2011 AHA management

156 Pages·2011·8.2 MB·English

2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for
the Management of Patients With Unstable Angina/Non- ST-Elevation Myocardial
Infarction : A Report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines
Jeffrey L. Anderson, Cynthia D. Adams, Elliott M. Antman, Charles R. Bridges, Robert M.
Califf, Donald E. Casey, Jr, William E. Chavey II, Francis M. Fesmire, Judith S. Hochman,
Thomas N. Levin, A. Michael Lincoff, Eric D. Peterson, Pierre Theroux, Nanette Kass Wenger
and R. Scott Wright
Circulation. 2011;123:e426-e579; originally published online March 28, 2011;
doi: 10.1161/CIR.0b013e318212bb8b
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ACC/AHA Practice Guideline
Thisguidelinecontainshyperlinkstorecommendationsandsupportingtextthathavebeenupdatedbythe“2011ACCF/AHAFocusedUpdateontheManagement
of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction” (Circulation. 2011;123:2022–2060; doi:10.1161/CIR.0b013e31820f2f3e). Updated
sectionsareindicatedintheTableofContentsandtext.
2011 ACCF/AHA Focused Update Incorporated Into the
ACC/AHA 2007 Guidelines for the Management of Patients With
Unstable Angina/Non–ST-Elevation Myocardial Infarction
A Report of the American College of Cardiology Foundation/American
Heart Association Task Force on Practice Guidelines
2007 WRITING COMMITTEE MEMBERS
DevelopedinCollaborationwiththeAmericanCollegeofEmergencyPhysicians,theSocietyfor
CardiovascularAngiographyandInterventions,andtheSocietyofThoracicSurgeons
Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the
Society for Academic Emergency Medicine
Jeffrey L. Anderson, MD, FACC, FAHA, Chair; Cynthia D. Adams, RN, PhD, FAHA;
Elliott M. Antman, MD, FACC, FAHA; Charles R. Bridges, ScD, MD, FACC, FAHA(cid:1);
Robert M. Califf, MD, MACC; Donald E. Casey, Jr, MD, MPH, MBA, FACP†;
William E. Chavey II, MD, MS‡; Francis M. Fesmire, MD, FACEP§;
Judith S. Hochman, MD, FACC, FAHA; Thomas N. Levin, MD, FACC, FSCAI(cid:1);
A. Michael Lincoff, MD, FACC; Eric D. Peterson, MD, MPH, FACC, FAHA;
Pierre Theroux, MD, FACC, FAHA; Nanette Kass Wenger, MD, FACC, FAHA;
R. Scott Wright, MD, FACC, FAHA
2011 WRITING GROUP MEMBERS
Developed in Collaboration With the American College of Emergency Physicians, Society for
Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons
R. Scott Wright, MD, FACC, FAHA, Chair¶; Jeffrey L. Anderson, MD, FACC, FAHA, Vice Chair¶#;
Cynthia D. Adams, RN, PhD, FAHA¶; Charles R. Bridges, MD, ScD, FACC, FAHA*#;
Donald E. Casey, Jr, MD, MPH, MBA, FACP, FAHA†; Steven M. Ettinger, MD, FACC**;
Francis M. Fesmire, MD, FACEP§; Theodore G. Ganiats, MD†; Hani Jneid, MD, FACC, FAHA¶;
A. Michael Lincoff, MD, FACC¶#; Eric D. Peterson, MD, MPH, FACC, FAHA*‡# ††;
George J. Philippides, MD, FACC, FAHA¶; Pierre Theroux, MD, FACC, FAHA¶#;
Nanette K. Wenger, MD, MACC, FAHA¶#; James Patrick Zidar, MD, FACC, FSCAI(cid:1)#
*Society of Thoracic Surgeons Representative. †American College of Physicians Representative. ‡American Academy of Family Physicians
Representative.§AmericanCollegeofEmergencyPhysiciansRepresentative.(cid:1)SocietyforCardiovascularAngiographyandInterventionsRepresentative.
¶ACCF/AHARepresentative.#RecusedfromvotingonSection3.2,AntiplateletandAnticoagulantTherapy,andSection5.2.1,AntiplateletTherapy.
**ACCF/AHATaskForceonPracticeGuidelinesLiaison.††ACCF/AHATaskForceonPerformanceMeasuresLiaison.
ThisdocumentwasapprovedbytheAmericanCollegeofCardiologyFoundationBoardofTrusteesandbytheAmericanHeartAssociationScienceAdvisoryand
CoordinatingCommittee,andthesectionsthathavebeenupdatedareindicatedwithhyperlinkstothefocusedupdatewhereapplicable.
Whencitingthisdocument,theAmericanHeartAssociationrequeststhatthefollowingcitationformatbeused:AndersonJL,AdamsCD,AntmanEM,BridgesCR,
CaliffRM,CaseyDEJr,ChaveyWE2nd,FesmireFM,HochmanJS,LevinTN,LincoffAM,PetersonED,TherouxP,WengerNK,WrightRS.2011ACCF/AHA
focusedupdateincorporatedintothe2007ACC/AHAguidelinesforthemanagementofpatientswithunstableangina/non–ST-elevationmyocardialinfarction:areport
oftheAmericanCollegeofCardiologyFoundation/AmericanHeartAssociationTaskForceonPracticeGuidelines.Circulation.2011;123:e426–e579.
ThisarticlehasbeencopublishedintheJournaloftheAmericanCollegeofCardiology.
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Association(my.americanheart.org).Acopyofthedocumentisalsoavailableathttp://www.americanheart.org/presenter.jhtml?identifier(cid:1)3003999byselecting
eitherthe“topiclist”linkorthe“chronologicallist”link.Topurchaseadditionalreprints,[email protected].
ExpertpeerreviewofAHAScientificStatementsisconductedattheAHANationalCenter.FormoreonAHAstatementsandguidelinesdevelopment,
visithttp://www.americanheart.org/presenter.jhtml?identifier(cid:1)3023366.
