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ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary

2002; Elsevier BV; Volume: 21; Issue: 2 Linguagem: Inglês

10.1016/s1053-2498(01)00776-8

1557-3117

Sharon A. Hunt, David W. Baker, Marshall H. Chin, Michael P. Cinquegrani, Arthur M. Feldman, Gary S. Francis, Théodore G. Ganiats, Sidney Goldstein, Gabriel Gregoratos, Mariell Jessup, R.Joseph Noble, Milton Packer, Marc A. Silver, Lynne W. Stevenson, Raymond J. Gibbons, Elliott M. Antman, Joseph S. Alpert, David P. Faxon, Valentı́n Fuster, Gabriel Gregoratos, Alice K. Jacobs, Loren F. Hiratzka, Richard O. Russell, Sidney C. Smith,

Cardiac pacing and defibrillation studies

I. IntroductionHeart failure (HF) is a major public health problem in the United States. Nearly 5 million patients in this country have HF, and nearly 500,000 patients are diagnosed with HF for the first time each year. The disorder is the underlying reason for 12 to 15 million office visits and 6.5 million hospital days each year.1O’Connell J.B Bristow M Economic impact of heart failure in the United States time for a different approach.J Heart Lung Transplant. 1993; 13: S107-S112Google Scholar During the last 10 years, the annual number of hospitalizations has increased from approximately 550,000 to nearly 900,000 for HF as a primary diagnosis and from 1.7 to 2.6 million for HF as a primary or secondary diagnosis.2Haldeman G.A Croft J.B Giles W.H Rashidee A Hospitalization of patients with heart failure National Hospital Discharge Survey, 1985 to 1995.Am Heart J. 1999; 137: 352-360Abstract Full Text Full Text PDF PubMed Scopus (460) Google Scholar Nearly 300,000 patients die of HF as a primary or contributory cause each year, and the number of deaths has increased steadily despite advances in treatment.HF is primarily a disease of the elderly.3Kannel W.B Belanger A.J Epidemiology of heart failure.Am Heart J. 1991; 121: 951-957Abstract Full Text PDF PubMed Scopus (745) Google Scholar Approximately 6% to 10% of people older than 65 years have HF,4Kannel W.B Epidemiology and prevention of cardiac failure Framingham Study insights.Eur Heart J. 1987; 8: 23-26Crossref PubMed Google Scholar) and approximately 80% of patients hospitalized with HF are more than 65 years old.2Haldeman G.A Croft J.B Giles W.H Rashidee A Hospitalization of patients with heart failure National Hospital Discharge Survey, 1985 to 1995.Am Heart J. 1999; 137: 352-360Abstract Full Text Full Text PDF PubMed Scopus (460) Google Scholar HF is the most common Medicare diagnosis-related group, and more Medicare dollars are spent for the diagnosis and treatment of HF than for any other diagnosis.5Massie B.M Shah N.B Evolving trends in the epidemiologic factors of heart failure rationale for preventive strategies and comprehensive disease management.Am Heart J. 1997; 133: 703-712Abstract Full Text Full Text PDF PubMed Scopus (471) Google Scholar The total inpatient and outpatient costs for HF in 1991 were approximately $38.1 billion, which was approximately 5.4% of the healthcare budget that year.1O’Connell J.B Bristow M Economic impact of heart failure in the United States time for a different approach.J Heart Lung Transplant. 1993; 13: S107-S112Google Scholar In the United States, approximately $500 million annually is spent on drugs for the treatment of HF.The American College of Cardiology (ACC) and the American Heart Association (AHA) first published guidelines for the evaluation and management of HF in 1995.6Williams Jr, J.F Bristow M.R Fowler M.B et al.ACC/AHA guidelines for the evaluation and management of heart failure report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure).J Am Coll Cardiol. 1995; 26: 1376-1398Abstract Full Text PDF PubMed Scopus (28) Google Scholar Since that time, a great deal of progress has been made in the development of both pharmacological and nonpharmacological approaches to treatment for this common, costly, disabling, and generally fatal disorder. For this reason, the 2 organizations believed that the time was right to reassess and update these guidelines, fully recognizing that the optimal therapy of HF remains a work in progress and that future guidelines will supersede these.The writing committee was composed of 7 members who represented the ACC and AHA, as well as invited participants from the American College of Chest Physicians, the Heart Failure Society of America, the International Society for Heart and Lung Transplantation, the American Academy of Family Physicians, and the American College of Physicians-American Society of Internal Medicine. Both the academic and private practice sectors were represented. This document was reviewed by 3 official reviewers nominated by the ACC, 3 official reviewers nominated by the AHA, 1 reviewer nominated by the Heart Failure Society of America, 1 reviewer nominated by the International Society for Heart and Lung