2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and

90 Pages·2013·6.07 MB·English

JournaloftheAmericanCollegeofCardiology Vol.53,No.15,2009
©2009bytheAmericanCollegeofCardiologyFoundationandtheAmericanHeartAssociation,Inc. ISSN0735-1097/09/$36.00
PublishedbyElsevierInc. doi:10.1016/j.jacc.2008.11.013
PRACTICE GUIDELINE: FULL TEXT
2009 Focused Update Incorporated Into the
ACC/AHA 2005 Guidelines for the Diagnosis and
Management of Heart Failure in Adults
A Report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines
Developed in Collaboration With the International Society for Heart and Lung Transplantation
2005Writing Sharon Ann Hunt, MD, FACC, FAHA, Chair Marvin A. Konstam, MD, FACC
Committee
Donna M. Mancini, MD
Members
William T. Abraham, MD, FACC, FAHA Keith Michl, MD, FACP
Marshall H. Chin, MD, MPH, FACP John A. Oates, MD, FAHA
ArthurM.Feldman,MD,PHD,FACC,FAHA Peter S. Rahko, MD, FACC, FAHA
Gary S. Francis, MD, FACC, FAHA Marc A. Silver, MD, FACC, FAHA
Theodore G. Ganiats, MD Lynne Warner Stevenson, MD, FACC, FAHA
Mariell Jessup, MD, FACC, FAHA Clyde W. Yancy, MD, FACC, FAHA
2009 Mariell Jessup, MD, FACC, FAHA, Chair* LynneWarnerStevenson,MD,FACC,FAHA†
Focused
Clyde W. Yancy, MD, FACC, FAHA††
Update
Writing William T. Abraham, MD, FACC, FAHA†
Group Donald E. Casey, MD, MPH, MBA‡ *InternationalSocietyforHeartandLungTransplantationRepresen-
tative;†AmericanCollegeofCardiologyFoundation/AmericanHeart
Members ArthurM.Feldman,MD,PHD,FACC,FAHA§ AssociationRepresentative;‡AmericanCollegeofPhysiciansRepre-
Gary S. Francis, MD, FACC, FAHA§ sentative;§HeartFailureSocietyofAmericaRepresentative;(cid:1)American
Theodore G. Ganiats, MD(cid:1) AcademyofFamilyPhysiciansRepresentative;¶AmericanCollegeof
Cardiology Foundation/American Heart Association Performance
Marvin A. Konstam, MD, FACC¶ Measures Liaison; #Content Expert; **American College of Chest
PhysiciansRepresentative;††AmericanCollegeofCardiologyFounda-
Donna M. Mancini, MD#
tion/AmericanHeartAssociationTaskForceonPracticeGuidelines
Peter S. Rahko, MD, FACC, FAHA† Liaison
Marc A. Silver, MD, FACC, FAHA**
ThisdocumentwasapprovedbytheAmericanCollegeofCardiologyFoundation ThisarticlehasbeencopublishedelectronicallybyCirculation.
Board of Trustees and the American Heart Association Science Advisory and Copies:ThisdocumentisavailableontheWorldWideWebsitesoftheAmeri-
CoordinatingCommitteeinOctober2008. can College of Cardiology (www.acc.org) and American Heart Association (my.
TheAmericanCollegeofCardiologyFoundationrequeststhatthisdocument americanheart.org).Forcopiesofthisdocument,pleasecontactElsevierInc.Reprint
becitedasfollows:HuntSA,AbrahamWT,ChinMH,FeldmanAM,Francis Department,fax[phone],[email protected].
GS,GaniatsTG,JessupM,KonstamMA,ManciniDM,MichlK,OatesJA, Permissions:Multiplecopies,modification,alteration,enhancement,and/ordis-
Rahko PS, Silver MA, Stevenson LW, Yancy CW. 2009 focused update
tributionofthisdocumentarenotpermittedwithouttheexpresspermissionofthe
incorporatedintotheACC/AHA2005guidelinesforthediagnosisandmanage-
American College of Cardiology Foundation. Please contact Elsevier’s permission
mentofheartfailureinadults:areportoftheAmericanCollegeofCardiology
[email protected].
Foundation/American Heart Association Task Force on Practice Guidelines.
JAmCollCardiol2009;53:e1–90.
e2 Huntetal. JACCVol.53,No.15,2009
2009ACCF/AHAHeartFailureGuidelines April14,2009:e1–90
Task SidneyC.Smith,JR,MD,FACC,FAHA,Chair Bruce W. Lytle, MD, FACC, FAHA‡‡
Force
AliceK.Jacobs,MD,FACC,FAHA,Vice-Chair Rick A. Nishimura, MD, FACC, FAHA
Members
Richard L. Page, MD, FACC, FAHA
Christopher E. Buller, MD, FACC
Lynn G. Tarkington, RN
Mark A. Creager, MD, FACC, FAHA
Clyde W. Yancy, MD, FACC, FAHA
Steven M. Ettinger, MD, FACC
Harlan M. Krumholz, MD, FACC, FAHA ‡‡FormerTaskForcememberduringthewritingeffort
Frederick G. Kushner, MD, FACC, FAHA
4.1.1.2. TREATMENTOFDIABETES..........................e18
TABLE OF CONTENTS
4.1.1.3. MANAGEMENTOFTHEMETABOLICSYNDROME.........e18
4.1.1.4. MANAGEMENTOFATHEROSCLEROTICDISEASE.........e18
Preamble(UPDATED).........................................e3 4.1.1.5. CONTROLOFCONDITIONSTHATMAYCAUSE
CARDIACINJURY.................................e18
4.1.1.6. OTHERMEASURES................................e19
1. Introduction(UPDATED)..................................e5 4.1.2. EarlyDetectionofStructuralAbnormalities......e19
4.2. PatientsWithCardiacStructuralAbnormalities
1.1. EvidenceReview(UPDATED)........................e5 orRemodelingWhoHaveNotDeveloped
1.2. OrganizationofCommitteeand HeartFailureSymptoms(StageB)................e19
RelationshipsWithIndustry(UPDATED)...........e6 4.2.1. PreventionofCardiovascularEvents..............e20
1.3. ReviewandApproval(NEW) ........................e6 4.2.1.1. PATIENTSWITHANACUTEMYOCARDIAL
INFARCTION.....................................e20
1.4. StagesofHeartFailure(UPDATED)................e6
4.2.1.2. PATIENTSWITHAHISTORYOFMIBUTNORMALLEFT
2. CharacterizationofHeartFailureasa VENTRICULAREJECTIONFRACTION...................e20
ClinicalSyndrome.........................................e7 4.2.1.3. PATIENTSWITHHYPERTENSIONANDLEFTVENTRICULAR