Permissions:Multiplecopies,modification,alteration,enhancement,and/ordistributionofthisdocumentarenotpermittedwithouttheexpresspermissionofthe
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(Circulation.2011;123:e426-e579.)
©2011bytheAmericanCollegeofCardiologyFoundationandtheAmericanHeartAssociation,Inc.
Circulationisavailableathttp://circ.ahajournals.org DOI:10.1161/CIR.0b013e318212bb8b
Downloaded from http://circ.ahajournals.org/e 4at2 U6niversity of Washington on August 14, 2012
Anderson et al ACCF/AHA UA/NSTEMI Guideline Revision e427
ACCF/AHA TASK FORCE MEMBERS
Alice K. Jacobs, MD, FACC, FAHA, Chair; Jeffrey L. Anderson, MD, FACC, FAHA, Chair-Elect;
Nancy Albert, PhD, CCNS, CCRN, FAHA; Judith S. Hochman, MD, FACC, FAHA;
Mark A. Creager, MD, FACC, FAHA; Frederick G. Kushner, MD, FACC, FAHA;
Steven M. Ettinger, MD, FACC; Erik Magnus Ohman, MD, FACC; Robert A. Guyton, MD, FACC;
William G. Stevenson, MD, FACC, FAHA; Jonathan L. Halperin, MD, FACC, FAHA;
Clyde W. Yancy, MD, FACC, FAHA
TABLE OF CONTENTS 2.2.8.2.1.2. Bedside Testing for Cardiac
Markers.........................................e453
2.2.8.3. Myoglobin and CK-MB Subforms
Preamble (UPDATED) ...................................................e429 Compared With Troponins.......................e453
1. Introduction..................................................................e430 2.2.8.4. Summary Comparison of Biomarkers
1.1.Organization of Committee and Evidence of Necrosis: Singly and In
Review (UPDATED)...........................................e430 Combination.............................................e453
1.2. Purpose of These Guidelines...............................e431 2.2.9.Other Markers and Multimarker
1.3. OverviewoftheAcuteCoronarySyndromes..............e433 Approaches.....................................................e454
1.3.1. Definition of Terms........................................e433 2.2.9.1. Ischemia....................................................e454
1.3.2. Pathogenesis of UA/NSTEMI........................e434 2.2.9.2. Coagulation...............................................e455
1.3.3. Presentations of UA and NSTEMI................e434 2.2.9.3. Platelets.....................................................e455
1.4. Management Before UA/NSTEMI and 2.2.9.4. Inflammation.............................................e455
Onset of UA/NSTEMI.........................................e434 2.2.9.5. B-Type Natriuretic Peptides.....................e455
1.4.1.Identification of Patients at Risk of 2.3. Immediate Management.......................................e455
2.3.1. Chest Pain Units.............................................e456
UA/NSTEMI...................................................e435
2.3.2. DischargeFromEDorChestPainUnit...........e457
1.4.2.Interventions to Reduce Risk of
3. Early Hospital Care.....................................................e459
UA/NSTEMI...................................................e435
3.1. Anti-Ischemic and Analgesic Therapy................e459
1.5. Onset of UA/NSTEMI.........................................e436
3.1.1. General Care...................................................e463
1.5.1. Recognition of Symptoms by Patient............e436
3.1.2. Use of Anti-Ischemic Therapies....................e463
1.5.2. Silent and Unrecognized Events....................e437
3.1.2.1. Nitrates......................................................e463
2. Initial Evaluation and Management............................e437
3.1.2.2. Morphine Sulfate......................................e464
2.1. Clinical Assessment.............................................e437
3.1.2.3. Beta-Adrenergic Blockers........................e465
2.1.1. Emergency Department or Outpatient
3.1.2.4. Calcium Channel Blockers.......................e467
Facility Presentation.......................................e441
3.1.2.5. Inhibitors of The Renin-
2.1.2.Questions to Be Addressed at
Angiotensin-Aldosterone System.............e468
the Initial Evaluation......................................e441
3.1.2.6. Other Anti-Ischemic Therapies ...............e468
2.2. Early Risk Stratification.......................................e442
3.1.2.7.Intra-Aortic Balloon Pump
2.2.1. Estimation of the Level of Risk....................e443
Counterpulsation.......................................e468
2.2.2. Rationale for Risk Stratification....................e443
3.1.2.8. Analgesic Therapy....................................e469
2.2.3. History............................................................e444
3.2. Recommendations for Antiplatelet/
2.2.4.Anginal Symptoms and Anginal
Anticoagulant Therapy in Patients for
Equivalents.....................................................e444
Whom Diagnosis of UA/NSTEMI Is
2.2.5. DemographicsandHistoryinDiagnosis
Likely or Definite.................................................e469
andRiskStratification.........................................e445
3.2.1. Antiplatelet Therapy
2.2.6. EstimationofEarlyRiskatPresentation...........e446
Recommendations (UPDATED)....................e469
2.2.6.1. Electrocardiogram.....................................e447
3.2.2. Anticoagulant Therapy
2.2.6.2. Physical Examination...............................e449 Recommendations...........................................e472
2.2.7. Noncardiac Causes of Symptoms and 3.2.3. Additional Management Considerations
Secondary Causes of Myocardial for Antiplatelet and Anticoagulant
Ischemia..........................................................e449 Therapy (UPDATED)....................................e472
2.2.8. Cardiac Biomarkers of Necrosis and 3.2.4. Antiplatelet Agents and Trials
the Redefinition of AMI................................e449 (Aspirin, Ticlopidine, Clopidogrel)...............e473
2.2.8.1. Creatine Kinase-MB.................................e450 3.2.4.1. Aspirin......................................................e473
2.2.8.2. Cardiac Troponins....................................e450 3.2.4.2. Adenosine Diphosphate Receptor
2.2.8.2.1 Clinical Use.........................................e451 Antagonists and Other Antiplatelet
2.2.8.2.1.1. Clinical Use of Marker Agents.......................................................e476
Change Scores..............................e452 3.2.5. Anticoagulant Agents and Trials...................e479
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e428 Circulation May 10, 2011
3.2.5.1. Unfractionated Heparin............................e480 5.2.13. Patient Education..........................................e519
3.2.5.2. Low-Molecular-Weight Heparin .............e481 5.2.14. Influenza.......................................................e519
3.2.5.3. LMWH Versus UFH................................e481 5.2.15. Depression....................................................e520
3.2.5.3.1. Extended Therapy With 5.2.16. Nonsteroidal Anti-Inflammatory
LMWHS..............................................e485 Drugs.............................................................e520
3.2.5.4. Direct Thrombin Inhibitors......................e485 5.2.17. Hormone Therapy.........................................e520
3.2.5.5. Factor XA Inhibitors................................e488 5.2.18. AntioxidantVitaminsandFolicAcid..............e520
3.2.5.6. Long-Term Anticoagulation.....................e489 5.3. Postdischarge Follow-Up ....................................e520
3.2.6. Platelet GP IIb/IIIa Receptor 5.4. Cardiac Rehabilitation..........................................e522
Antagonists.....................................................e490 5.5. Return to Work and Disability ...........................e523
3.2.7. Fibrinolysis.....................................................e495 5.6. Other Activities ...................................................e523
