2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of

142 Pages·2016·2.92 MB·English

by  Robert O. Bonow

JournaloftheAmericanCollegeofCardiology Vol.52,No.13,2008
©2008bytheAmericanCollegeofCardiologyFoundationandtheAmericanHeartAssociation,Inc. ISSN0735-1097/08/$34.00
PublishedbyElsevierInc. doi:10.1016/j.jacc.2008.05.007
PRACTICE GUIDELINE
2008 Focused Update Incorporated Into the
ACC/AHA 2006 Guidelines for the Management
of Patients With Valvular Heart Disease
AReportoftheAmericanCollegeofCardiology/AmericanHeartAssociationTaskForceonPracticeGuidelines
(WritingCommitteetoRevisethe1998GuidelinesfortheManagementofPatientsWithValvularHeartDisease)
Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and
Interventions, and Society of Thoracic Surgeons
2006Writing Robert O. Bonow, MD, MACC, FAHA, Chair Rick A. Nishimura, MD, FACC, FAHA
Committee
Patrick T. O’Gara, MD, FACC, FAHA
Members
Blase A. Carabello, MD, FACC, FAHA Robert A. O’Rourke, MD, MACC, FAHA
Kanu Chatterjee, MB, FACC Catherine M. Otto, MD, FACC, FAHA
Antonio C. de Leon, JR, MD, FACC, FAHA Pravin M. Shah, MD, MACC, FAHA
David P. Faxon, MD, FACC, FAHA Jack S. Shanewise, MD*
Michael D. Freed, MD, FACC, FAHA
William H. Gaasch, MD, FACC, FAHA *SocietyofCardiovascularAnesthesiologistsRepresentative
Bruce W. Lytle, MD, FACC
2008 Rick A. Nishimura, MD, FACC, FAHA, Chair Bruce W. Lytle, MD, FACC, FAHA
Focused
Patrick T. O’Gara, MD, FACC, FAHA
Update
Writing Blase A. Carabello, MD, FACC, FAHA Robert A. O’Rourke, MD, FACC, FAHA
Group David P. Faxon, MD, FACC, FAHA Pravin M. Shah, MD, MACC, FAHA
Members Michael D. Freed, MD, FACC, FAHA
ThisdocumentwasapprovedbytheAmericanCollegeofCardiologyFoundation 2008;52:e1–142.
Board of Trustees in May 2008 and by the American Heart Association Science ThisarticleiscopublishedintheSeptember23,2008,issueofCirculation.
AdvisoryandCoordinatingCommitteeinMay2008. Copies:ThisdocumentisavailableontheWorldWideWebsitesoftheAmerican
TheAmericanCollegeofCardiologyFoundationrequeststhatthisdocumentbe CollegeofCardiology(www.acc.org)andtheAmericanHeartAssociation(www.
citedasfollows:BonowRO,CarabelloBA,ChatterjeeK,deLeonACJr.,FaxonDP, my.americanheart.org). For copies of this document, please contact Elsevier Inc.
FreedMD,GaaschWH,LytleBW,NishimuraRA,O’GaraPT,O’RourkeRA, ReprintDepartment,fax[phone],[e-mail].
Otto CM, Shah PM, Shanewise JS. 2008 focused update incorporated into the Permissions: Modification, alteration, enhancement and/or distribution of this
ACC/AHA 2006 guidelines for the management of patients with valvular heart
documentarenotpermittedwithouttheexpresspermissionoftheAmericanCollege
disease:areportoftheAmericanCollegeofCardiology/AmericanHeartAssociation
of Cardiology Foundation or the American Heart Association. Please contact
TaskForceonPracticeGuidelines(WritingCommitteetoDevelopGuidelinesfor
Elsevier’[e-mail].
the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol
e2 Bonowetal. JACCVol.52,No.13,2008
ACC/AHAVHDGuidelines:2008FocusedUpdateIncorporated September23,2008:e1–142
Task Sidney C. Smith, JR, MD, FACC, FAHA, Chair Frederick G. Kushner, MD, FACC, FAHA
Force
Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair Bruce W. Lytle, MD, FACC, FAHA†
Members
Rick A. Nishimura, MD, FACC, FAHA
Christopher E. Buller, MD, FACC
Richard L. Page, MD, FACC, FAHA
Mark A. Creager, MD, FACC, FAHA
Lynn G. Tarkington, RN
Steven M. Ettinger, MD, FACC
Clyde W. Yancy, JR, MD, FACC, FAHA
David P. Faxon, MD, FACC, FAHA†
Jonathan L. Halperin, MD, FACC, FAHA† †FormerTaskForcememberduringthiswritingeffort
Harlan M. Krumholz, MD, FACC, FAHA
3.1.4.1. ECHOCARDIOGRAPHY(IMAGING,SPECTRAL,AND
TABLE OF CONTENTS
COLORDOPPLER)INAORTICSTENOSIS....................e19
3.1.4.2. EXERCISETESTING....................................e21
PREAMBLE(UPDATED).......................................e5 3.1.4.3. SERIALEVALUATIONS..................................e21
3.1.4.4. MEDICALTHERAPY(UPDATED)..........................e21
1. INTRODUCTION.............................................e6 3.1.4.5. PHYSICALACTIVITYANDEXERCISE .......................e22
3.1.5. IndicationsforCardiacCatheterization..............e22
1.1. EvidenceReview(UPDATED).........................e6 3.1.6. Low-Flow/Low-GradientAorticStenosis...........e22
3.1.7. IndicationsforAorticValveReplacement...........e23
1.2. ScopeoftheDocument(UPDATED)..................e7 3.1.7.1. SYMPTOMATICPATIENTS ...............................e23
1.3. ReviewandApproval(NEW)..........................e8 3.1.7.2. ASYMPTOMATICPATIENTS..............................e24
3.1.7.3. PATIENTSUNDERGOINGCORONARYARTERYBYPASSOR
2. GENERALPRINCIPLES....................................e8 OTHERCARDIACSURGERY..............................e25
3.1.8. AorticBalloonValvotomy...........................e25
2.1. Evaluation of the Patient With a Cardiac 3.1.9. MedicalTherapyfortheInoperablePatient.........e25
Murmur.................................................e8 3.1.10. EvaluationAfterAorticValveReplacement........e26
2.1.1. Introduction(UPDATED) ..........................e8 3.1.11. SpecialConsiderationsintheElderly..............e26
2.1.2. ClassificationofMurmurs............................e8 3.2. AorticRegurgitation..................................e26
2.1.2.1. DYNAMICCARDIACAUSCULTATION.........................e9 3.2.1. Etiology.............................................e26
2.1.2.2. OTHERPHYSICALFINDINGS..............................e9 3.2.2. AcuteAorticRegurgitation..........................e26
2.1.2.3. ASSOCIATEDSYMPTOMS ...............................e10 3.2.2.1. PATHOPHYSIOLOGY....................................e26
2.1.3. ElectrocardiographyandChestRoentgenography......e11 3.2.2.2. DIAGNOSIS..........................................e27
2.1.4. Echocardiography...................................e11 3.2.2.3. TREATMENT..........................................e27
2.1.5. CardiacCatheterization.............................e12 3.2.3. ChronicAorticRegurgitation.......................e27
2.1.6. ExerciseTesting.....................................e12 3.2.3.1. PATHOPHYSIOLOGY....................................e27
2.1.7. ApproachtothePatient.............................e12 3.2.3.2. NATURALHISTORY....................................e29
2.2. ValveDiseaseSeverityTable.......................e13 3.2.3.2.1. ASYMPTOMATICPATIENTSWITHNORMALLEFT
VENTRICULARFUNCTION.............................e29