HYPERTROPHY...................................e20
4.2.1.4. PATIENTSWITHCHRONICREDUCTIONOFLEFTVENTRICULAR
2.1. DefinitionofHeartFailure...........................e7 EJECTIONFRACTIONBUTNOSYMPTOMS..............e20
2.2. HeartFailureasaSymptomaticDisorder .........e7 4.2.1.5. PATIENTSWITHSEVEREVALVULARDISEASEBUTNO
2.3. HeartFailureasaProgressiveDisorder...........e8 SYMPTOMS.....................................e20
4.2.2. EarlyDetectionofHeartFailure.................e21
3. InitialandSerialClinicalAssessmentof
4.3. PatientsWithCurrentorPriorSymptoms
PatientsPresentingWithHeartFailure ofHF(StageC)......................................e21
(UPDATED) .................................................e8 4.3.1. PatientsWithReducedLeftVentricular
EjectionFraction(UPDATED)..................e21
3.1. InitialEvaluationofPatients......................e10 4.3.1.1. GENERALMEASURES(UPDATED)....................e22
3.1.1. IdentificationofPatients(UPDATED)..........e10 4.3.1.2. DRUGSRECOMMENDEDFORROUTINEUSE............e24
3.1.2. IdentificationofaStructuralandFunctional 4.3.1.2.1. DIURETICS.................................e24
Abnormality(UPDATED).......................e11 4.3.1.2.2. INHIBITORSOFTHERENIN-ANGIOTENSIN-
3.1.3. EvaluationoftheCauseofHeartFailure.........e11 ALDOSTERONESYSTEM.......................e25
3.1.3.1. HISTORYANDPHYSICALEXAMINATION...............e11 4.3.1.2.2.1. AngiotensinConvertingEnzyme
3.1.3.2. LABORATORYTESTING(UPDATED)...................e12 InhibitorsintheManagementof
3.1.3.3. EVALUATIONOFTHEPOSSIBILITYOFCORONARY HeartFailure........................e26
ARTERYDISEASE.................................e13 4.3.1.2.2.2. AngiotensinReceptorBlockers........e28
3.1.3.4. EVALUATIONOFTHEPOSSIBILITYOFMYOCARDIAL 4.3.1.2.2.3. AldosteroneAntagonists..............e29
DISEASE........................................e13 4.3.1.2.3. BETA-ADRENERGICRECEPTORBLOCKERS ........e31
3.2. OngoingEvaluationofPatients ...................e14 4.3.1.2.4. DIGITALIS..................................e33
3.2.1. AssessmentofFunctionalCapacity...............e14 4.3.1.2.5. VENTRICULARARRHYTHMIASANDPREVENTION
3.2.2. AssessmentofVolumeStatus ....................e14 OFSUDDENDEATH(UPDATED).................e35
3.2.3. LaboratoryAssessment(UPDATED)............e15 4.3.1.3. INTERVENTIONSTOBECONSIDEREDFORUSEIN
3.2.4. AssessmentofPrognosis(UPDATED) ..........e16 SELECTEDPATIENTS..............................e37
4.3.1.3.1. ISOSORBIDEDINITRATE.......................e37
4. Therapy....................................................e16 4.3.1.3.2. HYDRALAZINE...............................e37
4.3.1.3.3. HYDRALAZINEANDISOSORBIDEDINITRATE
4.1. PatientsatHighRiskforDevelopingHeart (UPDATED).................................e37
Failure(StageA)....................................e16 4.3.1.3.4. CARDIACRESYNCHRONIZATIONTHERAPY
4.1.1. ControlofRisk...................................e17 (UPDATED).................................e38
4.1.1.1. TREATMENTOFHYPERTENSION.....................e17 4.3.1.3.5. EXERCISETRAINING..........................e39
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April14,2009:e1–90 2009ACCF/AHAHeartFailureGuidelines
4.3.1.4. DRUGSANDINTERVENTIONSUNDERACTIVE 8.2. Disease-ManagementSystems....................e61
INVESTIGATION...................................e39 8.3. PerformanceMeasures.............................e62
4.3.1.4.1. TECHNIQUESFORRESPIRATORYSUPPORT........e39
8.4. RolesofGeneralistPhysiciansand
4.3.1.4.2. EXTERNALCOUNTERPULSATION ................e39
4.3.1.4.3. VASOPRESSINRECEPTORANTAGONISTS.........e40 Cardiologists ........................................e62
4.3.1.4.4. IMPLANTABLEHEMODYNAMICMONITORS ........e40 References...................................................e63
4.3.1.4.5. CARDIACSUPPORTDEVICES...................e40
4.3.1.4.6. SURGICALAPPROACHESUNDERINVESTIGATION......e40
4.3.1.4.7. NESIRITIDE.................................e40 Appendix1....................................................e82
4.3.1.5. DRUGSANDINTERVENTIONSOFUNPROVEDVALUE
ANDNOTRECOMMENDED..........................e40 Appendix2....................................................e83
4.3.1.5.1. NUTRITIONALSUPPLEMENTSANDHORMONAL
THERAPIES.................................e40
4.3.1.5.2. INTERMITTENTINTRAVENOUSPOSITIVE Appendix3....................................................e86
INOTROPICTHERAPY(UPDATED)................e41
4.3.2. PatientsWithHeartFailureandNormal Appendix4....................................................e87
LeftVentricularEjectionFraction................e41
4.3.2.1. IDENTIFICATIONOFPATIENTS.......................e42
4.3.2.2. DIAGNOSIS......................................e43 Appendix5....................................................e88
4.3.2.3. PRINCIPLESOFTREATMENT........................e43
4.4. PatientsWithRefractoryEnd-StageHeart
Failure(StageD)(UPDATED).......................e44 Preamble (UPDATED)
4.4.1. ManagementofFluidStatus .....................e44
4.4.2. UtilizationofNeurohormonalInhibitors .........e45
4.4.3. IntravenousPeripheralVasodilatorsand Itisimportantthatthemedicalprofessionplayasignificant
PositiveInotropicAgents(UPDATED) .........e45 role in critically evaluating the use of diagnostic procedures