3.3. Initial Conservative Versus Initial Invasive 5.7. Patient Records and Other Information
Strategies (UPDATED)........................................e495 Systems ................................................................e524
3.3.1. General Principles..........................................e495 6. Special Groups ............................................................e525
3.3.2. Rationale for the Initial Conservative 6.1. Women ................................................................e525
Strategy...........................................................e496
6.1.1. Profile of UA/NSTEMI in Women...............e525
3.3.3. Rationale for the Invasive
6.1.2. Management...................................................e525
Strategy...........................................................e496
6.1.2.1. Pharmacological Therapy.........................e525
3.3.4. Immediate Angiography.................................e496
6.1.2.2. Coronary Artery
3.3.5. Deferred Angiography....................................e496
Revascularization......................................e526
3.3.6. Comparison of Early Invasive and
6.1.2.3. Initial Invasive Versus Initial
Initial Conservative Strategies.......................e496
Conservative Strategy .............................e526
3.3.7. Subgroups.......................................................e499
6.1.3. Stress Testing ................................................e528
3.3.8. Care Objectives..............................................e500
6.1.4. Conclusions ...................................................e528
3.4. Risk Stratification Before Discharge...................e502
6.2. Diabetes Mellitus (UPDATED)...........................e529
3.4.1. Care Objectives..............................................e503
6.2.1. Profile and Initial Management of
3.4.2. Noninvasive Test Selection............................e504
Diabetic and Hyperglycemic Patients
3.4.3. Selection for Coronary Angiography.............e505
With UA/NSTEMI.........................................e529
3.4.4. Patient Counseling..........................................e506
6.2.2. Coronary Revascularization ..........................e530
4. Coronary Revascularization.........................................e506
6.2.3. Conclusions ...................................................e531
4.1. Recommendations for Revascularization
6.3. Post-CABG Patients ............................................e531
With PCI and CABG in Patients With
6.3.1. Pathological Findings ....................................e531
UA/NSTEMI........................................................e506
6.3.2. Clinical Findings and Approach....................e532
4.1.1. Recommendations for PCI.............................e506
6.3.3. Conclusions ...................................................e532
4.1.2. Recommendations for CABG........................e506
6.4. Older Adults ........................................................e532
4.2. General Principles................................................e507
6.4.1. Pharmacological Management ......................e533
4.3. Percutaneous Coronary Intervention....................e508
6.4.2. Functional Studies..........................................e533
4.3.1. Platelet Inhibitors and Percutaneous
6.4.3. Percutaneous Coronary Intervention
Revascularization............................................e509
in Older Patients.............................................e533
4.4. Surgical Revascularization...................................e510
6.4.4. Contemporary Revascularization
4.5. Conclusions..........................................................e511
Strategies in Older Patients............................e534
5. Late Hospital Care, Hospital Discharge, and
6.4.5. Conclusions.....................................................e534
Post-Hospital Discharge Care......................................e512
6.5. Chronic Kidney Disease (UPDATED)................e534
5.1. MedicalRegimenandUseofMedications.............e512
5.2. Long-Term Medical Therapy and 6.6. Cocaine and Methamphetamine Users................e535
Secondary Prevention...........................................e513 6.6.1. Coronary Artery Spasm With
5.2.1. Antiplatelet Therapy (UPDATED)..............e513 Cocaine Use....................................................e536
5.2.2. Beta Blockers...............................................e514 6.6.2. Treatment........................................................e537
5.2.3. Inhibition of the Renin-Angiotensin- 6.6.3. Methamphetamine Use and
Aldosterone System......................................e514 UA/NSTEMI...................................................e537
5.2.4. Nitroglycerin.................................................e514 6.7. Variant (Prinzmetal's) Angina..............................e537
5.2.5. Calcium Channel Blockers...........................e515 6.7.1. Clinical Picture...............................................e538
5.2.6. Warfarin Therapy (UPDATED)...................e515 6.7.2. Pathogenesis...................................................e538
5.2.7. Lipid Management.......................................e515 6.7.3. Diagnosis........................................................e538
5.2.8. Blood Pressure Control ...............................e517 6.7.4. Treatment........................................................e539
5.2.9. Diabetes Mellitus..........................................e517 6.7.5. Prognosis.........................................................e539
5.2.10. Smoking Cessation.......................................e518 6.8. Cardiovascular “Syndrome X”............................e539
5.2.11. Weight Management....................................e518 6.8.1. Definition and Clinical Picture......................e539
5.2.12. Physical Activity..........................................e518 6.8.2. Treatment........................................................e540
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Anderson et al ACCF/AHA UA/NSTEMI Guideline Revision e429
6.9. Takotsubo Cardiomyopathy.................................e541 document, were asked to provide disclosure statements of
7.Conclusions and Future Directions..............................e541 all such relationships that may be perceived as real or
7.1. Recommendations for Quality of Care potentialconflictsofinterest.WritingCommitteemembers
and Outcomes for Acute Coronary are also strongly encouraged to declare a previous rela-
Syndromes (NEW SECTION) ............................e542 tionshipwithindustrythatmaybeperceivedasrelevantto
Appendix 1.......................................................................e543 guideline development. If a Writing Committee member
Appendix 2.......................................................................e548 develops a new relationship with industry during their
Appendix 3 (UPDATED)................................................e553 tenure, they are required to notify guideline staff in
Appendixes 4-8 (NEW SECTION).................................e555 writing. The continued participation of the Writing Com-
References........................................................................e556 mittee member will be reviewed. These statements are
reviewed by the parent task force, reported orally to all
Preamble (UPDATED) members of the Writing Committee at each meeting, and
For new or updated text, view the 2011 Focused Update updated and reviewed by the Writing Committee as
(http://circ.ahajournals.org/cgi/reprint/CIR.0b013e31820f2f3e). changesoccur.Pleaserefertothemethodologymanualfor
Text supporting unchanged recommendations has not been ACC/AHAGuidelineWritingCommitteesfurtherdescrip-
updated. tion of relationships with industry policy, available on the
It is important that the medical profession play a ACC and AHA World Wide Web sites (http://www.
