2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis ... · PRACTICE GUIDELINE: FOCUSED UPDATE 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart

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Journal of the American College of Cardiology Vol. 53, No. 15, 2009© 2009 by the American College of Cardiology Foundation and the American Heart Association, Inc. ISSN 0735-1097/09/$36.00P

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PRACTICE GUIDELINE: FOCUSED UPDATE

2009 Focused Update: ACCF/AHA Guidelines for theDiagnosis and Management of Heart Failure in AdultsA Report of the American College of Cardiology Foundation/American Heart Association Task Forceon Practice Guidelines

Developed in Collaboration With the International Society for Heart and Lung Transplantation

2009 Writing Group to Review New Evidence and Update the2005 Guideline for the Management of Patients With Chronic Heart Failure

Writing on Behalf of the 2005 Heart Failure Writing Committee

ublished by Elsevier Inc. doi:10.1016/j.jacc.2008.11.009

*i‡RCst

Mariell Jessup, MD, FACC, FAHA, Chair*

William T. Abraham, MD, FACC, FAHA†Donald E. Casey, MD, MPH, MBA‡Arthur M. Feldman, MD, PHD, FACC, FAHA§Gary S. Francis, MD, FACC, FAHA§Theodore G. Ganiats, MD�Marvin A. Konstam, MD, FACC¶Donna M. Mancini, MD#

anagement of Chronic Heart Failure in the Adult Writing Committee. 2009ocused update: ACCF/AHA guidelines for the diagnosis and management of heart

Ad

ded From: http://content.onlinejacc.org/ on 01/08/2013

Marc A. Silver, MD, FACC, FAHA**Lynne Warner Stevenson, MD, FACC, FAHA†Clyde W. Yancy, MD, FACC, FAHA††

International Society for Heart and Lung Transplantation Representative; †Amer-can College of Cardiology Foundation/American Heart Association Representative;American College of Physicians Representative; §Heart Failure Society of Americaepresentative; �American Academy of Family Physicians Representative; ¶Americanollege of Cardiology Foundation/American Heart Association Performance Mea-

ures Liaison; #Content Expert; **American College of Chest Physicians Represen-ative; ††American College of Cardiology Foundation/American Heart Association

Peter S. Rahko, MD, FACC, FAHA† Task Force on Practice Guidelines Liaison

2005 WritingCommitteeMembers

Sharon Ann Hunt, MD, FACC, FAHA,Chair

William T. Abraham, MD, FACC, FAHAMarshall H. Chin, MD, MPH, FACPArthur M. Feldman, MD, PHD, FACC,

FAHAGary S. Francis, MD, FACC, FAHATheodore G. Ganiats, MD

Mariell Jessup, MD, FACC, FAHAMarvin A. Konstam, MD, FACCDonna M. Mancini, MDKeith Michl, MD, FACPJohn A. Oates, MD, FAHAPeter S. Rahko, MD, FACC, FAHAMarc A. Silver, MD, FACC, FAHALynne Warner Stevenson, MD, FACC, FAHAClyde W. Yancy, MD, FACC, FAHA

his document is a limited update to the 2005 guideline update and is based on aeview of certain evidence, not a full literature review. This document was approvedy the American College of Cardiology Foundation Board of Trustees and by themerican Heart Association Science Advisory and Coordinating Committee inctober 2008.The American College of Cardiology Foundation requests that this document be

ited as follows: Jessup M, Abraham WT, Casey DE, Feldman AM, Francis GS,aniats TG, Konstam MA, Mancini DM, Rahko PS, Silver MA, Stevenson LW,ancy CW, writing on behalf of the 2005 Guideline Update for the Diagnosis and

failure in adults: a report of the American College of Cardiology/American HeartAssociation Task Force on Practice Guidelines. J Am Coll Cardiol 2009;53:1343–82.

This article has been copublished in the April 14, 2009, issue of Circulation.Copies: This document is available on the World Wide Web sites of the

American College of Cardiology (www.acc.org) and American Heart Association(my.americanheart.org). For copies of this document, please contact Elsevier Inc.Reprint Department, fax (212) 633-3820, e-mail [email protected].

Permissions: Multiple copies, modification, alteration, enhancement, and/or dis-tribution of this document are not permitted without the express permission of the

merican College of Cardiology Foundation. Please contact Elsevier’s permissionepartment at [email protected].

http://www.acc.org

http://my.americanheart.org

mailto:[email protected]

mailto:[email protected]

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1344 Jessup et al. JACC Vol. 53, No. 15, 20092009 Guideline Focused Update on Heart Failure April 14, 2009:1343–82

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Task ForceMembers

Sidney C. Smith, JR, MD, FACC, FAHA, ChairAlice K. Jacobs, MD, FACC, FAHA, Vice-Chair

Christopher E. Buller, MD, FACCMark A. Creager, MD, FACC, FAHASteven M. Ettinger, MD, FACCHarlan M. Krumholz, MD, FACC, FAHAFrederick G. Kushner, MD, FACC, FAHA

Bruce W. Lytle, MD, FACC, FAHA‡‡Rick A. Nishimura, MD, FACC, FAHARichard L. Page, MD, FACC, FAHALynn G. Tarkington, RNClyde W. Yancy, MD, FACC, FAHA

‡‡Former Task Force member during the writing effort

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TABLE OF CONTENTS

reamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1344

. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1346

1.1. Evidence Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1346

1.2. Organization of Committee and RelationshipsWith Industry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1347

1.3. Review and Approval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1347

1.4. Stages of Heart Failure: InformationFrom the 2005 Guideline . . . . . . . . . . . . . . . . . . . . . . . . . .1347

. Initial and Serial Clinical Assessment of PatientsPresenting With Heart Failure . . . . . . . . . . . . . . . . . . . . . . . .1348

3.1. Initial Evaluation of Patients . . . . . . . . . . . . . . . . . . . . .13503.1.1. Identification of Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . .13503.1.2. Identification of a Structural and Functional

Abnormality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13503.1.3.2. LABORATORY TESTING . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1351

3.2.3. Laboratory Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13523.2.4. Assessment of Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . .1352

. Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1353

4.3.1. Patients With Reduced Left Ventricular EjectionFraction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1353

4.3.1.1. GENERAL MEASURES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13564.3.1.2.5. VENTRICULAR ARRHYTHMIAS AND PREVENTION OF

SUDDEN DEATH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13574.3.1.3.3. HYDRALAZINE AND ISOSORBIDE DINITRATE . . . . . . . . . . . . . .13594.3.1.3.4. CARDIAC RESYNCHRONIZATION THERAPY . . . . . . . . . . . . . . . .13594.3.1.5.2. INTERMITTENT INTRAVENOUS POSITIVE

INOTROPIC THERAPY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1360

4.4. Patients With Refractory End-Stage HeartFailure (Stage D) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1360

4.4.3. Intravenous Peripheral Vasodilators and PositiveInotropic Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1362

4.5. The Hospitalized Patient (New Section). . . . . . . . .13624.5.1. Diagnostic Strategies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13644.5.2. Treatment in the Hospital . . . . . . . . . . . . . . . . . . . . . . . . . .1365

4.5.2.1. DIURETICS: THE PATIENT WITH VOLUME OVERLOAD . . . . . . . . . . .13654.5.2.2. VASODILATORS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13664.5.2.3. INOTROPES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13664.5.2.4. OTHER CONSIDERATIONS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1367

4.5.3. The Hospital Discharge. . . . . . . . . . . . . . . . . . . . . . . . . . . . .1367

. Treatment of Special Populations . . . . . . . . . . . . . . . . . . .1368c


. Patients With Heart Failure Who HaveConcomitant Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1369

6.1.3. Supraventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . .1369

eferences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1370

ppendix 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1379

ppendix 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1380

reamble

primary challenge in the development of clinical practiceuidelines is keeping pace with the stream of new data onhich recommendations are based. In an effort to respondore quickly to new evidence, the American College ofardiology Foundation/American Heart Association

ACCF/AHA) Task Force on Practice Guidelines hasreated a “focused update” process to revise the existinguideline recommendations that are affected by the evolvingata or opinion. Prior to the initiation of this focusedpproach, periodic updates and revisions of existing guidelinesequired up to 3 years to complete. Now, however, newvidence is reviewed in an ongoing fashion to more efficientlyespond to important science and treatment trends that couldave a major impact on patient outcomes and quality of care.vidence is reviewed at least twice a year, and updates will be

nitiated on an as-needed basis as quickly as possible, whileaintaining the rigorous methodology that the ACCF andHA have developed during their more than 20 years ofartnership.These updated guideline recommendations reflect a con-

ensus of expert opinion after a thorough review primarily ofate-breaking clinical trials identified through a broad-basedetting process as important to the relevant patient popu-ation, as well as of other new data deemed to have anmpact on patient care (see Section 1.1., Evidence Review,or details regarding this focused update). It is important toote that this focused update is not intended to representn update based on a full literature review from the datef the previous guideline publication. Specific criteria/
onsiderations for inclusion of new data include the following:

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1345JACC Vol. 53, No. 15, 2009 Jessup et al.April 14, 2009:1343–82 2009 Guideline Focused Update on Heart Failure

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Publication in a peer-reviewed journalLarge randomized, placebo-controlled trial(s)Nonrandomized data deemed important on the basis ofresults affecting current safety and efficacy assumptionsStrength/weakness of research methodology and findingsLikelihood of additional studies influencing current findingsImpact on current performance measure(s) and/or like-lihood of need to develop new performance measure(s)Requests and requirements for review and update from thepractice community, key stakeholders, and other sourcesfree of relationships with industry or other potential biasNumber of previous trials showing consistent resultsNeed for consistency with a new guideline or guidelinerevision

In analyzing the data and developing updated recommen-ations and supporting text, the focused update writingroup used evidence-based methodologies developed by theCCF/AHA Task Force on Practice Guidelines, which areescribed elsewhere (1).The schema for class of recommendation and level of

able 1. Applying Classification of Recommendations and Leve

Data available from clinical trials or registries about the usefulness/efficacy in different subpopailure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply thend themselves to clinical trials. Even though randomized trials are not available, there may bCC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when wrcomplete thought, such that a recommendation, even if separated and presented apart from

ull intent of the recommendation. It is hoped that this will increase readers’ comprehension of

vidence is summarized in Table 1, which also illustrates i


ow the grading system provides an estimate of the size ofhe treatment effect and an estimate of the certainty of thereatment effect. Note that a recommendation with Level ofvidence B or C does not imply that the recommendation

s weak. Many important clinical questions addressed inuidelines do not lend themselves to clinical trials. Althoughandomized trials may not be available, there may be a verylear clinical consensus that a particular test or therapy isseful and effective. Both the class of recommendation andevel of evidence listed in the focused updates are based ononsideration of the evidence reviewed in previous iterationsf the guideline as well as the focused update. Of note, themplications of older studies that have informed recommen-ations but have not been repeated in contemporary settingsre carefully considered.

The ACCF/AHA practice guidelines address patientopulations (and healthcare providers) residing in Northmerica. As such, drugs that are not currently available

n North America are discussed in the text without apecific class of recommendation. For studies performed

vidence

, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heartecommendation is weak. Many important clinical questions addressed in the guidelines do noty clear clinical consensus that a particular test or therapy is useful or effective. †In 2003, thecommendations. All guideline recommendations have been written in full sentences that expresst of the document (including headings above sets of recommendations), would still convey theidelines and will allow quires at the individual recommendation level.

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n large numbers of subjects outside of North America,

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ach writing committee reviews the potential impact ofifferent practice patterns and patient populations on the

reatment effect and on the relevance to the ACCF/AHA targetopulation to determine whether the findings should inform apecific recommendation.

The ACCF/AHA practice guidelines are intended tossist healthcare providers in clinical decision making byescribing a range of generally acceptable approaches for theiagnosis, management, and prevention of specific diseasesr conditions. The guidelines attempt to define practiceshat meet the needs of most patients in most circumstances.he ultimate judgment regarding care of a particular patientust be made by the healthcare provider and patient in light of

ll the circumstances presented by that patient. Thus, there areircumstances in which deviations from these guidelines maye appropriate. Clinical decision making should consider theuality and availability of expertise in the area where care isrovided. These guidelines may be used as the basis foregulatory or payer decisions, but the ultimate goals are qualityf care and serving the patient’s best interests.

Prescribed courses of treatment in accordance with theseecommendations are effective only if they are followed byhe patient. Because lack of patient adherence may adverselyffect treatment outcomes, healthcare providers shouldake every effort to engage the patient in active participa-

ion with prescribed treatment.The ACCF/AHA Task Force on Practice Guidelinesakes every effort to avoid actual, potential, or perceived

onflict of interest that may arise as a result of industryelationships or personal interests among the writing com-ittee. Specifically, all members of the writing committee,

s well as peer reviewers of the document, are asked toisclose all such relationships pertaining to the trials andther evidence under consideration (see Appendixes 1 and). Final recommendations were balloted to all writingommittee members. Writing committee members with sig-ificant (greater than $10 000) relevant relationships with

ndustry were required to recuse themselves from voting onhat recommendation. Writing committee members who didot participate are not listed as authors of this focused update.With the exception of the recommendations presented

ere, the full guideline remains current. Only the recom-endations from the affected section(s) of the full guideline

re included in this focused update. For easy reference, allecommendations from any section of a guideline affected by

change are presented with notation as to whether theyemain current, are new, or have been modified. Whenvidence affects recommendations in more than 1 set ofuidelines, those guidelines are updated concurrently.

The recommendations in this focused update are consideredurrent until they are superseded by another focused update orhe full-text guidelines are revised. This focused update isublished in the April 14, 2009, issues of the Journal of themerican College of Cardiology and Circulation as an update to

he full-text guideline and is also posted on the ACCF
www.acc.org, www.cardiosource.com) and AHA (my.ameri- A

anheart.org) Web sites. A revised version of the ACC/AHA005 Guideline Update for the Diagnosis and Management ofhronic Heart Failure in the Adult (2) full-text guideline that

ncorporates the focused update has also been e-published inhese issues and is available on the respective Web sites (3). Forasy reference, that online-only version denotes sections thatave been updated.

Sidney C. Smith, Jr, MD, FACC, FAHAChair, ACCF/AHA Task Force on Practice Guidelines

Alice K. Jacobs, MD, FACC, FAHAVice-Chair, ACCF/AHA Task Force on Practice Guidelines

. Introduction

.1. Evidence Review

ate-breaking clinical trials presented at the 2005, 2006,nd 2007 annual scientific meetings of the ACCF, AHA,nd European Society of Cardiology, as well as selectedther data, were reviewed by the standing guideline writingommittee along with the parent task force and otherxperts to identify those trials and other key data that mightmpact guideline recommendations. On the basis of theriteria/considerations noted earlier, recent trial data andther clinical information were considered importantnough to prompt a focused update of the ACC/AHA 2005uideline Update for the Diagnosis and Management ofhronic Heart Failure in the Adult (2). In addition, the

uidelines writing committee thought that a new section onhe management of the hospitalized patient with heart failureHF) should be included in this update. A number of recent

F trials reviewed for this update, were, in fact, performed onospitalized patients, and a number of newer therapies arender development for this population. Moreover, there isncreasing government and other third-party payer interest inhe prevention of HF hospitalizations, and rehospitalizations.uality indicators about the process of discharging the HF

atient have already been developed, and data about rehospi-alizations for HF by hospital have already been made public.hus, the committee thought that a new section about this

mportant aspect of HF care should be added to this update.When considering the new data for this focused update,

he writing group faced the task of weighing evidence fromtudies enrolling large numbers of subjects outside Northmerica. While noting that practice patterns and the rigor

pplied to data collection, as well as the genetic makeup ofubjects, might influence the observed magnitude of areatment’s effect, the writing group believed that the dataere relevant to formulation of recommendations for theanagement of HF in North America.Policy on clinical areas not covered by the present

ocused update can be found in the 2009 Focused Updatencorporated into the ACC/AHA 2005 Guidelines forhe Diagnosis and Management of Heart Failure in
dults (3).
http://www.acc.org

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.2. Organization of Committee andelationships With Industry

or this focused update, all members of the 2005 HFriting committee were invited to participate; those who

greed (referred to as the 2009 Focused Update Writingroup) were required to disclose all relationships with

ndustry relevant to the data under consideration (1). Eachecommendation required a confidential vote by the writingroup members before and after external review of theocument. Writing group members who had a significantgreater than $10 000) relationship with industry relevant torecommendation were required to recuse themselves from

oting on that recommendation.

.3. Review and Approval

his document was reviewed by 2 external reviewers nom-nated by the ACCF and 2 external reviewers nominated byhe AHA, as well as a reviewer from the ACCF/AHA Taskorce on Practice Guidelines, 10 organizational reviewers

epresenting the American College of Chest Physicians, themerican College of Physicians, the American Academyf Family Physicians, the Heart Failure Society of Amer-ca, and the International Society for Heart and Lungransplantation, and 14 individual content reviewers. All

igure 1. Stages in the Development of Heart Failure/Recommend

CEI indicates angiotensin-converting enzyme inhibitors; ARB, angiotensin II receptorre; LVH, left ventricular hypertrophy; and MI, myocardial infarction.

nformation about reviewers’ relationships with industry L


as collected and distributed to the writing committeend is published in this document (see Appendix 2 foretails).This document was approved for publication by the govern-

ng bodies of the ACCF and the AHA and endorsed by thenternational Society for Heart and Lung Transplantation.