4.4.4. MechanicalandSurgicalStrategies...............e46 and therapies as they are introduced and tested in the
4.5. TheHospitalizedPatient(NEW)...................e47 detection, management, or prevention of disease states.
4.5.1. DiagnosticStrategies.............................e49 Rigorous and expert analysis of the available data docu-
4.5.2. TreatmentintheHospital........................e49 menting relative benefits and risks of those procedures and
4.5.2.1. DIURETICS:THEPATIENTWITHVOLUMEOVERLOAD.......e49
4.5.2.2. VASODILATORS..................................e50 therapies can produce helpful guidelines that improve the
4.5.2.3. INOTROPES.....................................e51 effectiveness of care, optimize patient outcomes, and favor-
4.5.2.4. OTHERCONSIDERATIONS ..........................e51 ably affect the overall cost of care by focusing resources on
4.5.3. TheHospitalDischarge..........................e52 the most effective strategies.
5. TreatmentofSpecialPopulations(UPDATED)......e52 The American College of Cardiology Foundation
(ACCF)andtheAmericanHeartAssociation(AHA)have
5.1. WomenandMen ....................................e53 jointly engaged in the production of such guidelines in the
5.2. EthnicConsiderations..............................e53 area of cardiovascular disease since 1980. This effort is
5.3. ElderlyPatients.....................................e54 directedbytheACCF/AHATaskForceonPracticeGuide-
lines, whose charge is to develop and revise practice guide-
6. PatientsWithHeartFailureWhoHave
lines for important cardiovascular diseases and procedures.
ConcomitantDisorders .................................e54 Experts in the subject under consideration are selected
from both organizations and charged with examining
6.1. CardiovascularDisorders...........................e55
subject-specific data and writing or updating these guide-
6.1.1. Hypertension,Hyperlipidemia,and
DiabetesMellitus.................................e55 lines. The process includes additional representatives from
6.1.2. CoronaryArteryDisease .........................e56 other medical practitioner and specialty groups where ap-
6.1.3. SupraventricularArrhythmias(UPDATED) .....e56 propriate. Writing groups are specifically charged to per-
6.1.4. PreventionofThromboembolicEvents...........e57 form a formal literature review, weigh the strength of
6.2. NoncardiovascularDisorders......................e58 evidence for or against a particular treatment or procedure,
6.2.1. PatientsWithRenalInsufficiency ................e58
and include estimates of expected health outcomes where
6.2.2. PatientsWithPulmonaryDisease................e58
6.2.3. PatientsWithCancer ............................e58 data exist. Patient-specific modifiers, comorbidities, and
6.2.4. PatientsWithThyroidDisease...................e59 issues of patient preference that might influence the choice
6.2.5. PatientsWithHepatitisCandHuman of particular tests or therapies are considered, as are fre-
ImmunodeficiencyVirus..........................e59 quencyoffollow-upandcost-effectiveness.Whenavailable,
6.2.6. PatientsWithAnemia............................e59
information from studies on cost will be considered; how-
7. End-of-LifeConsiderations.............................e59 ever, review of data on efficacy and clinical outcomes will
constitutetheprimarybasisforpreparingrecommendations
8. ImplementationofPracticeGuidelines..............e61 in these guidelines.
The ACCF/AHA Task Force on Practice Guidelines
8.1. IsolatedProviderInterventions ...................e61 makes every effort to avoid any actual, potential, or per-
e4 Huntetal. JACCVol.53,No.15,2009
2009ACCF/AHAHeartFailureGuidelines April14,2009:e1–90
Table1. ApplyingClassificationofRecommendationsandLevelofEvidence
*Dataavailablefromclinicaltrialsorregistriesabouttheusefulness/efficacyindifferentsubpopulations,suchasgender,age,historyofdiabetes,historyofpriormyocardialinfarction,historyofheart
failure,andprioraspirinuse.ArecommendationwithLevelofEvidenceBorCdoesnotimplythattherecommendationisweak.Manyimportantclinicalquestionsaddressedintheguidelinesdonot
lendthemselvestoclinicaltrials.Eventhoughrandomizedtrialsarenotavailable,theremaybeaveryclearclinicalconsensusthataparticulartestortherapyisusefuloreffective.†In2003,the
ACCF/AHATaskForceonPracticeGuidelinesdevelopedalistofsuggestedphrasestousewhenwritingrecommendations.Allguidelinerecommendationshavebeenwritteninfullsentencesthat
expressacompletethought,suchthatarecommendation,evenifseparatedandpresentedapartfromtherestofthedocument(includingheadingsabovesetsofrecommendations),wouldstillconvey
thefullintentoftherecommendation.Itishopedthatthiswillincreasereaders’comprehensionoftheguidelinesandwillallowqueriesattheindividualrecommendationlevel.
ceived conflicts of interest that might arise as a result of an dix 2 for a listing of peer reviewer relationships with
outsiderelationshiporpersonalinterestofamemberofthe industry that are pertinent to this guideline.
writing committee. Specifically, all members of the writing The practice guidelines produced are intended to assist
committee, as well as peer reviewers of the document, are healthcare providers in clinical decision making by describ-
asked to provide disclosure statements of all such relation- ing a range of generally acceptable approaches for the
shipsthatmightbeperceivedasrealorpotentialconflictsof diagnosis,management,orpreventionofspecificdiseasesor
interest. Writing committee members are also strongly conditions.Theseguidelinesattempttodefinepracticesthat
encouraged to declare a previous relationship with industry meet the needs of most patients in most circumstances.
thatmaybeperceivedasrelevanttoguidelinedevelopment. These guideline recommendations reflect a consensus of
Ifawritingcommitteememberdevelopsanewrelationship expert opinion after a thorough review of the available,
during his or her tenure, he or she is required to notify the current scientific evidence and are intended to improve
guideline writing staff in writing. The continued participa- patient care. If these guidelines are used as the basis for
tion of the writing committee member will be reviewed by regulatory/payer decisions, the ultimate goal is quality of
the parent task force, reported orally to all members of the care and serving the patient’s best interests. The ultimate
writingpanelateachmeeting,andupdatedandreviewedby judgment regarding care of a particular patient must be
the writing committee as changes occur. Please refer to the madebythehealthcareproviderandpatientinlightofallof
methodology manual for the ACCF/AHA guideline writ- the circumstances presented by that patient.