2.3. EndocarditisandRheumaticFeverProphylaxis
3.2.3.2.2. ASYMPTOMATICPATIENTSWITHDEPRESSEDSYSTOLIC
(UPDATED).............................................e13 FUNCTION.........................................e30
2.3.1. EndocarditisProphylaxis(UPDATED).............e13 3.2.3.2.3. SYMPTOMATICPATIENTS.............................e30
Table5(DELETED)
3.2.3.3. DIAGNOSISANDINITIALEVALUATION......................e30
Table 6 (UPDATED)
3.2.3.4. MEDICALTHERAPY....................................e31
Table 7 (UPDATED)
3.2.3.5. PHYSICALACTIVITYANDEXERCISE .......................e33
Table8(DELETED)
3.2.3.6. SERIALTESTING......................................e33
2.32..23..2.R1.hGeEuNmERaAtLicCOFNeSvIDerERPArToIOpNhSy.l.a.x.is.................................................ee1177 3.2.3.7. INDICATIONSFORCARDIACCATHETERIZATION..............e34
3.2.3.8. INDICATIONSFORAORTICVALVEREPLACEMENTOR
2.3.2.2. PRIMARYPREVENTION.................................e17
AORTICVALVEREPAIR.................................e35
2.3.2.3. SECONDARYPREVENTION...............................e17
3.2.3.8.1. SYMPTOMATICPATIENTSWITHNORMALLEFT
3. SPECIFICVALVELESIONS..............................e18 VENTRICULARSYSTOLICFUNCTION.....................e35
3.2.3.8.2. SYMPTOMATICPATIENTSWITHLEFTVENTRICULAR
3.1. AorticStenosis .......................................e18 DYSFUNCTION......................................e35
3.1.1. Introduction........................................e18 3.2.3.8.3. ASYMPTOMATICPATIENTS............................e36
3.1.1.1. GRADINGTHEDEGREEOFSTENOSIS......................e18 3.2.4. ConcomitantAorticRootDisease...................e37
3.1.2. Pathophysiology.....................................e18 3.2.5. EvaluationofPatientsAfterAorticValve
3.1.3. NaturalHistory .....................................e19 Replacement ........................................e37
3.1.4. ManagementoftheAsymptomaticPatient..........e19 3.2.6. SpecialConsiderationsintheElderly................e38
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3.3. BicuspidAorticValveWithDilatedAscending 3.7.2.2.1. TWO-DIMENSIONALANDDOPPLERECHOCARDIOGRAPHIC
Aorta...................................................e38 STUDIES..........................................e64
3.4. MitralStenosis........................................e39 3.7.2.2.2. CARDIACCATHETERIZATION...........................e64
3.7.2.3. MANAGEMENT........................................e65
3.4.1. PathophysiologyandNaturalHistory ...............e39 3.7.3. CombinedMitralStenosisandAorticRegurgitation.....e65
3.4.2. IndicationsforEchocardiographyinMitral
3.7.3.1. PATHOPHYSIOLOGY....................................e65
Stenosis.............................................e40 3.7.3.2. MANAGEMENT........................................e65
3.4.3. MedicalTherapy....................................e42 3.7.4. CombinedMitralStenosisandTricuspid
3.4.3.1. MEDICALTHERAPY:GENERAL(UPDATED)..................e42 Regurgitation........................................e65
3.4.3.2. MEDICALTHERAPY:ATRIALFIBRILLATION..................e43 3.7.4.1. PATHOPHYSIOLOGY....................................e65
3.4.3.3. MEDICALTHERAPY:PREVENTIONOFSYSTEMIC 3.7.4.2. DIAGNOSIS..........................................e65
EMBOLIZATION.......................................e43 3.7.4.3. MANAGEMENT........................................e65
3.4.4. RecommendationsRegardingPhysicalActivity 3.7.5. CombinedMitralRegurgitationandAortic
andExercise.........................................e44 Regurgitation........................................e66
3.4.5. SerialTesting.......................................e44 3.7.5.1. PATHOPHYSIOLOGY....................................e66
3.4.6. EvaluationoftheSymptomaticPatient..............e44 3.7.5.2. DIAGNOSISANDTHERAPY..............................e66
3.4.7. Indications for Invasive Hemodynamic 3.7.6. CombinedMitralStenosisandAorticStenosis......e66
Evaluation..........................................e45 3.7.6.1. PATHOPHYSIOLOGY....................................e66
3.4.8. IndicationsforPercutaneousMitralBalloon 3.7.6.2. DIAGNOSISANDTHERAPY..............................e66
Valvotomy...........................................e47 3.7.7. CombinedAorticStenosisandMitralRegurgitation.....e66
3.4.9. IndicationsforSurgeryforMitralStenosis..........e50 3.7.7.1. PATHOPHYSIOLOGY....................................e66
3.4.10. ManagementofPatientsAfterValvotomyor 3.7.7.2. DIAGNOSISANDTHERAPY..............................e66
Commissurotomy..................................e51 3.8. TricuspidValveDisease..............................e66
3.4.11. SpecialConsiderations.............................e52 3.8.1. Pathophysiology.....................................e66
3.4.11.1. PREGNANTPATIENTS.................................e52 3.8.2. Diagnosis ...........................................e67
3.4.11.2. OLDERPATIENTS ....................................e52 3.8.3. Management........................................e67
3.5. MitralValveProlapse................................e52 3.9. Drug-RelatedValvularHeartDisease...............e68
3.5.1. PathophysiologyandNaturalHistory ...............e52 3.10. RadiationHeartDisease ...........................e68
3.5.2. EvaluationandManagementofthe
AsymptomaticPatient(UPDATED)...............e53 4. EVALUATIONANDMANAGEMENTOFINFECTIVE
3.5.3. EvaluationandManagementofthe ENDOCARDITIS...............................................e69
SymptomaticPatient(UPDATED).................e54
3.5.4. SurgicalConsiderations .............................e55 4.1. AntimicrobialTherapy................................e69
3.6. MitralRegurgitation..................................e55 4.2. Culture-NegativeEndocarditis ......................e71
3.6.1. Etiology.............................................e55
3.6.2. AcuteSevereMitralRegurgitation..................e56 4.3. EndocarditisinHIV-SeropositivePatients.........e71
3.6.2.1. PATHOPHYSIOLOGY....................................e56 4.4. IndicationsforEchocardiographyin
3.6.2.2. DIAGNOSIS..........................................e56 SuspectedorKnownEndocarditis..................e71
3.6.2.3. MEDICALTHERAPY....................................e56 4.4.1. TransthoracicEchocardiographyinEndocarditis......e73
3.6.3. ChronicAsymptomaticMitralRegurgitation........e56 4.4.2. Transesophageal Echocardiography in