.4. Stages of Heart Failure:nformation From the 2005 Guideline

he HF writing committee previously developed a newpproach to the classification of HF (2), one that empha-ized both the development and progression of the disease.n doing so, they identified 4 stages involved in theevelopment of the HF syndrome (Figure 1). The first 2tages (A and B) are clearly not HF but are an attempt toelp healthcare providers with the early identification ofatients who are at risk for developing HF. Stages A and Batients are best defined as those with risk factors thatlearly predispose toward the development of HF. Forxample, patients with coronary artery disease, hyperten-ion, or diabetes mellitus who do not yet demonstratempaired left ventricular (LV) function, hypertrophy, oreometric chamber distortion would be considered Stage A,hereas patients who are asymptomatic but demonstrate

herapy by Stage

er; EF, ejection fraction; FHx CM, family history of cardiomyopathy; HF, heart fail-

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esignated as Stage B. Stage C then denotes patients withurrent or past symptoms of HF associated with underlyingtructural heart disease (the bulk of patients with HF), andtage D designates patients with truly refractory HF whoight be eligible for specialized, advanced treatment strat-

gies, such as mechanical circulatory support, procedures toacilitate fluid removal, continuous inotropic infusions, orardiac transplantation or other innovative or experimental


. Initial and Serial Clinical Assessment ofatients Presenting With Heart Failure

he changes in this section are made to clarify the role ofunctional assessment of the HF patient, beyond the New York

eart Association (NYHA) classification, and to expand on these of B-type natriuretic peptide (BNP) and N-terminalro-B-type natriuretic peptide (NT-proBNP) testing within

urgical procedures, or for end-of-life care, such as hospice. the context of the overall evaluation of the patient (Table 2).

able 2. Updates to Section 3. Initial and Serial Clinical Assessment of Patients Presenting With Heart Failure

2005 Guideline Recommendations 2009 Focused Update Recommendations Comments

3. Recommendations for the Initial Clinical Assessment of Patients Presenting With Heart Failure

Class I

thorough history and physical examination should beobtained/performed in patients presenting with HF toidentify cardiac and noncardiac disorders or behaviors thatmight cause or accelerate the development or progression ofHF. (Level of Evidence: C)

1. A thorough history and physical examination should beobtained/performed in patients presenting with HF toidentify cardiac and noncardiac disorders or behaviorsthat might cause or accelerate the development orprogression of HF. (Level of Evidence: C)

2005 recommendation remainscurrent in the 2009 update.

careful history of current and past use of alcohol, illicit drugs,current or past standard or “alternative therapies,” andchemotherapy drugs should be obtained from patientspresenting with HF. (Level of Evidence: C)

2. A careful history of current and past use of alcohol, illicitdrugs, current or past standard or “alternativetherapies,” and chemotherapy drugs should be obtainedfrom patients presenting with HF. (Level of Evidence: C)


n patients presenting with HF, initial assessment should bemade of the patient’s ability to perform routine and desiredactivities of daily living. (Level of Evidence: C)

3. In patients presenting with HF, initial assessment shouldbe made of the patient’s ability to perform routine anddesired activities of daily living. (Level of Evidence: C)


nitial examination of patients presenting with HF shouldinclude assessment of the patient’s volume status,orthostatic blood pressure changes, measurement of weightand height, and calculation of body mass index. (Level ofEvidence: C)

4. Initial examination of patients presenting with HF shouldinclude assessment of the patient’s volume status,orthostatic blood pressure changes, measurement ofweight and height, and calculation of body mass index.(Level of Evidence: C)


nitial laboratory evaluation of patients presenting with HFshould include complete blood count, urinalysis, serumelectrolytes (including calcium and magnesium), blood ureanitrogen, serum creatinine, fasting blood glucose(glycohemoglobin), lipid profile, liver function tests, andthyroid-stimulating hormone. (Level of Evidence: C)

5. Initial laboratory evaluation of patients presenting with HFshould include complete blood count, urinalysis, serumelectrolytes (including calcium and magnesium), bloodurea nitrogen, serum creatinine, fasting blood glucose(glycohemoglobin), lipid profile, liver function tests, andthyroid-stimulating hormone. (Level of Evidence: C)


welve-lead electrocardiogram and chest radiograph (posterior toanterior [PA] and lateral) should be performed initially in allpatients presenting with HF. (Level of Evidence: C)

6. Twelve-lead electrocardiogram and chest radiograph (PAand lateral) should be performed initially in all patientspresenting with HF. (Level of Evidence: C)


wo-dimensional echocardiography with Doppler should beperformed during initial evaluation of patients presentingwith HF to assess left ventricular ejection fraction (LVEF),LV size, wall thickness, and valve function. Radionuclideventriculography can be performed to assess LVEF andvolumes. (Level of Evidence: C)

7. Two-dimensional echocardiography with Doppler shouldbe performed during initial evaluation of patientspresenting with HF to assess LVEF, left ventricular size,wall thickness, and valve function. Radionuclideventriculography can be performed to assess LVEF andvolumes. (Level of Evidence: C)


oronary arteriography should be performed in patientspresenting with HF who have angina or significant ischemiaunless the patient is not eligible for revascularization of anykind. (Level of Evidence: B)

8. Coronary arteriography should be performed in patientspresenting with HF who have angina or significantischemia unless the patient is not eligible forrevascularization of any kind (4–8). (Level of Evidence: B)


Class IIa

oronary arteriography is reasonable for patients presentingwith HF who have chest pain that may or may not be ofcardiac origin who have not had evaluation of their coronaryanatomy and who have no contraindications to coronaryrevascularization. (Level of Evidence: C)

1. Coronary arteriography is reasonable for patientspresenting with HF who have chest pain that may ormay not be of cardiac origin who have not hadevaluation of their coronary anatomy and who have nocontraindications to coronary revascularization. (Level ofEvidence: C)


oronary arteriography is reasonable for patients presenting withHF who have known or suspected coronary artery disease butwho do not have angina unless the patient is not eligible forrevascularization of any kind. (Level of Evidence: C)

2. Coronary arteriography is reasonable for patientspresenting with HF who have known or suspectedcoronary artery disease but who do not have anginaunless the patient is not eligible for revascularization ofany kind. (Level of Evidence: C)


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able 2. Continued


Class IIa (Continued)

oninvasive imaging to detect myocardial ischemia andviability is reasonable in patients presenting with HF whohave known coronary artery disease and no angina unlessthe patient is not eligible for revascularization of any kind.(Level of Evidence: B)

3. Noninvasive imaging to detect myocardial ischemia andviability is reasonable in patients presenting with HF whohave known coronary artery disease and no anginaunless the patient is not eligible for revascularization ofany kind (9). (Level of Evidence: B)


aximal exercise testing with or without measurement ofrespiratory gas exchange and/or blood oxygen saturation isreasonable in patients presenting with HF to help determinewhether HF is the cause of exercise limitation when thecontribution of HF is uncertain. (Level of Evidence: C)

4. Maximal exercise testing with or without measurementof respiratory gas exchange and/or blood oxygensaturation is reasonable in patients presenting with HFto help determine whether HF is the cause of exerciselimitation when the contribution of HF is uncertain.(Level of Evidence: C)


aximal exercise testing with measurement of respiratory gasexchange is reasonable to identify high-risk patientspresenting with HF who are candidates for cardiactransplantation or other advanced treatments. (Level ofEvidence: B)

5. Maximal exercise testing with measurement ofrespiratory gas exchange is reasonable to identify high-risk patients presenting with HF who are candidates forcardiac transplantation or other advanced treatments(10–12). (Level of Evidence: B)


creening for hemochromatosis, sleep-disturbed breathing, orhuman immunodeficiency virus is reasonable in selectedpatients who present with HF. (Level of Evidence: C)

6. Screening for hemochromatosis, sleep-disturbedbreathing, or human immunodeficiency virus isreasonable in selected patients who present with HF.(Level of Evidence: C)


iagnostic tests for rheumatologic diseases, amyloidosis, orpheochromocytoma are reasonable in patients presentingwith HF in whom there is a clinical suspicion of thesediseases. (Level of Evidence: C)

7. Diagnostic tests for rheumatologic diseases,amyloidosis, or pheochromocytoma are reasonable inpatients presenting with HF in whom there is a clinicalsuspicion of these diseases. (Level of Evidence: C)


ndomyocardial biopsy can be useful in patients presentingwith HF when a specific diagnosis is suspected that wouldinfluence therapy. (Level of Evidence: C)

8. Endomyocardial biopsy can be useful in patientspresenting with HF when a specific diagnosis issuspected that would influence therapy (13). (Level ofEvidence: C)


easurement of BNP can be useful in the evaluation ofpatients presenting in the urgent care setting in whom theclinical diagnosis of HF is uncertain. (Level of Evidence: A)

9. Measurement of natriuretic peptides (BNP and NT-proBNP) can be useful in the evaluation of patientspresenting in the urgent care setting in whom theclinical diagnosis of HF is uncertain. Measurement ofnatriuretic peptides (BNP and NT-proBNP) can be usefulin risk stratification (14–21). (Level of Evidence: A)

Modified recommendation(added a caveat onnatriuretic peptides and theirrole as part of totalevaluation, in both diastolicand systolic dysfunction).

Class IIb

oninvasive imaging may be considered to define thelikelihood of coronary artery disease in patients with HF andLV dysfunction. (Level of Evidence: C)

1. Noninvasive imaging may be considered to define thelikelihood of coronary artery disease in patients with HFand LV dysfunction. (Level of Evidence: C)


olter monitoring might be considered in patients presentingwith HF who have a history of myocardial infarction (MI) andare being considered for electrophysiologic study todocument ventricular tachycardia (VT) inducibility. (Level ofEvidence: C)

2. Holter monitoring might be considered in patientspresenting with HF who have a history of MI and arebeing considered for electrophysiologic study todocument VT inducibility. (Level of Evidence: C)


Class III

ndomyocardial biopsy should not be performed in the routineevaluation of patients with HF. (Level of Evidence: C)

1. Endomyocardial biopsy should not be performed in theroutine evaluation of patients with HF (13). (Level ofEvidence: C)


outine use of signal-averaged electrocardiography is notrecommended for the evaluation of patients presenting withHF. (Level of Evidence: C)

2. Routine use of signal-averaged electrocardiography isnot recommended for the evaluation of patientspresenting with HF. (Level of Evidence: C)


outine measurement of circulating levels of neurohormones(e.g., norepinephrine or endothelin) is not recommended forpatients presenting with HF. (Level of Evidence: C)

3. Routine measurement of circulating levels ofneurohormones (e.g., norepinephrine or endothelin) isnot recommended for patients presenting with HF.(Level of Evidence: C)


3. Recommendations for Serial Clinical Assessment of Patients Presenting With Heart Failure

Class I

ssessment should be made at each visit of the ability of apatient with HF to perform routine and desired activities ofdaily living. (Level of Evidence: C)

1. Assessment should be made at each visit of the abilityof a patient with HF to perform routine and desiredactivities of daily living. (Level of Evidence: C)


ssessment should be made at each visit of the volume statusand weight of a patient with HF. (Level of Evidence: C)

2. Assessment should be made at each visit of the volumestatus and weight of a patient with HF. (Level ofEvidence: C)


areful history of current use of alcohol, tobacco, illicit drugs,“alternative therapies,” and chemotherapy drugs, as well asdiet and sodium intake, should be obtained at each visit of apatient with HF. (Level of Evidence: C)

3. Careful history of current use of alcohol, tobacco, illicitdrugs, “alternative therapies,” and chemotherapy drugs,as well as diet and sodium intake, should be obtained ateach visit of a patient with HF. (Level of Evidence: C)



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.1. Initial Evaluation of Patients

.1.1. Identification of Patients

n general, patients with LV dysfunction or HF present tohe healthcare provider in 1 of 3 ways:

. With a syndrome of decreased exercise tolerance. Mostpatients with HF seek medical attention with complaints ofa reduction in their effort tolerance due to dyspnea and/orfatigue. These symptoms, which may occur at rest or duringexercise, may be attributed inappropriately by the patientand/or healthcare provider to aging, other physiologicalabnormalities (e.g., deconditioning), or other medical dis-orders (e.g., pulmonary disease). Therefore, in a patientwhose exercise capacity is limited by dyspnea or fatigue, thehealthcare provider must determine whether the principalcause is HF or another abnormality. Elucidation of theprecise reason for exercise intolerance can be difficultbecause several disorders may coexist in the same patient. Aclear distinction can sometimes be made only by measure-ments of gas exchange or blood oxygen saturation or byinvasive hemodynamic measurements during graded levelsof exercise (see ACC/AHA 2002 Guideline Update forExercise Testing [22]).

. With a syndrome of fluid retention. Patients may presentwith complaints of leg or abdominal swelling as theirprimary (or only) symptom. In these patients, the impair-ment of exercise tolerance may occur so gradually that itmay not be noted unless the patient is questioned carefullyand specifically about a change in activities of daily living.

. With no symptoms or symptoms of another cardiac ornoncardiac disorder. During their evaluation for adisorder other than HF (e.g., abnormal heart sounds orabnormal electrocardiogram or chest x-ray, hypertensionor hypotension, diabetes mellitus, an acute myocardialinfarction (MI), an arrhythmia, or a pulmonary orsystemic thromboembolic event), patients may be foundto have evidence of cardiac enlargement or dysfunction.

A variety of approaches have been used to quantify theegree of functional limitation imposed by HF. The mostidely used scale is the NYHA functional classification (23),

able 2. Continued

2005 Guideline Recommendations 200

Cl

epeat measurement of ejection fraction (EF) and the severityof structural remodeling can provide useful information inpatients with HF who have had a change in clinical status orwho have experienced or recovered from a clinical event orreceived treatment that might have had a significant effecton cardiac function. (Level of Evidence: C)

1. Repeat mremodelipatientsstatus orclinical ea significEvidence

Cl

he value of serial measurements of BNP to guide therapy forpatients with HF is not well established. (Level of Evidence: C)

1. The valuetherapy f(Level of

ut this system is subject to considerable interobserver variabil- c


ty and is insensitive to important changes in exercise capacity.hese limitations may be overcome by formal tests of exercise

olerance. Measurement of the distance that a patient can walkn 6 minutes may have prognostic significance and may help tossess the level of functional impairment in the very sick, buterial changes in walking distance may not parallel changes inlinical status. Maximal exercise testing, with measurement ofeak oxygen uptake, has been used to identify appropriateandidates for cardiac transplantation, to determine disability,nd to assist in the formulation of an exercise prescription, butts role in the general management of patients with HF has noteen defined.

.1.2. Identification of a Structural and Functionalbnormality

complete history and physical examination are the first stepsn evaluating the structural abnormality or cause responsible forhe development of HF. Direct inquiry may reveal prior orurrent evidence of MI, valvular disease, or congenital heartisease, whereas examination of the heart may suggest theresence of cardiac enlargement, murmurs, or a third heartound. Although the history and physical examination mayrovide important clues about the nature of the underlyingardiac abnormality, identification of the structural abnormal-ty leading to HF generally requires invasive or noninvasivemaging of the cardiac chambers or great vessels.

The single most useful diagnostic test in the evaluation ofatients with HF is the comprehensive 2-dimensional echo-ardiogram coupled with Doppler flow studies to determinehether abnormalities of myocardium, heart valves, or pericar-ium are present and which chambers are involved. Threeundamental questions must be addressed: 1) Is the LVjection fraction (EF) preserved or reduced? 2) Is the structuref the LV normal or abnormal? 3) Are there other structuralbnormalities such as valvular, pericardial, or right ventricularbnormalities that could account for the clinical presentation?his information should be quantified with a numerical esti-ate of EF, measurement of ventricular dimensions and/or

olumes, measurement of wall thickness, and evaluation of

used Update Recommendations Comments

a

rement of EF and the severity of structuralbe useful to provide information in

F who have had a change in clinicalave experienced or recovered from ar received treatment that might have hadfect on cardiac function. (Level of


b

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Right ventricular size and systolic performance should bessessed. Atrial size should also be determined semiquantita-ively and left atrial dimensions and/or volumes measured. Allalves should be evaluated for anatomic and flow abnormalitieso exclude the presence of primary valve disease. Secondaryhanges in valve function, particularly the severity of mitral andricuspid valve insufficiency, should be determined.

Noninvasive hemodynamic data acquired at the time ofchocardiography are an important additional correlate foratients with preserved or reduced EF. Combined quantifica-ion of the mitral valve inflow pattern, pulmonary venousnflow pattern, and mitral annular velocity provides data aboutharacteristics of LV filling and left atrial pressure. Evaluationf the tricuspid valve regurgitant gradient coupled with mea-urement of inferior vena caval dimension and its responseuring respiration provides an estimate of systolic pulmonaryrtery pressure and central venous pressure. Stroke volume maye determined with combined dimension measurement andulsed Doppler in the LV outflow tract (24). However,bnormalities can be present in any of these parameters in thebsence of HF. No single parameter necessarily correlatespecifically with HF; however, a totally normal filling patternrgues against clinical HF.

A comprehensive echocardiographic evaluation is impor-ant, because it is common for patients to have more than 1ardiac abnormality that contributes to the development ofF. Furthermore, the study may serve as a baseline for

omparison, because measurement of EF and the severity oftructural remodeling can provide useful information in pa-ients who have had a change in clinical status or who havexperienced or recovered from a clinical event or receivedreatment that might have had a significant effect on cardiacunction.

Other tests may be used to provide information regardinghe nature and severity of the cardiac abnormality. Radio-uclide ventriculography can provide highly accurate mea-urements of LV function and right ventricular EF, but it isnable to directly assess valvular abnormalities or cardiacypertrophy. Magnetic resonance imaging or computedomography may be useful in evaluating chamber size andentricular mass, detecting right ventricular dysplasia, orecognizing the presence of pericardial disease, as well as inssessing cardiac function and wall motion (25).