ingcommitteesforfurtherdescriptionandtherelationships The2005guidelineswereapprovedforpublicationbythe
withindustrypolicy(1).SeeAppendix1foralistofwriting governingbodiesoftheACCFandtheAHAandhavebeen
committeememberrelationshipswithindustryandAppen- officially endorsed by the American College of Chest
JACCVol.53,No.15,2009 Huntetal. e5
April14,2009:e1–90 2009ACCF/AHAHeartFailureGuidelines
Physicians, the International Society for Heart and Lung pital discharge diagnosis), and more Medicare dollars are
Transplantation,andtheHeartRhythmSociety.Thesum- spent for the diagnosis and treatment of HF than for any
mary article including recommendations was published in other diagnosis (9). The total estimated direct and indirect
the September 20, 2005, issues of both the Journal of the costs for HF in 2005 were approximately $27.9 billion (4).
AmericanCollegeofCardiologyandCirculation.Thefull-text IntheUnitedStates,approximately$2.9billionannuallyis
guideline is posted on the World Wide Web sites of the spent on drugs for the treatment of HF (4).
ACC (www.acc.org) and the AHA (my.americanheart.org).
Copiesofthefulltextandthesummaryarticleareavailable 1.1. Evidence Review (UPDATED)
from both organizations.
TheACCFandtheAHAfirstpublishedguidelinesforthe
The current document is a re-publication of the “ACC/
evaluation and management of HF in 1995 and published
AHA 2005 Guideline Update for the Diagnosis and Man-
revisedguidelinesin2001(10).Sincethattime,agreatdeal
agementofChronicHeartFailureintheAdult”(2),revised
of progress has been made in the development of both
to incorporate updated recommendations and text from a
pharmacological and nonpharmacological approaches to
focused update performed during 2008 (3). Recommenda-
treatment for this common, costly, disabling, and poten-
tions have been updated with new information that has
tiallyfataldisorder.Thenumberofavailabletreatmentshas
emergedfromclinicaltrialsorotherACCF/AHAguideline
increased, but this increase has rendered clinical decision
orconsensusdocuments.Inaddition,thewritingcommittee
making far more complex. The timing and sequence of
felt that a new section, the Hospitalized Patient, was
initiatingtreatmentsandtheappropriatenessofprescribing
necessarytoaddresstheincreasinglyrecognizedproblemof
them in combination are uncertain. The increasing recog-
the patient with acute decompensated heart failure, as
nition of the existence of clinical HF in patients with a
opposed to the patient with chronic heart failure. Heart
normal ejection fraction (EF) (see Section 4.3.2.1) has also
failureisnowthesinglemostcommonreasonwhypatients
led to heightened awareness of the limitations of evidence-
over65yearsareadmittedtothehospital,andtheupdated
basedtherapyforthisimportantgroupofpatients.Forthese
guidelinesreviewimportantmanagementprinciplesforthis
reasons,the2organizationsbelievedthatitwasappropriate
population. For easy reference, this online-only version
to reassess and update these guidelines, fully recognizing
denotes sections that have been updated.
that the optimal therapy of HF remains a work in progress
Elliott M. Antman, MD, FACC, FAHA
and that future advances will require that the guideline be
Chair,ACCF/AHATaskForceonPracticeGuidelines,2003–2005
updated again.
Sidney C. Smith, Jr, MD, FACC, FAHA The recommendations listed in the 2005 guideline are
Chair,ACCF/AHATaskForceonPracticeGuidelines,2006–2008 evidence based whenever possible. Pertinent medical liter-
atureintheEnglishlanguagewasidentifiedthroughaseries
1. Introduction (UPDATED)
of computerized literature searches (including Medline and
EMBASE)andamanualsearchofselectedarticles.Refer-
Heart failure (HF) is a major and growing public health encesselectedandpublishedinthisdocumentarerepresen-
problem in the United States. Approximately 5 million tative but not all inclusive. Recommendations relevant to a
patientsinthiscountryhaveHF,andover550000patients class of drugs specify the use of the drugs shown to be
arediagnosedwithHFforthefirsttimeeachyear(4).The effectiveinclinicaltrialsunlessthereisreasontobelievethat
disorder is the primary reason for 12 to 15 million office such drugs have a broad class effect.
visitsand6.5millionhospitaldayseachyear(5).From1990 In2005,thecommitteeelectedtofocusthisdocumenton
to 1999, the annual number of hospitalizations has in- thepreventionofHFandonthediagnosisandmanagement
creased from approximately 810 000 to over 1 million for of chronic HF in the adult patient with normal or low
HF as a primary diagnosis and from 2.4 to 3.6 million for LVEF.OtherguidelinesarerelevanttotheHFpopulation,
HFasaprimaryorsecondarydiagnosis(6).In2001,nearly and include the ACC/AHA Guidelines for the Manage-
53000patientsdiedofHFasaprimarycause.Thenumber mentofPatientsWithST-ElevationMyocardialInfarction
of HF deaths has increased steadily despite advances in (11)andtheACC/AHA2002UpdateoftheGuidelinesfor
treatment,inpartbecauseofincreasingnumbersofpatients the Management of Unstable Angina and Non-ST Eleva-
with HF due to better treatment and “salvage” of patients tion Myocardial Infarction (12). These guidelines have
with acute myocardial infarctions (MIs) earlier in life (4). excluded HF in children, both because the underlying
Heart failure is primarily a condition of the elderly (7), causes of HF in children differ from those in adults and
and thus the widely recognized “aging of the population” because none of the controlled trials of treatments for HF
also contributes to the increasing incidence of HF. The have included children. We have not considered the man-
incidence of HF approaches 10 per 1000 population after agement of HF due to primary valvular disease (see ACC/
age 65 (4), and approximately 80% of patients hospitalized AHA Guidelines on the Management of Patients With
withHFaremorethan65yearsold(8).Heartfailureisthe Valvular Heart Disease [13]) or congenital malformations,
most common Medicare diagnosis-related group (i.e., hos- and we have not included recommendations for the treat-
e6 Huntetal. JACCVol.53,No.15,2009
2009ACCF/AHAHeartFailureGuidelines April14,2009:e1–90
mentofspecificmyocardialdisorders(e.g.,hemochromato- FocusedUpdateWritingGroupandpeerreviewers,respec-
sis, sarcoidosis, or amyloidosis). tively). Each recommendation required a confidential vote
For the 2009 focused update, late-breaking clinical trials by the writing group members before and after external
presented at the 2005, 2006, and 2007 annual scientific review of the document. Writing group members who had
meetings of the ACCF, AHA, and European Society of asignificant(greaterthan$10000)relationshipwithindus-
Cardiology, as well as selected other data, from 2005 try relevant to a recommendation were required to recuse
through November 2007, were reviewed by the standing themselves from voting on that recommendation.