3.6.3.1. PATHOPHYSIOLOGYANDNATURALHISTORY................e56
Endocarditis........................................e73
3.6.3.2. DIAGNOSIS..........................................e57
3.6.3.3. INDICATIONSFORTRANSTHORACICECHOCARDIOGRAPHY .....e57 4.5. OutpatientTreatment................................e74
3.6.3.4. INDICATIONSFORTRANSESOPHAGEALECHOCARDIOGRAPHY......e58 4.6. IndicationsforSurgeryinPatientsWith
3.6.3.5. SERIALTESTING......................................e58 AcuteInfectiveEndocarditis........................e75
3.6.3.6. GUIDELINESFORPHYSICALACTIVITYANDEXERCISE.........e58 4.6.1. SurgeryforNativeValveEndocarditis...............e75
3.6.3.7. MEDICALTHERAPY....................................e58 4.6.2. SurgeryforProstheticValveEndocarditis...........e77
3.6.3.8. INDICATIONSFORCARDIACCATHETERIZATION..............e59
3.6.4. IndicationsforSurgery..............................e59 5. MANAGEMENTOFVALVULARDISEASEIN
3.6.4.1. TYPESOFSURGERY...................................e59 PREGNANCY..................................................e77
3.6.4.2. INDICATIONSFORMITRALVALVEOPERATION...............e60
3.6.4.2.1. SYMPTOMATICPATIENTSWITHNORMALLEFT 5.1. PhysiologicalChangesofPregnancy...............e77
VENTRICULARFUNCTION.............................e61
3.6.4.2.2. ASYMPTOMATICORSYMPTOMATICPATIENTSWITH 5.2. PhysicalExamination................................e77
LEFTVENTRICULARDYSFUNCTION......................e61 5.3. Echocardiography.....................................e78
3.6.4.2.3. ASYMPTOMATICPATIENTSWITHNORMALLEFT 5.4. GeneralManagementGuidelines ...................e78
VENTRICULARFUNCTION.............................e62
3.6.4.2.4. ATRIALFIBRILLATION ................................e63 5.5. SpecificLesions......................................e80
5.5.1. MitralStenosis......................................e80
3.6.5. IschemicMitralRegurgitation.......................e63
5.5.2. MitralRegurgitation................................e80
3.6.6. EvaluationofPatientsAfterMitralValve
5.5.3. AorticStenosis......................................e80
ReplacementorRepair..............................e63
5.5.4. AorticRegurgitation................................e80
3.6.7. SpecialConsiderationsintheElderly................e64
5.5.5. PulmonicStenosis...................................e80
3.7. MultipleValveDisease ..............................e64 5.5.6. TricuspidValveDisease.............................e81
3.7.1. Introduction.........................................e64 5.5.7. MarfanSyndrome...................................e81
3.73..27..2.M1. PixAeTdHOSPiHnYgSlIOeLVOGaYlv.e..D..i.s.e.a.s.e...................................................ee6644 5.6. EndocarditisProphylaxis(UPDATED)...............e81
3.7.2.2. DIAGNOSIS..........................................e64 5.7. CardiacValveSurgery ...............................e81
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5.8. AnticoagulationDuringPregnancy..................e81 7.3.2.1. SELECTIONOFAMITRALVALVEPROSTHESIS..............e100
5.8.1. Warfarin............................................e81 7.3.2.2. CHOICEOFMITRALVALVEOPERATION...................e100
5.8.2. UnfractionatedHeparin.............................e82 7.4. TricuspidValveSurgery.............................e101
5.8.3. Low-Molecular-WeightHeparins...................e82
5.8.4. SelectionofAnticoagulationRegimeninPregnant 7.5. ValveSelectionforWomenofChildbearingAge.....e101
PatientsWithMechanicalProstheticValves ........e82 8. INTRAOPERATIVEASSESSMENT......................e101
5.9. SelectionofValveProsthesesinYoungWomen.....e84
6. MANAGEMENTOFCONGENITALVALVULARHEART 8.1. SpecificValveLesions..............................e102
DISEASEINADOLESCENTSANDYOUNGADULTS 8.1.1. AorticStenosis.....................................e102
(UPDATED)....................................................e84 88..11..23.. AMoirtrtiaclRSteegnuorsgiist.a.t.io.n................................................................ee110023
8.1.4. MitralRegurgitation...............................e103
6.1. AorticStenosis .......................................e84 8.1.5. TricuspidRegurgitation............................e103
6.1.1. Pathophysiology.....................................e84 8.1.6. TricuspidStenosis..................................e103
6.1.2. EvaluationofAsymptomaticAdolescentsor
8.1.7. PulmonicValveLesions............................e103
YoungAdultsWithAorticStenosis.................e85
6.1.3. IndicationsforAorticBalloonValvotomyin 8.2. SpecificClinicalScenarios.........................e104
8.2.1. PreviouslyUndetectedAorticStenosisDuring
AdolescentsandYoungAdults......................e85
CABG.............................................e104
6.2. AorticRegurgitation..................................e86 8.2.2. PreviouslyUndetectedMitralRegurgitation
6.3. MitralRegurgitation..................................e87 DuringCABG.....................................e104
6.4. MitralStenosis........................................e87
9. MANAGEMENTOFPATIENTSWITHPROSTHETIC
6.56..5T.1r.icPuastphiodphVyaslivoelogDyi.s.e.a..s.e.............................................................ee8888 HEARTVALVES..............................................e104
6.5.2. EvaluationofTricuspidValveDiseasein
AdolescentsandYoungAdults......................e89 9.1. AntibioticProphylaxis ..............................e104
6.5.3. IndicationsforInterventioninTricuspid 9.1.1. InfectiveEndocarditis..............................e104
Regurgitation........................................e89 9.1.2. RecurrenceofRheumaticCarditis..................e104
6.6. PulmonicStenosis....................................e89 9.2. AntithromboticTherapy.............................e104
6.6.1. Pathophysiology.....................................e89 9.2.1. MechanicalValves .................................e105
6.6.2. EvaluationofPulmonicStenosisinAdolescents 9.2.2. BiologicalValves...................................e106
andYoungAdults...................................e90 9.2.3. EmbolicEventsDuringAdequateAntithrombotic
6.6.3. IndicationsforBalloonValvotomyinPulmonic Therapy............................................e106
Stenosis(UPDATED)..............................e90 9.2.4. ExcessiveAnticoagulation..........................e106
9.2.5. BridgingTherapyinPatientsWith
6.7. PulmonaryRegurgitation............................e91
MechanicalValvesWhoRequireInterruption
