Abstract

HomeCirculationVol. 112, No. 12ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult—Summary Article Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult—Summary ArticleA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society WRITING COMMITTEE MEMBERS Sharon Ann Hunt, William T. Abraham, Marshall H. Chin, Arthur M. Feldman, Gary S. Francis, Theodore G. Ganiats, Mariell Jessup, Marvin A. Konstam, Donna M. Mancini, Keith Michl, John A. Oates, Peter S. Rahko, Marc A. Silver, Lynne Warner Stevenson, Clyde W. Yancy, Elliott M. Antman, Sidney C. SmithJr, Cynthia D. Adams, Jeffrey L. Anderson, David P. Faxon, Valentin Fuster, Jonathan L. Halperin, Loren F. Hiratzka, Sharon Ann Hunt, Alice K. Jacobs, Rick Nishimura, Joseph P. Ornato, Richard L. Page and Barbara Riegel WRITING COMMITTEE MEMBERS , Sharon Ann HuntSharon Ann Hunt , William T. AbrahamWilliam T. Abraham , Marshall H. ChinMarshall H. Chin , Arthur M. FeldmanArthur M. Feldman , Gary S. FrancisGary S. Francis , Theodore G. GaniatsTheodore G. Ganiats , Mariell JessupMariell Jessup , Marvin A. KonstamMarvin A. Konstam , Donna M. ManciniDonna M. Mancini , Keith MichlKeith Michl , John A. OatesJohn A. Oates , Peter S. RahkoPeter S. Rahko , Marc A. SilverMarc A. Silver , Lynne Warner StevensonLynne Warner Stevenson , Clyde W. YancyClyde W. Yancy , Elliott M. AntmanElliott M. Antman , Sidney C. SmithJrSidney C. SmithJr , Cynthia D. AdamsCynthia D. Adams , Jeffrey L. AndersonJeffrey L. Anderson , David P. FaxonDavid P. Faxon , Valentin FusterValentin Fuster , Jonathan L. HalperinJonathan L. Halperin , Loren F. HiratzkaLoren F. Hiratzka , Sharon Ann HuntSharon Ann Hunt , Alice K. JacobsAlice K. Jacobs , Rick NishimuraRick Nishimura , Joseph P. OrnatoJoseph P. Ornato , Richard L. PageRichard L. Page and Barbara RiegelBarbara Riegel Originally published13 Sep 2005https://doi.org/10.1161/CIRCULATIONAHA.105.167587Circulation. 2005;112:1825–1852is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 13, 2005: Previous Version 1 Table of ContentsI. Introduction 1826II. Characterization of HF as a Clinical Syndrome 1828A. Definition of HF 1828B. HF as a Symptomatic Disorder 1828C. HF as a Progressive Disorder 1829III. Initial and Serial Clinical Assessment of Patients Presenting With HF 1829A. Initial Evaluation of Patients 18311. Identification of a Structural and Functional Abnormality 18312. Evaluation of the Cause of HF 1831a. History and Physical Examination 1831b. Laboratory Testing 1831B. Ongoing Evaluation of Patients 18321. Assessment of Volume Status 18322. Laboratory Assessment 18323. Assessment of Prognosis 1832IV. Therapy 1832A. Patients at High Risk for Developing HF (Stage A) 18321. Control of Risk 1833a. Treatment of Hypertension 1833b. Treatment of Diabetes 1834c. Management of the Metabolic Syndrome 1834d. Management of Atherosclerotic Disease 1834e. Control of Conditions That May Cause Cardiac Injury 1834f. Other Measures 18342. Early Detection of Structural Abnormalities 1834B. Patients With Cardiac Structural Abnormalities or Remodeling Who Have Not Developed HF Symptoms (Stage B) 18351. Prevention of Cardiovascular Events 1835a. Patients With an Acute MI 1835b. Patients With Chronic Reduction of LVEF but No Symptoms 1835C. Patients With Current or Prior Symptoms of HF (Stage C) 18361. Patients With Reduced LVEF 1836a. General Measures 1837b. Drugs Recommended for Routine Use 1837c. Interventions to be Considered for Use in Selected Patients 1842d. Drugs and Interventions Under Active Investigation 1842e. Drugs and Interventions of Unproved Value and Not Recommended 18422. Patients With HF and Normal LVEF 1843a. Identification of Patients 1843b. Diagnosis 1843c. Principles of Treatment 1843D. Patients With Refractory End-Stage HF (Stage D) 18441. Management of Fluid Status 18442. Intravenous Peripheral Vasodilators and Positive Inotropic Agents 18443. Mechanical and Surgical Strategies 1844V. Treatment of Special Populations 1845A. Women and Men 1845B. Ethnic Considerations 1845C. Elderly Patients 1845VI. Patients With HF Who Have Concomitant Disorders 1846A. Cardiovascular Disorders 18461. Hypertension, Hyperlipidemia, and Diabetes Mellitus 18462. Supraventricular Arrhythmias 18463. Prevention of Thromboembolic Events 1846B. Noncardiovascular Disorders 18461. Patients With Pulmonary Disease 18462. Patients With Cancer 18473. Patients With Thyroid Disease 18474. Patients With Hepatitis C and Human Immunodeficiency Virus 18475. Patients With Anemia 1847VII. End-of-Life Considerations 1847VIII. Implementation of Practice Guidelines 1847A. Performance Measures 1848References 1848I. IntroductionThe American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. This process gives priority to areas where major changes in text, particularly recommendations, are required on the basis of new understanding of evidence. Minor changes in verbiage and references are discouraged. The ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult published in 2001 have now been updated. The full-text guidelines incorporating the updated material are e-published in the Journal of the American College of Cardiology and Circulation on the ACC Web site (www.acc.org) and the AHA Web site (www.americanheart.org) in 2 versions: a version highlighting the changes in recommendations (i.e., deleted text struck through, new