significant role in critically evaluating the use of diagnos- acc.org/qualityandscience/clinical/manual/manual%
ticproceduresandtherapiesinthedetection,management, 5Fi.htmandhttp://www.circ.ahajournals.org/manual/).See
or prevention of disease states. Rigorous and expert Appendix 1 for a list of Writing Committee member
analysis of the available data documenting absolute and relationshipswithindustryandAppendix2foralistingof
relative benefits and risks of those procedures and thera- peerreviewerrelationshipswithindustrythatarepertinent
pies can produce helpful guidelines that improve the to this guideline.
effectiveness of care, optimize patient outcomes, and Thesepracticeguidelinesareintendedtoassisthealthcare
favorably affect the overall cost of care by focusing providersinclinicaldecisionmakingbydescribingarangeof
resources on the most effective strategies. generally acceptable approaches for the diagnosis, manage-
TheAmericanCollegeofCardiologyFoundation(ACCF) ment, and prevention of specific diseases or conditions.
and the American Heart Association (AHA) have jointly Clinical decision making should consider the quality and
engaged in the production of such guidelines in the area of availability of expertise in the area where care is provided.
cardiovasculardiseasesince1980.TheAmericanCollegeof These guidelines attempt to define practices that meet the
Cardiology (ACC)/AHA Task Force on Practice Guidelines, needs of most patients in most circumstances. These guide-
whose charge is to develop, update, or revise practice line recommendations reflect a consensus of expert opinion
guidelines for important cardiovascular diseases and proce- after a thorough review of the available, current scientific
dures, directs this effort. Writing committees are charged evidence and are intended to improve patient care.
withthetaskofperforminganassessmentoftheevidenceand Patient adherence to prescribed and agreed upon medical
actingasanindependentgroupofauthorstodevelop,update, regimens and lifestyles is an important aspect of treatment.
or revise written recommendations for clinical practice. Prescribed courses of treatment in accordance with these
Experts in the subject under consideration have been recommendationswillonlybeeffectiveiftheyarefollowed.
selectedfrombothorganizationstoexaminesubject-specific Since lack of patient understanding and adherence may
data and write guidelines. The process includes additional adversely affect treatment outcomes, physicians and other
representativesfromothermedicalpractitionerandspecialty healthcareprovidersshouldmakeeveryefforttoengagethe
groupswhenappropriate.Writingcommitteesarespecifically patient in active participation with prescribed medical regi-
charged to perform a formal literature review, weigh the mens and lifestyles.
strength of evidence for or against a particular treatment or If these guidelines are used as the basis for regulatory/
procedure,andincludeestimatesofexpectedhealthoutcomes payer decisions, the ultimate goal is quality of care and
where data exist. Patient-specific modifiers, comorbidities, serving the patients best interests. The ultimate judgment
and issues of patient preference that might influence the regarding care of a particular patient must be made by the
choiceofparticulartestsortherapiesareconsidered,aswell health care provider and patient in light of all the circum-
as frequency of follow-up and cost effectiveness. When stancespresentedbythatpatient.Therearecircumstancesin
available, information from studies on cost will be consid- which derivations from these guidelines are appropriate.
ered; however, review of data on efficacy and clinical The guidelines will be reviewed annually by the ACC/
outcomes will constitute the primary basis for preparing AHATaskForceonPracticeGuidelinesandwillbeconsid-
recommendations in these guidelines. eredcurrentunlesstheyareupdated,revised,orsunsettedand
The ACC/AHA Task Force on Practice Guidelines withdrawn from distribution. The executive summary and
makes every effort to avoid any actual, potential, or recommendationsarepublishedintheAugust7,2007,issue
perceived conflict of interest that may arise as a result of of the Journal of the American College of Cardiology and
anindustryrelationshiporpersonalinterestofamemberof August7,2007,issueofCirculation.Thefull-textguidelines
the Writing Committee. Specifically, all members of the aree-publishedinthesameissueofthejournalsnotedabove,
Writing Committee, as well as peer reviewers of the as well as posted on the ACC (www.acc.org) and AHA
Downloaded from http://circ.ahajournals.org/ at University of Washington on August 14, 2012
e430 Circulation May 10, 2011
Table1. ApplyingClassificationofRecommendationsandLevelofEvidence†(UPDATED)(seethe2011FocusedUpdate)
*Dataavailablefromclinicaltrialsorregistriesabouttheusefulness/efficacyindifferentsubpopulations,suchasgender,age,historyofdiabetes,historyofprior
myocardialinfarction,historyofheartfailure,andprioraspirinuse.ArecommendationwithLevelofEvidenceBorCdoesnotimplythattherecommendationisweak.