guideline writing committee along with the parent task
1.3. Review and Approval (NEW)
force to identify those trials and other key data that might
impact guideline recommendations. On the basis of the The 2005 Guideline document was reviewed by 3 official
criteria/considerations noted earlier, recent trial data and reviewers nominated by the ACCF, 3 official reviewers
other clinical information were considered important nominated by the AHA, 1 reviewer nominated by the
enough to prompt a focused update of the ACCF/AHA AmericanAcademyofFamilyPhysicians,2reviewersnom-
2005GuidelineUpdatefortheDiagnosisandManagement inated by the American College of Chest Physicians, 1
of Chronic Heart Failure in the Adult (2). In addition, the reviewernominatedbytheAmericanCollegeofPhysicians,
guidelineswritingcommitteethoughtthatanewsectionon 4 reviewers nominated by the Heart Failure Society of
themanagementofthehospitalizedpatientwithHFshould America, and 1 reviewer nominated by the International
be included in this update. A number of recent HF trials SocietyforHeartandLungTransplantation.Inaddition,9
reviewed for this update, were, in fact, performed on content reviewers and the following committees reviewed
hospitalized patients, and a number of newer therapies are the document: ACCF/AHA Committee to Develop Per-
under development for this population. Moreover, there is formance Measures for Heart Failure, ACCF/AHA Com-
increasing government and other third-party payer interest mitteetoReviseGuidelinesfortheManagementofPatients
inthepreventionofHFhospitalizations,andrehospitaliza- With Acute Myocardial Infarction, ACCF/AHA/ESC
tions. Quality indicators about the process of discharging Committee to Update Guidelines on the Management of
theHFpatienthavealreadybeendeveloped,anddataabout Patients with Atrial Fibrillation, ACCF/AHA Committee
rehospitalizations for HF by hospital have been made to Update Guidelines on Coronary Artery Bypass Graft
public. Thus, the committee thought that a new section Surgery,ACCFCommitteetoDevelopDataStandardson
about this important aspect of HF care should be added to Heart Failure, AHA Quality of Care and Outcomes Re-
the update. searchInterdisciplinaryWorkingGroupSteeringCommit-
When considering the new data for the focused update, tee, and AHA Council on Clinical Cardiology Committee
thewritinggroupfacedthetaskofweighingevidencefrom on Heart Failure and Transplantation.
studies enrolling large numbers of subjects outside North The 2009 focused update was reviewed by 2 external
America. While noting that practice patterns and the rigor reviewersnominatedbyboththeACCFandAHA,aswell
applied to data collection, as well as the genetic makeup of asareviewerfromtheACCF/AHATaskForceonPractice
subjects, might influence the observed magnitude of a Guidelines, 10 organizational reviewers representing the
treatment’s effect, the writing group believed that the data American College of Chest Physicians, the American Col-
were relevant to formulation of recommendations for the lege of Physicians, the American Academy of Family
management of HF in North America. Physicians, the Heart Failure Society of America, and the
International Society for Heart and Lung Transplantation,
1.2. Organization of Committee and Relationships
and 14 individual content reviewers. All information about
With Industry (UPDATED)
reviewers’ relationships with industry was collected and
The2005writingcommitteewascomposedof15members distributedtothewritingcommitteeandispublishedinthis
who represented the ACCF and AHA, as well as invited document (see Appendix 5 for details).
participants from the American College of Chest Physi- The2009focusedupdatewasapprovedforpublicationby
cians, the Heart Failure Society of America, the Interna- the governing bodies of the ACCF and the AHA and
tional Society for Heart and Lung Transplantation, the endorsed by the International Society for Heart and Lung
American Academy of Family Physicians, and the Ameri- Transplantation.
can College of Physicians. Both the academic and private
1.4. Stages of Heart Failure (UPDATED)
practice sectors were represented.
For the 2009 focused update, all members of the 2005 The HF writing committee previously developed a new
HF writing committee were invited to participate; those approach to the classification of HF (2), one that em-
who agreed (referred to as the 2009 Focused Update phasized both the development and progression of the
Writing Group) were required to disclose all relationships disease. In doing so, they identified 4 stages involved in
withindustryrelevanttothedataunderconsideration(1)as the development of the HF syndrome. The first 2 stages
were all peer reviewers of the document (see Appendixes 4 (A and B) are clearly not HF but are an attempt to help
and5foralistingofrelationshipswithindustryforthe2009 healthcare providers with the early identification of
JACCVol.53,No.15,2009 Huntetal. e7
April14,2009:e1–90 2009ACCF/AHAHeartFailureGuidelines
patients who are at risk for developing HF. Stages A and 2. Characterization of Heart Failure as a
B patients are best defined as those with risk factors that Clinical Syndrome
clearly predispose toward the development of HF. For
example, patients with coronary artery disease, hyperten-
2.1. Definition of Heart Failure
sion, or diabetes mellitus who do not yet demonstrate
impaired left ventricular (LV) function, hypertrophy, or Heart failure is a complex clinical syndrome that can result
geometric chamber distortion would be considered Stage from any structural or functional cardiac disorder that
A, whereas patients who are asymptomatic but demon- impairstheabilityoftheventricletofillwithorejectblood.
strate LV hypertrophy (LVH) and/or impaired LV func- ThecardinalmanifestationsofHFaredyspneaandfatigue,
which may limit exercise tolerance, and fluid retention,
tion would be designated as Stage B. Stage C then
which may lead to pulmonary congestion and peripheral
denotes patients with current or past symptoms of HF
edema.Bothabnormalitiescanimpairthefunctionalcapac-
associated with underlying structural heart disease (the
ityandqualityoflifeofaffectedindividuals,buttheydonot
bulk of patients with HF), and Stage D designates
necessarily dominate the clinical picture at the same time.
patients with truly refractory HF who might be eligible
Somepatientshaveexerciseintolerancebutlittleevidenceof
for specialized, advanced treatment strategies, such as
fluidretention,whereasotherscomplainprimarilyofedema
mechanical circulatory support, procedures to facilitate
andreportfewsymptomsofdyspneaorfatigue.Becausenot
fluid removal, continuous inotropic infusions, or cardiac
all patients have volume overload at the time of initial or
transplantation or other innovative or experimental sur-
subsequent evaluation, the term “heart failure” is preferred
gical procedures, or for end-of-life care, such as hospice.
over the older term “congestive heart failure.”