text underlined) from the 2001 guideline to the 2005 guideline and a "clean" version that incorporates all changes in the recommendations. (The "track change" version only highlights changes to the recommendations; it does not show changes to supporting text, tables, or figures.) This article describes the major areas of change reflected in the update. Please note we have changed the Table of Contents headings in the 2001 guidelines from roman numerals to unique identifying numbers. Interested readers are referred to the full-text guideline to completely understand the context of these changes.Heart failure (HF) is a major and growing public health problem in the United States. Approximately 5 million patients in this country have HF, and more than 550 000 patients are diagnosed with HF for the first time each year (1). The disorder is the primary reason for 12 to 15 million office visits and 6.5 million hospital days each year (2). From 1990 to 1999, the annual number of hospitalizations has increased from approximately 810 000 to over 1 million for HF as a primary diagnosis and from 2.4 to 3.6 million for HF as a primary or secondary diagnosis (3). In 2001, nearly 53 000 patients died of HF as a primary cause. The number of HF deaths has increased steadily despite advances in treatment, in part because of increasing numbers of patients with HF due to better treatment and "salvage" of patients with acute myocardial infarctions (MIs) earlier in life (1).Heart failure is primarily a condition of the elderly (4), and thus the widely recognized "aging of the population" also contributes to the increasing incidence of HF. The incidence of HF approaches 10 per 1000 population after age 65 (1) and approximately 80% of patients hospitalized with HF are more than 65 years old (5). Heart failure is the most common Medicare diagnosis-related group (i.e., hospital discharge diagnosis), and more Medicare dollars are spent for the diagnosis and treatment of HF than for any other diagnosis (6). It has been estimated that in 2005, the total direct and indirect cost of HF in the United States will be equal to $27.9 billion (1). In the United States, approximately $2.9 billion annually is spent on drugs for the treatment of HF (1).The ACC and the AHA first published guidelines for the evaluation and management of HF in 1995 (7) and published revised guidelines in 2001 (8). 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 potentially fatal disorder. Available treatments have increased, but this increase has rendered clinical decision making far more complex. The timing and sequence of initiating treatments and the appropriateness of prescribing them in combination are uncertain. The increasing recognition of the existence of clinical HF in patients with a normal ejection fraction (EF) has also led to heightened awareness of the limitations of evidence-based therapy for this important group of patients. For these reasons, the 2 organizations believed that it was appropriate to reassess and update these guidelines, fully recognizing that the optimal therapy of HF remains a work in progress and that future advances will require that the guideline be updated again.In formulating the 2001 document, the writing committee decided to take a new approach to the classification of HF, one that emphasized both the development and progression of the disease. In doing so, the 2001 document identified 4 stages involved in the development of the HF syndrome. The first 2 stages (A and B) are clearly not HF but are an attempt to help healthcare providers identify patients early who are at risk for developing HF. Stages A and B patients are best defined as those with risk factors that clearly predispose toward the development of HF. For example, patients with coronary artery disease, hypertension, or diabetes mellitus who do not yet demonstrate impaired left ventricular (LV) function, hypertrophy, or geometric chamber distortion would be considered Stage A, whereas patients who are asymptomatic but demonstrate LV hypertrophy (LVH) and/or impaired LV function would be designated as Stage B. Stage C then denotes patients with current or past symptoms of HF associated with underlying structural heart disease (the bulk of patients with HF), and Stage D designates patients with truly refractory HF who might be eligible for specialized, advanced treatment strategies such as mechanical circulatory support, procedures to facilitate fluid removal, continuous inotropic infusions, or cardiac transplantation or other innovative or experimental surgical procedures, or for end-of-life care, such as hospice.This classification recognizes that there are established risk factors and structural prerequisites for the development of HF and that therapeutic interventions introduced even before the appearance of LV dysfunction or symptoms can reduce the population morbidity and mortality of HF. This classification system is intended to complement but in no way 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 that the NYHA functional classification reflects a subjective assessment by a healthcare provider and can change frequently over short periods of time. It has also been recognized that the treatments used may not differ significantly across the classes. Therefore, the committee believed that a staging system was