Manyimportantclinicalquestionsaddressedintheguidelinesdonotlendthemselvestoclinicaltrials.Eventhoughrandomizedtrialsarenotavailable,theremay
beaveryclearclinicalconsensusthataparticulartestortherapyisusefuloreffective.†In2003,theACC/AHATaskForceonPracticeGuidelinesdevelopedalist
ofsuggestedphrasestousewhenwritingrecommendations.Allguidelinerecommendationshavebeenwritteninfullsentencesthatexpressacompletethought,
suchthatarecommendation,evenifseparatedandpresentedapartfromtherestofthedocument(includingheadingsabovesetsofrecommendations),wouldstill
conveythefullintentoftherecommendation.Itishopedthatthiswillincreasereaders’comprehensionoftheguidelinesandwillallowqueriesattheindividual
recommendationlevel.
(www.americanheart.org) World Wide Web sites. Copies of leading cause of death in the United States. Unstable angina
the full text and the executive summary are available from (UA) and the closely related condition of non–ST-segment
both organizations. elevationmyocardialinfarction(NSTEMI)areverycommon
Sidney C. Smith, Jr, MD, FACC, FAHA manifestations of this disease.
Chair, ACC/AHA Task Force on Practice Guidelines The committee members reviewed and compiled published
reports through a series of computerized literature searches of
1. Introduction the English-language literature since 2002 and a final manual
search of selected articles. Details of the specific searches
1.1. Organization of Committee and
conductedforparticularsectionsareprovidedwhenappropriate.
Evidence Review (UPDATED) Detailed evidence tables were developed whenever necessary
For new or updated text, view the 2011 Focused Update. withthespecificcriteriaoutlinedintheindividualsections.The
Textsupportingunchangedrecommendationshasnotbeen recommendationsmadewerebasedprimarilyonthesepublished
updated. data. The weight of the evidence was ranked highest (A) to
The ACC/AHA Task Force on Practice Guidelines was lowest (C). The final recommendations for indications for a
formed to make recommendations regarding the diagnosis diagnosticprocedure,aparticulartherapy,oraninterventionin
andtreatmentofpatientswithknownorsuspectedcardiovas- patients with UA/NSTEMI summarize both clinical evidence
cular disease (CVD). Coronary artery disease (CAD) is the andexpertopinion.
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Anderson et al ACCF/AHA UA/NSTEMI Guideline Revision e431
Table2. GuidelinesfortheIdentificationofACSPatientsbyEDRegistrationClerksorTriageNurses
Registration/clericalstaff
Patientswiththefollowingchiefcomplaintsrequireimmediateassessmentbythetriagenurseandshouldbereferredforfurtherevaluation:
•Chestpain,pressure,tightness,orheaviness;painthatradiatestoneck,jaw,shoulders,back,or1orbotharms
•Indigestionor"heartburn"nauseaand/orvomitingassociatedwithchestdiscomfort
•Persistentshortnessofbreath
•Weakness,dizziness,lightheadedness,lossofconsciousness
Triagenurse
PatientswiththefollowingsymptomsandsignsrequireimmediateassessmentbythetriagenursefortheinitiationoftheACSprotocol:
•Chestpainorsevereepigastricpain,nontraumaticinorigin,withcomponentstypicalofmyocardialischemiaorMI:
(cid:2)Central/substernalcompressionorcrushingchestpain
(cid:2)Pressure,tightness,heaviness,cramping,burning,achingsensation
(cid:2)Unexplainedindigestion,belching,epigastricpain
(cid:2)Radiatingpaininneck,jaw,shoulders,back,or1orbotharms
•Associateddyspnea
•Associatednauseaand/orvomiting
•Associateddiaphoresis
Ifthesesymptomsarepresent,obtainstatECG.
Medicalhistory
Thetriagenurseshouldtakeabrief,targeted,initialhistorywithanassessmentofcurrentorpasthistoryof:
•CABG,PCI,CAD,anginaoneffort,orMI
•NTGusetorelievechestdiscomfort
•Riskfactors,includingsmoking,hyperlipidemia,hypertension,diabetesmellitus,familyhistory,andcocaineormethamphetamineuse
•Regularandrecentmedicationuse
ThebriefhistorymustnotdelayentryintotheACSprotocol.
Specialconsiderations
Womenmaypresentmorefrequentlythanmenwithatypicalchestpainandsymptoms.
Diabeticpatientsmayhaveatypicalpresentationsduetoautonomicdysfunction.
Elderlypatientsmayhaveatypicalsymptomssuchasgeneralizedweakness,stroke,syncope,orachangeinmentalstatus.
AdaptedfromNationalHeartAttackAlertProgram.EmergencyDepartment:rapididentificationandtreatmentofpatientswithacutemyocardialinfarction.Bethesda,
MD:USDepartmentofHealthandHumanServices.USPublicHealthService.NationalInstitutesofHealth.NationalHeart,LungandBloodInstitute,September1993.
NIHPublicationNo.93-32786
ACS(cid:1)acutecoronarysyndrome;CABG(cid:1)coronaryarterybypassgraftsurgery;CAD(cid:1)coronaryarterydisease;ECG(cid:1)electrocardiogram;ED(cid:1)emergency
department;MI(cid:1)myocardialinfarction;NTG(cid:1)nitroglycerin;PCI(cid:1)percutaneouscoronaryintervention.
