most useful method for evaluating systolic and diastolic dysfunction. The following investigations are considered appropriate in patients with HF. However, the recommendations largely represent expert consensus opinion without adequate documented evidence. Level of evidence C applies unless otherwise stated. An electrocardiogram (ECG) should be performed in every patient with suspected heart failure. Electrocardiographic changes are common in patients suspected of having HF (Table 12). An abnormal ECG has little predictive value for the presence of HF. If the ECG is completely normal, HF, especially with systolic dysfunction, is unlikely (<10%). Chest X-ray is an essential component of the diagnostic work-up in heart failure. It permits assessment of pulmonary congestion and may demonstrate important pulmonary or thoracic causes of dyspnoea. The chest X-ray (in two planes) is useful to detect cardiomegaly, pulmonary congestion, and pleural fluid accumulation, and can demonstrate the presence of pulmonary disease or infection causing or contributing to dyspnoea (Table 13). Apart from congestion, findings are predictive of HF only in the context of typical signs and symptoms. Cardiomegaly can be absent not only in acute but also in chronic HF. A routine diagnostic evaluation of patients with suspected HF includes a complete blood count (haemoglobin, leukocytes, and platelets), serum electrolytes, serum creatinine, estimated glomerular filtration rate (GFR), glucose, liver function tests, and urinalysis. Additional tests should be considered according to the clinical picture (Table 14). Marked haematological or electrolyte abnormalities are uncommon in untreated mild to moderate HF, although mild anaemia, hyponatraemia, hyperkalaemia, and reduced renal function are common, especially in patients treated with diuretics and ACEI/ARB/aldosterone antagonist therapy. Appropriate laboratory monitoring is essential during the initiation, titration, and follow-up phases in patients receiving drug therapy for HF. Plasma concentrations of natriuretic peptides are useful biomarkers in the diagnosis of HF and in the management of patients with established chronic HF. Evidence exists supporting their use for diagnosing, staging, making hospitalization/discharge decisions, and identifying patients at risk for clinical events. The evidence for their use in monitoring and adjusting drug therapy is less clearly established. A normal concentration in an untreated patient has a high negative predictive value and makes HF an unlikely cause of symptoms. This may play an important role especially in primary care. High levels of natriuretic peptides despite optimal treatment indicate a poor prognosis. B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) measurements were introduced as tools for diagnosis59 and management60 of HF (Figure 1). They rise in response to an increase in myocardial wall stress. Usually, lower levels are observed in patients with preserved LV systolic function. There is no definitive cut-off value recognized for either of the two natriuretic peptides commonly assessed for the diagnosis of HF in the emergency department. Due to the relatively long half-lives of natriuretic peptides, abrupt changes in LV filling pressures may not be reflected by rapid changes in peptides. Conditions other than HF associated with elevated natriuretic peptide levels include: LV hypertrophy, tachycardia, right ventricular overload, myocardial ischaemia, hypoxaemia, renal dysfunction, advanced age, liver cirrhosis, sepsis, and infection. Obesity and treatment may decrease natriuretic peptide levels. Natriuretic peptides may also be useful in assessing prognosis prior to hospital discharge and in monitoring the effectiveness of HF therapy.61,62 Troponin I or T should be sampled in suspected HF when the clinical picture suggests an acute coronary syndrome (ACS). An increase in cardiac troponins indicates myocyte necrosis and, if indicated, the potential for revascularization should be considered and an appropriate diagnostic work-up performed. An increase in troponin also occurs in acute myocarditis. Mild increases in cardiac troponins are frequently seen in severe HF or during episodes of HF decompensation in patients without evidence of myocardial ischaemia due to ACS and in situations such as sepsis. An elevated troponin is a strong prognostic marker in HF, especially in the presence of elevated natriuretic peptides.63 HF is accompanied by an increase in various other neurohormonal markers (norepinephrine, renin, aldosterone, endothelin, arginine vasopressin). Although useful in research, evaluation of neuroendocrine activation is not required for diagnostic or prognostic purposes in individual patients. The term echocardiography is used to refer to all cardiac ultrasound imaging techniques, including pulsed and continuous wave Doppler, colour Doppler and tissue Doppler imaging (TDI). Confirmation by echocardiography of the diagnosis of heart failure and/or cardiac dysfunction is mandatory and should be performed shortly following suspicion of the diagnosis of HF. Echocardiography is widely available, rapid, non-invasive, and safe, and provides extensive information on cardiac anatomy (volumes, geometry, mass), wall motion, and valvular function. The study provides essential information on the aetiology of HF. In general a diagnosis of heart failure should include an echocardiogram. The most practical measurement of ventricular function for distinguishing between patients with systolic dysfunction and patients with preserved systolic function is the LVEF (normal >45–50%). This cut-off is somewhat arbitrary. LVEF is not synonymous with indices of contractility as it is strongly dependent on volumes, preload, afterload, heart rate, and valvular function. Stroke volume may be maintained by cardiac dilatation and increased volumes. Tables 15 and 16 present the most common echocardiographic and Doppler abnormalities in HF. Assessment of diastolic function using evaluation of the ventricular filling pattern is important for detecting abnormalities of diastolic function or filling in patients with HF. This can be the predominant functional abnormality of the heart, thus fulfilling the third component necessary for the diagnosis of heart failure. This is especially true in symptomatic patients with preserved LVEF. A recent consensus paper from the Heart Failure Association has focused on the assessment of diastolic dysfunction in HFPEF.64 There are three types of abnormal filling patterns recognized conventionally in patients in sinus rhythm. Doppler echocardiography allows estimation of the systolic pulmonary artery pressure. This is derived from calculation of the right ventricular systolic pressure estimated from the peak velocity of the tricuspid regurgitant jet velocity present in most subjects. It also permits an assessment of stroke volume and cardiac output by measurement of the velocity time integral (VTI) of the aortic flow. Echocardiography plays a major role in confirming the diagnosis of HFPEF. The diagnosis of HFPEF requires three conditions to be satisfied: Transoesophageal echocardiography (TOE) is recommended in patients who have an inadequate transthoracic echo window (obesity, ventilated patients), in complicated valvular patients (especially aortic, mitral, and mechanical valves), in suspected endocarditis, in congenital heart disease, or to exclude a thrombus in the left atrial appendage in patients with AF. Stress echocardiography (dobutamine or exercise echo) is used to detect ventricular dysfunction caused by ischaemia and to assess myocardial viability in the presence of marked hypokinesis or akinesis. It may also be useful in identifying myocardial stunning, hibernation, and in relating HF symptoms to valvular abnormalities. In patients with HF, stress echo may have a lower sensitivity and specificity due to LV dilatation or the presence of bundle branch block. In patients in whom echocardiography at rest has not provided adequate information and in patients with suspected CAD, further non-invasive imaging may include cardiac magnetic resonance imaging (CMR), cardiac CT, or radionuclide imaging. CMR is a versatile, highly accurate, reproducible, non-invasive imaging technique for the assessment of left and right ventricular volumes, global function, regional wall motion, myocardial thickness, thickening, myocardial mass and tumours, cardiac valves, congenital defects, and pericardial disease.65,66 It has become the gold standard of accurac" @default.
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W2181350280 date "2008-10-01" @default.
W2181350280 modified "2023-10-14" @default.
W2181350280 title "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008‡" @default.
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