Thisclassificationrecognizesthatthereareestablished
TheclinicalsyndromeofHFmayresultfromdisordersof
risk factors and structural prerequisites for the develop-
the pericardium, myocardium, endocardium, or great ves-
ment of HF and that therapeutic interventions intro-
sels, but the majority of patients with HF have symptoms
duced even before the appearance of LV dysfunction or
due to an impairment of LV myocardial function. Heart
symptoms can reduce the population morbidity and
failure may be associated with a wide spectrum of LV
mortality of HF. This classification system is intended to
functional abnormalities, which may range from patients
complement but in no way to replace the New York
withnormalLVsizeandpreservedEFtothosewithsevere
Heart Association (NYHA) functional classification,
dilatation and/or markedly reduced EF. In most patients,
which primarily gauges the severity of symptoms in
abnormalities of systolic and diastolic dysfunction coexist,
patients who are in Stage C or Stage D. It has been
regardless of EF. Patients with normal EF may have a
recognized for many years that the NYHA functional
differentnaturalhistoryandmayrequiredifferenttreatment
classification reflects a subjective assessment by a health-
strategies than patients with reduced EF, although such
care provider and can change frequently over short
differences remain controversial (see Section 4.3.2.1).
periods of time. It has also been recognized that the
Coronary artery disease, hypertension, and dilated car-
treatments used may not differ significantly across the
diomyopathy are the causes of HF in a substantial propor-
classes. Therefore, the committee believed that a staging
tion of patients in the Western world. As many as 30% of
system was needed that would reliably and objectively patients with dilated cardiomyopathy may have a genetic
identify patients during the course of their developing cause(14).Valvularheartdiseaseisstillacommoncauseof
disease and that would be linked to treatments uniquely HF.Infact,nearlyanyformofheartdiseasemayultimately
appropriateateachstageofillness.Accordingtothisnew lead to the HF syndrome.
staging approach, patients would only be expected to It should be emphasized that HF is not equivalent to
either not advance at all or to advance from one stage to cardiomyopathy or to LV dysfunction; these latter terms
the next, unless progression of the disease was slowed or describe possible structural or functional reasons for the
stopped by treatment, and spontaneous reversal of this development of HF. Instead, HF is defined as a clinical
progression would be considered unusual. For instance, syndrome that is characterized by specific symptoms (dys-
although symptoms (NYHA functional class) might vary pnea and fatigue) in the medical history and signs (edema,
widelyovertime(inresponsetotherapyortoprogression rales) on the physical examination. There is no single
of disease) in a patient who has already developed the diagnostic test for HF because it is largely a clinical
clinical syndrome of HF (Stage C), the patient could diagnosis that is based on a careful history and physical
never return to Stage B (never had HF), and therapies examination.
recommendedforStageCwillbeappropriateevenifthis
2.2. Heart Failure as a Symptomatic Disorder
patient is in NYHA class I. This new classification
scheme adds a useful dimension to our thinking about The approach that is most commonly used to quantify the
HF that is similar to that achieved by staging or risk degree of functional limitation imposed by HF is one first
assessmentsystemsforotherdisorders(e.g.,thoseusedin developedbytheNYHA.Thissystemassignspatientsto1
the approach to cancer). of 4 functional classes, depending on the degree of effort
e8 Huntetal. JACCVol.53,No.15,2009
2009ACCF/AHAHeartFailureGuidelines April14,2009:e1–90
needed to elicit symptoms: patients may have symptoms of These effects, in turn, serve to sustain and exacerbate the
HF at rest (class IV), on less-than-ordinary exertion (class remodeling process. Cardiac remodeling generally precedes
III), on ordinary exertion (class II), or only at levels of the development of symptoms (occasionally by months or
exertion that would limit normal individuals (class I). even years), continues after the appearance of symptoms,
Although the functional class tends to deteriorate over and contributes substantially to worsening of symptoms
periods of time, most patients with HF do not typically despite treatment. Progression of coronary artery disease,
show an uninterrupted and inexorable worsening of symp- diabetes mellitus, hypertension, or the onset of atrial fibril-
toms. Instead, the severity of symptoms characteristically lation may also contribute to the progression of HF. The
fluctuates even in the absence of changes in medications, development of structural abnormalities can have 1 of 3
and changes in medications and diet can have either outcomes: 1) patients die before developing symptoms (in
favorable or adverse effects on functional capacity in the StageAorB),2)patientsdevelopsymptomscontrolledby
absence of measurable changes in ventricular function. treatment, or 3) patients die of progressive HF. Sudden
Somepatientsmaydemonstrateremarkablerecovery,some- death can interrupt this course at any time.
times associated with improvement in structural and func- AlthoughseveralfactorscanacceleratetheprocessofLV
tional abnormalities. Usually, sustained improvement is remodeling,thereissubstantialevidencethattheactivation
associated with drug therapy, and that therapy should be of endogenous neurohormonal systems plays an important
continued indefinitely. roleincardiacremodelingandtherebyintheprogressionof
The mechanisms responsible for the exercise intolerance HF. Patients with HF have elevated circulating or tissue
of patients with chronic HF have not been defined clearly. levelsofnorepinephrine,angiotensinII,aldosterone,endo-
Although HF is generally regarded as a hemodynamic thelin,vasopressin,andcytokines,whichcanact(aloneorin
disorder, many studies have indicated that there is a poor concert)toadverselyaffectthestructureandfunctionofthe
relation between measures of cardiac performance and the heart. These neurohormonal factors not only increase the
symptomsproducedbythedisease.Patientswithaverylow hemodynamic stresses on the ventricle by causing sodium
EF (see Section 4.3.2.1) may be asymptomatic, whereas retentionandperipheralvasoconstrictionbutmayalsoexert
patients with preserved LVEF may have severe disability. directtoxiceffectsoncardiaccellsandstimulatemyocardial
The apparent discordance between EF and the degree of fibrosis,whichcanfurtheralterthearchitectureand impair
functional impairment is not well understood but may be the performance of the failing heart. Neurohormonal acti-
explained in part by alterations in ventricular distensibility, vationalsohasdirectdeleteriouseffectsonthemyocytesand
valvular regurgitation, pericardial restraint, cardiac rhythm, interstitium, altering the performance and phenotype of
conduction abnormalities, and right ventricular function these cells.