ClassificationofRecommendations These guidelines overlap several previously published
The schema for classification of recommendations and level ACC/AHA practice guidelines, including the ACC/AHA
of evidence is summarized in Table 1, which also illustrates Guidelines for the Management of Patients With ST-
howthegradingsystemprovidesanestimateofthesizeofthe ElevationMyocardialInfarction,1theACC/AHA/SCAI2005
treatment effect and an estimate of the certainty of the Guideline Update for Percutaneous Coronary Intervention,2
treatment effect. the AHA/ACC Guidelines for Secondary Prevention for
Acompletelistofthethousandsofpublicationsonvarious Patients With Coronary and Other Atherosclerotic Vascular
aspectsofthissubjectisbeyondthescopeoftheseguidelines; Disease: 2006 Update,3 and the ACC/AHA 2002 Guideline
only selected references are included. The Committee con- UpdatefortheManagementofPatientsWithChronicStable
sisted of acknowledged experts in general internal medicine Angina.4
representing the American College of Physicians (ACP),
family medicine from the American Academy of Family 1.2. Purpose of These Guidelines
Physicians(AAFP),emergencymedicinefromtheAmerican These guidelines address the diagnosis and management of
College of Emergency Physicians (ACEP), thoracic surgery patients with UA and the closely related condition of
fromtheSocietyofThoracicSurgeons(STS),interventional NSTEMI. These life-threatening disorders are a major cause
cardiologyfromtheSocietyforCardiovascularAngiography of emergency medical care and hospitalization in the United
and Interventions (SCAI), and general and critical care States. In 2004, the National Center for Health Statistics
cardiology, as well as individuals with recognized expertise reported1,565,000hospitalizationsforprimaryorsecondary
in more specialized areas, including noninvasive testing, diagnosisofanacutecoronarysyndrome(ACS),669,000for
preventive cardiology, coronary intervention, and cardiovas- UAand896,000formyocardialinfarction(MI).5Theaverage
cularsurgery.Boththeacademicandprivatepracticesectors age of a person having a first heart attack is 65.8 years for
wererepresented.Thisdocumentwasreviewedby2outside menand70.4yearsforwomen,and43%ofACSpatientsof
reviewersnominatedbyeachoftheACCandAHAandby49 all ages are women. In 2003, there were 4,497,000 visits to
peer reviewers. These guidelines will be considered current US emergency departments (EDs) for primary diagnosis of
unless the Task Force revises them or withdraws them from CVD.5 The prevalence of this presentation of CVD ensures
distribution. that many health care providers who are not cardiovascular
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e432 Circulation May 10, 2011
Figure1.AcuteCoronarySyndromes.Thetophalfofthefigureillustratesthechronologyoftheinterfacebetweenthepatientandthe
clinicianthroughtheprogressionofplaqueformation,onset,andcomplicationsofUA/NSTEMI,alongwithrelevantmanagementcon-
siderationsateachstage.Thelongitudinalsectionofanarterydepictsthe“timeline”ofatherogenesisfrom(1)anormalarteryto(2)
lesioninitiationandaccumulationofextracellularlipidintheintima,to(3)theevolutiontothefibrofattystage,to(4)lesionprogression
withprocoagulantexpressionandweakeningofthefibrouscap.Anacutecoronarysyndrome(ACS)developswhenthevulnerableor
high-riskplaqueundergoesdisruptionofthefibrouscap(5);disruptionoftheplaqueisthestimulusforthrombogenesis.Thrombus
resorptionmaybefollowedbycollagenaccumulationandsmoothmusclecellgrowth(6).Afterdisruptionofavulnerableorhigh-risk
plaque,patientsexperienceischemicdiscomfortthatresultsfromareductionofflowthroughtheaffectedepicardialcoronaryartery.
Theflowreductionmaybecausedbyacompletelyocclusivethrombus(bottomhalf,rightside)orsubtotallyocclusivethrombus(bot-
tomhalf,leftside).PatientswithischemicdiscomfortmaypresentwithorwithoutST-segmentelevationontheECG.Amongpatients
withST-segmentelevation,most(thickwhitearrowinbottompanel)ultimatelydevelopaQ-waveMI(QwMI),althoughafew(thinwhite
arrow)developanon–Q-waveMI(NQMI).PatientswhopresentwithoutST-segmentelevationaresufferingfromeitherunstableangina
(UA)oranon–ST-segmentelevationMI(NSTEMI)(thickredarrows),adistinctionthatisultimatelymadeonthebasisofthepresence
orabsenceofaserumcardiacmarkersuchasCK-MBoracardiactroponindetectedintheblood.Mostpatientspresentingwith
NSTEMIultimatelydevelopaNQMIontheECG;afewmaydevelopaQwMI.ThespectrumofclinicalpresentationsrangingfromUA
throughNSTEMIandSTEMIisreferredtoastheacutecoronarysyndromes.ThisUA/NSTEMIguideline,asdiagrammedintheupper
panel,includessectionsoninitialmanagementbeforeUA/NSTEMI,attheonsetofUA/NSTEMI,andduringthehospitalphase.Sec-
ondarypreventionandplansforlong-termmanagementbeginearlyduringthehospitalphaseoftreatment.(cid:1)Positiveserumcardiac
marker.ModifiedwithpermissionfromLibbyP.Currentconceptsofthepathogenesisoftheacutecoronarysyndromes.Circulation
2001;104:365;(7)©2001Lippincott,Williams&Wilkins;TheLancet,358,HammCW,BertrandM,BraunwaldE.Acutecoronarysyn-
dromewithoutSTelevation:implementationofnewguidelines,1533–8.Copyright2001,withpermissionfromElsevier8;andDavies
MJ.Thepathophysiologyofacutecoronarysyndromes.Heart2000;83:361–6.9©2000Lippincott,Williams&Wilkins.CK-MB(cid:1)MB
fractionofcreatinekinase;Dx(cid:1)diagnosis;ECG(cid:1)electrocardiogram.