7. SURGICALCONSIDERATIONS...........................e91 ofWarfarinTherapyforNoncardiacSurgery,
InvasiveProcedures,orDentalCare................e106
7.1. AmericanAssociationforThoracicSurgery/ 9.2.6. AntithromboticTherapyinPatientsWhoNeed
SocietyofThoracicSurgeonsGuidelinesfor CardiacCatheterization/Angiography..............e107
Clinical Reporting of Heart Valve 9.2.7. ThrombosisofProstheticHeartValves ............e108
Complications........................................e92 9.3. Follow-UpVisits......................................e109
7.2. AorticValveSurgery.................................e93 9.3.1. FirstOutpatientPostoperativeVisit................e109
7.2.1. RisksandStrategiesinAorticValveSurgery........e94 9.3.2. Follow-UpVisitsinPatientsWithout
7.2.2. MechanicalAorticValveProstheses.................e94 Complications ......................................e109
7.2.2.1. ANTITHROMBOTICTHERAPYFORPATIENTSWITHAORTIC 9.3.3. Follow-UpVisitsinPatientsWithComplications......e110
7.2.3. SteMnEtCeHdANaInCAdLNHEoAnRsTteVnALtVeEdSH..e.t.e.r.o.g.r.a.f.t.s...............................ee9944 9.4. ReoperationtoReplaceaProstheticValve......e110
7.2.3.1. AORTICVALVEREPLACEMENTWITHSTENTEDHETEROGRAFTS.....e94 10. EVALUATIONANDTREATMENTOFCORONARY
7.2.3.2. AORTICVALVEREPLACEMENTWITHSTENTLESS
ARTERYDISEASEINPATIENTSWITHVALVULAR
HETEROGRAFTS......................................e95
7.2.4. AorticValveHomografts............................e96 HEARTDISEASE.............................................e110
7.2.5. PulmonicValveAutotransplantation................e96
7.2.6. AorticValveRepair.................................e97 10.1. ProbabilityofCoronaryArteryDiseasein
7.2.7. LeftVentricle–to–DescendingAortaShunt.........e97 PatientsWithValvularHeartDisease...........e110
7.2.8. ComparativeTrialsandSelectionofAortic
10.2. DiagnosisofCoronaryArteryDisease...........e111
ValveProstheses.....................................e97
10.3. TreatmentofCoronaryArteryDiseaseat
7.2.9. MajorCriteriaforAorticValveSelection ...........e98
7.3. MitralValveSurgery .................................e98 theTimeofAorticValveReplacement ..........e112
7.3.1. MitralValveRepair.................................e99 10.4. AorticValveReplacementinPatients
7.3.1.1. MYXOMATOUSMITRALVALVE............................e99 UndergoingCoronaryArteryBypassSurgery ...e112
7.3.1.2. RHEUMATICHEARTDISEASE ............................e99 10.5. ManagementofConcomitantMVDisease
7.3.1.3. ISCHEMICMITRALVALVEDISEASE........................e99 andCoronaryArteryDisease.....................e113
7.3.1.4. MITRALVALVEENDOCARDITIS..........................e100
7.3.2. MitralValveProstheses(Mechanicalor REFERENCES...............................................e113
Bioprostheses)......................................e100
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APPENDIX 1................................................e137 may be perceived as real or potential conflicts of interest.
Writing committee members are also strongly encouraged
APPENDIX 2................................................e138 to declare a previous relationship with industry that may be
perceived as relevant to guideline development. If a writing
APPENDIX 3................................................e140
committee member develops a new relationship with indus-
try during his or her tenure, he or she is required to notify
APPENDIX 4 (NEW) .......................................e140
guideline staff in writing. The continued participation of the
APPENDIX 5 (NEW) .......................................e141 writing committee member will be reviewed. These state-
ments are reviewed by the parent task force, reported orally
to all members of the writing panel at each meeting, and
updated and reviewed by the writing committee as changes
PREAMBLE (UPDATED)
occur. Please refer to the methodology manual for the ACC/
AHA guideline writing committees for further description and
It is important that the medical profession play a significant the relationships with industry policy (1067). See Appendix 1
role in critically evaluating the use of diagnostic procedures
for a list of writing committee member relationships with
and therapies as they are introduced in the detection,
industry and Appendix 2 for a listing of peer reviewer relation-
management, or prevention of disease states. Rigorous and
ships with industry that are pertinent to this guideline.
expert analysis of the available data documenting the abso-
These practice guidelines are intended to assist healthcare
lute and relative benefits and risks of those procedures and
providers in clinical decision making by describing a range
therapies can produce helpful guidelines that improve the
of generally acceptable approaches for the diagnosis, man-
effectiveness of care, optimize patient outcomes, and favor-
agement, and prevention of specific diseases or conditions.
ably affect the overall cost of care by focusing resources on
See Appendix 3 for a list of abbreviated terms used in this
the most effective strategies.
guideline. These guidelines attempt to define practices that
The American College of Cardiology (ACC) and the
meet the needs of most patients in most circumstances.
American Heart Association (AHA) have jointly engaged
These guideline recommendations reflect a consensus of expert
in the production of such guidelines in the area of cardio-
opinion after a thorough review of the available, current
vascular disease since 1980. This effort is directed by the
scientific evidence and are intended to improve patient care. If
ACC/AHA Task Force on Practice Guidelines, whose
these guidelines are used as the basis for regulatory/payer
charge is to develop, update, or revise practice guidelines for
decisions, the ultimate goal is quality of care and serving the
important cardiovascular diseases and procedures. Writing
patient’s best interests. The ultimate judgment regarding care
committees are charged with the task of performing an
of a particular patient must be made by the healthcare provider
assessment of the evidence and acting as an independent
and patient in light of all of the circumstances presented by that
group of authors to develop and update written recommen-
patient. There are circumstances in which deviations from
dations for clinical practice.
these guidelines are appropriate.