Magnetic resonance imaging may also be used to identifyyocardial viability and scar tissue (26). Chest radiography can

e used to estimate the degree of cardiac enlargement andulmonary congestion or to detect the presence of pulmonaryisease. A 12-lead electrocardiogram may demonstrate evi-ence of prior MI, LV hypertrophy, cardiac conduction ab-ormality (e.g., left bundle-branch block), or a cardiac arrhyth-ia. However, because of their low sensitivity and specificity,

either the chest x-ray nor the electrocardiogram should formhe primary basis for determining the specific cardiac abnor-
ality responsible for the development of HF. i

.1.3.2. LABORATORY TESTING

aboratory testing may reveal the presence of disorders oronditions that can lead to or exacerbate HF. The initialvaluation of patients with HF should include a completelood count, urinalysis, serum electrolytes (including cal-ium and magnesium), glycohemoglobin, and blood lipids,s well as tests of both renal and hepatic function, a chestadiograph, and a 12-lead electrocardiogram. Thyroid func-ion tests (especially thyroid-stimulating hormone) shoulde measured, because both hyperthyroidism and hypothy-oidism can be a primary or contributory cause of HF. Aasting transferrin saturation is useful to screen for hemo-hromatosis; several mutated alleles for this disorder areommon in individuals of Northern European descent, andffected patients may show improvement in LV functionfter treatment with phlebotomy and chelating agents.

agnetic resonance imaging of the heart or liver may beeeded to confirm the presence of iron overload. Screeningor human immunodeficiency virus (HIV) is reasonable andhould be considered for all high-risk patients. However,ther clinical signs of HIV infection typically precede anyF symptoms in those patients who develop HIV cardio-yopathy. Serum titers of antibodies developed in response

o infectious organisms are occasionally measured in pa-ients with a recent onset of HF (especially in those with aecent viral syndrome), but the yield of such testing is low,nd the therapeutic implications of a positive result arencertain (see a recent review of the role of endomyocardialiopsy (13), and Section 3.1.3.4, Evaluation of the Possi-ility of Myocardial Disease, in the full-text guideline.ssays for connective tissue diseases and for pheochromo-

ytoma should be performed if these diagnoses are sus-ected, and serum titers of Chagas disease antibodies shoulde checked in patients with nonischemic cardiomyopathyho have traveled in or emigrated from an endemic region.Several recent assays have been developed for natriuretic

eptides (BNP and NT-proBNP). Several of the natriureticeptides are synthesized by and released from the heart.levated plasma BNP levels have been associated with

educed LVEF (27), LV hypertrophy, elevated LV fillingressures, and acute MI and ischemia, although they canccur in other settings, such as pulmonary embolism andhronic obstructive pulmonary disease.

Natriuretic peptides are sensitive to other biological factors,uch as age, sex, weight, and renal function (28). Elevatedevels lend support to a diagnosis of abnormal ventricularunction or hemodynamics causing symptomatic HF (29).rials with these diagnostic markers suggest use in the urgent-

are setting, where they have been used in combination withlinical evaluation to differentiate dyspnea due to HF fromyspnea of other causes (4), and suggest that its use may reduceoth the time to hospital discharge and the cost of treatment30). BNP levels tend to be less elevated in HF with preservedF than in HF with low EF and are lower in obese patients

31,32). Levels of natriuretic peptides may be elevated mean-
ngfully in women and in people over 60 years of age who do

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ot have HF, and thus these levels should be interpretedautiously in such individuals when distinguishing betweenardiac and noncardiac causes of dyspnea. Elevated natriureticeptide levels may lend weight to a suspected diagnosis of HFr trigger consideration of HF when the diagnosis is unknownut should not be used in isolation to confirm or exclude theresence of HF (30,33).

.2.3. Laboratory Assessment

erum electrolytes and renal function should be monitoredoutinely in patients with HF. Of particular importance ishe serial measurement of serum potassium concentration,ecause hypokalemia is a common adverse effect of treat-ent with diuretics and may cause fatal arrhythmias and

ncrease the risk of digitalis toxicity, whereas hyperkalemiaay complicate therapy with angiotensin-converting en-

yme (ACE) inhibitors, angiotensin II receptor blockersARBs), and aldosterone antagonists. Worsening renalunction may require adjustment of the doses of diuretics,enin-angiotensin-aldosterone system antagonists, digoxin,nd noncardiac medications. Development of hyponatremiar anemia may be a sign of disease progression and isssociated with impaired survival.

Serum BNP levels have been shown to parallel the clinicaleverity of HF as assessed by NYHA class in broadopulations. Levels are higher in hospitalized patients andend to decrease during aggressive therapy for decompen-ation (see Section 3.1.3.2. in the full-text guideline, Lab-ratory Testing) (29). Indeed, there is an increasing body ofvidence demonstrating the power of the addition of BNPor NT-proBNP) levels in the assessment of prognosis in aariety of cardiovascular disorders. However, it cannot bessumed that BNP levels can be used effectively as targetsor adjustment of therapy in individual patients. Manyatients taking optimal doses of medications continue tohow markedly elevated levels of BNP, and some patientsemonstrate BNP levels within the normal range despitedvanced HF. The use of BNP measurements to guide theitration of drug doses has not been shown conclusively tomprove outcomes more effectively than achievement of thearget doses of drugs shown in clinical trials to prolong life34). Ongoing trials will help to determine the role of serialNP (or other natriuretic peptides) measurements in bothiagnosis and management of HF.Serial chest radiographs are not recommended in theanagement of chronic HF. Although the cardiothoracic

atio is commonly believed to reflect the cardiac dilatationhat is characteristic of HF, enlargement of the cardiacilhouette primarily reflects changes in right ventricularolume rather than LV function, because the right ventricleorms most of the border of dilated hearts on radiographs.imilarly, changes in the radiographic assessment of pulmo-ary vascular congestion are too insensitive to detect any buthe most extreme changes in fluid status (35).

Repeat assessment of EF may be most useful when the
atient has demonstrated a major change in clinical status. a

oth improvement and deterioration may have importantmplications for future care, although the recommended

edical regimen should be continued in most cases. Im-rovement may reflect recovery from a previous condition,uch as viral myocarditis or hypothyroidism, or may occurfter titration of recommended therapies for chronic HF.hus, it is appropriate to obtain a repeat EF after someeriod of optimal medical therapy, typically 4 to 6 months,o decide about the implantation of an implantableardioverter-defibrillator (ICD). Deterioration may reflectradual disease progression or a new event, such as recurrentI. Routine assessment of EF at frequent, regular, or

rbitrary intervals is not recommended.There has been no established role for periodic invasive or

oninvasive hemodynamic measurements in the manage-ent of HF. Most drugs used for the treatment of HF are

rescribed on the basis of their ability to improve symptomsr survival rather than their effect on hemodynamic vari-bles. Moreover, the initial and target doses of these drugsre selected on the basis of experience in controlled trialsnd are not based on the changes they may produce inardiac output or pulmonary wedge pressure. Nevertheless,nvasive hemodynamic measurements may assist in theetermination of volume status and in distinguishing HFrom other disorders that may cause circulatory instability,uch as pulmonary diseases and sepsis. Measurements ofardiac output and pulmonary wedge pressure through aulmonary artery catheter have also been used in patientsith refractory HF to assess pulmonary vascular resistance,determinant of eligibility for heart transplantation. Car-

iac output can also be measured by noninvasive methods.

.2.4. Assessment of Prognosis

lthough both healthcare providers and patients may benterested in defining the prognosis of an individual patientith HF, the likelihood of survival can be determined

eliably only in populations and not in individuals. How-ver, some attempt at prognostication in HF may provideetter information for patients and their families to helphem appropriately plan for their futures. It also identifiesatients in whom cardiac transplantation or mechanicalevice therapy should be considered.Multivariate analysis of clinical variables has helped to

dentify the most significant predictors of survival, and prog-ostic models have been developed and validated (36). De-reasing LVEF, worsening NYHA functional status, degree ofyponatremia, decreasing peak exercise oxygen uptake, de-reasing hematocrit, widened QRS on 12-lead electrocardio-ram, chronic hypotension, resting tachycardia, renal insuffi-iency, intolerance to conventional therapy, and refractoryolume overload are all generally recognized key prognosticarameters, although the actual prognostic models incorporat-ng them are not widely used in clinical practice (36,37).lthough elevated circulating levels of neurohormonal factorsave also been associated with high mortality rates, the routine
ssessment of neurohormones such as norepinephrine or en-

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othelin is neither feasible nor helpful in clinical management.ikewise, elevated BNP (or NT-proBNP) levels predict higher

isk of HF and other events after MI, whereas markedlevation in BNP levels during hospitalization for HF mayredict rehospitalization and death. Nonetheless, the BNPeasurement has not been clearly shown to supplement careful

linical assessment for management.Because treatment of HF has improved over the past 10

ears, the older prognostic models need to be revalidated (38),nd newer prognostic models may have to be developed.utcomes have been improved for most high-risk patients,hich has resulted in a shift in the selection process for patients

eferred for heart transplantation (38). Routine use of ambu-atory electrocardiographic monitoring, T-wave alternans anal-sis, heart rate variability measurement, and signal-averagedlectrocardiography have not been shown to provide incremen-al value in assessing overall prognosis, although ambulatorylectrocardiographic monitoring can be useful in decision
aking regarding placement of ICDs (39). fi

. Therapy

.3.1. Patients With Reduced Left Ventricularjection Fraction

hanges in this section focused on 3 areas: recommendationsbout electrical device therapy (e.g., cardiac resynchronizationherapy [CRT] and ICDs), the use of a fixed dose combinationf hydralazine and isosorbide dinitrate in self-identified Africanmericans, and the management of atrial fibrillation in pa-

ients with HF. The previous version of the guidelines had aumber of possibly confusing recommendations about selectionf patients for ICD implantation. The writing group hasried to simplify the recommendations, and keep them con-ordant with the most recent guidelines covering the samessue (39,40). Updated trial information has led to thehange in the recommendations about the use of hydralazine/sosorbide dinitrate and about the management of atrial
brillation (Table 3).
able 3. Updates to Section 4.3.1. Patients With Reduced Lefjection Fraction

2005 Guideline Recommendations 2009

4.3.1. Patients With Reduced

C

easures listed as Class I recommendations for patients instages A and B are also appropriate for patients in StageC. (Levels of Evidence: A, B, and C as appropriate)

1. Measurespatientspatientsappropria

iuretics and salt restriction are indicated in patients withcurrent or prior symptoms of HF and reduced LVEF whohave evidence of fluid retention (see Table 4). (Level ofEvidence: C)

2. Diureticswith currwho havefull-text g

ngiotensin converting enzyme inhibitors are recommendedfor all patients with current or prior symptoms of HF andreduced LVEF, unless contraindicated (see text, Table 3 inthe full-text guidelines). (Level of Evidence: A)

3. Angiotenrecommesymptomcontraindguideline

eta blockers (using 1 of the 3 proven to reduce mortality,i.e., bisoprolol, carvedilol, and sustained releasemetoprolol succinate) are recommended for all stablepatients with current or prior symptoms of HF andreduced LVEF, unless contraindicated (see text, Table 3 inthe full-text guidelines). (Level of Evidence: A)

4. Beta blocmortalityrelease mstable paand reduTable 3 inEvidence

ngiotensin II receptor blockers approved for thetreatment of HF (see Table 3) are recommended inpatients with current or prior symptoms of HF andreduced LVEF who are ACE inhibitor-intolerant (see textfor information regarding patients with angioedema).(Level of Evidence: A)

5. Angiotentext guidecurrent oare ACE iregardingEvidence

rugs known to adversely affect the clinical status ofpatients with current or prior symptoms of HF andreduced LVEF should be avoided or withdrawn wheneverpossible (e.g., nonsteroidal anti-inflammatory drugs, mostantiarrhythmic drugs, and most calcium channel blockingdrugs; see text). (Level of Evidence: B)

6. Drugs knpatientsreduced Lwhenevedrugs, mchannel bEvidence

t Ventricular

Focused Update Recommendations Comments

Left Ventricular Ejection Fraction

lass I

listed as Class I recommendations forin stages A and B are also appropriate forin Stage C. (Levels of Evidence: A, B, and C aste)

2005 recommendation remainscurrent in 2009 update.

and salt restriction are indicated in patientsent or prior symptoms of HF and reduced LVEF

evidence of fluid retention (see Table 4 in theuidelines). (Level of Evidence: C)


sin-converting enzyme inhibitors arended for all patients with current or priors of HF and reduced LVEF, unlessicated (see text, Table 3 in the full-texts) (41–53). (Level of Evidence: A)


kers (using 1 of the 3 proven to reduce, i.e., bisoprolol, carvedilol, and sustainedetoprolol succinate) are recommended for all

tients with current or prior symptoms of HFced LVEF, unless contraindicated (see text,

the full-text guidelines) (54–72). (Level of: A)


sin II receptor blockers (see Table 3 in the full-lines) are recommended in patients with

r prior symptoms of HF and reduced LVEF whonhibitor-intolerant (see text for informationpatients with angioedema) (73–83). (Level of

: A)

2005 recommendation remainscurrent but text modified toeliminate specific agentstested.

own to adversely affect the clinical status ofwith current or prior symptoms of HF andVEF should be avoided or withdrawn

r possible (e.g., nonsteroidal anti-inflammatoryost antiarrhythmic drugs, and most calciumlocking drugs; see text) (84–90). (Level of

: B)


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Class I (Continued)

aximal exercise testing with or without measurement ofrespiratory gas exchange is recommended to facilitateprescription of an appropriate exercise program forpatients with HF. (Level of Evidence: C)

2005 recommendation nolonger current. See 2009Class IIa No. 2recommendation below.

xercise training is beneficial as an adjunctive approach toimprove clinical status in ambulatory patients with currentor prior symptoms of HF and reduced LVEF. (Level ofEvidence: B)

7. Exercise training is beneficial as an adjunctiveapproach to improve clinical status in ambulatorypatients with current or prior symptoms of HF andreduced LVEF (90a–90d). (Level of Evidence: B)


n implantable cardioverter-defibrillator is recommended assecondary prevention to prolong survival in patients withcurrent or prior symptoms of HF and reduced LVEF whohave a history of cardiac arrest, ventricular fibrillation, orhemodynamically destabilizing ventricular tachycardia.(Level of Evidence: A)

8. An implantable cardioverter-defibrillator isrecommended as secondary prevention to prolongsurvival in patients with current or prior symptoms ofHF and reduced LVEF who have a history of cardiacarrest, ventricular fibrillation, or hemodynamicallydestabilizing ventricular tachycardia (91–93). (Level ofEvidence: A)


mplantable cardioverter-defibrillator therapy isrecommended for primary prevention to reduce totalmortality by a reduction in sudden cardiac death inpatients with ischemic heart disease who are at least 40days post-MI, have an LVEF less than or equal to 30%,with NYHA functional class II or III symptoms whileundergoing chronic optimal medical therapy, and havereasonable expectation of survival with a good functionalstatus for more than 1 year. (Level of Evidence: A)

9. Implantable cardioverter-defibrillator therapy isrecommended for primary prevention of suddencardiac death to reduce total mortality in patients withnon-ischemic dilated cardiomyopathy or ischemic heartdisease at least 40 days post-MI, a LVEF less than orequal to 35%, and NYHA functional class II or IIIsymptoms while receiving chronic optimal medicaltherapy, and who have reasonable expectation ofsurvival with a good functional status for more than 1year (40,93–99). (Level of Evidence: A)

Modified recommendation to beconsistent with theACC/AHA/Heart RhythmSociety (HRS) 2008 Device-Based Therapy guidelines.

mplantable cardioverter-defibrillator therapy isrecommended for primary prevention to reduce totalmortality by a reduction in sudden cardiac death inpatients with nonischemic cardiomyopathy who have anLVEF less than or equal to 30%, with NYHA functionalclass II or III symptoms while undergoing chronic optimalmedical therapy, and who have reasonable expectation ofsurvival with a good functional status for more than 1year. (Level of Evidence: B)

2005 recommendation nolonger current. See 2009Class I No. 9recommendation above.

atients with LVEF less than or equal to 35%, sinus rhythm,and NYHA functional class III or ambulatory class IVsymptoms despite recommended, optimal medicaltherapy and who have cardiac dyssynchrony, which iscurrently defined as a QRS duration greater than 120 ms,should receive cardiac resynchronization therapy unlesscontraindicated. (Level of Evidence: A)

10. Patients with LVEF of less than or equal to 35%, sinusrhythm, and NYHA functional class III or ambulatoryclass IV symptoms despite recommended, optimalmedical therapy and who have cardiac dyssynchrony,which is currently defined as a QRS duration greaterthan or equal to 0.12 seconds, should receive cardiacresynchronization therapy, with or without an ICD, unlesscontraindicated (100–115). (Level of Evidence: A)

Clarified recommendation(includes therapy with orwithout an ICD).

ddition of an aldosterone antagonist is reasonable inselected patients with moderately severe to severesymptoms of HF and reduced LVEF who can be carefullymonitored for preserved renal function and normalpotassium concentration. Creatinine should be less thanor equal to 2.5 mg per dL in men or less than or equal to2.0 mg per dL in women and potassium should be lessthan 5.0 mEq per liter. Under circumstances wheremonitoring for hyperkalemia or renal dysfunction is notanticipated to be feasible, the risks may outweigh thebenefits of aldosterone antagonists. (Level of Evidence: B)

11. Addition of an aldosterone antagonist is recommendedin selected patients with moderately severe to severesymptoms of HF and reduced LVEF who can becarefully monitored for preserved renal function andnormal potassium concentration. Creatinine should be2.5 mg per dL or less in men or 2.0 mg per dL or lessin women and potassium should be less than 5.0mEq per liter. Under circumstances wheremonitoring for hyperkalemia or renal dysfunction isnot anticipated to be feasible, the risks mayoutweigh the benefits of aldosterone antagonists(116–118). (Level of Evidence: B)


12. The combination of hydralazine and nitrates isrecommended to improve outcomes for patients self-described as African-Americans, with moderate-severesymptoms on optimal therapy with ACE inhibitors,beta blockers, and diuretics (119,120). (Level ofEvidence: B)

New recommendation

Class IIa

1. It is reasonable to treat patients with atrial fibrillationand HF with a strategy to maintain sinus rhythm orwith a strategy to control ventricular rate alone (121–125). (Level of Evidence: A)

New recommendation

2. Maximal exercise testing with or without measurementof respiratory gas exchange is reasonable to facilitateprescription of an appropriate exercise program forpatients presenting with HF. (Level of Evidence: C)

Modified recommendation(changed class ofrecommendation from I toIIa).