(14). In addition, in ambulatory patients, many noncardiac The development of HF can be appropriately character-
factors may contribute substantially to exercise intolerance. ized by considering 4 stages of the disease, as described in
These factors include but are not limited to changes in the Introduction. This staging system recognizes that HF,
peripheral vascular function, skeletal muscle physiology, like coronary artery disease, has established risk factors and
pulmonary dynamics, neurohormonal and reflex autonomic
structural prerequisites; that the development of HF has
activity, and renal sodium handling. The existence of these
asymptomatic and symptomatic phases; and that specific
noncardiac factors may explain why the hemodynamic
treatments targeted at each stage can reduce the morbidity
improvement produced by therapeutic agents in patients
and mortality of HF (Figure 1).
with chronic HF may not be immediately or necessarily
translated into clinical improvement. Although pharmaco- 3. Initial and Serial Clinical Assessment of
logical interventions may produce rapid changes in hemo- Patients Presenting With Heart Failure
dynamicvariables,signsandsymptomsmayimproveslowly
(UPDATED)
over weeks or months or not at all.
2.3. Heart Failure as a Progressive Disorder
The changes in this section are made to clarify the role of
Left ventricular dysfunction begins with some injury to, or functional assessment of the HF patient, beyond the NYHA
stress on, the myocardium and is generally a progressive functional classification, and to expand on the use of B-type
process, even in the absence of a new identifiable insult to natriuretic peptide (BNP) and N-terminal pro-B-type natri-
theheart.Theprincipalmanifestationofsuchprogressionis uretic peptide (NT-proBNP) testing within the context of the
achangeinthegeometryandstructureoftheLV,suchthat overall evaluation of the patient (Table 2).
the chamber dilates and/or hypertrophies and becomes
Recommendations for Initial Clinical Assessment of
morespherical—aprocessreferredtoascardiacremodeling.
Patients Presenting With Heart Failure
This change in chamber size and structure not only in-
creasesthehemodynamicstressesonthewallsofthefailing CLASSI
heart and depresses its mechanical performance but may 1. Athoroughhistoryandphysicalexaminationshouldbeobtained/
also increase regurgitant flow through the mitral valve. performedinpatientspresentingwithHFtoidentifycardiacand
JACCVol.53,No.15,2009 Huntetal. e9
April14,2009:e1–90 2009ACCF/AHAHeartFailureGuidelines
Figure1. StagesintheDevelopmentofHeartFailure/RecommendedTherapybyStage
ACEIindicatesangiotensin-convertingenzymeinhibitor;ARB,angiotensinIIreceptorblocker;EF,ejectionfraction;FHxCM,familyhistoryofcardiomyopathy;HF,heartfailure;
LV,leftventricular;LVH,leftventricularhypertrophy;andMI,myocardialinfarction.
noncardiacdisordersorbehaviorsthatmightcauseoraccelerate 8. Coronaryarteriographyshouldbeperformedinpatientspresent-
thedevelopmentorprogressionofHF.(LevelofEvidence:C) ingwithHFwhohaveanginaorsignificantischemiaunlessthe
2. Acarefulhistoryofcurrentandpastuseofalcohol,illicitdrugs, patientisnoteligibleforrevascularizationofanykind(15–19).
currentorpaststandardor“alternativetherapies,”andchemo- (LevelofEvidence:B)
therapydrugsshouldbeobtainedfrompatientspresentingwith
HF.(LevelofEvidence:C) CLASSIIa
3. In patients presenting with HF, initial assessment should be 1. Coronaryarteriographyisreasonableforpatientspresentingwith
made of the patient’s ability to perform routine and desired HFwhohavechestpainthatmayormaynotbeofcardiacorigin
activitiesofdailyliving.(LevelofEvidence:C) whohavenothadevaluationoftheircoronaryanatomyandwho
4. InitialexaminationofpatientspresentingwithHFshouldinclude havenocontraindicationstocoronaryrevascularization.(Levelof
assessment of the patient’s volume status, orthostatic blood Evidence:C)
pressure changes, measurement of weight and height, and 2. Coronaryarteriographyisreasonableforpatientspresentingwith
calculationofbodymassindex.(LevelofEvidence:C) HF who have known or suspected coronary artery disease but
5. Initial laboratory evaluation of patients presenting with HF who do not have angina unless the patient is not eligible for
shouldincludecompletebloodcount,urinalysis,serumelectro- revascularizationofanykind.(LevelofEvidence:C)
lytes (including calcium and magnesium), blood urea nitrogen, 3. Noninvasive imaging to detect myocardial ischemia and via-
serumcreatinine,fastingbloodglucose(glycohemoglobin),lipid bility is reasonable in patients presenting with HF who have
profile,liverfunctiontests,andthyroid-stimulatinghormone.(Level known coronary artery disease and no angina unless the
ofEvidence:C) patientisnoteligibleforrevascularizationofanykind(20).(Level
6. Twelve-leadelectrocardiogramandchestradiograph(posterior- ofEvidence:B)
anteriorandlateral)shouldbeperformedinitiallyinallpatients 4. Maximalexercisetestingwithorwithoutmeasurementofrespi-
presentingwithHF.(LevelofEvidence:C) ratorygasexchangeand/orbloodoxygensaturationisreason-
7. Two-dimensional echocardiography with Doppler should be per- ableinpatientspresentingwithHFtohelpdeterminewhetherHF
formedduringinitialevaluationofpatientspresentingwithHFto isthecauseofexerciselimitationwhenthecontributionofHFis
assess LVEF, left ventricular size, wall thickness, and valve uncertain.(LevelofEvidence:C)
function. Radionuclide ventriculography can be performed to 5. Maximalexercisetestingwithmeasurementofrespiratorygas
assessLVEFandvolumes.(LevelofEvidence:C) exchangeisreasonabletoidentifyhigh-riskpatientspresenting
e10 Huntetal. JACCVol.53,No.15,2009
2009ACCF/AHAHeartFailureGuidelines April14,2009:e1–90
withHFwhoarecandidatesforcardiactransplantationorother 3.1. Initial Evaluation of Patients
advancedtreatments(21–23).(LevelofEvidence:B)
3.1.1. Identification of Patients (UPDATED)
6. Screening for hemochromatosis, sleep-disturbed breathing, or
humanimmunodeficiencyvirusisreasonableinselectedpatients In general, patients with LV dysfunction or HF present to
whopresentwithHF.(LevelofEvidence:C)
the healthcare provider in 1 of 3 ways:
7. Diagnostic tests for rheumatologic diseases, amyloidosis, or
pheochromocytoma are reasonable in patients presenting with 1. With a syndrome of decreased exercise tolerance.