needed that would reliably and objectively identify patients during the course of their developing disease and that would be linked to treatments uniquely appropriate at each stage of illness. According to this new staging approach, patients would only be expected to either not advance at all or to advance from one stage to the next, unless progression of the disease was slowed or stopped by treatment, and spontaneous reversal of this progression would be considered unusual. For instance, although symptoms (NYHA class) might vary widely over time (in response to therapy or to progression of disease) in a patient who has already developed the clinical syndrome of HF (Stage C), the patient could never return to Stage B (never had HF), and therapies recommended for Stage C will be appropriate even if this patient is in NYHA class I. This new classification scheme adds a useful dimension to our thinking about HF that is similar to that achieved by staging or risk assessment systems for other disorders (e.g., those used in the approach to cancer).A classification of recommendation and level of evidence have been assigned to each recommendation. Classification of recommendations and levels of evidence are expressed in the ACC/AHA format as follows. Please refer to Table 1 in the full-text guidelines for more details. TABLE 1. Evaluation of the Cause of Heart Failure: The HistoryHF indicates heart failure; Hx, history; MI, myocardial infarction; and PAD, peripheral arterial disease.History to include inquiry regarding: Hypertension Diabetes Dyslipidemia Valvular heart disease Coronary or peripheral vascular disease Myopathy Rheumatic fever Mediastinal irradiation History or symptoms of sleep-disordered breathing Exposure to cardiotoxic agents Current and past alcohol consumption Smoking Collagen vascular disease Exposure to sexually transmitted diseases Thyroid disorder Pheochromocytoma ObesityFamily history to include inquiry regarding: Predisposition to atherosclerotic disease (Hx of MIs, strokes, PAD) Sudden cardiac death Myopathy Conduction system disease (need for pacemaker) Tachyarrhythmias Cardiomyopathy (unexplained HF) Skeletal myopathiesClassification of RecommendationsClass I: Conditions for which there is evidence and/or general agreement that a given procedure/therapy is beneficial, useful, and/or effective.Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure/therapy.IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.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.Level of EvidenceLevel of Evidence A: Data are derived from multiple randomized clinical trials or meta-analyses.Level of Evidence B: Data are derived from a single randomized trial, or nonrandomized studies.Level of Evidence C: Only consensus opinion of experts, case studies, or standard of care.This document focuses on the prevention of HF and on the evaluation and management of chronic HF in the adult patient with normal or reduced LVEF. It specifically did not consider acute HF, which might merit a separate set of guidelines and is addressed in part in the ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (9) and the ACC/AHA 2002 Guideline Update for the Management of Patients with Unstable Angina and Non-ST Elevation Myocardial Infarction (10). 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 the Management of Patients With Valvular Heart Disease (11)] or congenital malformations, and we have not included recommendations for the treatment of specific myocardial disorders (e.g., hemochromatosis, sarcoidosis, or amyloidosis).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.All of the recommendations in this guideline update were written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document, would still convey the full intent of the recommendation. It is hoped that this will increase readers' comprehension of the guidelines. The rewritten recommendations appear under their respective headings.Use of boldfaced type in the recommendations shows where the intent of the recommendations has changed from the 2001 guidelines.II. Characterization of HF as a Clinical SyndromeA. Definition of HFHeart failure 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 congestion and peripheral edema. Both abnormalities can impair the functional capacity and quality of life of affected individuals, but they do not necessarily dominate the clinical picture at the same time. Some patients have exercise intolerance but little evidence of fluid retention, whereas others complain primarily of edema and report few symptoms of dyspnea or fatigue. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" is preferred over the older term "congestive heart failure."The clinical syndrome of HF may result from disorders of the pericardium, myocardium, endocardium, or great vessels, but the majority of patients with HF have symptoms due to an impairment of LV myocardial function. Heart failure may be associated with a wide spectrum of LV functional abnormalities, which may range from patients with normal LV size and preserved EF to those with severe dilatation and/or markedly reduced EF. In most patients, abnormalities of systolic and diastolic dysfunction coexist, regardless of EF. Patients with normal EF may have a different natural history and may require different treatment strategies than patients with reduced EF, although such differences remain controversial (see Section 4.3.2 in the full-text guidelines).Coronary artery disease, hypertension, and dilated cardiomyopathy are the causes of HF in a substantial proportion of patients in the Western world. As many as 30% of patients with dilated cardiomyopathy may have a genetic cause (12). Valvular heart disease is still a common cause of HF. In fact, nearly any form of heart disease may ultimately lead to the HF syndrome.It should be emphasized that HF is not equivalent to cardiomyopathy or to LV dysfunction; these latter terms describe possible structural or functional reasons for the development of HF. Instead, HF is defined as a clinical syndrome that is characterized by specific symptoms (dyspnea and fatigue) in the medical history and signs (edema, rales) on the physical examination. There is no single diagnostic test for HF because it is largely a clinical diagnosis that is based on a careful history and physical examination.B. Heart Failure as a Symptomatic DisorderThe approach that is most commonly used to quantify the degree of functional limitation imposed by HF is one first developed by the NYHA. 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 of exertion that would limit normal individuals (class I). Although the functional class tends to deteriorate over periods of time, most patients with HF do not typically show an uninterrupted and inexorable worsening of symptoms. Instead, the severity of symptoms characteristically fluctuates even in the absence of changes in medications, and changes in medications and diet can have either favorable or adverse effects on functional capacity in the absence of measurable changes in ventricular function. Some patients may demonstrate remarkable recovery, sometimes associated with improvement in structural and functional abnormalities. Usually, sustained improvement is associated with drug therapy, and that therapy should be continued indefinitely.The mechanisms responsible for the exercise intolerance of patients with chronic HF have not been defined clearly. Although HF is generally regarded as a hemodynamic disorder, many studies have indicated that there is a poor relation between measures of cardiac performance and the symptoms produced by the disease. Patients with a very low EF may be asymptomatic, whereas patients with preserved LVEF may have severe disability. The apparent discordance between EF and the degree of functional impairment is not well understood but may be explained in part by alterations in ventricular distensibility, valvular regurgitation, pericardial restraint, cardiac rhythm, conduction abnormalities, and right ventricular function (12). In addition, in ambulatory patients, many noncardiac factors may contribute substantially to exercise intolerance. These factors include but are not limited to changes in peripheral vascular function, skeletal muscle physiology, pulmonary dynamics, neurohormonal and reflex autonomic activity, and renal sodium handling. The existence of these noncardiac factors may explain why the hemodynamic improvement produced by therapeutic agents in patients with chronic HF may not be immediately or necessarily translated into clinical improvement. Although pharmacological interventions may produce rapid changes in hemodynamic variables, signs and symptoms may improve slowly over weeks or months or not at all.C. Heart Failure as a Progressive DisorderLeft ventricular dysfunction begins with some injury to, or stress on, the myocardium and is generally a progressive process, even in the absence of a new identifiable insult to the heart. The principal manifestation of such progression is a change in the geometry and structure of the LV, such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as cardiac remodeling. This change in chamber size and structure not only increases the hemodynamic stresses on the walls of the failing heart and depresses its mechanical performance but may also increase regurgitant flow through the mitral valve. These effects, in turn, serve to sustain and exacerbate the remodeling process. Cardiac remodeling generally precedes the development of symptoms (occasionally by months or even years), continues after the appearance of symptoms, and contributes substantially to worsening of symptoms despite treatment. Progression of coronary artery disease, diabetes mellitus, hypertension, or the onset of atrial fibrillation may also contribute to the progression of HF. The development of structural abnormalities can have 1 of 3 outcomes: 1) patients die before developing symptoms (in stage A or B), 2) patients develop symptoms controlled by treatment, or 3) patients die of progressive HF. Sudden death can interrupt this course at any time.Although several factors can accelerate the process of LV remodeling, there is substantial evidence that the activation of endogenous neurohormonal systems plays an important role in cardiac remodeling and thereby in the progression of HF. Patients with HF have elevated circulating or tissue levels of norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines, which can act (alone or in concert) to adversely affect the structure and function of the heart. These neurohormonal factors not only increase the hemodynamic stresses on the ventricle by causing sodium retention and peripheral vasoconstriction but may also exert direct toxic effects on cardiac cells and stimulate myocardial fibrosis, which can further alter the architecture and impair the performance of the failing heart. Neurohormonal activation also has direct deleterious effects on the myocytes and interstitium, altering the performance and phenotype of these cells.The development of HF can be appropriately characterized by considering 4 stages of the disease, as described in the Introduction. This staging system recognizes that HF, like coronary artery disease, has established risk factors and structural prerequisites; that the development of HF has asymptomatic and symptomatic phases; and that specific treatments targeted at each stage can reduce the morbidity and mortality of HF (Figure). Download figureDownload PowerPointStages in the development of HF/recommended therapy by stage. FHx CM indicates family history of cardiomyopathy; ACEI, angiotensin converting enzyme inhibitors; and ARB, angiotensin receptor blocker.Stages in the development of HF/recommended therapy by stage. FHx CM indicates family history of cardiomyopathy; ACEI, angiotensin converting enzyme inhibitors; and ARB, angiotensin receptor blocker.III. Initial and Serial Clinical Assessment of Patients Presenting With HFIn this section, recommendations for the evaluation of patients with HF have been separated into 2 sets of recommendations: 1) for the initial clinical assessment of patients presenting with HF and 2) for the serial clinical assessment of patients presenting with HF.Recommendations for the Initial Clinical Assessment of Patients Presenting With Heart FailureClass IA thorough history and physical examination should be obtained/performed in patients presenting with HF to identify cardiac and noncardiac disorders or behaviors that might cause or accelerate the development or progression of HF. (Level of Evidence: C)A careful history of current and past use of alcohol, illicit drugs, current or past standard or "alternative therapies," and chemotherapy drugs should be obtained from patients presenting with HF. (Level of Evidence: C)In patients presenting with HF, initial assessment should be made of the patient's ability to perform routine and desired activities of daily living. (Level of Evidence: C)Initial examination of patients presenting with HF should include assessment of the patient's volume status, orthostatic blood pressure changes, measurement of weight and height, and calculation of body mass index.(Level of Evidence: C)Initial laboratory evaluation of patients presenting with HF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, fasting blood glucose (glycohemoglobin), lipid profile, liver function tests, and thyroid-stimulating hormone. (Level of Evidence: C)Twelve-lead electrocardiogram and chest radiograph (PA and lateral) should be performed initially in all patients presenting with HF. (Level of Evidence: C)Two-dimensional echocardiography with Doppler should be performed during initial evaluation of patients presenting with HF to assess LVEF, LV size, wall thickness, and valve function. Radionuclide ventriculography can be performed to assess LVEF and volumes. (Level of Evidence: C)Coronary arteriography should be performed in patients presenting with HF who have angina or significant ischemia unless the patient is not eligible for revascularization of any kind.(Level of Evidence: B)Class IIaCoronary arteriography is reasonable for patients presenting with HF who have chest pain that may or may not be of cardiac origin who have not had evaluation of their coronary anatomy and who have no contraindications to coronary revascularization. (Level of Evidence: C)Coronary arteriography is reasonable for patients presenting with HF who have known or suspected coronary artery disease but who do not have angina unless the patient is not eligible for revascularization of any kind.(Level of Evidence: C)Noninvasive imaging to detect myocardial ischemia and viability is reasonable in patients presenting with HF who have known coronary artery disease and no angina unless the patient is not eligible for revascularization of any kind. (Level of Evidence: B)Maximal exercise testing with or without measurement of respiratory gas exchange and/or blood oxygen saturation is reasonable in patients presenting with HF to help determine whether HF is the cause of exercise limitation when the contribution of HF is uncertain. (Level of Evidence: C)Maximal exercise testing with measurement of respiratory gas exchange is reasonable to identify high-risk patients presenting with HF who are candidates for cardiac transplantation or other advanced treatments. (Level of Evidence: B)Screening for hemochromatosis, sleep-disturbed breathing, or human immunodeficiency virus is reasonable in selected patients who present with HF. (Level of Evidence: C)Diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma are reasonable in patients presenting with HF in whom there is a clinical suspicion of these diseases. (Level of Evidence: C)Endomyocardial biopsy can be useful in patients presenting with HF when a specific diagnosis is suspected that would influence therapy. (Level of Evidence: C)Measurement of B-type natriuretic peptide (BNP*) can be useful in the evaluation of patients presenting in the urgent