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ngiotensin II receptor blockers are reasonable to use asalternatives to ACE inhibitors as first-line therapy forpatients with mild to moderate HF and reduced LVEF,especially for patients already taking ARBs for otherindications. (Level of Evidence: A)

3. Angiotensin II receptor blockers are reasonable to useas alternatives to ACE inhibitors as first-line therapy forpatients with mild to moderate HF and reduced LVEF,especially for patients already taking ARBs for otherindications (73–82). (Level of Evidence: A)


igitalis can be beneficial in patients with current or priorsymptoms of HF and reduced LVEF to decreasehospitalizations for HF. (Level of Evidence: B)

4. Digitalis can be beneficial in patients with current orprior symptoms of HF and reduced LVEF to decreasehospitalizations for HF (126–133). (Level ofEvidence: B)


he addition of a combination of hydralazine and a nitrate isreasonable for patients with reduced LVEF who arealready taking an ACE inhibitor and beta-blocker forsymptomatic HF and who have persistent symptoms.(Level of Evidence: B)

5. The addition of a combination of hydralazine and anitrate is reasonable for patients with reduced LVEFwho are already taking an ACE inhibitor and betablocker for symptomatic HF and who have persistentsymptoms (119,134). (Level of Evidence: B)


lacement of an implantable cardioverter-defibrillator isreasonable in patients with LVEF of 30% to 35% of anyorigin with NYHA functional class II or III symptoms whoare taking chronic optimal medical therapy and who havereasonable expectation of survival with good functionalstatus of more than 1 year. (Level of Evidence: B)

2005 recommendation nolonger current. See 2009Class I No. 9recommendation above.

6. For patients who have LVEF less than or equal to 35%,a QRS duration of greater than or equal to 0.12seconds, and atrial fibrillation (AF), CRT with or withoutan ICD is reasonable for the treatment of NYHAfunctional class III or ambulatory class IV heart failuresymptoms on optimal recommended medical therapy(3,135). (Level of Evidence: B)

New recommendation added tobe consistent with the ACC/AHA/HRS 2008 Device-BasedTherapy guidelines (40).

7. For patients with LVEF of less than or equal to 35%with NYHA functional class III or ambulatory class IVsymptoms who are receiving optimal recommendedmedical therapy and who have frequent dependence onventricular pacing, CRT is reasonable (3). (Level ofEvidence: C)

New recommendation added tobe consistent with the ACC/AHA/HRS 2008 Device-BasedTherapy guidelines.

Class IIb

combination of hydralazine and a nitrate might bereasonable in patients with current or prior symptoms ofHF and reduced LVEF who cannot be given an ACEinhibitor or ARB because of drug intolerance, hypotension,or renal insufficiency. (Level of Evidence: C)

1. A combination of hydralazine and a nitrate might bereasonable in patients with current or prior symptomsof HF and reduced LVEF who cannot be given an ACEinhibitor or ARB because of drug intolerance,hypotension, or renal insufficiency (119,136,137).(Level of Evidence: C)


he addition of an ARB may be considered in persistentlysymptomatic patients with reduced LVEF who are alreadybeing treated with conventional therapy. (Level ofEvidence: B)

2. The addition of an ARB may be considered inpersistently symptomatic patients with reduced LVEFwho are already being treated with conventionaltherapy (73–82). (Level of Evidence: B)


Class III

outine combined use of an ACE inhibitor, ARB, andaldosterone antagonist is not recommended for patientswith current or prior symptoms of HF and reduced LVEF.(Level of Evidence: C)

1. Routine combined use of an ACE inhibitor, ARB, andaldosterone antagonist is not recommended forpatients with current or prior symptoms of HF andreduced LVEF. (Level of Evidence: C)


alcium channel blocking drugs are not indicated as routinetreatment for HF in patients with current or priorsymptoms of HF and reduced LVEF. (Level of Evidence: A)

2. Calcium channel blocking drugs are not indicated asroutine treatment for HF in patients with current orprior symptoms of HF and reduced LVEF (138–141).(Level of Evidence: A)


ong-term use of an infusion of a positive inotropic drugmay be harmful and is not recommended for patientswith current or prior symptoms of HF and reduced LVEF,except as palliation for patients with end-stage diseasewho cannot be stabilized with standard medical treatment(see recommendations for Stage D). (Level of Evidence: C)

3. Long-term use of an infusion of a positive inotropicdrug may be harmful and is not recommended forpatients with current or prior symptoms of HF andreduced LVEF, except as palliation for patients withend-stage disease who cannot be stabilized withstandard medical treatment (see recommendations forStage D). (Level of Evidence: C)


se of nutritional supplements as treatment for HF is notindicated in patients with current or prior symptoms of HFand reduced LVEF. (Level of Evidence: C)

4. Use of nutritional supplements as treatment for HF isnot indicated in patients with current or priorsymptoms of HF and reduced LVEF. (Level ofEvidence: C)


ormonal therapies other than to replete deficiencies arenot recommended and may be harmful to patients withcurrent or prior symptoms of HF and reduced LVEF. (Levelof Evidence: C)

5. Hormonal therapies other than to replete deficienciesare not recommended and may be harmful to patientswith current or prior symptoms of HF and reducedLVEF. (Level of Evidence: C)



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.3.1.1. GENERAL MEASURES

easures listed as Class I recommendations for patients intage A or B are also appropriate for patients with current orrior symptoms of HF (also see Section 5, Treatment ofpecial Populations). In addition, moderate sodium restric-ion, along with daily measurement of weight, is indicatedo permit effective use of lower and safer doses of diureticrugs, even if overt sodium retention can be controlled byhe use of diuretics. Immunization with influenza andneumococcal vaccines may reduce the risk of a respiratorynfection. Although most patients should not participate ineavy labor or exhaustive sports, physical activity should bencouraged (except during periods of acute exacerbation ofhe signs and symptoms of HF, or in patients with suspectedyocarditis), because restriction of activity promotes phys-

cal deconditioning, which may adversely affect clinicaltatus and contribute to the exercise intolerance of patientsith HF (142–145).Three classes of drugs can exacerbate the syndrome of HF

nd should be avoided in most patients:

. Antiarrhythmic agents (146) can exert important car-diodepressant and proarrhythmic effects. Of availableagents, only amiodarone and dofetilide (147) have beenshown not to adversely affect survival.

. Calcium channel blockers can lead to worsening HF andhave been associated with an increased risk of cardiovas-cular events (148). Of available calcium channel blockers,only the vasoselective ones have been shown not toadversely affect survival (139,149).

. Nonsteroidal anti-inflammatory drugs can cause sodiumretention and peripheral vasoconstriction and can atten-uate the efficacy and enhance the toxicity of diuretics andACE inhibitors (84–87). A discussion of the use ofaspirin as a unique agent is found later in this section (seeSection 4.3.1.2.2.1., Angiotensin Converting EnzymeInhibitors in the Management of Heart Failure, in thefull-text guideline).

Patients with HF should be monitored carefully forhanges in serum potassium, and every effort should beade to prevent the occurrence of either hypokalemia or

yperkalemia, both of which may adversely affect cardiacxcitability and conduction and may lead to sudden death150). Activation of both the sympathetic nervous systemnd renin-angiotensin system can lead to hypokalemia151,152), and most drugs used for the treatment of HF canlter serum potassium (153). Even modest decreases inerum potassium can increase the risks of using digitalis andntiarrhythmic drugs (150,154), and even modest increasesn serum potassium may prevent the use of treatmentsnown to prolong life (155). Hence, many experts believehat serum potassium concentrations should be targeted inhe 4.0 to 5.0 mmol per liter range. In some patients,orrection of potassium deficits may require supplementa-ion of magnesium and potassium (156). In others (partic-
larly those taking ACE inhibitors alone or in combination o

ith aldosterone antagonists), the routine prescription of po-assium salts may be unnecessary and potentially deleterious.

Of the general measures that should be used in patientsith HF, possibly the most effective yet least used is closebservation and follow-up. Nonadherence with diet andedications can rapidly and profoundly affect the clinical

tatus of patients, and increases in body weight and minorhanges in symptoms commonly precede by several days theccurrence of major clinical episodes that require emergencyare or hospitalization. Patient education and close super-ision, which includes surveillance by the patient and his orer family, can reduce the likelihood of nonadherence and

ead to the detection of changes in body weight or clinicaltatus early enough to allow the patient or a healthcarerovider an opportunity to institute treatments that canrevent clinical deterioration. Supervision need not beerformed by a physician and may ideally be accomplishedy a nurse or physician’s assistant with special training in theare of patients with HF. Such an approach has beeneported to have significant clinical benefits (157–160).ecommendations Concerning Aldosterone Antagonists. The

ddition of low-dose aldosterone antagonists is recom-ended in carefully selected patients with moderately severe

r severe HF symptoms and recent decompensation or withV dysfunction early after MI. These recommendations areased on the strong data demonstrating reduced death andehospitalization in 2 clinical trial populations (155,161).he entry criteria for these trials describe a broader popu-

ation than was actually enrolled, such that the favorablefficacy/ toxicity ratio may not be as applicable to patients athe margins of trial eligibility. For both of these major trials,atients were excluded for a serum creatinine level in excessf 2.5 mg per dL, but few patients were actually enrolledith serum creatinine levels over 1.5 mg per dL. In the trialf patients after MI, there was a significant interactionetween serum creatinine and benefit of eplerenone. Theverage serum creatinine of enrolled patients was 1.1 mg perL, above which there was no demonstrable benefit forurvival.

To minimize the risk of life-threatening hyperkalemia inatients with low LVEF and symptoms of HF, patientshould have initial serum creatinine less than 2.0 to 2.5 mger dL without recent worsening and serum potassium lesshan 5.0 mEq per liter without a history of severe hyperka-emia. In view of the consistency of evidence for patientsith low LVEF early after MI and patients with recentecompensation and severe symptoms, it may be reasonableo consider addition of aldosterone antagonists to loopiuretics for some patients with mild to moderate symptomsf HF; however, the writing committee strongly believeshat there are insufficient data or experience to provide apecific or strong recommendation. Because the safety andfficacy of aldosterone antagonist therapy have not beenhown in the absence of loop diuretic therapy, it is noturrently recommended that such therapy be given without
ther concomitant diuretic therapy in chronic HF. Al-

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hough 17% of patients in the CHARM (Candesartan ineart Failure: Assessment of Reduction in Mortality andorbidity) add-on trial (83) were receiving spironolactone,

he safety of the combination of ACE inhibitors, ARBs,nd aldosterone antagonists has not been explored ade-uately, and this combination cannot be recommended..3.1.2.5. VENTRICULAR ARRHYTHMIAS AND PREVENTION OF SUDDEN DEATH.

atients with LV dilation and reduced LVEF frequentlyanifest ventricular tachyarrhythmias, both nonsustained

entricular tachycardia (VT) and sustained VT. The cardiacortality of patients with all types of ventricular tachyar-

hythmias is high. The high mortality results from progres-ive HF, as well as from sudden death. Sudden death isften equated with a primary arrhythmic event, but multipleauses of sudden death have been documented and includeschemic events such as acute MI (162), electrolyte distur-ances, pulmonary or systemic emboli, or other vascularvents. Although ventricular tachyarrhythmias are the mostommon rhythms associated with unexpected sudden death,radycardia and other pulseless supraventricular rhythms areommon in patients with advanced HF (163).

Sudden death can be decreased meaningfully by theherapies that decrease disease progression, as discussedlsewhere in these guidelines. For instance, clinical trialsith beta blockers have shown a reduction in sudden death,

s well as in all-cause mortality, in both postinfarctionatients and patients with HF regardless of cause54,58,60,164,165). Aldosterone antagonists decrease sud-en death and overall mortality in HF early after MI and indvanced HF (161). Sudden unexpected death can beecreased further by the use of implanted devices thaterminate sustained arrhythmias (40,102). Even whenpecific antiarrhythmic therapy is necessary to diminishecurrent ventricular tachyarrhythmias and device firings,he frequency and tolerance of arrhythmias may bemproved with appropriate therapy for HF. In someases, definitive therapy of myocardial ischemia or othereversible factors may prevent recurrence of tachyarrhyth-ia, particularly polymorphic VT, ventricular fibrillation,

nd nonsustained VT. Nonetheless, implantable defibril-ators should be recommended in all patients who havead a life-threatening tachyarrhythmia and have an other-ise good prognosis.The absolute frequency of sudden death is highest in

atients with severe symptoms, or Stage D HF. Manyatients with end-stage symptoms experience “suddeneath” that is nonetheless expected. Prevention of suddeneath in this population could potentially shift the mode ofeath from sudden to that of progressive HF withoutecreasing total mortality, as competing risks of deathmerge. On the other hand, prevention of sudden death inild HF may allow many years of meaningful survival. Thisakes it imperative for physicians to not only assess an

ndividual patient’s risk for sudden death but also assessverall prognosis and functional capacity before consider-
tion of device implantation. a

econdary Prevention of Sudden Death. Patients with previousardiac arrest or documented sustained ventricular arrhyth-ias have a high risk of recurrent events. Implantation of an

CD has been shown to reduce mortality in cardiac arresturvivors. An ICD is indicated for secondary prevention ofeath from ventricular tachyarrhythmias in patients withtherwise good clinical function and prognosis, for whomrolongation of survival is a goal. Patients with chronic HFnd a low EF who experience syncope of unclear origin havehigh rate of subsequent sudden death and should also be

onsidered for placement of an ICD (95). However, whenentricular tachyarrhythmias occur in a patient with arogressive and irreversible downward spiral of clinical HFecompensation, placement of an ICD is not indicated torevent recurrence of sudden death, because death is likelymminent regardless of mode. An exception may exist forhe small minority of patients for whom definitive therapyuch as cardiac transplantation is planned.rimary Prevention of Sudden Death. Patients with low EFithout prior history of cardiac arrest, spontaneous VT, or

nducible VT (positive programmed electrical stimulationtudy) have a risk of sudden death that is lower than forhose who have experienced previous events, but it remainsignificant. Within this group, it has not yet been possible todentify those patients at highest risk, especially in thebsence of prior MI. Approximately 50% to 70% of patientsith low EF and symptomatic HF have episodes of non-

ustained VT on routine ambulatory electrocardiographiconitoring; however, it is not clear whether the occurrence

f complex ventricular arrhythmias in these patients withF contributes to the high frequency of sudden death or,

lternatively, simply reflects the underlying disease process166–168). Antiarrhythmic drugs to suppress prematureentricular depolarizations and nonsustained ventricular ar-hythmias have not improved survival (88,89), althoughonsustained VT may play a role in triggering ventricularachyarrhythmias. Furthermore, most antiarrhythmic drugsave negative inotropic effects and can increase the risk oferious arrhythmia; these adverse cardiovascular effects arearticularly pronounced in patients with low EF (90,146,69). This risk is especially high with the use of class IAgents (quinidine and procainamide), class IC agents (fle-ainide and propafenone), and some class III agents (D-otalol) (88,89,170,171), which have increased mortality inost-MI trials (172). Amiodarone is a class III antiarrhyth-ic agent but differs from other drugs in this class in havingsympatholytic effect on the heart (173). Amiodarone has

een associated with overall neutral effects on survival whendministered to patients with low EF and HF (93,174–76). Amiodarone therapy may also act through mecha-isms other than antiarrhythmic effects, because amioda-one has been shown in some trials to increase LVEF andecrease the incidence of worsening HF (175,176). Sideffects of amiodarone have included thyroid abnormalities,ulmonary toxicity, hepatotoxicity, neuropathy, insomnia,
nd numerous other reactions. Therefore, amiodarone

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hould not be considered as part of the routine treatment ofatients with HF, with or without frequent prematureentricular depolarizations or asymptomatic nonsustainedT; however, it remains the agent most likely to be safe and

ffective when antiarrhythmic therapy is necessary to pre-ent recurrent atrial fibrillation or symptomatic ventricularrrhythmias. Other pharmacological antiarrhythmic thera-ies, apart from beta blockers, are rarely indicated in HF butay occasionally be used to suppress recurrent ICD shockshen amiodarone has been ineffective or discontinuedwing to toxicity.The role of ICDs in the primary prevention of sudden death

n patients without prior history of symptomatic arrhythmiasas been explored recently in a number of trials. If sustainedentricular tachyarrhythmias can be induced in the electro-hysiology laboratory in patients with previous MI or chronicschemic heart disease, the risk of sudden death in theseatients is in the range of 5% to 6% per year and can bemproved by ICD implantation (96).