Experts in the subject under consideration are selected from
The current document is a republication of the “ACC/
both organizations to examine subject-specific data and write
AHA 2006 Guidelines for the Management of Patients
guidelines. The process includes additional representatives
With Valvular Heart Disease” (1068), revised to incorporate
from other medical practitioner and specialty groups where
individual recommendations from a 2008 focused update
appropriate. Writing committees are specifically charged to
(1069), which spotlights the 2007 AHA Guidelines for
perform a formal literature review, weigh the strength of
Infective Endocarditis Prophylaxis. For easy reference, this
evidence for or against a particular treatment or procedure, and
online-only version denotes sections that have been up-
include estimates of expected health outcomes where data exist.
Patient-specific modifiers, comorbidities, and issues of patient dated. All members of the 2006 Valvular Heart Disease
preference that may influence the choice of particular tests or Writing Committee were invited to participate in the
therapies are considered, as well as frequency of follow-up. writing group; those who agreed were required to disclose
When available, information from studies on cost will be all relationships with industry relevant to the data under
considered; however, review of data on efficacy and clinical consideration (1067), as were all peer reviewers of the
outcomes will be the primary basis for preparing recommen- document. (See Appendixes 4 and 5 for a listing of
dation in these guidelines. relationships with industry for the 2008 Focused Update
The ACC/AHA Task Force on Practice Guidelines Writing Group and peer reviewers, respectively.) Each
makes every effort to avoid any actual, potential, or per- recommendationrequiredaconfidentialvotebythewriting
ceived conflicts of interest that may arise as a result of an group members before and after external review of the
outside relationship or personal interest of a member of the document. Any writing group member with a significant
writing committee. Specifically, all members of the writing (greaterthan$10000)relationshipwithindustryrelevantto
committee and peer reviewers of the document are asked to the recommendation was recused from voting on that
provide disclosure statements of all such relationships that recommendation.
e6 Bonowetal. JACCVol.52,No.13,2008
ACC/AHAVHDGuidelines:2008FocusedUpdateIncorporated September23,2008:e1–142
Guidelines are reviewed annually by the ACC/AHA tionscoveringthetreatmentofvalvularheartdiseaseisbeyond
Task Force on Practice Guidelines and are considered the scope of this document; the document includes those
currentunlesstheyareupdatedorsunsettedandwithdrawn reports that the committee believes represent the most com-
from distribution. prehensiveorconvincingdatathatarenecessarytosupportits
Sidney C. Smith, Jr., MD, FACC, FAHA conclusions.However,evidencetableswereupdatedtoreflect
Chair, ACC/AHA Task Force on Practice Guidelines major advances over this time period. Inaccuracies or incon-
sistencies present in the original publication were identified
1. INTRODUCTION and corrected when possible. Recommendations provided in
thisdocumentarebasedprimarilyonpublisheddata.Because
randomized trials are unavailable in many facets of valvular
1.1. Evidence Review (UPDATED)
heart disease treatment, observational studies, and in some
The ACC and the AHA have long been involved in the areas,expertopinionsformthebasisforrecommendationsthat
joint development of practice guidelines designed to assist areoffered.
healthcare providers in the management of selected cardio- All of the recommendations in this guideline revision
vascular disorders or the selection of certain cardiovascular were converted from the tabular format used in the 1998
procedures. The determination of the disorders or proce- guideline to a listing of recommendations that has been
dures to develop guidelines is based on several factors, writteninfullsentencestoexpressacompletethought,such
including importance to healthcare providers and whether that a recommendation, even if separated and presented
there are sufficient data from which to derive accepted apartfromtherestofthedocument,wouldstillconveythe
guidelines.Oneimportantcategoryofcardiacdisordersthat fullintentoftherecommendation.Itishopedthatthiswill
affect a large number of patients who require diagnostic increasethereaders’comprehensionoftheguidelines.Also,
proceduresanddecisionsregardinglong-termmanagement the level of evidence, either A, B, or C, for each recom-
is valvular heart disease. mendation is now provided.
Duringthepast2decades,majoradvanceshaveoccurred Classification of recommendations and level of evidence
in diagnostic techniques, the understanding of natural are expressed in the ACC/AHA format as follows:
history, and interventional cardiology and surgical proce- • CLASSI:Conditionsforwhichthereisevidenceforand/or
dures for patients with valvular heart disease. These ad-
general agreement that the procedure or treatment is
vances have resulted in enhanced diagnosis, more scientific
beneficial, useful, and effective.
selection of patients for surgery or catheter-based interven- • CLASS II: Conditions for which there is conflicting evi-
tion versus medical management, and increased survival of
dence and/or a divergence of opinion about the useful-
patients with these disorders. The information base from
ness/efficacy of a procedure or treatment.
which to make clinical management decisions has greatly • CLASS IIA: Weight of evidence/opinion is in favor of
expandedinrecentyears,yetinmanysituations,management
usefulness/efficacy.
issues remain controversial or uncertain. Unlike many other • CLASS IIB: Usefulness/efficacy is less well established by
formsofcardiovasculardisease,thereisascarcityoflarge-scale
evidence/opinion.
multicenter trials addressing the diagnosis and treatment of • CLASS III: Conditions for which there is evidence and/or
patients with valvular disease from which to derive definitive
general agreement that the procedure/treatment is not
conclusions, and the information available in the literature
useful/effective and in some cases may be harmful.
representsprimarilytheexperiencesreportedbysingleinstitu-
tionsinrelativelysmallnumbersofpatients. In addition, the weight of evidence in support of the
The 1998 Committee on Management of Patients With recommendation is listed as follows:
Valvular Heart Disease reviewed and compiled this informa- • Level of Evidence A: Data derived from multiple ran-
tion base and made recommendations for diagnostic testing,
domized clinical trials.
treatment,andphysicalactivity.Fortopicsforwhichtherewas • Level of Evidence B: Data derived from a single ran-
an absence of multiple randomized, controlled trials, the
domized trial or nonrandomized studies.
preferredbasisformedicaldecisionmakinginclinicalpractice • LevelofEvidenceC:Onlyconsensusopinionofexperts,
(evidence-basedmedicine),thecommittee’srecommendations
case studies, or standard-of-care.