HFinwhomthereisaclinicalsuspicionofthesediseases.(Level Most patients with HF seek medical attention with
ofEvidence:C) complaintsofareductionintheirefforttolerancedueto
8. Endomyocardialbiopsycanbeusefulinpatientspresentingwith dyspnea and/or fatigue. These symptoms, which may
HFwhenaspecificdiagnosisissuspectedthatwouldinfluence occur at rest or during exercise, may be attributed
therapy(24).(LevelofEvidence:C)
inappropriatelybythepatientand/orhealthcareprovider
9. Measurementofnatriureticpeptides(BNPandNT-proBNP)can
to aging, other physiological abnormalities (e.g., decon-
beusefulintheevaluationofpatientspresentingintheurgent
ditioning), or other medical disorders (e.g., pulmonary
care setting in whom the clinical diagnosis of HF is uncertain.
disease). Therefore, in a patient whose exercise capacity
Measurementofnatriureticpeptides(BNPandNT-proBNP)can
is limited by dyspnea or fatigue, the healthcare provider
behelpfulinriskstratification(25–32).(LevelofEvidence:A)
must determine whether the principal cause is HF or
CLASSIIb another abnormality. Elucidation of the precise reason
1. Noninvasiveimagingmaybeconsideredtodefinethelikelihood for exercise intolerance can be difficult because several
of coronary artery disease in patients with HF and LV dysfunc- disorders may coexist in the same patient. A clear
tion.(LevelofEvidence:C) distinction can sometimes be made only by measure-
2. Holter monitoring might be considered in patients presenting
ments of gas exchange or blood oxygen saturation or by
withHFwhohaveahistoryofMIandarebeingconsideredfor
invasivehemodynamicmeasurementsduringgradedlev-
electrophysiologic study to document VT inducibility. (Level of
els of exercise (see ACC/AHA 2002 Guideline Update
Evidence:C)
for Exercise Testing [33]).
CLASSIII 2. With a syndrome of fluid retention. Patients may
1. Endomyocardial biopsy should not be performed in the routine presentwithcomplaintsoflegorabdominalswellingas
evaluationofpatientswithHF(24).(LevelofEvidence:C) their primary (or only) symptom. In these patients, the
2. Routineuseofsignal-averagedelectrocardiographyisnotrecom- impairmentofexercisetolerancemayoccursogradually
mendedfortheevaluationofpatientspresentingwithHF.(Level thatitmaynotbenotedunlessthepatientisquestioned
ofEvidence:C)
carefully and specifically about a change in activities of
3. Routine measurement of circulating levels of neurohormones
daily living.
(e.g., norepinephrine or endothelin) is not recommended for
3. With no symptoms or symptoms of another cardiac
patientspresentingwithHF.(LevelofEvidence:C)
or noncardiac disorder. During their evaluation for a
Recommendations for Serial Clinical Assessment of disorderotherthanHF(e.g.,abnormalheartsoundsor
Patients Presenting With Heart Failure abnormal electrocardiogram or chest x-ray, hyperten-
sion or hypotension, diabetes mellitus, an acute myo-
CLASSI
cardial infarction (MI), an arrhythmia, or a pulmonary
1. Assessment should be made at each visit of the ability of a
or systemic thromboembolic event), patients may be
patientwithHFtoperformroutineanddesiredactivitiesofdaily
found to have evidence of cardiac enlargement or
living.(LevelofEvidence:C)
dysfunction.
2. Assessmentshouldbemadeateachvisitofthevolumestatus
andweightofapatientwithHF.(LevelofEvidence:C)
A variety of approaches have been used to quantify the
3. Careful history of current use of alcohol, tobacco, illicit drugs,
degree of functional limitation imposed by HF. The most
“alternativetherapies,”andchemotherapydrugs,aswellasdiet
widely used scale is the NYHA functional classification
andsodiumintake,shouldbeobtainedateachvisitofapatient
(34),butthissystemissubjecttoconsiderableinterobserver
withHF.(LevelofEvidence:C)
variabilityandisinsensitivetoimportantchangesinexercise
CLASSIIa capacity.Theselimitationsmaybeovercomebyformaltests
1. RepeatmeasurementofEFandtheseverityofstructuralremod- of exercise tolerance. Measurement of the distance that a
elingcanbeusefultoprovideinformationinpatientswithHFwho patient can walk in 6 minutes may have prognostic signif-
havehadachangeinclinicalstatusorwhohaveexperiencedor icance and may help to assess the level of functional
recoveredfromaclinicaleventorreceivedtreatmentthatmight impairment in the very sick, but serial changes in walking
have had a significant effect on cardiac function. (Level of
distancemaynotparallelchangesinclinicalstatus.Maximal
Evidence:C)
exercise testing, with measurement of peak oxygen uptake,
CLASSIIb hasbeenusedtoidentifyappropriatecandidatesforcardiac
1. The value of serial measurements of BNP to guide therapy for transplantation, to determine disability, and to assist in the
patientswithHFisnotwellestablished.(LevelofEvidence:C) formulation of an exercise prescription, but its role in the