The role of ICD implantation for the primary preventionf sudden death in patients with HF and low EF and noistory of spontaneous or inducible VT has been addressedy several large trials that used only readily available clinicalata as entry criteria (93,97,98). The first of these demon-trated that ICDs, compared with standard medical therapy,ecreased the occurrence of total mortality for patients withF of 30% or less after remote MI (97). Absolute mortalityas decreased in the ICD arm by 5.6%, a relative decreasef 31% over 20 months. In a second trial, a survival benefitas not demonstrated with devices implanted within 6 to 40ays after an acute MI in patients who at that time had anF less than 35% and abnormal heart rate variability.lthough sudden deaths were decreased, there was an

ncrease in other events, and ICD implantation did notonfer any survival benefit in this setting (98). A third trialxamining the benefit of ICD implantation for patients withF less than 35% and NYHA functional class II to III

ymptoms of HF included both ischemic and nonischemicauses of HF; absolute mortality was decreased by 7.2% over5-year period in the arm that received a simple “shock-

ox” ICD with backup pacing at a rate of 40 bpm. Thisepresented a relative mortality decrease of 23%, which wassurvival increase of 11% (93). There was no improvement

n survival during the first year, with a 1.8% absolute survivalenefit per year averaged over the next 4 years. TheEFINITE (Defibrillators in Non-Ischemic Cardiomyop-

thy Treatment Evaluation) trial compared medical therapylone with medical therapy plus an ICD in patients withonischemic cardiomyopathy, NYHA class I to III HF, andn LVEF less than 36% (177). The ICD was associatedith a reduction in all-cause mortality that did not reach

tatistical significance but was consistent in terms of mag-itude of effect (30%) with the findings of the MADIT IIMulticenter Automatic Defibrillator Implantation II) (97)
nd the SCD-HeFT (Sudden Cardiac Death in Heart t

ailure: Trial of prophylactic amiodarone versus implant-ble defibrillator therapy) (92).

There is an intrinsic variability in measurement of EFarticularly shortly after recovery from an acute coronaryyndrome event. Moreover, as reviewed earlier, the pivotalrimary prevention trials used a variable inclusion EF,anging below 30% or 36%. Given the totality of the dataemonstrating the efficacy of an ICD in reducing overallortality in a population with dilated cardiomyopathy of

ither ischemic or nonischemic origins, the current recom-endation is to include all such patients with an LVEF of

ess than or equal to 35%.ICDs are highly effective in preventing death due to

entricular tachyarrhythmias; however, frequent shocksrom an ICD can lead to a reduced quality of life, whetherriggered appropriately by life-threatening rhythms or inap-ropriately by sinus or other supraventricular tachycardia.or symptoms from recurrent discharges triggered by ven-

ricular arrhythmias or atrial fibrillation, antiarrhythmicherapy, most often amiodarone, may be added. For recur-ent ICD discharges from VT despite antiarrhythmic ther-py, catheter ablation may be effective (178).

It is important to recognize that ICDs have the potentialo aggravate HF and have been associated with an increasen HF hospitalizations (97,99). This may result from rightentricular pacing that produces dyssynchronous cardiacontraction; however, the occurrence of excess nonsuddenvents with ICDs placed early after MI suggests that otheractors may also limit the overall benefit from ICDs. Carefulttention to the details of ICD implantation, programming,nd pacing function is important for all patients with lowF who are treated with an ICD. The ACC/AHA/HRS008 Guidelines for Device-Based Therapy of Cardiachythm Abnormalities (40) provides further discussion of

he potential problem of worsening HF and LV function inll patients with right ventricular pacing.

The decision regarding the balance of potential risks andenefits of ICD implantation for an individual patient thusemains a complex one. A decrease in incidence of suddeneath does not necessarily translate into decreased totalortality, and decreased total mortality does not guaranteeprolongation of survival with meaningful quality of life.his concept is particularly important in patients with

imited prognosis owing to advanced HF or other seriousomorbidities, because there was no survival benefit ob-erved from ICD implantation until after the first year in 2f the major trials (93,97). Furthermore, the average age ofatients with HF and low EF is over 70 years, a populationot well represented in any of the ICD trials. Comorbiditiesommon in the elderly population, such as prior stroke,hronic pulmonary disease, and crippling arthritic condi-ions, as well as nursing home residence, should be factorednto discussions regarding ICD. Atrial fibrillation, a com-

on trigger for inappropriate shocks, is more prevalent inhe elderly population. The gap between community and
rial populations is particularly important for a device

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herapy that may prolong survival but has no positive impactn function or quality of life. Some patients may suffer aiminished quality of life because of device-site complica-ions, such as bleeding, hematoma, or infections, or afterCD discharges, particularly those that are inappropriate.

Consideration of ICD implantation is thus recom-ended in patients with EF less than or equal to 35% andild to moderate symptoms of HF and in whom survivalith good functional capacity is otherwise anticipated to

xtend beyond 1 year. Because medical therapy may sub-tantially improve EF, consideration of ICD implantshould follow documentation of sustained reduction of EFespite a course of beta blockers and ACE inhibitors orRBs; however, ICDs are not warranted in patients with

efractory symptoms of HF (Stage D) or in patients withoncomitant diseases that would shorten their life expect-ncy independent of HF. Before implantation, patientshould be fully informed of their cardiac prognosis, includ-ng the risk of both sudden and nonsudden mortality; thefficacy, safety, and risks of an ICD; and the morbidityssociated with an ICD shock. Patients and families shouldlearly understand that the ICD does not improve clinicalunction or delay HF progression. Most important, theossible reasons and process for potential future deactivationf defibrillator features should be discussed long beforeunctional capacity or outlook for survival is severelyeduced..3.1.3.3. HYDRALAZINE AND ISOSORBIDE DINITRATE. In a large-scalerial that compared the vasodilator combination with pla-ebo, the use of hydralazine and isosorbide dinitrate reducedortality but not hospitalizations in patients with HF

reated with digoxin and diuretics but not an ACE inhibitorr beta blocker (136,137). However, in another large-scalerial that compared the vasodilator combination with anCE inhibitor, the ACE inhibitor produced more favorable

ffects on survival (52), a benefit not evident in the subgroupf patients with Class III to IV HF. In both trials, the usef hydralazine and isosorbide dinitrate produced frequentdverse reactions (primarily headache and gastrointestinalomplaints), and many patients could not continue treat-ent at target doses.Of note, a post hoc retrospective analysis of both vaso-

ilator trials demonstrated particular efficacy of isosorbideinitrate and hydralazine in the African American cohort119). A confirmatory trial has been done. In that trial,hich was limited to the patients self-described as Africanmerican, the addition of hydralazine and isosorbide dini-

rate to standard therapy with an ACE inhibitor and/or aeta blocker was shown to be of significant benefit (120).he benefit was presumed to be related to enhanced nitricxide bioavailability. Accordingly, this combination is rec-mmended for African Americans who remain symptom-tic despite optimal medical therapy. Whether this benefit isvident in other patients with HF remains to be investi-ated. The combination of hydralazine and isosorbide
initrate should not be used for the treatment of HF in t

atients who have no prior use of an ACE inhibitor andhould not be substituted for ACE inhibitors in patientsho are tolerating ACE inhibitors without difficulty.Despite the lack of data with the vasodilator combination

n patients who are intolerant of ACE inhibitors, theombined use of hydralazine and isosorbide dinitrate may beonsidered as a therapeutic option in such patients. How-ver, compliance with this combination has generally beenoor because of the large number of tablets required and theigh incidence of adverse reactions (52,136). For patientsith more severe HF symptoms and ACE inhibitor intol-

rance, the combination of hydralazine and nitrates is usedrequently, particularly when ACE inhibitor therapy isimited by hypotension or renal insufficiency. There are,owever, no trials addressing the use of isosorbide dinitratend hydralazine specifically in the population of patientsho have persistent symptoms and intolerance to inhibitorsf the renin-angiotensin system..3.1.3.4. CARDIAC RESYNCHRONIZATION THERAPY. Approximatelyne-third of patients with low EF and Class III to IVymptoms of HF manifest a QRS duration greater than 0.12econds (179–181). This electrocardiographic representa-ion of abnormal cardiac conduction has been used todentify patients with dyssynchronous ventricular contrac-ion. While imperfect, no other consensus definition ofardiac dyssynchrony exists as yet, although several echo-ardiographic measures appear promising. The mechanicalonsequences of dyssynchrony include suboptimal ventric-lar filling, a reduction in LV dP/dt (rate of rise ofentricular contractile force or pressure), prolonged durationand therefore greater severity) of mitral regurgitation, andaradoxical septal wall motion (182–184). Ventricular dys-ynchrony has also been associated with increased mortalityn HF patients (103–105). Dyssynchronous contraction cane addressed by electrically activating the right and leftentricles in a synchronized manner with a biventricularacemaker device. This approach to HF therapy, commonlyalled cardiac resynchronization therapy (CRT), may en-ance ventricular contraction and reduce the degree ofecondary mitral regurgitation (106–108). In addition, thehort-term use of CRT has been associated with improve-ents in cardiac function and hemodynamics without an

ccompanying increase in oxygen use (109), as well as adaptivehanges in the biochemistry of the failing heart (107).

To date, more than 4000 HF patients with ventricularyssynchrony have been evaluated in randomized controlledrials of optimal medical therapy alone versus optimaledical therapy plus CRT with or without an ICD. CRT,hen added to optimal medical therapy in persistently

ymptomatic patients, has resulted in significant improve-ents in quality of life, functional class, exercise capacity (by

eak oxygen uptake) and exercise distance during a-minute walk test, and EF in patients randomized to CRT110) or to the combination of CRT and ICD (102,111,12). In a meta-analysis of several CRT trials, HF hospi-
alizations were reduced by 32% and all-cause mortality by

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5% (112). The effect on mortality in this meta-analysisecame apparent after approximately 3 months of therapy112). In 1 study, subjects were randomized to optimalharmacological therapy alone, optimal medical therapylus CRT alone, or optimal medical therapy plus theombination of CRT and an ICD. Compared with optimaledical therapy alone, both device arms significantly de-

reased the combined risk of all-cause hospitalization andll-cause mortality by approximately 20%, whereas theombination of a CRT and an ICD decreased all-causeortality significantly by 36% (113). More recently, in a

andomized controlled trial comparing optimal medicalherapy alone with optimal medical therapy plus CRT alonewithout a defibrillator), CRT significantly reduced theombined risk of death of any cause or unplanned hospitaldmission for a major cardiovascular event (analyzed as timeo first event) by 37% (101). In that trial, all-cause mortalityas significantly reduced by 36% and HF hospitalizationsy 52% with the addition of CRT.Thus, there is strong evidence to support the use of CRT

o improve symptoms, exercise capacity, quality of life,VEF, and survival and to decrease hospitalizations inatients with persistently symptomatic HF undergoingptimal medical therapy who have cardiac dyssynchrony (asvidenced by a prolonged QRS duration). The use of anCD in combination with CRT should be based on thendications for ICD therapy.

With few exceptions, resynchronization trials have en-olled patients in normal sinus rhythm. Although the entryriteria specified QRS duration only longer than 0.12econds, the average QRS duration in the large trials wasonger than 0.15 seconds, with less information demonstrat-ng benefit in patients with lesser prolongation of QRS.wo small studies, one randomized (114) and the otherbservational (115), evaluated the potential benefit of CRTn HF patients with ventricular dyssynchrony and atrialbrillation. Although both studies demonstrated the benefitf CRT in these patients, the total number of patientsxamined (fewer than 100) precludes a recommendation forRT in otherwise eligible patients with atrial fibrillation.o date, only a small number of patients with “pure” rightundle-branch block have been enrolled in CRT trials.imilarly, the prolonged QRS duration associated with rightentricular pacing has also been associated with ventricularyssynchrony that may be improved by CRT, but noublished studies have addressed this situation as yet.ecommendations regarding CRT for patients with LVEFf less than or equal to 35%, NYHA functional class III, andmbulatory class IV symptoms or dependence on ventricularacing have been updated to be consistent with the ACC/HA/HRS 2008 Guidelines for Device-Based Therapy ofardiac Rhythm Abnormalities (40).Ten studies have reported on CRT peri-implant morbid-

ty and mortality. There were 13 deaths in 3113 patients0.4%). From a pooled assessment of 3475 patients in 17
tudies, the success rate of implantation was approximately m

0% (112). Device-related problems during the first 6onths after implantation reported in 13 studies included

ead malfunction or dislodgement in 8.5%, pacemakerroblems in 6.7%, and infection in 1.4% of cases. Theseorbidity and mortality data are derived from trials that

sed expert centers. Results in individual clinical centersay vary considerably and are subject to a significant

earning curve for each center; however, as implantationechniques evolve and equipment improves, complicationates may also decline (112)..3.1.5.2. INTERMITTENT INTRAVENOUS POSITIVE INOTROPIC THERAPY.

lthough positive inotropic agents can improve cardiacerformance during short- and long-term therapy185,186), long-term oral therapy with these drugs has notmproved symptoms or clinical status (131,187–197) andas been associated with a significant increase in mortality,specially in patients with advanced HF (195,198–203).espite these data, some physicians have proposed that the

egularly scheduled intermittent use of intravenous positivenotropic drugs (e.g., dobutamine or milrinone) in a super-ised outpatient setting might be associated with somelinical benefits (204–206).

However, there has been little experience with intermit-ent home infusions of positive inotropic agents in con-rolled clinical trials. Nearly all of the available data areerived from open-label and uncontrolled studies or fromrials that have compared one inotropic agent with another,ithout a placebo group (204–207). Most trials have been

mall and short in duration and thus have not been able torovide reliable information about the effect of treatment onhe risk of serious cardiac events. Much, if not all, of theenefit seen in these uncontrolled reports may have beenelated to the increased surveillance of the patient’s statusnd intensification of concomitant therapy and not to these of positive inotropic agents. Only 1 placebo-controlledrial of intermittent intravenous positive inotropic therapyas been published (208), and its findings are consistentith the results of long-term studies with continuous oralositive inotropic therapy in HF (e.g., with milrinone),hich showed little efficacy and were terminated earlyecause of an increased risk of death.Given the lack of evidence to support their efficacy and

oncerns about their toxicity, intermittent infusions ofositive inotropic agents (whether at home, in an outpatientlinic, or in a short-stay unit) should not be used in theong-term treatment of HF, even in its advanced stages.he use of continuous infusions of positive inotropic agents

s palliative therapy in patients with end-stage diseaseStage D) is discussed later in this document (123,124).

.4. Patients With Refractory End-Stageeart Failure (Stage D)

he role of intermittent infusions as effective treatment fordvanced HF has been further clarified by an additional
ulticenter trial (Table 4).

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Most patients with HF due to reduced LVEF respondavorably to pharmacological and nonpharmacological treat-ents and enjoy a good quality of life and enhanced

urvival; however, some patients do not improve or experi-nce rapid recurrence of symptoms despite optimal medicalherapy. Such patients characteristically have symptoms atest or on minimal exertion, including profound fatigue;annot perform most activities of daily living; frequentlyave evidence of cardiac cachexia; and typically requireepeated and/or prolonged hospitalizations for intensive

able 4. Updates to Section 4.4. Patients With Refractory End

2005 Guideline Recommendations 2009 F

Updates to Section 4.4. Patients With R

C

eticulous identification and control of fluid retention isrecommended in patients with refractory end-stageHF. (Level of Evidence: B)

1. Meticulous idrecommende(209–216). (

eferral for cardiac transplantation in potentiallyeligible patients is recommended for patients withrefractory end-stage HF. (Level of Evidence: B)

2. Referral forpatients is reend-stage HF

eferral of patients with refractory end-stage HF to anHF program with expertise in the management ofrefractory HF is useful. (Level of Evidence: A)

3. Referral of pprogram witHF is useful

ptions for end-of-life care should be discussed with thepatient and family when severe symptoms in patientswith refractory end-stage HF persist despiteapplication of all recommended therapies. (Level ofEvidence: C)

4. Options for epatient andwith refractoof all recomm

atients with refractory end-stage HF andimplantable defibrillators should receiveinformation about the option to inactivatedefibrillation. (Level of Evidence: C)

5. Patients withdefibrillatorsinactivate the

Cl

onsideration of an LV assist device as permanent or“destination” therapy is reasonable in highly selectedpatients with refractory end-stage HF and anestimated 1-year mortality over 50% with medicaltherapy. (Level of Evidence: B)

1. Consideratio“destination”patients with1-year morta(222,223). (

Cl

ulmonary artery catheter placement may bereasonable to guide therapy in patients withrefractory end-stage HF and persistently severesymptoms. (Level of Evidence: C)

1. Pulmonary areasonable tend-stage HF(217,224). (

he effectiveness of mitral valve repair or replacementis not established for severe secondary mitralregurgitation in refractory end-stage HF. (Level ofEvidence: C)

2. The effectiveis not well esregurgitation(Level of Evid

ontinuous intravenous infusion of a positive inotropicagent may be considered for palliation of symptomsin patients with refractory end-stage HF. (Level ofEvidence: C)

3. Continuous iagent may bpatients withof Evidence:

C

artial left ventriculectomy is not recommended inpatients with nonischemic cardiomyopathy andrefractory end-stage HF. (Level of Evidence: C)

1. Partial left vpatients withrefractory en

outine intermittent infusions of positive inotropicagents are not recommended for patients withrefractory end-stage HF. (Level of Evidence: B)

2. Routine inteinotropic agerefractory en

anagement. These individuals represent the most ad- S


anced stage of HF and should be considered for specializedreatment strategies, such as mechanical circulatory support,ontinuous intravenous positive inotropic therapy, referralor cardiac transplantation, or hospice care. Before a patients considered to have refractory HF, physicians shouldonfirm the accuracy of the diagnosis, identify any contrib-ting conditions, and ensure that all conventional medicaltrategies have been optimally employed. Measures listed aslass I recommendations for patients in stages A, B, and C

re also appropriate for patients in end-stage HF (also see

e Heart Failure (Stage D)

d Update Recommendations Comments

tory End-Stage Heart Failure (Stage D)

cation and control of fluid retention isatients with refractory end-stage HFof Evidence: B)


c transplantation in potentially eligibleended for patients with refractory

). (Level of Evidence: B)


s with refractory end-stage HF to a HFrtise in the management of refractory221). (Level of Evidence: A)


life care should be discussed with thewhen severe symptoms in patients-stage HF persist despite applicationd therapies. (Level of Evidence: C)


tory end-stage HF and implantablereceive information about the option to

rillator. (Level of Evidence: C)


a

n LV assist device as permanent orpy is reasonable in highly selectedctory end-stage HF and an estimateder 50% with medical therapyf Evidence: B)


b

atheter placement may bee therapy in patients with refractorypersistently severe symptomsf Evidence: C)


of mitral valve repair or replacementhed for severe secondary mitralractory end-stage HF (225–227).C)


nous infusion of a positive inotropicidered for palliation of symptoms in

ctory end-stage HF (228,229). (Level


I

lectomy is not recommended inchemic cardiomyopathy ande HF. (Level of Evidence: C)


nt infusions of vasoactive and positivee not recommended for patients withe HF (230,231). (Level of Evidence: A)

Modified recommendation(changed Level of Evidencefrom B to A).