Downloaded from http://circ.ahajournals.org/ at University of Washington on August 14, 2012
Anderson et al ACCF/AHA UA/NSTEMI Guideline Revision e433
specialists will encounter patients with UA/NSTEMI in the MI(STEMI)whoshouldbeconsideredforimmediatereper-
course of the treatment of other diseases, especially in fusiontherapyandtorecognizeotherpotentiallycatastrophic
outpatient and ED settings. These guidelines are intended to causes of patient symptoms, such as aortic dissection.
assistbothcardiovascularspecialistsandnonspecialistsinthe Patients diagnosed as having STEMI are excluded from
proper evaluation and management of patients with an acute managementaccordingtotheseguidelinesandshouldbeman-
onset of symptoms suggestive of these conditions. These agedasindicatedaccordingtotheACC/AHAGuidelinesforthe
clinical practice guidelines also provide recommendations Management of Patients With ST-Elevation Myocardial
and supporting evidence for the continued management of Infarction.1,10 Similarly, management of electrocardiographic
patientswiththeseconditionsinbothinpatientandoutpatient true posterior MI, which can masquerade as NSTEMI, is
settings. The diagnostic and therapeutic strategies that are coveredintheSTEMIguidelines.1Themanagementofpatients
recommended are supported by the best available evidence whoexperienceperiproceduralmyocardialdamage,asreflected
and expert opinion. The application of these principles with in the release of biomarkers of necrosis, such as the MB
carefully reasoned clinical judgment reduces but does not isoenzymeofcreatinekinase(CK-MB)ortroponin,alsoisnot
eliminate the risk of cardiac damage and death in patients consideredhere.
who present with symptoms suggestive of UA/NSTEMI. PatientswithMIandwithdefiniteischemicECGchanges
forwhomacutereperfusiontherapyisnotsuitableshouldbe
1.3. Overview of the Acute Coronary Syndromes diagnosed and managed as patients with UA. The residual
groupofpatientswithaninitialdiagnosisofACSwillinclude
1.3.1. Definition of Terms
Unstable angina/NSTEMI constitutes a clinical syndrome many patients who will ultimately be proven to have a
subset of the ACS that is usually, but not always, caused by noncardiaccausefortheinitialclinicalpresentationthatwas
atheroscleroticCADandisassociatedwithanincreasedrisk suggestiveofACS.Therefore,attheconclusionoftheinitial
ofcardiacdeathandsubsequentMI.InthespectrumofACS, evaluation, which is frequently performed in the ED but
UA/NSTEMI is defined by electrocardiographic (ECG) ST- sometimesoccursduringtheinitialhoursofinpatienthospi-
talization,eachpatientshouldhaveaprovisionaldiagnosisof
segment depression or prominent T-wave inversion and/or
1) ACS (Fig. 1), which in turn is classified as a) STEMI, a
positivebiomarkersofnecrosis(e.g.,troponin)intheabsence
condition for which immediate reperfusion therapy (fibrino-
ofST-segmentelevationandinanappropriateclinicalsetting
lysisorpercutaneouscoronaryintervention[PCI])shouldbe
(chestdiscomfortoranginalequivalent)(Table2,Fig.1).The
considered, b) NSTEMI, or c) UA (definite, probable, or
results of angiographic and angioscopic studies suggest that
possible);2)anon-ACScardiovascularcondition(e.g.,acute
UA/NSTEMI often results from the disruption or erosion of
pericarditis);3)anoncardiacconditionwithanotherspecific
an atherosclerotic plaque and a subsequent cascade of path-
disease (e.g., chest pain secondary to esophageal spasm); or
ological processes that decrease coronary blood flow. Most
4) a noncardiac condition that is undefined. In addition, the
patients who die during UA/NSTEMI do so because of
initialevaluationshouldbeusedtodetermineriskandtotreat
suddendeathorthedevelopment(orrecurrence)ofacuteMI.
life-threatening events.
The efficient diagnosis and optimal management of these
patientsmustderivefrominformationreadilyavailableatthe
Table3. CausesofUA/NSTEMI*
time of the initial clinical presentation. The clinical presen-
tation of patients with a life-threatening ACS often overlaps Thrombusorthromboembolism,usuallyarisingondisruptedoreroded
thatofpatientssubsequentlyfoundnottohaveCAD.More- plaque
over,someformsofMIcannotalwaysbedifferentiatedfrom •Occlusivethrombus,usuallywithcollateralvessels†
UA at the time of initial presentation. •Subtotallyocclusivethrombusonpre-existingplaque
•Distalmicrovascularthromboembolismfromplaque-associatedthrombus
“Acute coronary syndrome” has evolved as a useful oper-
ationaltermtorefertoanyconstellationofclinicalsymptoms Thromboembolismfromplaqueerosion
•Non-plaque-associatedcoronarythromboembolism
that are compatible with acute myocardial ischemia (Fig. 1).
ItencompassesMI(ST-segmentelevationanddepression,Q Dynamicobstruction(coronaryspasm‡orvasoconstriction)ofepicardial
and/ormicrovascularvessels
waveandnon-Qwave)andUA.Theseguidelinesfocuson2
componentsofthissyndrome:UAandNSTEMI.Inpractice, Progressivemechanicalobstructiontocoronaryflow
the term “possible ACS” is often assigned first by ancillary Coronaryarterialinflammation
personnel,suchasemergencymedicaltechniciansandtriage SecondaryUA
nurses, early in the evaluation process. A guideline of the Coronaryarterydissection§
National Heart Attack Alert Program6 summarizes the clini-
*Thesecausesarenotmutuallyexclusive;somepatientshave2ormore
cal information needed to make the diagnosis of possible causes.
ACSattheearliestphaseofclinicalevaluation(Table2).The †DeWoodMA,StifterWF,SimpsonCS,etal.Coronaryarteriographicfindings
implicationofthisearlydiagnosisforclinicalmanagementis soon after non-Q-wave myocardial infarction. N Engl J Med 1986;315:417–
that a patient who is considered to have an ACS should be 23.13
‡Mayoccurontopofanatheroscleroticplaque,producingmissed-etiology
placed in an environment with continuous ECG monitoring
anginaorUA/NSTEMI.
and defibrillation capability, where a 12-lead ECG can be
§Rare. Modified with permission from Braunwald E. Unstable angina: an
obtained expeditiously and definitively interpreted, ideally
etiologicapproachtomanagement.Circulation1998;98:2219–22.12
within10minofarrivalintheED.Themosturgentpriority UA (cid:1) unstable angina; UA/NSTEMI (cid:1) unstable angina/non-ST-elevation
of early evaluation is to identify patients with ST-elevation myocardialinfarction.