were based on data derived from single randomized trials or
nonrandomizedstudiesorwerebasedonaconsensusopinion The schema for classification of recommendations and
of experts. The 2006 writing committee was charged with level of evidence is summarized in Figure 1, which also
revising the guidelines published in 1998. The committee illustrates how the grading system provides an estimate of
reviewedpertinentpublications,includingabstracts,througha the size of the treatment effect and an estimate of the
computerized search of the English literature since 1998 and certainty of the treatment effect.
performed a manual search of final articles. Special attention Writing committee membership consisted of cardiovas-
was devoted to identification of randomized trials published cular disease specialists and representatives of the cardiac
sincetheoriginaldocument.Acompletelistingofallpublica- surgeryandcardiacanesthesiologyfields;boththeacademic
JACCVol.52,No.13,2008 Bonowetal. e7
September23,2008:e1–142 ACC/AHAVHDGuidelines:2008FocusedUpdateIncorporated
Figure1. ApplyingClassificationofRecommendationsandLevelofEvidence
*Dataavailablefromclinicaltrialsorregistriesabouttheusefulness/efficacyindifferentsubpopulations,suchasgender,age,historyofdiabetes,historyofpriormyocardial
infarction,historyofheartfailure,andprioraspirinuse.ArecommendationwithLevelofEvidenceBorCdoesnotimplythattherecommendationisweak.Manyimportant
clinicalquestionsaddressedintheguidelinesdonotlendthemselvestoclinicaltrials.Eventhoughrandomizedtrialsarenotavailable,theremaybeaveryclearclinical
consensusthataparticulartestortherapyisusefuloreffective.†In2003theACC/AHATaskForceonPracticeGuidelinesrecentlyprovidedalistofsuggestedphrasesto
usewhenwritingrecommendations.Allrecommendationsinthisguidelinehavebeenwritteninfullsentencesthatexpressacompletethought,suchthatarecommenda-
tion,evenifseparatedandpresentedapartfromtherestofthedocument(includingheadingsabovesetsofrecommendations),wouldstillconveythefullintentoftherec-
ommendation.Itishopedthatthiswillincreasereaders’comprehensionoftheguidelinesandwillallowqueriesattheindividualrecommendationlevel.
andprivatepracticesectorswererepresented.TheSocietyof diagnostic testing, including the guidelines for the clinical
Cardiovascular Anesthesiologists assigned an official repre- use of cardiac radionuclide imaging (1), the clinical appli-
sentative to the writing committee. cation of echocardiography (2), exercise testing (3), and
percutaneous coronary intervention (4). Although these
1.2. Scope of the Document (UPDATED)
guidelines are not intended to include detailed information
The guidelines attempt to deal with general issues of
covered in previous guidelines on the use of imaging and
treatment of patients with heart valve disorders, such as
diagnostic testing, an essential component of this report is
evaluation of patients with heart murmurs, prevention and
thediscussionofindicationsforthesetestsintheevaluation
treatment of endocarditis, management of valve disease in
and treatment of patients with valvular heart disease.
pregnancy, and treatment of patients with concomitant
The committee emphasizes the fact that many factors
coronary artery disease (CAD), as well as more specialized
ultimately determine the most appropriate treatment of
issues that pertain to specific valve lesions. The guidelines
individualpatientswithvalvularheartdiseasewithinagiven
focusprimarilyonvalvularheartdiseaseintheadult,witha
community. These include the availability of diagnostic
separate section dealing with specific recommendations for
valve disorders in adolescents and young adults. The diag- equipmentandexpertdiagnosticians,theexpertiseofinter-
nosis and management of infants and young children with ventional cardiologists and surgeons, and notably, the
congenital valvular abnormalities are significantly different wishesofwell-informedpatients.Therefore,deviationfrom
from those of the adolescent or adult and are beyond the theseguidelinesmaybeappropriateinsomecircumstances.
scope of these guidelines. These guidelines are written with the assumption that a
This task force report overlaps with several previously diagnostic test can be performed and interpreted with skill
publishedACC/AHAguidelinesaboutcardiacimagingand levelsconsistentwithpreviouslyreportedACCtrainingand
e8 Bonowetal. JACCVol.52,No.13,2008
ACC/AHAVHDGuidelines:2008FocusedUpdateIncorporated September23,2008:e1–142
competency statements and ACC/AHA guidelines, that Table1. ClassificationofCardiacMurmurs
interventional cardiological and surgical procedures can be
1.Systolicmurmurs
performed by highly trained practitioners within acceptable
a.Holosystolic(pansystolic)murmurs
safety standards, and that the resources necessary to perform b.Midsystolic(systolicejection)murmurs
these diagnostic procedures and provide this care are readily c.Earlysystolicmurmurs
available. This is not true in all geographic areas, which d.Midtolatesystolicmurmurs
further underscores the committee’s position that its recom- 2.Diastolicmurmurs
mendations are guidelines and not rigid requirements. a.Earlyhigh-pitcheddiastolicmurmurs
b.Middiastolicmurmurs
1.3. Review and Approval (NEW)
c.Presystolicmurmurs
The 2006 document (1068) was reviewed by 2 official reviewers 3.Continuousmurmurs
nominated by the ACC; 2 official reviewers nominated by the
AHA; 1 official reviewer from the ACC/AHA Task Force on
Practice Guidelines; reviewers nominated by the Society of • highbloodflowratethroughnormalorabnormalorifices
Cardiovascular Anesthesiologists, the Society for Cardiovascu- • forwardflowthroughanarrowedorirregularorificeinto
lar Angiography and Interventions, and the Society of Tho-
a dilated vessel or chamber
racic Surgeons (STS); and individual content reviewers, includ- • backward or regurgitant flow through an incompetent
ing members of the ACCF Cardiac Catheterization and
valve
Intervention Committee, ACCF Cardiovascular Imaging
Committee, ACCF Cardiovascular Surgery Committee, Often, more than 1 of these factors is operative (5–7).
AHA Endocarditis Committee, AHA Cardiac Clinical Im- Aheartmurmurmayhavenopathologicalsignificanceor
aging Committee, AHA Cardiovascular Intervention and may be an important clue to the presence of valvular,
Imaging Committee, and AHA Cerebrovascular Imaging and congenital,orotherstructuralabnormalitiesoftheheart(8).