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urther therapies are appropriate, careful discussion of therognosis and options for end-of-life care should be initi-ted (see Section 7, End-of-Life Considerations, in theull-text guideline) (2).

.4.3. Intravenous Peripheral Vasodilators andositive Inotropic Agents

atients with refractory HF are hospitalized frequently forlinical deterioration, and during such admissions, they com-only receive infusions of both positive inotropic agents

dobutamine, dopamine, or milrinone) and vasodilator drugsnitroglycerin, nitroprusside, or nesiritide) in an effort tomprove cardiac performance, facilitate diuresis, and promotelinical stability. Some physicians have advocated the place-ent of pulmonary artery catheters in patients with refractoryF, with the goal of obtaining hemodynamic measurements

hat might be used to guide the selection and titration ofherapeutic agents (224). However, the logic of this approachas been questioned, because many useful drugs for HFroduce benefits by mechanisms that cannot be evaluated byeasuring their short-term hemodynamic effects (232,233).egardless of whether invasive hemodynamic monitoring issed, once the clinical status of the patient has stabilized, everyffort should be made to devise an oral regimen that canaintain symptomatic improvement and reduce the subse-

uent risk of deterioration. Assessment of the adequacy andolerability of orally based strategies may necessitate observa-ion in the hospital for at least 48 hours after the infusions are


Patients who cannot be weaned from intravenous toral therapy despite repeated attempts may require place-ent of an indwelling intravenous catheter to allow for

he continuous infusion of dobutamine or milrinone or,s has been used more recently, nesiritide. Such a strategys commonly used in patients who are awaiting cardiacransplantation, but it may also be used in the outpatientetting in patients who otherwise cannot be dischargedrom the hospital. The decision to continue intravenousnfusions at home should not be made until all alternativettempts to achieve stability have failed repeatedly, be-ause such an approach can present a major burden to theamily and health services and may ultimately increase theisk of death. However, continuous intravenous supportay provide palliation of symptoms as part of an overall

lan to allow the patient to die with comfort at home228,229). The use of continuous intravenous support tollow hospital discharge should be distinguished from thentermittent administration of infusions of such agents toatients who have been successfully weaned from inotro-ic support (220). Intermittent outpatient infusions ofither vasoactive drugs such as nesiritide or positivenotropic drugs have not shown to improve symptoms orurvival in patients with advanced HF (220,230,231).

.5. The Hospitalized Patient (New)

ew recommendations and text have been developed on the
iscontinued (234). hospitalized patient (Table 5).
able 5. Recommendations for the Hospitalized Patient

2009 Focused Update Recommendations Comments

Class I

1. The diagnosis of HF is primarily based on signs and symptoms derived from a thorough history and physical examination. Cliniciansshould determine the following:

New recommendation

a. adequacy of systemic perfusion;

b. volume status;

c. the contribution of precipitating factors and/or comorbidities;

d. if the heart failure is new onset or an exacerbation of chronic disease; and

e. whether it is associated with preserved ejection fraction.

Chest radiographs, electrocardiogram, and echocardiography are key tests in this assessment. (Level of Evidence: C)

2. Concentrations of B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) should be measured inpatients being evaluated for dyspnea in which the contribution of HF is not known. Final diagnosis requires interpreting theseresults in the context of all available clinical data and ought not to be considered a stand alone test (235,236). (Level of Evidence: A)

New recommendation

3. Acute coronary syndrome precipitating HF hospitalization should be promptly identified by electrocardiogram and cardiac troponintesting, and treated, as appropriate to the overall condition and prognosis of the patient. (Level of Evidence: C)

New recommendation

4. It is recommended that the following common potential precipitating factors for acute HF be identified as recognition of thesecomorbidities is critical to guide therapy:

New recommendation

● acute coronary syndromes/coronary ischemia;

● severe hypertension;

● atrial and ventricular arrhythmias;

● infections;

● pulmonary emboli;

● renal failure; and

● medical or dietary noncompliance. (Level of Evidence: C)

5. Oxygen therapy should be administered to relieve symptoms related to hypoxemia. (Level of Evidence: C) New recommendation

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able 5. Continued

2009 Focused Update Recommendations Comments

Class I (Continued)

6. Whether the diagnosis of HF is new or chronic, patients who present with rapid decompensation and hypoperfusion associated withdecreasing urine output and other manifestations of shock are critically ill and rapid intervention should be used to improvesystemic perfusion. (Level of Evidence: C)

New recommendation

7. Patients admitted with HF and with evidence of significant fluid overload should be treated with intravenous loop diuretics. Therapyshould begin in the emergency department or outpatient clinic without delay, as early intervention may be associated with betteroutcomes for patients hospitalized with decompensated HF (21,237,238). (Level of Evidence: B) If patients are already receivingloop diuretic therapy, the initial intravenous dose should equal or exceed their chronic oral daily dose. Urine output and signs andsymptoms of congestion should be serially assessed, and diuretic dose should be titrated accordingly to relieve symptoms and toreduce extracellular fluid volume excess. (Level of Evidence: C)

New recommendation

8. Effect of HF treatment should be monitored with careful measurement of fluid intake and output; vital signs; body weight,determined at the same time each day; clinical signs (supine and standing) and symptoms of systemic perfusion and congestion.Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of IV diuretics or activetitration of HF medications. (Level of Evidence: C)

New recommendation

9. When diuresis is inadequate to relieve congestion, as evidenced by clinical evaluation, the diuretic regimen should be intensifiedusing either:

New recommendation

a. higher doses of loop diuretics;

b. addition of a second diuretic (such as metolazone, spironolactone or intravenous chlorothiazide); or

c. continuous infusion of a loop diuretic. (Level of Evidence: C)

0. In patients with clinical evidence of hypotension associated with hypoperfusion and obvious evidence of elevated cardiac fillingpressures (e.g., elevated jugular venous pressure; elevated pulmonary artery wedge pressure), intravenous inotropic or vasopressordrugs should be administered to maintain systemic perfusion and preserve end-organ performance while more definitive therapy isconsidered. (Level of Evidence: C)

New recommendation

1. Invasive hemodynamic monitoring should be performed to guide therapy in patients who are in respiratory distress or with clinicalevidence of impaired perfusion in whom the adequacy or excess of intracardiac filling pressures cannot be determined fromclinical assessment. (Level of Evidence: C)

New recommendation

2. Medications should be reconciled in every patient and adjusted as appropriate on admission to and discharge from the hospital.(Level of Evidence: C)

New recommendation

3. In patients with reduced ejection fraction experiencing a symptomatic exacerbation of HF requiring hospitalization during chronicmaintenance treatment with oral therapies known to improve outcomes, particularly ACE inhibitors or ARBs and beta-blockertherapy, it is recommended that these therapies be continued in most patients in the absence of hemodynamic instability orcontraindications. (Level of Evidence: C)

New recommendation

4. In patients hospitalized with HF with reduced ejection fraction not treated with oral therapies known to improve outcomes,particularly ACE inhibitors or ARBs and beta-blocker therapy, initiation of these therapies is recommended in stable patients priorto hospital discharge (239,240). (Level of Evidence: B)

New recommendation

5. Initiation of beta-blocker therapy is recommended after optimization of volume status and successful discontinuation ofintravenous diuretics, vasodilators, and inotropic agents. Beta-blocker therapy should be initiated at a low dose and only in stablepatients. Particular caution should be used when initiating beta blockers in patients who have required inotropes during theirhospital course (239,240). (Level of Evidence: B)

New recommendation

6. In all patients hospitalized with HF, both with preserved (see Section 4.3.2., Patients With HF and Normal LVEF, in the full-textguideline) and low EF, transition should be made from intravenous to oral diuretic therapy with careful attention to oral diureticdosing and monitoring of electrolytes. With all medication changes, the patient should be monitored for supine and uprighthypotension, worsening renal function and HF signs/symptoms. (Level of Evidence: C)

New recommendation

7. Comprehensive written discharge instructions for all patients with a hospitalization for HF and their caregivers is stronglyrecommended, with special emphasis on the following 6 aspects of care: diet, discharge medications, with a special focus onadherence, persistence, and uptitration to recommended doses of ACE inhibitor/ARB and beta-blocker medication, activity level,follow-up appointments, daily weight monitoring, and what to do if HF symptoms worsen. (Level of Evidence: C)

New recommendation

8. Postdischarge systems of care, if available, should be used to facilitate the transition to effective outpatient care for patientshospitalized with HF (112,241–247). (Level of Evidence: B)

New recommendation

Class IIa

1. When patients present with acute HF and known or suspected acute myocardial ischemia due to occlusive coronary disease,especially when there are signs and symptoms of inadequate systemic perfusion, urgent cardiac catheterization andrevascularization is reasonable where it is likely to prolong meaningful survival. (Level of Evidence: C)

New recommendation

2. In patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension, vasodilators such asintravenous nitroglycerin, nitroprusside or nesiritide can be beneficial when added to diuretics and/or in those who do not respondto diuretics alone. (Level of Evidence: C)

New recommendation

3. Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF who have persistent symptomsdespite empiric adjustment of standard therapies, and

New recommendation

a. whose fluid status, perfusion, or systemic or pulmonary vascular resistances are uncertain.

b. whose systolic pressure remains low, or is associated with symptoms, despite initial therapy,

c. whose renal function is worsening with therapy

d. who require parenteral vasoactive agents or

e. who may need consideration for advanced device therapy or transplantation. (Level of Evidence: C)


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A patient may develop acute or progressive symptoms ofF and require hospitalization. In general, there are 3

linical profiles that describe the hospitalized patient withF: 1) the patient with volume overload, manifested by

ulmonary and/or systemic congestion, frequently precipi-ated by an acute increase in chronic hypertension; 2) theatient with profound depression of cardiac output mani-ested by hypotension, renal insufficiency, and/or a shockyndrome, and 3) the patient with signs and symptoms ofoth fluid overload and shock. Irrespective of the presentinglinical picture, there have been a confusing variety of termsn the literature used to describe these patients, includingcute HF syndrome, acute decompensated HF, or cardio-enic shock. However different these 3 groups of patientsay be in outcome, they can all be characterized as havingchange in HF signs and symptoms resulting in a need forrgent therapy. Patients with HF and preserved LVEF (seeection 4.3.2, Patients With Heart Failure and Normal Leftentricular Ejection Fraction in the full-text guideline) are just

s likely to be admitted to hospital as those with HF and lowVEF (251). Admission with HF is often triggered by aoncomitant cardiovascular event such as a symptomatic tachy-rrhythmia, unstable coronary syndrome, or a cerebrovascularvent; often the admission is related to medical or dietaryoncompliance. The threshold for admission may also be

owered when HF exacerbation is accompanied with a non-ardiac condition such as pneumonia or newly diagnosednemia. Indeed, it is important to note that concurrent con-itions and comorbidities such as coronary artery disease,ypertension, valvular heart disease, arrhythmias, renal dys-unction, diabetes, thromboembolism, and anemia are oftenresent, more so than has usually been described in clinicalrials, and may precipitate or contribute to the pathophysiologyf the syndrome. Unfortunately, the precipitating event leadingo hospitalization is not always readily apparent.

ommon Factors That Precipitate Hospitalization foreart Failure

Noncompliance with medical regimen, sodium and/orfluid restrictionAcute myocardial ischemia

able 5. Continued

2009 Focused Update Recomme

Class IIa

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C

1. Use of parenteral inotropes in normotensive patients with acute decompensis not recommended (249). (Level of Evidence: B)

2. Routine use of invasive hemodynamic monitoring in normotensive patientssymptomatic response to diuretics and vasodilators is not recommended (2

Uncorrected high blood pressure w


Atrial fibrillation and other arrhythmiasRecent addition of negative inotropic drugs (e.g., vera-pamil, nifedipine, diltiazem, beta blockers)Pulmonary embolusNonsteroidal anti-inflammatory drugsExcessive alcohol or illicit drug useEndocrine abnormalities (e.g., diabetes mellitus, hyper-thyroidism, hypothyroidism)Concurrent infections (e.g., pneumonia, viral illnesses)

HF hospitalizations account for a substantial portion ofhe overall costs of caring for patients with HF and may bessociated with a staggering degree of morbidity and mor-ality, particularly in the elderly population. It is evident thathe prognosis after an index hospitalization for HF isminous, with a 50% rate of readmission at 6 months and a5% to 35% incidence of death at 12 months (252–256).ndeed, many HF trials now incorporate the need forospitalization as an important endpoint with which tovaluate a new therapy; government agencies and insuranceompanies are increasingly interested in understanding therequency of repeat HF hospitalizations. Thus, it is impor-ant to outline what should occur in the hospital for the HFatient requiring therapy. The scope of these recommenda-ions are based on evidence from the few available random-zed trials evaluating management strategies in the acuteecompensated HF patient (248–250,257,258), analyses of

arge registries, and consensus opinion. Additional andore comprehensive information on this subject may be

ound in the guidelines from the Heart Failure Society ofmerica and the European Society of Cardiology

259,260,260a).

.5.1. Diagnostic Strategies

he diagnosis of HF in the hospitalized patient should beased primarily on signs and symptoms, as discussed inection 3.1., Initial Evaluation of Patients. Clinicians needo determine as accurately and as quickly as possible 1) theolume status of the patient, 2) the adequacy of circulatoryupport or perfusion, and 3) the role or presence ofrecipitating factors and/or comorbidities. In the patient

ons Comments

tinued)

to medical therapy (248). (Level of Evidence: B) New recommendation

b

reasonable for those patients presenting withcardiac output, with or without congestion, tonce: C)

New recommendation

I

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irected toward understanding what has caused the appar-nt acute worsening of clinical symptoms. Many of the stepsn this investigation are identical to those used in the initialvaluation of HF (see Sections 3.1.3., Evaluation of theause of Heart Failure and 3.2., Ongoing Evaluation ofatients, in the full-text guideline). When the diagnosis ofF is uncertain, determination of plasma BNP or NT-

roBNP concentration should be considered in patientseing evaluated for dyspnea who have signs and symptomsompatible with HF. The natriuretic peptide concentrationhould not be interpreted in isolation but in the context ofll available clinical data bearing on the diagnosis of HF.

An important cause of worsening HF, and for new-onsetF, is an acute MI. Because many patients admitted with

cute HF have coronary artery disease, troponins are typi-ally evaluated at admission for acute exacerbation. Actualriteria for an acute coronary event that may indicate theeed for further intervention may be present in up to 20% ofatients (261,262). However, many other patients may have

ow levels of detectable troponins not meeting criteria for ancute ischemic event but typical of chronic HF with an acutexacerbation (263). Registry data have suggested that these of coronary angiography is low for patients hospitalizedith decompensated HF and opportunities to diagnose

mportant coronary artery disease may be missed. Symptomsf HF or cardiogenic shock associated with an ischemicvent are covered in other guidelines (264,265) and areeyond the scope of this update. For the patient with newlyiscovered HF, clinicians should be aware of the importantole of coronary artery disease in causing HF and should beertain that coronary structure and function are well delin-ated (see Section 3.1.2., Identification of a Structural andunctional Abnormality) while simultaneously beginning

reatment. Coronary visualization may be an important partf the evaluation of patients hospitalized with HF.Often, patients with chronic HF are admitted with acute

ecompensation from a number of possible precipitatingauses. Clinicians should carefully review the patient’saintenance HF medications and decide whether adjust-ents should be made as a result of the hospitalization. The

arge majority of patients with HF admitted to the hospital,specially those with concomitant hypertension, should haveheir oral therapy continued, or even uptitrated, duringospitalization. It is important to note that it has beenhown that continuation of beta blockers for most patientss well tolerated and results in better outcomes (239,240).

ithholding of or reduction in beta-blocker therapy shoulde considered only in patients hospitalized after recentnitiation or increase in beta-blocker therapy or with markedolume overload. Patients admitted with worseningzotemia should be considered for a reduction in or tempo-ary discontinuation of their ACE inhibitors, ARBs, and/orldosterone antagonists until renal function improves. Pa-ients with marked volume overload will require intravenousiuretic therapy with uptitration of diuretic dose and/or
ddition of synergistic diuretic agents. It should be noted r

hat uptitration of ACE inhibitors or beta blockers duringecompensation may reduce the efficacy of the acute inter-entions to relieve congestion. Although it is important tonsure that evidence-based medications are instituted prioro the patient leaving the hospital, it is equally as critical toeassess medications on admission and to adjust theirdministration in light of the worsening HF.