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e434 Circulation May 10, 2011
Intheseguidelines,UAandNSTEMIareconsideredtobe Table4. ThreePrincipalPresentationsofUA
closely related conditions whose pathogenesis and clinical
Class Presentation
presentationsaresimilarbutofdifferingseverity;thatis,they
Restangina* Anginaoccurringatrestandprolonged,usuallygreater
differ primarily in whether the ischemia is severe enough to
than20min
cause sufficient myocardial damage to release detectable
New-onsetangina New-onsetanginaofatleastCCSclassIIIseverity
quantitiesofamarkerofmyocardialinjury,mostcommonly
troponin I (TnI), troponin T (TnT), or CK-MB. Once it has Increasingangina Previouslydiagnosedanginathathasbecome
distinctlymorefrequent,longerinduration,orlower
been established that no biomarker of myocardial necrosis
inthreshold(i.e.,increasedby1ormoreCCSclass
has been released (based on 2 or more samples collected at
toatleastCCSclassIIIseverity)
least6hapart,withareferencelimitofthe99thpercentileof
*Patients with non-ST-elevated myocardial infarction usually present with
the normal population),11 the patient with ACS may be
anginaatrest.AdaptedwithpermissionfromBraunwaldE.Unstableangina:a
consideredtohaveexperiencedUA,whereasthediagnosisof
classification.Circulation1989;80:410–4.14
NSTEMI is established if a biomarker has been released. CCS (cid:1) Canadian Cardiovascular Society classification; UA (cid:1) unstable
Markers of myocardial injury can be detected in the blood- angina.
stream with a delay of up to several hours after the onset of
ischemic chest pain, which then allows the differentiation can occur on top of obstructive or destabilized plaque,
between UA (i.e., no biomarkers in circulation; usually resulting in angina of “mixed” origin or UA/NSTEMI. Dy-
transient, if any, ECG changes of ischemia) and NSTEMI namic coronary obstruction can also be caused by diffuse
(i.e.,elevatedbiomarkers).Thus,atthetimeofpresentation, microvascular dysfunction; for example, due to endothelial
patientswithUAandNSTEMIcanbeindistinguishableand dysfunctionortheabnormalconstrictionofsmallintramural
therefore are considered together in these guidelines. resistance vessels. Coronary spasm also is the presumed
mechanismunderlyingcocaine-inducedUA/NSTEMI.
1.3.2. Pathogenesis of UA/NSTEMI
● AthirdcauseofUA/NSTEMIisseverenarrowingwithout
Theseconditionsarecharacterizedbyanimbalancebetween
spasm or thrombus. This occurs in some patients with
myocardial oxygen supply and demand. They are not a
progressive atherosclerosis or with restenosis after a PCI.
specificdisease,suchaspneumococcalpneumonia,butrather
● A fourth cause of UA/NSTEMI is coronary artery dissec-
a syndrome, analogous to hypertension. A relatively few
tion (e.g., as a cause of ACS in peripartal women).
nonexclusive causes are recognized12 (Table 3).
● The fifth mechanism is secondary UA, in which the
Themostcommonmechanismsinvolveanimbalancethat
precipitating condition is extrinsic to the coronary arterial
is caused primarily by a reduction in oxygen supply to the
bed. Patients with secondary UA usually, but not always,
myocardium,whereaswiththefifthmechanismnotedbelow,
have underlying coronary atherosclerotic narrowing that
the imbalance is principally due to increased myocardial
limits myocardial perfusion, and they often have chronic
oxygen requirements, usually in the presence of a fixed,
stable angina. Secondary UA is precipitated by conditions
restricted oxygen supply:
that 1) increase myocardial oxygen requirements, such as
● The most common cause of UA/NSTEMI is reduced fever, tachycardia, or thyrotoxicosis; 2) reduce coronary
myocardial perfusion that results from coronary artery blood flow, such as hypotension; or 3) reduce myocardial
narrowing caused by a thrombus that developed on a oxygen delivery, such as anemia or hypoxemia.
disrupted atherosclerotic plaque and is usually nonocclu-
These causes of UA/NSTEMI are not mutually exclusive.
sive.Microembolizationofplateletaggregatesandcompo-
nentsofthedisruptedplaquearebelievedtoberesponsible 1.3.3. Presentations of UA and NSTEMI
for the release of myocardial markers in many of these There are 3 principal presentations of UA: 1) rest angina
patients.Anocclusivethrombus/plaquealsocancausethis (anginacommencingwhenthepatientisatrest),2)new-onset
syndrome in the presence of an extensive collateral blood (lessthan2months)severeangina,and3)increasingangina
supply. (increasing in intensity, duration, and/or frequency) (Table
● The most common underlying molecular and cellular 4).14 Criteria for the diagnosis of UA are based on the
pathophysiology of disrupted atherosclerotic plaque is duration and intensity of angina as graded according to the
arterial inflammation, caused by noninfectious (e.g., oxi- Canadian Cardiovascular Society classification (Table 5).15
dized lipids) and, possibly, infectious stimuli, which can Non–ST-elevationMIgenerallypresentsasprolonged,more
lead to plaque expansion and destabilization, rupture or intense rest angina or angina equivalent.
erosion, and thrombogenesis. Activated macrophages and
Tlymphocyteslocatedattheshoulderofaplaqueincrease 1.4. Management Before UA/NSTEMI and Onset
theexpressionofenzymessuchasmetalloproteinasesthat of UA/NSTEMI
causethinninganddisruptionoftheplaque,whichinturn The ACS spectrum (UA/MI) has a variable but potentially
can lead to UA/NSTEMI. serious prognosis. The major risk factors for development of
● Alesscommoncauseisdynamicobstruction,whichmaybe coronaryheartdisease(CHD)andUA/NSTEMIarewellestab-
triggeredbyintensefocalspasmofasegmentofanepicardial lished. Clinical trials have demonstrated that modification of
coronary artery (Prinzmetals angina) (see Section 6.7). This thoseriskfactorscanpreventthedevelopmentofCHD(primary
localspasmiscausedbyhypercontractilityofvascularsmooth prevention)orreducetheriskofexperiencingUA/NSTEMIin
muscleand/orbyendothelialdysfunction.Large-vesselspasm patients who have CHD (secondary prevention). All practitio-
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