Intervention Committee. Mostsystolicheartmurmursdonotsignifycardiacdisease,
As mentioned previously, this document also incorporates andmanyarerelatedtophysiologicalincreasesinbloodflow
a 2008 focused update of the “ACC/AHA 2006 Guidelines velocity (9). In other instances, a heart murmur may be an
for the Management of Patients With Valvular Heart importantcluetothediagnosisofundetectedcardiacdisease
Disease” (1069), which spotlights the 2007 AHA Guide- (e.g., valvular aortic stenosis [AS]) that may be important
lines for Infective Endocarditis Prophylaxis (1070). Only even when asymptomatic or that may define the reason for
recommendations related to infective endocarditis have cardiac symptoms. In these situations, various noninvasive
been revised. This document was reviewed by 2 external orinvasivecardiactestsmaybenecessarytoestablishafirm
reviewers nominated by the ACC and 2 external reviewers diagnosis and form the basis for rational treatment of an
nominated by the AHA, as well as 3 reviewers from the underlyingdisorder.Echocardiographyisparticularlyuseful
ACCF Congenital Heart Disease and Pediatric Commit- in this regard, as discussed in the “ACC/AHA/ASE 2003
tee, 2 reviewers from the ACCF Cardiovascular Surgery Guidelines for the Clinical Application of Echocardiogra-
Committee, 5 reviewers from the AHA Heart Failure and phy” (2). Diastolic murmurs virtually always represent
Transplant Committee, and 3 reviewers from the Rheu- pathological conditions and require further cardiac evalua-
maticFever,Endocarditis,andKawasakiDiseaseCommit- tion, as do most continuous murmurs. Continuous “inno-
tee. All information about reviewers’ relationships with cent”murmursincludevenoushumsandmammarysouffles.
industry was collected and distributed to the writing com- The traditional auscultation method of assessing cardiac
mittee and is published in this document (see Appendix 5 murmurshasbeenbasedontheirtiminginthecardiaccycle,
fordetails).Thisdocumentwasapprovedforpublicationby configuration, location and radiation, pitch, intensity
the governing bodies of the ACCF and the AHA in May (grades1through6),andduration(5–9).Theconfiguration
2008 and endorsed by the Society of Cardiovascular Anes- of a murmur may be crescendo, decrescendo, crescendo-
thesiologists, the Society for Cardiovascular Angiography
decrescendo (diamond-shaped), or plateau. The precise
and Interventions, and the Society of Thoracic Surgeons.
times of onset and cessation of a murmur associated with
cardiac pathology depend on the period of time in the
2. GENERAL PRINCIPLES
cardiac cycle in which a physiologically important pressure
differencebetween2chambersoccurs(5–9).Aclassification
2.1. Evaluation of the Patient With of cardiac murmurs is listed in Table 1.
a Cardiac Murmur
2.1.2. Classification of Murmurs
2.1.1. Introduction (UPDATED)
Holosystolic (pansystolic) murmurs are generated when
Cardiac auscultation remains the most widely used method there is flow between chambers that have widely different
ofscreeningforvalvularheartdisease(VHD).Theproduc- pressures throughout systole, such as the left ventricle and
tion of murmurs is due to 3 main factors: either the left atrium or right ventricle. With an abnormal
JACCVol.52,No.13,2008 Bonowetal. e9
September23,2008:e1–142 ACC/AHAVHDGuidelines:2008FocusedUpdateIncorporated
regurgitantorifice,thepressuregradientandregurgitantjet responsiblefortheregurgitationisminimal.Suchmurmurs
beginearlyincontractionandlastuntilrelaxationisalmost are common late after repair of tetralogy of Fallot.
complete. Middiastolic murmurs usually originate from the mitral
Midsystolic(systolicejection)murmurs,oftencrescendo- and tricuspid valves, occur early during ventricular filling,
decrescendo in configuration, occur when blood is ejected andareduetoarelativedisproportionbetweenvalveorifice
across the aortic or pulmonic outflow tracts. The murmurs size and diastolic blood flow volume. Although they are
start shortly after S , when the ventricular pressure rises usually due to mitral or tricuspid stenosis, middiastolic
1
sufficiently to open the semilunar valve. As ejection in- murmurs may also be due to increased diastolic blood flow
creases,themurmurisaugmented,andasejectiondeclines, across the mitral or tricuspid valve when such valves are
it diminishes. severelyregurgitant,acrossthenormalmitralvalve(MV)in
In the presence of normal semilunar valves, this murmur patients with ventricular septal defect or patent ductus
maybecausedbyanincreasedflowratesuchasthatwhich arteriosus, and across the normal tricuspid valve in patients
occurswithelevatedcardiacoutput(e.g.,pregnancy,thyro- with atrial septal defect. In severe, chronic AR, a low-
toxicosis, anemia, and arteriovenous fistula), ejection of pitched,rumblingdiastolicmurmur(Austin-Flintmurmur)
blood into a dilated vessel beyond the valve, or increased isoftenpresentattheLVapex;itmaybeeithermiddiastolic
transmission of sound through a thin chest wall. Most or presystolic. An opening snap is absent in isolated AR.
innocent murmurs that occur in children and young adults Presystolic murmurs begin during the period of ventric-
are midsystolic and originate either from the aortic or ularfillingthatfollowsatrialcontractionandthereforeoccur
pulmonic outflow tracts. Valvular, supravalvular, or subval- insinusrhythm.Theyareusuallyduetomitralortricuspid
vularobstruction(stenosis)ofeitherventriclemayalsocause stenosis. A right or left atrial myxoma may cause either
a midsystolic murmur, the intensity of which depends in middiastolic or presystolic murmurs similar to tricuspid or
partonthevelocityofbloodflowacrossthenarrowedarea. mitral stenosis (MS).
Midsystolic murmurs also occur in certain patients with Continuous murmurs arise from high- to low-pressure
functional mitral regurgitation (MR) or, less frequently, shunts that persist through the end of systole and the
tricuspid regurgitation (TR). Echocardiography is often beginningofdiastole.Thus,theybegininsystole,peaknear
necessarytoseparateaprominentandexaggerated(grade3) S ,andcontinueintoallorpartofdiastole.Therearemany
2
benign midsystolic murmur from one due to valvular AS. causes of continuous murmurs, but they are uncommon in
Earlysystolicmurmursarelesscommon;theybeginwith patients with valvular heart disease (5–9).
the first sound and end in midsystole. An early systolic
2.1.2.1. DYNAMICCARDIACAUSCULTATION
murmur is often due to TR that occurs in the absence of
Attentive cardiac auscultation during dynamic changes in
pulmonary hypertension, but it also occurs in patients with
cardiachemodynamicsoftenenablestheobservertodeduce
acute MR. In large ventricular septal defects with pulmo-
the correct origin and significance of a cardiac murmur
nary hypertension and small muscular ventricular septal
(10–13).Changesintheintensityofheartmurmursduring
defects, the shunting at the end of systole may be insignif-
various maneuvers are indicated in Table 2.
icant, with the murmur limited to early and midsystole.
Late systolic murmurs are soft or moderately loud, 2.1.2.2. OTHERPHYSICALFINDINGS
high-pitchedmurmursattheleftventricular(LV)apexthat The presence of other physical findings, either cardiac or
start well after ejection and end before or at S . They are noncardiac,mayprovideimportantcluestothesignificance
2
oftenduetoapicaltetheringandmalcoaptationofthemitral of a cardiac murmur and the need for further testing (Fig.
leaflets due to anatomic and functional changes of the 2).Forexample,arightheartmurmurinearlytomidsystole
annulus and ventricle. Late systolic murmurs in patients atthelowerleftsternalborderlikelyrepresentsTRwithout
withmidsystolicclicksresultfromlatesystolicregurgitation pulmonary hypertension in an injection drug user who
due to prolapse of the mitral leaflet(s) into the left atrium. presents with fever, petechiae, Osler’s nodes, and Janeway
Suchlatesystolicmurmurscanalsooccurintheabsenceof lesions.
clicks. Associated cardiac findings frequently provide important
Early diastolic murmurs begin with or shortly after S , information about cardiac murmurs. Fixed splitting of the
2
when the associated ventricular pressure drops sufficiently second heart sound during inspiration and expiration in a
below that in the aorta or pulmonary artery. High-pitched patient with a grade 2/6 midsystolic murmur in the pul-
murmursofaorticregurgitation(AR)orpulmonicregurgi- monic area and left sternal border should suggest the
tation due to pulmonary hypertension are generally decre- possibility of an atrial septal defect. A soft or absent A or
2
scendo, consistent with the rapid decline in volume or rate reversed splitting of S may denote severe AS. An early
2
of regurgitation during diastole. The diastolic murmur of aortic systolic ejection sound heard during inspiration and
pulmonic regurgitation without pulmonary hypertension is expiration suggests a bicuspid aortic valve, whereas an
low to medium pitched, and the onset of this murmur is ejection sound heard only in the pulmonic area and at the
slightly delayed because regurgitant flow is minimal at left sternal border during expiration usually denotes pul-
pulmonic valve closure, when the reverse pressure gradient monic valve stenosis. LV dilatation on precordial palpation
e10 Bonowetal. JACCVol.52,No.13,2008
ACC/AHAVHDGuidelines:2008FocusedUpdateIncorporated September23,2008:e1–142
Table2. InterventionsUsedtoAltertheIntensityofCardiacMurmurs
Respiration
Right-sidedmurmursgenerallyincreasewithinspiration.Left-sidedmurmursusuallyarelouderduringexpiration.
Valsalvamaneuver
Mostmurmursdecreaseinlengthandintensity.TwoexceptionsarethesystolicmurmurofHCM,whichusuallybecomesmuchlouder,andthatofMVP,which
becomeslongerandoftenlouder.AfterreleaseoftheValsalva,right-sidedmurmurstendtoreturntobaselineintensityearlierthanleft-sidedmurmurs.
Exercise
Murmurscausedbybloodflowacrossnormalorobstructedvalves(e.g.,PSandMS)becomelouderwithbothisotonicandisometric(handgrip)exercise.Murmurs
ofMR,VSD,andARalsoincreasewithhandgripexercise.
Positionalchanges
Withstanding,mostmurmursdiminish,2exceptionsbeingthemurmurofHCM,whichbecomeslouder,andthatofMVP,whichlengthensandoftenisintensified.
Withbrisksquatting,mostmurmursbecomelouder,butthoseofHCMandMVPusuallysoftenandmaydisappear.Passivelegraisingusuallyproducesthe
sameresultsasbrisksquatting.
Postventricularprematurebeatoratrialfibrillation
MurmursoriginatingatnormalorstenoticsemilunarvalvesincreaseinintensityduringthecardiaccycleafteraVPBorinthebeatafteralongcyclelengthinAF.
Bycontrast,systolicmurmursduetoatrioventricularvalveregurgitationdonotchange,diminish(papillarymuscledysfunction),orbecomeshorter(MVP).
Pharmacologicalinterventions
Duringtheinitialrelativehypotensionafteramylnitriteinhalation,murmursofMR,VSD,andARdecrease,whereasmurmursofASincreasebecauseofincreased
strokevolume.Duringthelatertachycardiaphase,murmursofMSandright-sidedlesionsalsoincrease.Thisinterventionmaythusdistinguishthemurmurof
theAustin-FlintphenomenonfromthatofMS.TheresponseinMVPoftenisbiphasic(softerthenlouderthancontrol).
Transientarterialocclusion
Transientexternalcompressionofbotharmsbybilateralcuffinflationto20mmHggreaterthanpeaksystolicpressureaugmentsthemurmursofMR,VSD,and
ARbutnotmurmursduetoothercauses.
AFindicatesatrialfibrillation;AR,aorticregurgitation;AS,aorticstenosis;HCM,hypertrophiccardiomyopathy;MR,mitralregurgitation;MS,mitralstenosis;MVP,mitralvalveprolapse;PS,pulmonic
stenosis;VPB,ventricularprematurebeat;andVSD,ventricularseptaldefect.
and bibasilar pulmonary rales favor the diagnosis of severe, corroborative information. For example, regurgitant cv
chronic MR in a patient with a grade 2/6 holosystolic wavesareindicativeofTRandareoftenpresentwithoutan
murmur at the cardiac apex. A slow-rising, diminished audible murmur.
arterial pulse suggests severe AS in a patient with a grade
2/6 midsystolic murmur at the second right intercostal 2.1.2.3. ASSOCIATEDSYMPTOMS
space. The typical parvus et tardus pulse may be absent in An important consideration in the patient with a cardiac
the elderly, even in those with severe AS, secondary to the murmur is the presence or absence of symptoms (15) (Fig.
effects of aging on the vasculature. Pulsus parvus may also 2). For example, symptoms of syncope, angina pectoris, or
occur with severely reduced cardiac output from any cause. heart failure in a patient with a midsystolic murmur will
Factors that aid in the differential diagnosis of LV outflow usuallyresultinamoreaggressivediagnosticapproachthan
tract obstruction are listed in Table 3 (14). Examination of in a patient with a similar midsystolic murmur who has
the jugular venous wave forms may provide additional or none of these symptoms. An echocardiogram to rule in or
Figure2. StrategyforEvaluatingHeartMurmurs
*IfanelectrocardiogramorchestX-rayhasbeenobtainedandisabnormal,echocardiographyisindicated.