.5.2. Treatment in the Hospital

.5.2.1. DIURETICS: THE PATIENT WITH VOLUME OVERLOAD

atients admitted with evidence of significant fluid overloadhould initially be treated with loop diuretics, usually givenntravenously. Therapy for this compelling presentation of

F should begin in the emergency department and shoulde initiated without delay. Early intervention has beenssociated with better outcomes for patients hospitalizedith decompensated HF (266,267). After admission to theospital, patients should be carefully monitored in accor-ance with the severity of their symptoms and the results ofnitial findings on the physical examination and laboratoryssessment. Careful and frequent serial evaluation of theatient is important primarily to assess volume status (seeection 3.2.2., Assessment of Volume Status, in the full-textuideline,) and adequacy of circulatory support. Laboratoryarameters are likewise necessary to judge efficacy of treat-ent (see Sections 3.1.3.2., Laboratory Testing, and 3.2.3.,aboratory Assessment). Monitoring of daily weight, su-ine and standing vital signs, fluid input, and output is aecessary part of daily management; assessment of dailylectrolytes and renal function should be done while intra-enous diuretics or active HF medication titration is beingndertaken.Intravenous loop diuretics have the potential to reduce

lomerular filtration rate (GFR), further worsen neurohu-oral activation, and produce electrolyte disturbances.hus, although the use of diuretics may result in the

ffective relief of symptoms, their impact on mortality hasot been well studied. Diuretics should be administered atoses sufficient to produce a rate of diuresis that willptimize volume status and relieve signs and symptoms ofongestion without inducing an excessively rapid reductionn intravascular volume, which could result in hypotension,enal dysfunction, or both (see Sections 4.3.1.2.1., Diuret-cs, and 4.4.1., Management of Fluid Status, in the full-textuideline). Because loop diuretics have a relatively shortalf-life, sodium reabsorption in the tubules will occur oncehe tubular concentration of the diuretics declines. There-ore, strictly limiting sodium intake and dosing the diureticultiple times per day will enhance effectiveness of the

iuresis (209,268–274). Some patients may present withongestion and moderate to severe renal dysfunction. Theesponse to diuretics may be significantly blunted, requiringigher initial doses. In many cases, reduction of fluidverload may improve not only congestion but also renalysfunction, particularly if significant venous congestion is
educed (275).

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Clinical experience suggests it is difficult to determinehether congestion has been adequately treated in manyatients, and registry data have confirmed that patients arerequently discharged after a net weight loss of only a fewounds. Although patients may rapidly improve symptom-tically, they may remain hemodynamically compromised.nfortunately, the routine use of serial natriuretic peptideeasurement (BNP or NT-proBNP) or even a Swan-Ganz

atheter to monitor hemodynamics has not been shown toe helpful in improving the outcomes of the hospitalizedatient with HF. Nevertheless, careful evaluation of allhysical findings, laboratory parameters, weight change, andet fluid change should be considered before dischargelanning is commenced.When a patient with congestion fails to respond to initial

oses of intravenous diuretics, several options may beonsidered. Efforts should be taken to make certain that,ndeed, congestion persists and that another hemodynamicrofile or perhaps another disease process is not evident.his is particularly important for the patient with progres-

ive renal insufficiency. If there is substantial doubt abouthe fluid status of the patient, HF experts suggest that it isn appropriate time for a formal hemodynamic assessmentf ventricular filling pressures and cardiac output, typicallyone with a right heart catheterization. If volume overload

s confirmed, the dose of the loop diuretic should be initiallyncreased to ensure that adequate drug levels reach theidney. If this is inadequate, a second type of diuretic,ypically a thiazide (metolazone or intravenous chlorothia-ide) or spironolactone, can be added to improve diureticesponsiveness. As a third strategy, continuous infusion ofhe loop diuretic may be considered. By continuous deliveryf the diuretic to the nephron, rebound resorption occurringuring the time blood levels of diuretic are low is avoidednd ototoxicity risk may actually be reduced (see Sections.3.1.2.1., Diuretics, and 4.4.1., Management of Fluidtatus) (209,210,274,276–282). If all diuretic strategies arensuccessful, ultrafiltration or another renal replacementtrategy may be reasonable. Ultrafiltration moves water andmall to medium-weight solutes across a semipermeableembrane to reduce volume overload. Because the electro-

yte concentration is similar to plasma, relatively moreodium can be removed than by diuretics (213,248,283–85). Consultation with a kidney specialist may be appro-riate before opting for any mechanical strategy to affectiuresis.

.5.2.2. VASODILATORS

here are a number of clinical scenarios whereby theddition of vasodilators to the HF regimen of the hospital-zed patient might be appropriate. For patients with ade-uate blood pressure and ongoing congestion not sufficientlyesponsive to diuretics and standard oral therapy (e.g.,aintenance of prior HF medications, if applicable), intra-

enous vasodilators such as nitroprusside, nitroglycerin, or
esiritide may be added to the treatment regimen. Regard- r

ess of the agent used, the clinician should make certain thatntravascular volume is, in fact, expanded and that theatient’s blood pressure can tolerate the addition of theasodilating drug.

Intravenous nitroglycerin, primarily through venodilationffects, lowers preload and may help to more rapidly reduceulmonary congestion. Patients with HF and hypertension,oronary ischemia, or significant mitral regurgitation areften cited as ideal candidates for the use of intravenousitroglycerin. However, tachyphylaxis to nitroglycerin mayevelop rather quickly and up to 20% of those with HF mayevelop resistance to even high doses (286–288). Sodiumitroprusside is a balanced preload-reducing venodilator andfterload-reducing arteriodilator that also dilates the pulmo-ary vasculature. Data demonstrating efficacy are limited,nd invasive hemodynamic blood pressure monitoring isypically required. Nitroprusside has the potential for pro-ucing marked hypotension and is usually used in thentensive care setting as well; longer infusions of the drugave been associated with thiocyanate toxicity, particularly

n the setting of renal insufficiency. Nitroprusside is poten-ially of value in severely congested patients with hyperten-ion or severe mitral valve regurgitation complicating LVysfunction. Nesiritide (human BNP) reduces LV fillingressure but has variable effects on cardiac output, urinaryutput, and sodium excretion. The severity of dyspnea iseduced more rapidly compared to diuretics alone. Becauseesiritide has a longer effective half-life than nitroglycerin oritroprusside, side effects such as hypotension may persist

onger. Conservative dosing of the drug (i.e., no bolus) andse of only the recommended doses may reduce complica-ions. Adverse renal consequences with nesiritide have beenuggested; careful monitoring of renal function is mandatory257,289–294). The effects of nesiritide on mortality remainncertain and active clinical investigation is ongoing.The role of intravenous vasodilators for the patient

ospitalized with HF cannot be generalized. The goals ofF therapy with vasodilators, in the absence of more

efinitive data, include a more rapid resolution of congestiveymptoms; relief of anginal symptoms while awaiting cor-nary intervention; control of hypertension complicatingF; and, in conjunction with ongoing hemodynamic mon-

toring while the intravenous drug is administered, improve-ent of hemodynamic abnormalities prior to instituting oralF medications.

.5.2.3. INOTROPES

atients presenting with either predominantly low outputyndrome (e.g., symptomatic hypotension) or combinedongestion and low output may be considered for intrave-ous inotropes such as dopamine, dobutamine, and milri-one. These agents may help relieve symptoms due to poorerfusion and preserve end-organ function in patients withevere systolic dysfunction and dilated cardiomyopathy.notropic agents are of greatest value in patients with
elative hypotension and intolerance or no response to

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asodilators and diuretics. Clinicians should be cautionedgain that the use of these drugs portends a very poorrognosis for their patients; a thorough hemodynamicssessment must be undertaken to ensure that the lowutput syndrome is responsible for the presenting clinicaligns and symptoms. Likewise, clinicians should not use apecific blood pressure value that might or might not meanypotension, to dictate the use of inotropic agents. Rather,depressed blood pressure associated with signs of poor

ardiac output or hypoperfusion (e.g., cold clammy skin,ool extremities, decreased urine output, altered mentation)hould prompt a consideration for more aggressive intrave-ous therapy. Dobutamine requires the beta-receptor for its

notropic effects, while milrinone does not. This may be aignificant consideration for patients already maintained oneta-blocking drugs. Furthermore, milrinone has vasodilat-ng properties for both the systemic circulation and theulmonary circulation. Despite these considerations, there iso evidence of benefit for routine use of inotropic support inatients presenting with acute HF due to congestion only249,295–297). Indeed, data from several studies suggest anncrease in adverse outcomes when inotropes are used.hus, inotropes should be confined to carefully selectedatients with low blood pressure and reduced cardiac outputho can have blood pressure and heart rhythm monitored

losely (see Section 4.4.3., Intravenous Peripheral Vasodi-ators and Positive Inotropic Agents).

Routine invasive hemodynamic monitoring is not indicatedor most patients hospitalized with symptoms of worsening

F. Recent evaluations of the use of right heart catheterizationo improve outcomes have been essentially neutral with regardo overall benefit (250,298). However, hemodynamic monitor-ng should be strongly considered in patients whose volumend filling pressures are uncertain or who are refractory tonitial therapy, particularly in those whose filling pressures andardiac output are unclear. Patients with clinically significantypotension (systolic blood pressure typically less than 90 mmg or symptomatic low systolic blood pressure) and/or wors-

ning renal function during initial therapy might also benefit.atients being considered for cardiac transplantation or place-ent of a mechanical circulatory support device are also

andidates for complete right heart catheterization, a necessaryart of the initial evaluation (see Section 4.4.4., Mechanicalnd Surgical Strategies, in the full-text guideline). Invasiveemodynamic monitoring should be performed in patientsith 1) presumed cardiogenic shock requiring escalating pres-

or therapy and consideration of mechanical support, 2) severelinical decompensation in which therapy is limited by uncer-ainty regarding relative contributions of elevated filling pres-ures, hypoperfusion, and vascular tone, 3) apparent depen-ence on intravenous inotropic infusions after initial clinical

mprovement, or 4) persistent severe symptoms despite adjust-ent of recommended therapies. This reinforces the concept

hat right heart catheterization is best reserved for thoseituations where a specific clinical or therapeutic question
eeds to be addressed. A

.5.2.4. OTHER CONSIDERATIONS

ther treatment or diagnostic strategies may be necessary forndividual patients after stabilization, particularly related to thenderlying cause of the acute event. Considerations are similaro those previously discussed in Section 3.1.3., Evaluation ofhe Cause of Heart Failure. The patient hospitalized with HFs at increased risk for thromboembolic complications and deepenous thrombosis and should receive prophylactic anticoagu-ation with either intravenous unfractionated heparin or sub-utaneous preparations of unfractionated or low-molecular-eight heparin, unless contraindicated (299).As the hospitalized patient becomes more clinically stable

nd volume status normalizes, oral HF therapy should benitiated or reintroduced (see Sections 4.3.1., Patients Witheduced Left Ventricular Ejection Fraction, and 4.3.2.,atients With HF and Normal LVEF, in the full-textuideline). Particular caution should be used when initiatingeta blockers in patients who have required inotropes duringheir hospital course or when initiating ACE inhibitors inhose patients who have experienced marked azotemia.uring additional hospital days, the patient should be fully

ransitioned off all intravenous therapy and oral therapyhould be adjusted and maximized. The clinical team shouldrovide further education about HF to both the patient andamily. The treating clinicians should also reassess overallrognosis once current functional status and precipitatingauses of the hospitalization have been determined. Theppropriateness of discussion about advanced therapy or endf life preferences should also be considered (see Sections.2.4., Assessment of Prognosis, and 7, End of Life Con-iderations, in the full-text guideline). On discharge, theatient, the family, and the patient’s primary physicianhould be aware and supportive of the follow-up plans.

.5.3. The Hospital Discharge

o ensure safe, high-quality, and efficient care for patientsollowing hospitalization for HF, the consistent use oflinical practice guidelines developed by the ACCF, theHA, and the Heart Failure Society of America should beromoted during and after the hospital stay. One criticalerformance measure for care coordination and transition ishat of written discharge instructions or educational mate-ial given to patient and/or caregiver at discharge to home oruring the hospital stay addressing all of the following:ctivity level, diet, discharge medications, follow-up ap-ointment, weight monitoring, and what to do if symptomsorsen (300). Education of HF patients and their families is

ritical and often complex. Failure of these patients tonderstand how best to comply with physician’s and otherealthcare providers’ instructions is often a cause of HFxacerbation leading to subsequent hospital readmission.

Large registries of hospitalized HF patients suggest thatany patients are discharged before optimal volume status

s achieved, or sent home without the benefit of life-savingherapies such as ACE/ARB and beta-blocker medications.
mong hospitals providing care for patients with HF, there

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s significant individual variability in conformity to quality-f-care indicators and clinical outcomes and a substantialap in overall performance (301). Patients are dischargedithout adequate control of their blood pressure or theentricular response to atrial fibrillation. Often, the treatinglinician fails to appreciate the severity of the HF process orelays diagnostic testing until the patient is seen as anutpatient. These problems, and others, may account for theigh rate of HF rehospitalizations seen in the United States.It is, therefore, incumbent on healthcare professionals to

e certain that patients and their families have an under-tanding of the causes of HF, prognosis, therapy, dietaryestrictions, activity, importance of compliance, and signsnd symptoms of recurrent HF. Thorough discharge plan-ing that includes a special emphasis on ensuring compli-nce with an evidence-based medication regimen (241) isssociated with improved patient outcomes (242,302,303).

Several studies have examined the effect of providingore intensive delivery of discharge instructions coupled

ightly with subsequent well-coordinated follow-up care foratients hospitalized with HF, many with positive results112,243–245). Comprehensive discharge planning plusostdischarge support for older patients with HF canignificantly reduce readmission rates and may improveealth outcomes such as survival and quality of life without

ncreasing costs. A meta-analysis (246) of 18 studies repre-enting data from 8 countries randomized 3304 oldernpatients with HF to comprehensive discharge planninglus postdischarge support or usual care. During a meanbservation period of 8 months, fewer intervention patientsere readmitted compared with controls. Analysis of studies

eporting secondary outcomes found a trend toward lowerll-cause mortality, length of stay, hospital costs, andmprovement in quality-of-life scores for patients assignedo an intervention compared with usual care. One othermportant study (247) focusing on hospital discharge foratients with HF demonstrated that the addition of a-hour, nurse educator–delivered teaching session at theime of hospital discharge using standardized instructions
esulted in improved clinical outcomes, increased self-care (

easure adherence, and reduced cost of care. Patientseceiving the education intervention had a lower risk ofehospitalization or death and lower costs of care.

The importance of patient safety for all patients hospi-alized with HF cannot be overemphasized. Meaningfulvidence has facilitated a much better understanding of theystems changes necessary to achieve safer care. This in-ludes the adoption by all US hospitals of a standardized setf 30 “Safe Practices” endorsed by the National Qualityorum (304), which overlap in many ways with the Nationalatient Safety Goals espoused by The Joint Commission

305). Improved communication between physicians andurses, medication reconciliation, transitions between careettings, and consistent documentation are examples ofatient safety standards that should be ensured for patientsischarged from the hospital with HF. Care information,specially changes in orders and new diagnostic informa-ion, must be transmitted in a timely and clearly under-tandable form to all of the patient’s current healthcareroviders who need that information to provide follow-up care.Hospitalization is in and of itself an independent risk

actor for shortened survival in patients with chronic HF.ence, appropriate levels of symptomatic relief, support,

nd palliative care for patients with chronic HF should beddressed as an ongoing key component of their plan ofare, especially when hospitalized with acute decompensa-ion (306). Fortunately, most US hospitals today have directccess to palliative care services (307). Good evidence existsor the critical importance of delivering comprehensiveupportive care to these patients, including the assessmentnd treatment of dyspnea and physiological issues includingnxiety and depression (308,309).

. Treatment of Special Populations

he recommendations for hydralazine/isosorbide dinitrate in apecific population have been clarified in this section and in arevious section (120,134), based on a recent multicenter trial
Table 6).

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. Patients With Heart Failure Who Haveoncomitant Disorders

.1.3. Supraventricular Arrhythmias

here have been additional trials investigating the appropriateanagement of atrial fibrillation in patients with HF. The text

as been modified to reflect the lessons learned from these trialssee Section 4.3.1, Patients With Reduced Left Ventricularjection Fraction). There is also an ACC/AHA/ESC guideline

n the management of atrial fibrillation (312).The course of patients with HF is frequently complicated

y supraventricular tachyarrhythmias, which may occurhen the myocardial disease process affects the atria orhen the atria are distended as a result of pressure or volumeverload of the right or left ventricles. The most commonreatable atrial arrhythmia is atrial fibrillation, which affects0% to 30% of patients with chronic HF and is associatedith a reduction in exercise capacity and a worse long-termrognosis (313–315).Supraventricular tachyarrhythmias may exert adverse ef-

ects via 4 different mechanisms: 1) the loss of atrialnhancement of ventricular filling may compromise cardiac

able 6. Updates to Section 5. Treatment of Special Populatio

2005 Guideline Recommendation 2009 Focused Upda

Updates to Section 5. Tre

C

1. The combination of adinitrate and hydralazmedical regimen for Hinhibitors and beta blin order to improve oudescribed as African Afunctional class III orbenefit similarly, buttested (120,134). (Le

roups of patients including a) high-risk ethnicminority groups (e.g., blacks), b) groupsunderrepresented in clinical trials, and c) anygroups believed to be underserved should, inthe absence of specific evidence to directotherwise, have clinical screening and therapyin a manner identical to that applied to thebroader population. (Level of Evidence: B)

2. Groups of patients inethnic minority groupunderrepresented in cgroups believed to bethe absence of specifiotherwise, have clinicin a manner identicalbroader population (3Evidence: B)

t is recommended that evidence-based therapyfor HF be used in the elderly patient, withindividualized consideration of the elderlypatient’s altered ability to metabolize ortolerate standard medications. (Level ofEvidence: C)

3. It is recommended ththerapy for HF be usewith individualized copatient’s altered abilitolerate standard meEvidence: C)

Cl

he addition of isosorbide dinitrate andhydralazine to a standard medical regimen forHF, including ACE inhibitors and beta blockers,is reasonable and can be effective in blackswith NYHA functional class III or IV HF. Othersmay benefit similarly, but this has not yet beentested. (Level of Evidence: A)

utput; 2) the rapid heart rate may increase demand and p


ecrease coronary perfusion (by shortening ventricular fill-ng time); 3) the rapidity of ventricular response mayiminish both cardiac contraction (by aggravating abnor-alities of the force-frequency relation) (316,317) and

ardiac relaxation (318,319); and 4) the stasis of blood in thebrillating atria may predispose patients to pulmonary orystemic emboli. In most patients with an ischemic oronischemic dilated cardiomyopathy, the rapidity of ven-ricular response is more important than the loss of atrialupport, because restoration of sinus rhythm does not resultn predictable clinical benefits (320). Rapid supraventricularrrhythmias may actually cause a cardiomyopathy (even inatients without an underlying contractile abnormality) ormay exacerbate a cardiomyopathy caused by another dis-rder (321,322). Hence, the control of ventricular rate andhe prevention of thromboembolic events are essentiallements of treatment of HF in patients with an underlyingupraventricular arrhythmia (323,324). Specific care andnitially low doses should be used when beta blockers arenstituted to control heart rate in patients with clinicalvidence of HF decompensation. The agent previously usedn clinical practice to slow the ventricular response in

commendation Comments

t of Special Populations

dose of isosorbidea standardluding ACE, is recommendedes for patients self-ans, with NYHAOthers mays not yet beenEvidence: A)

Modified recommendation (Class of recommendationelevated from IIa to I) based on A-HeFT (AfricanAmerican Heart Failure Trial) and robust secondaryanalyses of the original database and in anextended access study all confirm a substantialbenefit realized from the addition of isosorbidedinitrate and hydralazine to evidence-basedmedical and device therapy for African Americanswith HF.

g: a) high-risk, blacks), b) groupsl trials, and c) anyrserved should, inence to directening and therapyt applied to the1). (Level of

2005 recommendation remains current in 2009update.

dence-basede elderly patient,ation of the elderlyetabolize orns. (Level of

2005 recommendation remains current in 2009update.

a

Modified recommendation (Class of recommendationelevated from IIa to I) (see Class I, No. 1 above).