Transplantation, 1 reviewer nominated by the American Academy of Family Physicians, 1 reviewer nominated by the National Heart Foundation of Australia, the ACC Hypertensive Disease Committee and 16 content reviewers.In formulating the present document, the writing committee decided to take a new approach to the classification of HF that emphasized both the evolution and progression of the disease. In doing so, we identified 4 stages of HF. Stage A identifies the patient who is at high risk for developing HF but has no structural disorder of the heart; Stage B refers to a patient with a structural disorder of the heart but who has never developed symptoms of HF; Stage C denotes the patient with past or current symptoms of HF associated with underlying structural heart disease; and Stage D designates the patient with end-stage disease who requires specialized treatment strategies such as mechanical circulatory support, continuous inotropic infusions, cardiac transplantation, or hospice care (see Table 1 and Fig. 1 ). Only the latter 2 stages, of course, qualify for the traditional clinical diagnosis of HF for diagnostic or coding purposes. This classification recognizes that there are established risk factors and structural prerequisites for the development of HF and that therapeutic interventions performed even before the appearance of left ventricular dysfunction or symptoms can reduce the morbidity and mortality of HF. This classification system is intended to complement but not to replace the New York Heart Association (NYHA) functional classification, which primarily gauges the severity of symptoms in patients who are in stage C or D. It has been recognized for many years, however, that the NYHA functional classification reflects a subjective assessment by a physician and changes frequently over short periods of time and that the treatments used do not differ significantly across the classes. Therefore, the committee believed that a staging system was needed that would reliably and objectively identify patients in the course of their disease and would be linked to treatments that were uniquely appropriate at each stage of their illness. According to this new approach, patients would be expected to advance from one stage to the next unless progression of the disease was slowed or stopped by treatment. This new classification scheme adds a useful dimension to our thinking about HF similar to that achieved by staging systems for other disorders (e.g., those used in the classification of cancer).TABLEStages of HFStageDescriptionExamplesAPatients at high risk of developing HF because of the presence of conditions that are strongly associated with the development of HF. Such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of HF.Systemic hypertension; coronary artery disease; diabetes mellitus; history of cardiotoxic drug therapy or alcohol abuse; personal history of rheumatic fever; family history of cardiomyopathy.BPatients who have developed structural heart disease that is strongly associated with the development of HF but who have never shown signs or symptoms of HF.Left ventricular hypertrophy or fibrosis; left ventricular dilatation or hypocontractility; asymptomatic valvular heart disease; previous myocardial infarction.CPatients who have current or prior symptoms of HF associated with underlying structural heart disease.Dyspnea or fatigue due to left ventricular systolic dysfunction; asymptomatic patients who are undergoing treatment for prior symptoms of HF.DPatients with advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions.Patients who are frequently hospitalized for HF or cannot be safely discharged from the hospital; patients in the hospital awaiting heart transplantation; patients at home receiving continuous intravenous support for symptom relief or being supported with a mechanical circulatory assist device; patients in a hospice setting for the management of HF.HF indicates heart failure. Open table in a new tab All recommendations provided in this document follow the format of previous ACC/AHA guidelines:Class I:Conditions for which there is evidence and/or general agreement that a given procedure/therapy is useful and effective.Class II:Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure/therapy.Class IIa:Weight of evidence/opinion is in favor of usefulness/efficacy.Class IIb:Usefulness/efficacy is less well established by evidence/opinion.Class III:Conditions for which there is evidence and/or general agreement that a procedure/therapy is not useful/effective and in some cases may be harmful.The recommendations listed in this document are evidence based whenever possible. Pertinent medical literature in the English language was identified through a series of computerized literature searches (including Medline and EMBASE) and a manual search of selected articles. References selected and published in this document are representative but not all-inclusive.The levels of evidence on which these recommendations are based were ranked as level A if the data were derived from multiple randomized clinical trials, level B when data were derived from a single randomized trial or nonrandomized studies, and level C when the consensus opinion of experts was the primary source of recommendation. The strength of evidence does not necessarily reflect the strength of a recommendation. A treatment may be considered controversial although it has been evaluated in controlled clinical trials; conversely, a strong recommendation may be based on years of clinical experience and be supported only by historical data or by no data at all.The committee elected to focus this document on the prevention of HF, as well as the evaluation and management of chronic HF in the adult patient with left ventricular systolic and diastolic dysfunction. It specifically did not consider acute HF, which might merit a separate set of guidelines and which is addressed in part in the ACC/AHA guidelines for the management of patients with acute myocardial infarction.7Ryan T.J Antman E.M Brooks N.H et al.1999 update: ACC/AHA guidelines for the management of patients with acute myocardial infarction a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction).J Am Coll Cardiol. 1999; 34: 890-911Abstract Full Text Full Text PDF PubMed Scopus (726) Google Scholar We have also excluded HF in children, both because the underlying causes of HF in children differ from those in adults and because none of the controlled trials of treatments for HF have included children. We have not considered the management of HF due to primary valvular disease (see ACC/AHA guidelines on management of patients with valvular heart disease)8Bonow R.O Carabello B de Leon Jr, A.C et al.Guidelines for the management of patients with valvular heart disease: executive summary a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease).Circulation. 1998; 98: 1949-1984Crossref PubMed Scopus (812) Google Scholar or congenital malformations, and we have not included recommendations for the treatment of specific myocardial disorders (e.g., hemochromatosis, sarcoidosis, or amyloidosis).The ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult were approved for publication by the governing bodies of the ACC and AHA. These guidelines will be reviewed annually after publication and will be considered current unless the ACC/AHA Task Force on Practice Guidelines revises or withdraws them from circulation.These practice guidelines are intended to assist physicians in clinical decision making by describing a range of generally acceptable approaches for the prevention, diagnosis, and management of HF. The guidelines attempt to define practices that meet the needs of most patients under most circumstances. However, the ultimate judgment regarding the care of a particular patient must be made by the physician in light of all of the circumstances that are relevant to that patient. The various therapeutic strategies described in this document can be viewed as a checklist to be considered for each patient in an attempt to individualize treatment for an evolving disease process. Every patient is unique, not only in terms of his or her cause and course of HF, but also in terms of his or her personal and cultural approach to the disease. Guidelines can only provide an outline for evidence-based decisions or recommendations for individual care; these guidelines are meant to provide that outline.II. Characterization of HF as a clinical syndromeHF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and peripheral edema. Both abnormalities can impair the functional capacity and quality of life of affected individuals, but they may not necessarily dominate the clinical picture at the same time.Coronary artery disease is the underlying cause of HF in approximately two thirds of patients with left ventricular systolic dysfunction.9Gheorghiade M Bonow R.O Chronic heart failure in the United States a manifestation of coronary artery disease.Circulation. 1998; 97: 282-289Crossref PubMed Scopus (665) Google Scholar The remainder have nonischemic causes of systolic dysfunction and may have an identifiable cause (e.g., hypertension, valvular disease, myocardial toxins, or myocarditis) or may have no discernible cause (e.g., idiopathic dilated cardiomyopathy).The classification system that is most commonly used to quantify the degree of functional limitation imposed by HF is one first developed by the NYHA.10The Criteria Committee of the New York Heart AssociationDiseases of the Heart and Blood Vessels. 6th ed. Little Brown, Boston, MA1964Google Scholar This system assigns patients to 1 of 4 functional classes depending on the degree of effort needed to elicit symptoms: patients may have symptoms of HF at rest (class IV), on less-than-ordinary exertion (class III), on ordinary exertion (class II), or only at levels that would limit normal individuals (class I). The mechanisms responsible for exercise intolerance in patients with chronic HF have not been clearly defined. Patients with a very low ejection fraction may be asymptomatic, whereas patients with preserved left ventricular systolic function may have severe disability. The apparent discordance between the severity of systolic dysfunction and the degree of functional impairment is not well understood despite intense investigation.Left ventricular dysfunction begins with some injury to the myocardium and is usually a progressive process, even in the absence of a new identifiable insult to the myocardium. The principal manifestation of such progression is a process known as remodeling, which occurs in association with homeostatic attempts to decrease wall stress through increases in wall thickness. This ultimately results in a change in the geometry of the left ventricle such that the chamber dilates, hypertrophies, and becomes more spherical. The process of cardiac remodeling generally precedes the development of symptoms, occasionally by months or even years. The process of remodeling continues after the appearance of symptoms and may contribute importantly to worsening of symptoms despite treatment.The committee struggled with its perception that many clinicians do not appreciate the progressive nature of left ventricular dysfunction and HF or the importance of screening and prophylaxis for them, principles that are quite analogous to well-recognized strategies in the field of oncology. For this reason, it believed that the progression to and evolution of HF could appropriately be characterized by considering 4 stages in the evolution of the disease as described in the Introduction and Table 1. This classification scheme recognizes that HF, like coronary artery disease, has established risk factors; that the evolution of HF has asymptomatic and symptomatic phases; and that treatments prescribed at each stage can reduce the morbidity and mortality of HF.III. Assessment of patientsA Initial evaluation of patients and detection of predisposing conditions1 Identification of patientsIn general, patients with left ventricular dysfunction present to the physician in 1 of 3 ways: with a syndrome of decreased exercise tolerance; with a syndrome of fluid retention; or with no symptoms and incidentally discovered left ventricular dysfunction.2 Identification of structural abnormalityA complete history and physical examination are the first steps in evaluating the structural abnormality or cause responsible for the development of HF. Although the history and physical examination may provide important clues about the nature of the underlying cardiac abnormality, identification of the structural abnormality leading to HF generally requires either noninvasive or invasive imaging of the cardiac structures. The single most useful diagnostic test in the evaluation of patients with HF is the 2-dimensional echocardiogram, coupled with Doppler flow studies. Other tests may be used to provide information regarding the nature and severity of the cardiac abnormality. Radionuclide ventriculography can provide highly accurate measurements of global and regional function and assessment of ventricular enlargement, but it is unable to directly assess valvular abnormalities or cardiac hypertrophy. Both chest radiography and 12-lead electrocardiograms are considered to provide baseline information in most patients, but because they are both insensitive and nonspecific, neither the chest radiograph nor the electrocardiogram alone should form the primary basis for determining the specific cardiac abnormality responsible for the development of HF.Recently, the measurement of circulating levels of brain natriuretic peptide has become available as a means of identifying patients with elevated left ventricular filling pressures who are likely to exhibit signs and symptoms of HF. The assessment of this peptide cannot reliably distinguish patients with systolic from those with diastolic dysfunction. However, it has been widely investigated as a biochemical marker of morbidity and mortality in patients with known HF11Tsutamoto T Wada A Maeda K et al.Plasma brain natriuretic peptide level as a biochemical marker of morbidity and mortality in patients with asymptomatic or minimally symptomatic left ventricular dysfunction comparison with plasma angiotensin II and endothelin-1.Eur Heart J. 1999; 20: 1799-1807Crossref PubMed Scopus (230) Google Scholar and as an aid in differentiating dyspnea due to HF from dyspnea due to other causes in an emergency setting.12Dao Q Krishnaswamy P Kazanegra R et al.Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting.J Am Coll Cardiol. 2001; 37: 379-385Abstract Full Text Full Text PDF PubMed Scopus (726) Google Scholar The role of brain natriuretic peptide measurement in the identification and management of patients with symptomatic or asymptomatic left ventricular dysfunction remains to be fully clarified.3 Evaluation of the cause of ventricular dysfunctionIdentification of the disorder leading to HF may be important, because some causes of left ventricular dysfunction are reversible or treatable. However, it may not be possible to discern the cause of HF in many patients who present with this syndrome, and in others, the underlying condition may not be amenable to treatment. Hence, physicians should focus their efforts on diagnoses that have some potential for improvement with therapy directed at the underlying condition. Evaluation of potential causative factors should include taking a patient and family history, general laboratory testing, evaluation of the possibility of coronary artery disease, and evaluation of the possibility of primary myocardial disease.B Ongoing evaluation of HFOnce the nature and cause of the structural abnormalities leading to the development of HF have been defined, physicians should focus on the clinical assessment of patients, both during the initial presentation and during subsequent visits. This ongoing review of the patient’s clinical status is critical to the appropriate selection and monitoring of treatment. It should include assessment of functional capacity, assessment of volume status, laboratory evaluation, and assessment of prognosis.Recommendations for the evaluation of patients with HFClass I 1.Thorough history and physical examination to identify cardiac and noncardiac disorders that might lead to the development of HF or accelerate the progression of HF. (Level of Evidence: C)2.Initial and ongoing assessment of patient’s ability to perform routine and desired activities of daily living. (Level of Evidence: C)3.Initial and ongoing assessment of volume status. (Level of Evidence: C)4.Initial measurement of complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, blood glucose, liver function tests, and thyroid-stimulating hormone. (Level of Evidence: C)5.Serial monitoring of serum electrolytes and renal function. (Level of Evidence: C)6.Initial 12-lead electrocardiogram and chest radiograph. (Level of Evidence: C)7.Initial 2-dimensional echocardiography with Doppler or radionuclide ventriculography to assess left ventricular systolic function. (Level of Evidence: C)8.Cardiac catheterization with coronary arteriography in patients with angina who are candidates for revascularization. (Level of Evidence: B)Class IIa 1.Cardiac catheterization with coronary arteriography in patients with chest pain who have not had evaluation of their coronary anatomy and who have no contraindications to coronary revascularization. (Level of Evidence: C)2.Cardiac catheterization with coronary arteriography in patients with known or suspected coronary artery disease but without angina who are candidates for revascularization. (Level of Evidence: C)3.Noninvasive imaging to detect ischemia and viability in patients with known coronary artery disease and no angina who are being considered for revascularization. (Level of Evidence: C)4.Maximal exercise testing with measurement of respiratory gas exchange and/or blood oxygen saturation to help determine whether HF is the cause of exercise limitation when the contribution of HF is uncertain. (Level of Evidence: C)5.Maximal exercise testing with measurement of respiratory gas exchange to identify high-risk patients who are candidates for cardiac transplantation or other advanced treatments. (Level of Evidence: B)6.Echocardiography in asymptomatic first-degree relatives of patients with idiopathic dilated cardiomyopathy. (Level of Evidence: C)7.Repeat measurement of ejection fraction in patients who have had a change in clinical status or who have experienced or recovered from a clinical event or received treatment that might have had a significant effect on cardiac function. (Level of Evidence: C)8.Screening for hemochromatosis. (Level of Evidence: C)9.Measurement of serum antinuclear antibody, rheumatoid factor, urinary vanillylmandelic acid, and metanephrines in selected patients. (Level of Evidence: C)Class IIb 1.Noninvasive imaging to define the likelihood of coronary artery disease in patients with left ventricular dysfunction. (Level of Evidence: C)2.Maximal exercise testing with measurement of respiratory gas exchange to facilitate prescription of an appropriate exercise program. (Level of Evidence: C)3.Endomyocardial biopsy in patients in whom an inflammatory or infiltrative disorder of the heart is suspected. (Level of Evidence: C)4.Assessment of human immunodeficiency virus status. (Level of Evidence: C)Class III 1.Endomyocardial biopsy in the routine evaluation of patients with HF. (Level of Evidence: C)2.Routine Holter monitoring or signal-averaged electrocardiography. (Level of Evidence: C)3.Repeat coronary arteriography or noninvasive testing for ischemia in patients for whom coronary artery disease has previously been excluded as the cause of left ventricular dysfunction. (Level of Evidence: C)4.Routine measurement of circulating levels of norepinephrine or endothelin. (Level of Evidence: C)IV. TherapyA Patients at high risk of developing left ventricular dysfunction (stage A)Many conditions or behaviors that are associated with an increased risk of HF can be identified before patients show any evidence of structural heart disease. Because early modification of these factors can often reduce the risk of HF, working with patients with these risk factors provides the earliest opportunity to reduce the impact of HF on public and individual health.Recommendations for patients at high risk of developing HF (stage A)Class I 1.Control of systolic and diastolic hypertension in accordance with recommended guidelines. (Level of Evidence: A)2.Treatment of lipid disorders in accordance with recommended guidelines. (Level of Evidence: B)3.Avoidance of patient behaviors that may increase the risk of HF (e.g., smoking, alcohol consumption, and illicit drug use). (Level of Evidence: C)4.Angiotensin converting enzyme (ACE) inhibition in patients with a history of atherosclerotic vascular disease, diabetes mellitus, or hypertension and associated cardiovascular risk factors. (Level of Evidence: B)5.Control of ventricular rate in patients with supraventricular tachyarrhythmias. (Level of Evidence: B)6.Treatment of thyroid disorders. (Level of Evidence: C)7.Periodic evaluation for signs and symptoms of HF. (Level of Evidence: C)Class IIaNoninvasive evaluation of left ventricular function in patients with a strong family history of cardiomyopathy or in those receiving cardiotoxic interventions. (Level of Evidence: C)Class III 1.Exercise to prevent the development of HF. (Level of Evidence: C)2.Reduction of dietary salt beyond that which is prudent for healthy individuals in patients without hypertension or fluid retention. (Level of Evidence: C)3.Routine testing to detect left ventricular dysfunction in patients without signs or symptoms of HF or evidence of structural heart disease. (Level of Evidence: C)4.Routine use of nutritional supplements to prevent the development of structural heart disease. (Level of Evidence: C)B Patients with left ventricular dysfunction who have not developed symptoms (stage B)Patients without symptoms but who have had a myocardial infarction and patients without symptoms who have evidence of left ventricular dysfunction are at considerable risk of developing HF. The likelihood of developing clinical HF can be diminished by the use of therapies that reduce the risk of additional injury, the process of remodeling, and the progression of left ventricular dysfunction. However, as with patients with no structural heart disease, there is no evidence that control of dietary sodium, participation in regular exercise, or use of nutritional supplements can prevent the development of HF in patients with a recent or remote myocardial infarction with or without left ventricular systolic dysfunction.Recommendations for patients with asymptomatic left ventricular systolic dysfunction (stage B)Class I 1.ACE inhibition in patients with a recent or remote history of myocardial infarction regardless of ejection fraction. (Level of Evidence: A)2.ACE inhibition in patients with a reduced ejection fraction, whether or not they have experienced a myocardial infarction. (Level of Evidence: B)3.Beta-blockade in patients with a recent myocardial infarction regardless of ejection fraction. (Level of Evidence: A)4.Beta-blockade in patients with a reduced ejection fraction, whether or not they have experienced a myocardial infarction. (Level of Evidence: B)5.Valve replacement or repair for patients with hemodynamically significant valvular stenosis or regurgitation. (Level of Evidence: B)6.Regular evaluation for signs and symptoms of HF. (Level of Evidence: C)7.Measures listed as class I recommendations for patients in stage A. (Levels of Evidence: A, B, and C as appropriate).Class IIbLong-term treatment with systemic vasodilators in patients with severe aortic regurgitation. (Level of Evidence: B)Class III 1.Treatment with digoxin in patients with left ventricular dysfunction who are in sinus rhythm. (Level of Evidence: C)2.Reduction of dietary salt beyond that which is prudent for healthy individuals in patients without hypertension or fluid retention. (Level of Evidence: C)3.Exercise to prevent the development of HF. (Level of Evidence: C)4.Routine use of nutritional supplements to treat structural heart disease or prevent the development of symptoms of HF. (Level of Evidence: C)C Patients with left ventricular dysfunction with current or prior symptoms (stage C)1 General measuresMeasures listed as class I recommendations for patients in stages A and B are also appropriate for