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ardiac glycoside slows atrioventricular conduction moreffectively at rest than during exercise (325,326). Hence,igitalis does not block the excessive exercise-inducedachycardia that may limit the functional capacity of patientsith HF (325–328). Beta blockers are more effective thanigoxin during exercise (325,327) and are preferred becausef their favorable effects on the natural history of HF54,58,60). The combination of digoxin and beta blockersay be more effective than beta blockers alone for rate

ontrol. Although both verapamil and diltiazem can alsouppress the ventricular response during exercise, they canepress myocardial function and increase the risk of wors-ning HF, especially in patients with HF and low EF, inhom these drugs should be avoided (329,330). If beta-lockers are ineffective or contraindicated in patients withtrial fibrillation and HF, amiodarone may be a usefullternative (331). Atrioventricular nodal ablation may beeeded if tachycardia persists despite pharmacological ther-py (169). Catheter ablation for pulmonary vein isolationas been most effective in patients without structural heartisease; the benefit for patients with established HF is notnown (332–334). Regardless of the intervention used,very effort should be made to reduce the ventricularesponse to less than 80 to 90 bpm at rest and less than 110o 130 bpm during moderate exercise. Anticoagulationhould be maintained in all patients with HF and a historyf atrial fibrillation, regardless of whether sinus rhythm ischieved, because of the high rate of silent recurrence oftrial fibrillation with its attendant embolic risk, unless aontraindication exists (324).

Should patients with HF and atrial fibrillation be con-erted to and maintained in sinus rhythm? The efficacy andafety of restoring and maintaining sinus rhythm in patientsith atrial fibrillation were evaluated in a total of 5032atients in 4 separate trials (335). Both strategies for theanagement of atrial fibrillation, either to restore andaintain sinus rhythm by electrical or pharmacologic con-

ersion, or to control ventricular rate in atrial fibrillation,ave been shown to have equivalent outcomes. These resultsere confirmed in 2007 with the conclusion of a large trialf patients with both atrial fibrillation and HF (123,124,24). Most patients revert to atrial fibrillation within a shortime unless they are treated with a Class I or III antiar-hythmic drug (313). However, patients with HF are notikely to respond favorably to Class I drugs and may bearticularly predisposed to their cardiodepressant and proar-hythmic effects (90,146), which can increase the risk ofeath (88,89,170). Class III antiarrhythmic agents (e.g.,otalol, dofetilide, and amiodarone) can maintain sinushythm in some patients, but treatment with these drugs isssociated with an increased risk of organ toxicity (amioda-one) (336,337) and proarrhythmia (dofetilide) (147). Mostatients who had thromboembolic events, regardless of thetrategy used, were in atrial fibrillation at the time of thevent and either were not undergoing anticoagulation ther-
py or were undergoing therapy at subtherapeutic levels.

hus, it is reasonable to treat HF patients with atrialbrillation with a strategy of either scrupulous rate controlr an attempt at rhythm control.

taff

merican College of Cardiology Foundationohn C. Lewin, MD, Chief Executive Officerharlene May, Senior Director, Science and Clinical Policyisa Bradfield, Associate Director, Clinical Policy anduidelinesark D. Stewart, MPH, Associate Director, Evidence-

ased Medicineue Keller, BSN, MPH, Senior Specialist, Evidence-Basededicinellison McDougall, Senior Specialist, Practice Guidelinesrin A. Barrett, Senior Specialist, Science and Clinicalolicy

merican Heart Associationancy Brown, Chief Executive Officerayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Viceresident, Office of Science Operations

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tion of sinus rhythm. Am J Med. 1988;85:242–4. f

22. Grogan M, Smith HC, Gersh BJ, et al. Left ventricular dysfunctiondue to atrial fibrillation in patients initially believed to have idiopathicdilated cardiomyopathy. Am J Cardiol. 1992;69:1570–3.

23. Crijns HJ, Van den Berg MP, Van Gelder IC, et al. Management ofatrial fibrillation in the setting of heart failure. Eur Heart J. 1997;18Suppl C:C45–9.

24. Shivkumar K, Jafri SM, Gheorghiade M. Antithrombotic therapy inatrial fibrillation: a review of randomized trials with special referenceto the Stroke Prevention in Atrial Fibrillation II (SPAF II) Trial.Prog Cardiovasc Dis. 1996;38:337–42.

25. Farshi R, Kistner D, Sarma JS, et al. Ventricular rate control inchronic atrial fibrillation during daily activity and programmedexercise: a crossover open-label study of five drug regimens. J AmColl Cardiol. 1999;33:304–10.

26. Botker HE, Toft P, Klitgaard NA, et al. Influence of physical exerciseon serum digoxin concentration and heart rate in patients with atrialfibrillation. Br Heart J. 1991;65:337–41.

27. Matsuda M, Matsuda Y, Yamagishi T, et al. Effects of digoxin,propranolol, and verapamil on exercise in patients with chronicisolated atrial fibrillation. Cardiovasc Res. 1991;25:453–7.

28. David D, Segni ED, Klein HO, et al. Inefficacy of digitalis in thecontrol of heart rate in patients with chronic atrial fibrillation:beneficial effect of an added beta adrenergic blocking agent. Am JCardiol. 1979;44:1378–82.

29. Goldstein RE, Boccuzzi SJ, Cruess D, et al. Diltiazem increaseslate-onset congestive heart failure in postinfarction patients with earlyreduction in ejection fraction. The Adverse Experience Committee;and the Multicenter Diltiazem Postinfarction Research Group.Circulation. 1991;83:52–60.

30. Mohindra SK, Udeani GO. Long-acting verapamil and heart failure(letter). JAMA. 1989;261:994.

31. Deedwania PC, Singh BN, Ellenbogen K, et al. Spontaneousconversion and maintenance of sinus rhythm by amiodarone inpatients with heart failure and atrial fibrillation: observations from theVeterans Affairs congestive heart failure survival trial of antiarrhyth-mic therapy (CHF-STAT). The Department of Veterans AffairsCHF-STAT Investigators. Circulation. 1998;98:2574–9.

32. Wood MA, Brown-Mahoney C, Kay GN, et al. Clinical outcomesafter ablation and pacing therapy for atrial fibrillation: a meta-analysis. Circulation. 2000;101:1138–44.

33. Ozcan C, Jahangir A, Friedman PA, et al. Long-term survival afterablation of the atrioventricular node and implantation of a permanentpacemaker in patients with atrial fibrillation. N Engl J Med. 2001;344:1043–51.

34. Ozcan C, Jahangir A, Friedman PA, et al. Significant effects ofatrioventricular node ablation and pacemaker implantation on leftventricular function and long-term survival in patients with atrialfibrillation and left ventricular dysfunction. Am J Cardiol. 2003;92:33–7.

35. Boos CJ, Carlsson J, More RS. Rate or rhythm control in persistentatrial fibrillation? Q JM. 2003;96:881–92.

36. Naccarelli GV, Rinkenberger RL, Dougherty AH, et al. Adverseeffects of amiodarone. Pathogenesis, incidence and management.Med Toxicol Adverse Drug Exp. 1989;4:246–53.

37. Greene HL, Graham EL, Werner JA, et al. Toxic and therapeuticeffects of amiodarone in the treatment of cardiac arrhythmias. J AmColl Cardiol. 1983;2:1114–28.

ey Words: ACCF/AHA practice guideline y focused update y heart
ailure y hospitalized patient y refractory end-stage heart failure.
http://www.ahrq.gov/qual/30safe.htm

http://www.ahrq.gov/qual/30safe.htm

http://www.jointcommission.org/PatientSafety/NationalPatientSafetyGoals/08_hap_npsgs.htm

http://www.jointcommission.org/PatientSafety/NationalPatientSafetyGoals/08_hap_npsgs.htm

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PPENDIX 1. AUTHOR RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES—2009 FOCUSED UPDATE:CCF/AHA GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF HEART FAILURE IN ADULTS

CommitteeMember Consultant Speaker

Ownership/Partnership/

Principal Research

Institutional,Organizational, orOther Financial

Benefit Expert Witness

r. Mariell Jessup(Chair)

● Acorn● CardioMEMS● GlaxoSmithKline● Medtronic● Scios● Ventracor

None None None None None

r. William T.Abraham

● Arrow International● AstraZeneca● BioEnergy● Boehringer Ingelheim● CardioKine● CardioKinetix● CardioMEMS*● CHF Solutions● Department of Veterans

Affairs CooperativeStudies Program

● Edwards Lifesciences● Inovise● Medtronic*● Merck & Co.● National Institutes of

Health● Novartis● Paracor● Pfizer● ResMed● Respironics● Scios● St. Jude Medical*● Sunshine Heart

● Amgen● AstraZeneca● Boehringer

Ingelheim● CHF Solutions● GlaxoSmithKline● Guidant Corp.● Medtronic*● Merck & Co.● Novartis● Pfizer● ResMed● Respironics● Scios Inc.● St. Jude

Medical*

None ● Heart Failure Societyof America

● Medtronic Inc.*● National Institutes of

Health● Paracor Inc.*● St. Jude Medical*

None None

r. Donald E.Casey

None None None None None None

r. Arthur M.Feldman

● Alinea Pharmaceutical● Arca Discovery

None ● CardioKine* None ● CardioKine* None

r. Gary S.Francis

● Biosite● Boehringer Ingelheim● GlaxoSmithKline● Medtronic● NitroMed● Otsuka


r. Theodore G.Ganiats


r. Marvin A.Konstam

● AstraZeneca● CardioKine● GlaxoSmithKline● Merck*● Nitromed● Novartis*● Otsuka*● Sanofi

● Otsuka* ● Orqis* ● GlaxoSmithKline● Nitromed● Otsuka*

None None

r. Donna M.Mancini

● Acorn● Celladon



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CommitteeMember Consultant Speaker


Principal Research


Benefit Expert Witness

r. Peter S.Rahko

● Breast CancerInternational ResearchGroup

● BoehringerIngelheim

● GlaxoSmithKline● Novartis

None ● EnoxsivePharmaceuticals

None ● Deposition, Plaintiff,MyocardialInfarction PostMotor VehicleAccident

r. Marc A. Silver None ● GlaxoSmithKline● Johnson &

Johnson

None None None None

r. Lynne WarnerStevenson

None None None ● CardioMEMS● Medtronic

None ● CardioMEMS● Medtronic

r. Clyde W.Yancy

● Arc Discovery*● GlaxoSmithKline*● Nitromed● Scios, Inc.

● GlaxoSmithKline*● Novartis

None ● GlaxoSmithKline● Medtronic● Nitromed● Scios

None None

his table represents the relevant relationships of committee members with industry and other entities that were reported orally at the initial writing committee meeting and updated in conjunction with

ll meetings and conference calls of the writing committee during the document development process. It does not necessarily reflect relationships with industry at the time of publication. A person is

eemed to have a significant interest in a business if the interest represents ownership of 5% or more of the voting stock or share of the business entity, or ownership of $10 000 or more of the fair

arket value of the business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the previous year. A relationship is considered to be modest

f it is less than significant under the preceding definition. Relationships in this table are modest unless otherwise noted. *Significant (greater than $10 000) relationship.

PPENDIX 2. REVIEWER RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES—2009 FOCUSED UPDATE:CCF/AHA GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF HEART FAILURE IN ADULTS

PeerReviewer Representation Consultant Speaker


Principal Research


BenefitExpert

Witness

r. Steven M.Ettinger

Official—American Collegeof Cardiology/AmericanHeart Association TaskForce on PracticeGuidelines


r. Gregg G.Fonarow

Official—American HeartAssociation

● AstraZeneca● Bristol-Myers

Squibb-Sanofi*● GlaxoSmithKline*● Medtronic*● Merck*● Novartis*● Pfizer*

● AstraZeneca● Bristol-Myers

Squibb-Sanofi*● GlaxoSmithKline*● Medtronic*● Merck*● Novartis*● Pfizer*

None None None None

r. G. Harold Official—American Collegeof Cardiology Board ofTrustees


r. Robert E.Hobbs

Official—American Collegeof Cardiology Board ofGovernors

None ● Scios* None None None None

r. MichaelR. Zile

Official—American HeartAssociation

● Bristol-MyersSquibb-Sanofi

● Enoxsive● Medtronic● Novartis● Orqis● Ortho Clinical

Diagnostic● Synvista

None None ● Bristol-MyersSquibb-Sanofi

● Enoxsive● Medtronic● Novartis● Orqis● Ortho Clinical

Diagnostic● Synvista

None None


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Principal Research


BenefitExpert

Witness

r. DougCampos-Outcalt

Organizational—AmericanAcademy of FamilyPhysicians


r. Jun R.Chiong

Organizational—AmericanCollege of ChestPhysicians

● RocheDiagnostics

● GlaxoSmithKline None None None None

r. StevenDurning

Organizational—AmericanCollege of Physicians


r. KurtElward



r. MichaelFelker

Organizational—HeartFailure Society ofAmerica

● Amgen● Boston Scientific● Corthera● Cytokinetics● Geron● XDS

● Amgen● Cytokinetics● Roche

Diagnostics

None None None None

r. David D.Gutterman

Organizational—AmericanCollege of ChestPhysicians

None None ● Johnson &Johnson*

● NationalInstitutes ofHealth*

None None

r. Charin L.Hanlon

Organizational—AmericanCollege of Physicians


r. ThomasF. Koinis



r. Alan B.Miller

Organizational—HeartFailure Society ofAmerica

None ● AstraZeneca● Bristol-Myers

Squibb● CV Therapeutics● GlaxoSmithKline● Novartis

● CVTherapeutics

● Medtronic● Merck

None None None

r. SrinivasMurali

Organizational—InternationalSociety of Heart andLung Transplantation

None None None ● Jarvik Inc.● Novacardiac● Paracor Inc.● Scios● Thoratic Inc.● Ventrocor Inc.

● BostonScientific*(salary)

● Medtronic*(salary)

● St. JudeMedical*(salary)

None

r. Nancy M.Albert

Content—American HeartAssociation HeartFailure and TransplantCommittee

● Arco Biopharma● GlaxoSmithKline● Medtronic

● GlaxoSmithKline None ● GlaxoSmithKline*● Medtronic*

None None

r. John D.Bisognano

Content—AmericanCollege of CardiologyBoard of Governors


r. JavedButler

Content—AmericanCollege of CardiologyHeart Failure andTransplant Committee

None ● BoehringerIngelheim*

● GlaxoSmithKline*● Novartis*

None None None None

r. David E.Lanfear


● Thoratec None None ● Merck● Sanofi-Aventis

None None


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Principal Research


BenefitExpert

Witness

r. JoannLindenfeld


● Arca● CV Therapeutics*● Medtronic● Sanofi-Aventis● Takeda

None None ● Merck● Somalogic

None None

r. Wayne L.Miller



r. Judith E.Mitchell


● GlaxoSmithKline● NitroMed

● GlaxoSmithKline● NitroMed

None None None None

r. Rick A.Nishimura

Content—AmericanCollege of Cardiology/American HeartAssociation Task Forceon Practice Guidelines


r. Donna F.Petruccelli



r. WinKuangShen


None None None ● Medtronic* None None

r. Lynn G.Tarkington

Content—AmericanCollege of Cardiology/American HeartAssociation Task Forceon Practice Guidelines


r. Emily J.Tsai



his table represents the relevant relationships with industry and other entities that were disclosed at the time of peer review. It does not necessarily reflect relationships with industry at the time ofublication. A person is deemed to have a significant interest in a business if the interest represents ownership of 5% or more of the voting stock or share of the business entity, or ownership of $10 000r more of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the previous year. A relationship isonsidered to be modest if it is less than significant under the preceding definition. Relationships in this table are modest unless otherwise noted. Names are listed in alphabetical order within eachategory of review. *Significant (greater than $10 000) relationship.


Documents

2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis ... · PRACTICE GUIDELINE: FOCUSED UPDATE 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart