2012 ACCF/AHA Focused Update Incorporated Into the ACCF/AHA 2007 Guidelines for the

169 Pages·2013·7.72 MB·English

JournaloftheAmericanCollegeofCardiology Vol.61,No.23,2013
©2013bytheAmericanCollegeofCardiologyFoundationandtheAmericanHeartAssociation,Inc. ISSN0735-1097/$36.00
PublishedbyElsevierInc. http://dx.doi.org/10.1016/j.jacc.2013.01.014
PRACTICE GUIDELINE
2012 ACCF/AHA Focused Update Incorporated
Into the ACCF/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
Developed in Collaboration With the American College of Emergency Physicians,
Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.
Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the
Society for Academic Emergency Medicine
Jeffrey L. Anderson, MD, FACC, FAHAChair; Cynthia D. Adams, RN, PhD, FAHA;
Elliott M. Antman, MD, FACC, FAHA; Charles R. Bridges, MD, ScD, FACC, FAHA;
Robert M. Califf, MD, MACC; Donald E. Casey, Jr, MD, MPH, MBA, FACP, FAHA;
William E. Chavey, II, MD, MS; Francis M. Fesmire, MD, FACEP;
Judith S. Hochman, MD, FACC, FAHA; Thomas N. Levin, MD, FACC, FSCAI;
A. Michael Lincoff, MD, FACC; Eric D. Peterson, MD, MPH, FACC, FAHA;
Pierre Theroux, MD, FACC, FAHA; Nanette K. Wenger, MD; R. Scott Wright, MD, FACC, FAHA
2012 WRITING GROUP MEMBERS*
Developed in Collaboration With the American College of Emergency Physicians,
SocietyforCardiovascularAngiographyandInterventions,andSocietyofThoracicSurgeons
Hani Jneid, MD, FACC, FAHA, Chair†; Jeffrey L. Anderson, MD, FACC, FAHA, Vice Chair†‡;
R. Scott Wright, MD, FACC, FAHA, Vice Chair†; Cynthia D. Adams, RN, PhD, FAHA†;
CharlesR.Bridges,MD,ScD,FACC,FAHA§;DonaldE.Casey,Jr,MD,MPH,MBA,FACP,FAHA(cid:1);
Steven M. Ettinger, MD, FACC†; Francis M. Fesmire, MD, FACEP¶; Theodore G. Ganiats, MD#;
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
*Writingcommitteemembersarerequiredtorecusethemselvesfromvotingonsectionstowhichtheirspecificrelationshipswithindustryandother
entitiesmayapply;seeAppendix4for recusal information.†ACCF/AHARepresentative.‡ACCF/AHA TaskForceonPracticeGuidelinesLiaison.
§Society of Thoracic Surgeons Representative. (cid:1)American College of Physicians Representative. ¶American College of Emergency Physicians
Representative.#AmericanAcademyofFamilyPhysiciansRepresentative.**ACCF/AHATaskForceonPerformanceMeasuresLiaison.††Societyfor
CardiovascularAngiographyandInterventionsRepresentative.
ThisdocumentwasapprovedbytheAmericanCollegeofCardiologyFoundationBoardofTrusteesandtheAmericanHeartAssociationScience
AdvisoryandCoordinatingCommittee.
TheAmericanCollegeofCardiologyFoundationrequeststhatthisdocumentbecitedasfollows:AndersonJL,AdamsCD,AntmanEM,BridgesCR,
CaliffRM,CaseyDEJr,ChaveyWE2nd,FesmireFM,HochmanJS,LevinTN,LincoffAM,PetersonED,TherouxP,WengerNK,WrightRS.2012
ACCF/AHAfocusedupdateincorporatedintotheguidelineforthemanagementofpatientswithunstableangina/non–ST-elevationmyocardialinfarction:
a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol
2013;61:e179–347.doi:10.1016/j.jacc.2013.01.014.
ThisarticleiscopublishedinCirculation.
Copies: This document is available on the World Wide Web sites of the American College of Cardiology (http://www.cardiosource.org) and the
AmericanHeartAssociation(my.americanheart.org).Forcopiesofthisdocument,pleasecontactElsevierInc.ReprintDepartment,fax[phone],
[email protected].
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
permissionoftheAmericanCollegeofCardiologyFoundation.PleasecontactElsevier’[email protected].
e180 Andersonetal. JACCVol.61,No.23,2013
UA/NSTEMIGuideline:2012UpdateIncorporated June11,2013:e179–347
ACCF/AHA TASK FORCE MEMBERS
Jeffrey L. Anderson, MD, FACC, FAHA, Chair; Alice K. Jacobs, MD, FACC, FAHA,
Immediate Past Chair; Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect;
Nancy M. Albert, PhD, CCNS, CCRN; Mark A. Creager, MD, FACC, FAHA; David DeMets, PhD;
StevenM.Ettinger,MD,FACC;RobertA.Guyton,MD,FACC;JudithS.Hochman,MD,FACC,FAHA;
Frederick G. Kushner, MD, FACC, FAHA; E. Magnus Ohman, MD, FACC;
William Stevenson, MD, FACC, FAHA; Clyde W. Yancy, MD, FACC, FAHA
2.2.8.4. SUMMARYCOMPARISONOFBIOMARKERSOF
TABLE OF CONTENTS NECROSIS:SINGLYANDINCOMBINATION......e208
2.2.9. OtherMarkersandMultimarker
Preamble(UPDATED)............................e182 Approaches ..........................e208
2.2.9.1. ISCHEMIA.................................e208
1. Introduction(UPDATED) ......................e184 2.2.9.2. COAGULATION.............................e209
2.2.9.3. PLATELETS................................e209
1.1. OrganizationofCommitteeandEvidence 2.2.9.4. INFLAMMATION............................e209
Review(UPDATED)..........................e184 2.2.9.5. B-TYPENATRIURETICPEPTIDES..............e210
1.2. DocumentReviewandApproval(UPDATED).....e185 2.3. ImmediateManagement ....................e210
1.3. PurposeofTheseGuidelines................e185 2.3.1. ChestPainUnits......................e211
2.3.2. DischargeFromEDorChestPainUnit....e212
1.4. OverviewoftheAcuteCoronarySyndromes.....e186
1.4.1. DefinitionofTerms...................e186 3. EarlyHospitalCare...........................e213
1.4.2. PathogenesisofUA/NSTEMI...........e186
1.4.3. PresentationsofUAandNSTEMI.......e189 3.1. Anti-IschemicandAnalgesicTherapy ........e214
1.5. ManagementBeforeUA/NSTEMIand 3.1.1. GeneralCare.........................e215
OnsetofUA/NSTEMI........................e189 3.1.2. UseofAnti-IschemicTherapies .........e215
1.5.1. IdentificationofPatientsatRiskof 3.1.2.1. NITRATES.................................e215
UA/NSTEMI........................e189 3.1.2.2. MORPHINESULFATE........................e217
1.5.2. InterventionstoReduceRiskof 3.1.2.3. BETA-ADRENERGICBLOCKERS...............e217
UA/NSTEMI........................e190 3.1.2.4. CALCIUMCHANNELBLOCKERS...............e219
3.1.2.5. INHIBITORSOFTHERENIN-ANGIOTENSIN-
1.6. OnsetofUA/NSTEMI........................e191
ALDOSTERONESYSTEM.....................e220
1.6.1. RecognitionofSymptomsbyPatient .....e191
3.1.2.6. OTHERANTI-ISCHEMICTHERAPIES............e221
1.6.2. SilentandUnrecognizedEvents .........e191
3.1.2.7. INTRA-AORTICBALLOONPUMP
2. InitialEvaluationandManagement............e191
COUNTERPULSATION........................e221
3.1.2.8. ANALGESICTHERAPY.......................e221
2.1. ClinicalAssessment........................e191
3.2. RecommendationsforAntiplatelet/Anticoagulant
2.1.1. EmergencyDepartmentorOutpatient
TherapyinPatientsforWhomDiagnosisof
FacilityPresentation...................e195
2.1.2. QuestionstoBeAddressedatthe UA/NSTEMIIsLikelyorDefinite(UPDATED)....e221
InitialEvaluation......................e196 3.2.1. AntiplateletTherapy:Recommendations
(UPDATED) ........................e221
2.2. EarlyRiskStratification.....................e196
3.2.2. AnticoagulantTherapy:Recommendations....e223
2.2.1. EstimationoftheLevelofRisk..........e198
3.2.3. AdditionalManagementConsiderationsfor
2.2.2. RationaleforRiskStratification..........e198
AntiplateletandAnticoagulantTherapy:
2.2.3. History..............................e198
Recommendations(UPDATED).........e223
2.2.4. AnginalSymptomsandAnginal
3.2.3.1. ANTIPLATELET/ANTICOAGULANTTHERAPYIN
Equivalents ..........................e198
PATIENTSFORWHOMDIAGNOSISOFUA/NSTEMIIS
2.2.5. DemographicsandHistoryinDiagnosis
LIKELYORDEFINITE(NEWSECTION)..........e224
andRiskStratification .................e199
2.2.6. EstimationofEarlyRiskatPresentation.....e200 3.2.3.1.1. NEWERP2Y12RECEPTOR
INHIBITORS.....................e224
2.2.6.1. ELECTROCARDIOGRAM......................e202
2.2.6.2. PHYSICALEXAMINATION....................e203 3.2.3.1.2. CHOICEOFP2Y12RECEPTORINHIBITORS
2.2.7. NoncardiacCausesofSymptomsand FORPCIINUA/NSTEMI...........e227
SecondaryCausesofMyocardialIschemia...e204 3.2.3.1.2.1. TimingofDiscontinuationof
2.2.8. CardiacBiomarkersofNecrosisandthe P2Y ReceptorInhibitor
12
RedefinitionofAMI...................e204 TherapyforSurgical
2.2.8.1. CREATINEKINASE-MB.......................e205 Procedures...........e227
2.2.8.2. CARDIACTROPONINS.......................e205
3.2.3.1.3. INTERINDIVIDUALVARIABILITYIN
2.2.8.2.1. CLINICALUSE...................e205
RESPONSIVENESSTO
2.2.8.2.1.1. ClinicalUseofMarker CLOPIDOGREL...................e228
ChangeScores.......e207 3.2.3.1.4. OPTIMALLOADINGANDMAINTENANCE
2.2.8.2.1.2. BedsideTestingforCardiac DOSAGESOFCLOPIDOGREL......e228
Markers...........e208 3.2.3.1.5. PROTONPUMPINHIBITORSANDDUAL
2.2.8.3. MYOGLOBINANDCK-MBSUBFORMS ANTIPLATELETTHERAPY
COMPAREDWITHTROPONINS................e208 FORACS.......................e229
JACCVol.61,No.23,2013 Andersonetal. e181
June11,2013:e179–347 UA/NSTEMIGuideline:2012UpdateIncorporated
3.2.3.1.6. GLYCOPROTEINIIb/IIIaRECEPTOR 5.2.15. Depression...........................e272
ANTAGONISTS(UPDATEDTO 5.2.16. NonsteroidalAnti-InflammatoryDrugs ...e272
INCORPORATENEWERTRIALS 5.2.17. HormoneTherapy.....................e272
ANDEVIDENCE).................e230 5.2.18. AntioxidantVitaminsandFolicAcid.....e273
3.2.4. OlderAntiplateletAgentsandTrials 5.3. PostdischargeFollow-Up....................e273
(Aspirin,Ticlopidine,Clopidogrel).......e231
3.2.4.1. ASPIRIN..................................e231 5.4. CardiacRehabilitation ......................e274
3.2.4.2. ADENOSINEDIPHOSPHATERECEPTORANTAGONISTS 5.5. ReturntoWorkandDisability...............e275
ANDOTHERANTIPLATELETAGENTS...........e233 5.6. OtherActivities.............................e276
3.2.5. AnticoagulantAgentsandTrials.........e236
3.2.5.1. UNFRACTIONATEDHEPARIN.................e237 5.7. PatientRecordsandOther
3.2.5.2. LOW-MOLECULAR-WEIGHTHEPARIN..........e238 InformationSystems........................e277
3.2.5.3. LMWHVERSUSUFH........................e238 6. SpecialGroups...............................e277
3.2.5.3.1. EXTENDEDTHERAPY
WITHLMWHS...................e241 6.1. Women.....................................e277
3.2.5.4. DIRECTTHROMBININHIBITORS...............e241 6.1.1. ProfileofUA/NSTEMIinWomen......e278
3.2.5.5. FACTORXaInhibitors.......................e244 6.1.2. Management.........................e278
3.2.5.6. LONG-TERMANTICOAGULATION..............e245 6.1.2.1. PHARMACOLOGICALTHERAPY...............e278
3.2.6. PlateletGPIIb/IIIaReceptor 6.1.2.2. CORONARYARTERYREVASCULARIZATION.......e278
Antagonists..........................e246 6.1.2.3. INITIALINVASIVEVERSUSINITIAL
3.2.7. Fibrinolysis ..........................e251 CONSERVATIVESTRATEGY...................e279
3.3. InitialConservativeVersusInitialInvasive 6.1.3. StressTesting ........................e281
Strategies(UPDATED).......................e251 6.1.4. Conclusions..........................e281
3.3.1. GeneralPrinciples.....................e252 6.2. DiabetesMellitus(UPDATED)................e281
3.3.2. RationalefortheInitialConservative 6.2.1. ProfileandInitialManagementof
Strategy.............................e252 DiabeticandHyperglycemicPatientsWith
3.3.3. RationalefortheInvasiveStrategy .......e253 UA/NSTEMI........................e281
3.3.3.1. TIMINGOFINVASIVETHERAPY 6.2.1.1. INTENSIVEGLUCOSECONTROL
(NEWSECTION)............................e253 (NEWSECTION)............................e282
3.3.4. ImmediateAngiography................e254 6.2.2. CoronaryRevascularization .............e283
3.3.5. DeferredAngiography .................e254 6.2.3. Conclusions..........................e284
3.3.6. ComparisonofEarlyInvasiveand 6.3. Post-CABGPatients.........................e284
InitialConservativeStrategies ...........e254 6.3.1. PathologicalFindings..................e285
3.3.7. Subgroups ...........................e257 6.3.2. ClinicalFindingsandApproach .........e285
3.3.8. CareObjectives.......................e258 6.3.3. Conclusions..........................e285
3.4. RiskStratificationBeforeDischarge.........e260 6.4. OlderAdults................................e285
3.4.1. CareObjectives.......................e260 6.4.1. PharmacologicalManagement...........e286
3.4.2. NoninvasiveTestSelection..............e262 6.4.2. FunctionalStudies.....................e286
3.4.3. SelectionforCoronaryAngiography......e263 6.4.3. PercutaneousCoronaryInterventionin
3.4.4. PatientCounseling....................e263 OlderPatients........................e287
4. CoronaryRevascularization...................e263 6.4.4. ContemporaryRevascularizationStrategies
inOlderPatients......................e287
4.1. RecommendationsforRevascularizationWithPCI 6.4.5. Conclusions..........................e287
andCABGinPatientsWithUA/NSTEMI 6.5. ChronicKidneyDisease(UPDATED) .........e288
(UPDATED)..................................e263 6.5.1. AngiographyinPatientsWithCKD
5. LateHospitalCare,HospitalDischarge,and (NEWSECTION) ...................e288
Post-HospitalDischargeCare.................e263 6.6. CocaineandMethamphetamineUsers.......e290
6.6.1. CoronaryArterySpasmWith
5.1. MedicalRegimenandUseofMedications....e263 CocaineUse .........................e290
5.2. Long-TermMedicalTherapyandSecondary 6.6.2. Treatment ...........................e291
Prevention .................................e265 6.6.3. MethamphetamineUseand
5.2.1. ConvalescentandLong-Term UA/NSTEMI........................e292
AntiplateletTherapy(UPDATED).......e266 6.7. Variant(Prinzmetal’s)Angina ...............e292
5.2.2. BetaBlockers.........................e266 6.7.1. ClinicalPicture.......................e292
5.2.3. InhibitionoftheRenin-Angiotensin- 6.7.2. Pathogenesis .........................e292
AldosteroneSystem....................e267 6.7.3. Diagnosis............................e293
5.2.4. Nitroglycerin.........................e267 6.7.4. Treatment ...........................e293
5.2.5. CalciumChannelBlockers..............e267 6.7.5. Prognosis............................e293
5.2.6. WarfarinTherapy(UPDATED).........e267 6.8. Cardiovascular“SyndromeX”...............e294
5.2.7. LipidManagement....................e268
6.8.1. DefinitionandClinicalPicture ..........e294
5.2.8. BloodPressureControl ................e270
6.8.2. Treatment ...........................e295
5.2.9. DiabetesMellitus .....................e270
5.2.10. SmokingCessation....................e270 6.9. TakotsuboCardiomyopathy..................e295
5.2.11. WeightManagement ..................e271 7. ConclusionsandFutureDirections............e295
5.2.12. PhysicalActivity......................e271
5.2.13. PatientEducation.....................e272 7.1. RecommendationsforQualityofCareand
5.2.14. Influenza ............................e272 OutcomesforUA/NSTEMI(NEWSECTION) ...e297
e182 Andersonetal. JACCVol.61,No.23,2013
UA/NSTEMIGuideline:2012UpdateIncorporated June11,2013:e179–347
7.1.1. QualityCareandOutcomes groupofauthorstodevelop,update,orrevisewrittenrecom-
(NEWSECTION) ...................e297 mendations for clinical practice.
Experts in the subject under consideration have been
References.....................................e297
selected from both organizations to examine subject-specific
data and write guidelines. The process includes additional
Appendix1.2007AuthorRelationshipsWithIndustry representativesfromothermedicalpractitionerandspecialty
andOtherEntities...............................e325 groupswhenappropriate.Writingcommitteesarespecifically
chargedtoperformaliteraturereview,weighthestrengthof
evidence for or against a particular treatment or procedure,
Appendix2.2007ReviewerRelationshipsWith
and include estimates of expected health outcomes where
IndustryandOtherEntities......................e330
data exist. Patient-specific modifiers and comorbidities and
issues of patient preference that may influence the choice of
Appendix3.AbbreviationList....................e335 particular tests or therapies are considered, as well as fre-
quency of follow-up and cost-effectiveness. When available,
informationfromstudiesoncostwillbeconsidered;however,
Appendix4.2012AuthorRelationshipsWithIndustry
reviewofdataonefficacyandclinicaloutcomeswillconsti-
andOtherEntities(NEW)........................e338
tutetheprimarybasisforpreparingrecommendationsinthese
guidelines.
Appendix5.2012ReviewerRelationshipsWith The guidelines will be reviewed annually by the Task
IndustryandOtherEntities(NEW) ...............e340 Forceandwillbeconsideredcurrentunlesstheyareupdated,
revised,orsunsettedandwithdrawnfromdistribution.Keep-
ing pace with the stream of new data and evolving evidence
Appendix6.SelectionofInitialTreatmentStrategy:
onwhichguidelinerecommendationsarebasedisanongoing
InvasiveVersusConservativeStrategy(NEW)....e343
challenge to timely development of clinical practice guide-
lines. In an effort to respond promptly to new evidence, the
Appendix7.DosingTableforAntiplateletand Task Force has created a “focused update” process to revise
AnticoagulantTherapytoSupportPCIinUA/NSTEMI the existing guideline recommendations that are affected by
(NEW) ..........................................e344 evolving data or opinion. New evidence is reviewed in an
ongoing fashion to more efficiently respond to important
science and treatment trends that could have a major impact
Appendix8.ComparisonsAmongOrallyEffective
P2Y Inhibitors(NEW)..........................e346 on patient outcomes and quality of care.
12
Forthe2012focusedupdate,thestandingguidelinewriting
committee along with the parent Task Force identified trials
Appendix9.FlowchartforClassIandClassIIa
and other key data through October 2011 that may impact
RecommendationsforInitialManagementof
guideline recommendations, specifically in response to the
UA/NSTEMI(NEW) ..............................e347 approvalofneworalantiplatelets,andtoprovideguidanceon
how to incorporate these agents into daily practice (Section 1.1,
“MethodologyandEvidence”).Nowthatmultipleagentsare
Preamble (UPDATED)
available,acomparisonoftheiruseinvarioussettingswithin
clinical practice is provided. This iteration replaces the
It is important that the medical profession play a significant
sections in the 2007 ACC/AHA Guidelines for the Manage-
role in critically evaluating the use of diagnostic procedures
ment of Patients With Unstable Angina/Non–ST-Elevation
and therapies as they are introduced and tested in the
MyocardialInfarctionthatwereupdatedbythe2011ACCF/
detection, management, or prevention of disease states. Rig-
AHAFocusedUpdateoftheGuidelinesfortheManagement
orous and expert analysis of the available data documenting
of Patients With Unstable Angina/Non–ST-Elevation Myo-
absolute and relative benefits and risks of those procedures
cardialInfarction(1,2).Thefocusedupdateisnotintendedto
andtherapiescanproducehelpfulguidelinesthatimprovethe
bebasedonacompleteliteraturereviewfromthedateofthe
effectiveness of care, optimize patient outcomes, and favor-
previous guideline publication but rather to include pivotal
ably affect the overall cost of care by focusing resources on
new evidence that may affect changes to current recommen-
the most effective strategies.
dations. See the 2012 focused update for the complete
TheAmericanCollegeofCardiologyFoundation(ACCF) preamble and evidence review period (3).
and the American Heart Association (AHA) have jointly Inanalyzingthedataanddevelopingrecommendationsand
engaged in the production of such guidelines in the area of supportingtext,thewritinggroupusesevidence-basedmeth-
cardiovascular disease since 1980. The ACCF/AHA Task odologies developed by the Task Force (4). The Class of
ForceonPracticeGuidelines(TaskForce),whosechargeisto Recommendation (COR) is an estimate of the size of the
develop, update, or revise practice guidelines for important treatment effect, with consideration given to risks versus
cardiovascular diseases and procedures, directs this effort. benefits, as well as evidence and/or agreement that a given
Writing committees are charged with the task of performing treatment or procedure is or is not useful/effective and in
an assessment of the evidence and acting as an independent some situations may cause harm. The Level of Evidence
JACCVol.61,No.23,2013 Andersonetal. e183
June11,2013:e179–347 UA/NSTEMIGuideline:2012UpdateIncorporated
(LOE) is an estimate of the certainty or precision of the LOE is summarized in Table 1, which also provides sug-
treatment effect. The writing group reviews and ranks evi- gested phrases for writing recommendations within each
dence supporting each recommendation, with the weight of COR. A new addition to this methodology for the 2012
evidence ranked as LOE A, B, or C, according to specific focused update is separation of the Class III recommenda-
definitionsthatareincludedinTable1.Studiesareidentified tionstodelineatewhethertherecommendationisdetermined
as observational, retrospective, prospective, or randomized, to be of “no benefit” or is associated with “harm” to the
as appropriate. For certain conditions for which inadequate patient. In addition, in view of the increasing number of
data are available, recommendations are based on expert comparativeeffectivenessstudies,comparatorverbsandsug-
consensusandclinicalexperienceandarerankedasLOEC. gestedphrasesforwritingrecommendationsforthecompar-
WhenrecommendationsatLOECaresupportedbyhistorical ativeeffectivenessofonetreatmentorstrategyversusanother
clinical data, appropriate references (including clinical re- have been added for COR I and IIa, LOE A or B only.
views)arecitedifavailable.Forissuesforwhichsparsedata In view of the advances in medical therapy across the
are available, a survey of current practice among the clini- spectrumofcardiovasculardiseases,theTaskForcehasdesig-
ciansonthewritinggroupisthebasisforLOECrecommen- nated the term guideline-directed medical therapy (GDMT) to
dations,andnoreferencesarecited.TheschemaforCORand represent optimal medical therapy as defined by ACCF/AHA
Table1. ApplyingClassificationofRecommendationsandLevelofEvidence
ArecommendationwithLevelofEvidenceBorCdoesnotimplythattherecommendationisweak.Manyimportantclinicalquestionsaddressedintheguidelinesdonotlend
themselvestoclinicaltrials.Althoughrandomizedtrialsareunavailable,theremaybeaveryclearclinicalconsensusthataparticulartestortherapyisusefuloreffective.
*Dataavailablefromclinicaltrialsorregistriesabouttheusefulness/efficacyindifferentsubpopulations,suchassex,age,historyofdiabetes,historyofprior
myocardialinfarction,historyofheartfailure,andprioraspirinuse.
†Forcomparativeeffectivenessrecommendations(ClassIandIIa;LevelofEvidenceAandBonly),studiesthatsupporttheuseofcomparatorverbsshouldinvolve
directcomparisonsofthetreatmentsorstrategiesbeingevaluated.
e184 Andersonetal. JACCVol.61,No.23,2013
UA/NSTEMIGuideline:2012UpdateIncorporated June11,2013:e179–347
guideline(primarilyClassI)–recommendedtherapies.Thisnew vance).ThesestatementsarereviewedbytheTaskForceand
term,GDMT,isincorporatedintothe2012focusedupdateand all members during each conference call and/or meeting of
willbeusedthroughoutallfutureguidelines. the writing group and are updated as changes occur. All
Because the ACCF/AHA practice guidelines address pa- guideline recommendations require a confidential vote by
tient populations (and healthcare providers) residing in North thewritinggroupandmustbeapprovedbyaconsensusofthe
America,drugsthatarenotcurrentlyavailableinNorthAmerica votingmembers.Membersarenotpermittedtodraftorvote
are discussed in the text without a specific COR. For studies on any text or recommendations pertaining to their RWI.
performedinlargenumbersofsubjectsoutsideNorthAmerica, The2012memberswhorecusedthemselvesfromvotingare
each writing group reviews the potential impact of different indicated in the list of writing group members, and specific
practicepatternsandpatientpopulationsonthetreatmenteffect section recusals are noted in Appendix 4. 2007 and 2012
andrelevancetotheACCF/AHAtargetpopulationtodetermine authors’ and peer reviewers’ RWI pertinent to this guideline
whetherthefindingsshouldinformaspecificrecommendation. are disclosed in Appendixes 1, 2, 4, and 5, respectively.
TheACCF/AHApracticeguidelinesareintendedtoassist Additionally,toensurecompletetransparency,writinggroup
healthcare providers in clinical decision making by describ- members’ comprehensive disclosure informationincluding
ing a range of generally acceptable approaches to the diag- RWI not pertinent to this documentis available as an online
nosis, management, and prevention of specific diseases or supplement. Comprehensive disclosure information for the
conditions. The guidelines attempt to define practices that TaskForceisalsoavailableonlineatwww.cardiosource.org/
meet the needs of most patients in most circumstances. The ACC/About-ACC/Leadership/Guidelines-and-Documents-Task-
ultimate judgment about care of a particular patient must be Forces.aspx. The work of the 2012 writing group is supported
madebythehealthcareproviderandpatientinlightofallthe exclusivelybytheACCF,andAHA,withoutcommercialsupport.
circumstancespresentedbythatpatient.Asaresult,situations Writinggroupmembersvolunteeredtheirtimeforthisactivity.
may arise in which deviations from these guidelines may be InApril2011,theInstituteofMedicinereleased2reports:
appropriate. Clinical decision making should consider the Finding What Works in Health Care: Standards for System-
qualityandavailabilityofexpertiseintheareawherecareis aticReviewsandClinicalPracticeGuidelinesWeCanTrust
provided. When these guidelines are used as the basis for (5,6). It is noteworthy that the ACCF/AHA practice guide-
regulatory or payer decisions, the goal should be improve- lines were cited as being compliant with many of the
ment in quality of care. The Task Force recognizes that standards that were proposed. A thorough review of these
situationsariseinwhichadditionaldataareneededtoinform reports and our current methodology is under way, with
patient care more effectively; these areas will be identified further enhancements anticipated.
within each respective guideline when appropriate. The 2007 executive summary and recommendations are
Prescribed courses of treatment in accordance with these published in the August 7, 2007, issue of the Journal of the
recommendations are effective only if they are followed. Be- American College of Cardiology and August7,2007,issueof
cause lack of patient understanding and adherence may ad- Circulation. The full-text guidelines are e-published in the same
verselyaffectoutcomes,physiciansandotherhealthcareprovid- issueofthejournalsnotedabove,aswellaspostedontheACC
ers should make every effort to engage the patient’s active (http://www.cardiosource.org) and AHA (my.americanheart.org)
participation in prescribed medical regimens and lifestyles. In Web sites. Guidelines are official policy of both the ACCF
addition,patientsshouldbeinformedoftherisks,benefits,and and AHA.
alternativestoaparticulartreatmentandshouldbeinvolvedin Thecurrentdocumentisare-publicationofthe“ACCF/AHA
shareddecisionmakingwheneverfeasible,particularlyforCOR 2007GuidelinesfortheManagementofPatientsWithUnstable
IIaandIIb,forwhichthebenefit-to-riskratiomaybelower. Angina/Non–ST-Elevation Myocardial Infarction” (7), revised
TheTaskForcemakeseveryefforttoavoidactual,poten- toincorporateupdatedrecommendationsandtextfromthe2012
tial,orperceivedconflictsofinterestthatmayariseasaresult FocusedUpdate(3).Foreasyreference,thisonline-onlyversion
of industry relationships or personal interests among the denotessectionsthathavebeenupdated.Thesectionsthathave
members of the writing group. All writing group members not been updated could contain text or references that are not
andpeerreviewersoftheguidelinearerequiredtodiscloseall current,asthesesectionshavenotbeenmodified.
current healthcare–related relationships, including those ex- Jeffrey L. Anderson, MD, FACC, FAHA
isting 12 months before initiation of the writing effort. Chair, ACCF/AHA Task Force on Practice Guidelines
For the 2007 guidelines, all members of the writing
committee, as well as peer reviewers of the document, were 1. Introduction (UPDATED)
asked to provide disclosure statements of all such relation-
ships that may be perceived as real or potential conflicts of
interest. Writing committee members are also strongly en- 1.1. Organization of Committee and
couragedtodeclareapreviousrelationshipwithindustrythat Evidence Review (UPDATED)
may be perceived as relevant to guideline development. The ACC/AHA Task Force on Practice Guidelines was
In December 2009, the ACCF and AHA implemented a formed to make recommendations regarding the diagnosis
new policy for relationships with industry and other entities andtreatmentofpatientswithknownorsuspectedcardiovas-
(RWI) that requires the writing group chair plus a minimum cular disease (CVD). Coronary artery disease (CAD) is the
of 50% of the writing group to have no relevant RWI leading cause of death in the United States. Unstable angina
(Appendix 4 includes the ACCF/AHA definition of rele- (UA) and the closely related condition of non–ST-segment
JACCVol.61,No.23,2013 Andersonetal. e185
June11,2013:e179–347 UA/NSTEMIGuideline:2012UpdateIncorporated
elevationmyocardialinfarction(NSTEMI)areverycommon focused update was initiated to provide guidance on how to
manifestations of this disease. incorporate these agents into daily practice. Now that multi-
The 2007 guideline committee members reviewed and pleagentsareavailable,acomparisonisprovidedontheiruse
compiledpublishedreportsthroughaseriesofcomputerized in various settings within clinical practice.
literature searches of the English-language literature since
2002andafinalmanualsearchofselectedarticles.Detailsof
1.2. Document Review and Approval
the specific searches conducted for particular sections are
provided when appropriate. Detailed evidence tables were (UPDATED)
developed whenever necessary with the specific criteria The 2007 document was reviewed by 2 outside reviewers
outlined in the individual sections. The recommendations nominated by each of the ACC and AHA and by 49 peer
made were based primarily on these published data. The reviewers.
weightoftheevidencewasrankedhighest(A)tolowest(C). The 2012 focused update was reviewed by 2 official
The final recommendations for indications for a diagnostic reviewerseachnominatedbytheACCFandtheAHA,aswell
procedure,aparticulartherapy,oraninterventioninpatients as 1 or 2 reviewers each from the American College of
with UA/NSTEMI summarize both clinical evidence and Emergency Physicians, Society for Cardiovascular Angiog-
expert opinion. raphy and Interventions, and Society of Thoracic Surgeons,
The2007committeeconsistedofacknowledgedexpertsin and 29 individual content reviewers, including members of
generalinternalmedicinerepresentingtheAmericanCollege theACCFInterventionalScientificCouncil.Theinformation
of Physicians (ACP), family medicine from the American on reviewers’ RWI was distributed to the writing group and
AcademyofFamilyPhysicians(AAFP),emergencymedicine is published in this document (Appendix 5).
from the American College of Emergency Physicians This document was approved for publication by the gov-
(ACEP), thoracic surgery from the Society of Thoracic erningbodiesoftheACCFandtheAHAandendorsedbythe
Surgeons (STS), interventional cardiology from the Society American College of Emergency Physicians, Society for
for Cardiovascular Angiography and Interventions (SCAI), Cardiovascular Angiography and Interventions, and Society
andgeneralandcriticalcarecardiology,aswellasindividuals of Thoracic Surgeons.
with recognized expertise in more specialized areas, includ-
ing noninvasive testing, preventive cardiology, coronary in-
tervention, and cardiovascular surgery. Both the academic 1.3. Purpose of These Guidelines
and private practice sectors were represented. These guidelines address the diagnosis and management of
The 2007 guidelines overlap several previously published patients with UA and the closely related condition of
ACC/AHA practice guidelines, including the ACC/AHA NSTEMI. These life-threatening disorders are a major cause
Guidelines for the Management of Patients With ST- of emergency medical care and hospitalization in the United
Elevation Myocardial Infarction (8), the ACC/AHA/SCAI States. In 2004, the National Center for Health Statistics
2005GuidelineUpdateforPercutaneousCoronaryInterven- reported1,565,000hospitalizationsforprimaryorsecondary
tion(9),theAHA/ACCGuidelinesforSecondaryPrevention diagnosisofanacutecoronarysyndrome(ACS),669,000for
for Patients With Coronary and Other Atherosclerotic Vas- UA and 896,000 for myocardial infarction (MI) (12). The
cular Disease: 2006 Update (10), and the ACC/AHA 2002 average age of a person having a first heart attack is 65.8
Guideline Update for the Management of Patients With years for men and 70.4 years for women, and 43% of ACS
Chronic Stable Angina (11). patientsofallagesarewomen.In2003,therewere4,497,000
Forthe2012focusedupdate,membersofthe2011Unsta- visits to US emergency departments (EDs) for primary
ble Angina/Non–ST-Elevation Myocardial Infarction (UA/ diagnosisofCVD(12).Theprevalenceofthispresentationof
NSTEMI)focusedupdatewritinggroupwereinvitedandall CVD ensures that many health care providers who are not
agreed to participate (referred to as the 2012 focused update cardiovascular specialists will encounter patients with UA/
writing group). Members were required to disclose all RWI NSTEMI in the course of the treatment of other diseases,
relevant to the data under consideration. The 2012 writing especiallyinoutpatientandEDsettings.Theseguidelinesare
groupincludedrepresentativesfromtheACCF,AHA,Amer- intendedtoassistbothcardiovascularspecialistsandnonspe-
ican Academy of Family Physicians, American College of cialists in the proper evaluation and management of patients
Emergency Physicians, American College of Physicians, with an acute onset of symptoms suggestive of these condi-
Society for Cardiovascular Angiography and Interventions, tions. These clinical practice guidelines also provide recom-
and Society of Thoracic Surgeons. mendations and supporting evidence for the continued man-
For the 2012 focused update, late-breaking clinical trials agement of patients with these conditions in both inpatient
presented at the 2008, 2009, and 2010 annual scientific and outpatient settings. The diagnostic and therapeutic strat-
meetings of the ACC, AHA, and European Society of egies that are recommended are supported by the best
Cardiology, as well as selected other data through October available evidence and expert opinion. The application of
2011, were reviewed by the standing guideline writing these principles with carefully reasoned clinical judgment
committeealongwiththeparentTaskForcetoidentifythose reducesbutdoesnoteliminatetheriskofcardiacdamageand
trials and other key data that may impact guideline recom- death in patients who present with symptoms suggestive of
mendations.Onthebasisofthecriteria/considerationsnoted UA/NSTEMI. Appendix 3 lists the abbreviations found in
above, and the approval of new oral antiplatelets, the 2012 this document.
e186 Andersonetal. JACCVol.61,No.23,2013
UA/NSTEMIGuideline:2012UpdateIncorporated June11,2013:e179–347
1.4. Overview of the necrosis, such as the MB isoenzyme of creatine kinase
Acute Coronary Syndromes (CK-MB) or troponin, also is not considered here.
PatientswithMIandwithdefiniteischemicECGchanges
1.4.1. Definition of Terms forwhomacutereperfusiontherapyisnotsuitableshouldbe
Unstable angina/NSTEMI constitutes a clinical syndrome diagnosed and managed as patients with UA. The residual
subset of the ACS that is usually, but not always, caused by groupofpatientswithaninitialdiagnosisofACSwillinclude
atheroscleroticCADandisassociatedwithanincreasedrisk many patients who will ultimately be proven to have a
ofcardiacdeathandsubsequentMI.InthespectrumofACS, non-cardiaccausefortheinitialclinicalpresentationthatwas
UA/NSTEMI is defined by electrocardiographic (ECG) ST- suggestiveofACS.Therefore,attheconclusionoftheinitial
segment depression or prominent T-wave inversion and/or evaluation, which is frequently performed in the ED but
positivebiomarkersofnecrosis(e.g.,troponin)intheabsence sometimesoccursduringtheinitialhoursofinpatienthospi-
ofST-segmentelevationandinanappropriateclinicalsetting talization,eachpatientshouldhaveaprovisionaldiagnosisof
(chest discomfort or anginal equivalent) (Table 2, Figure 1). 1)ACS(Figure1),whichinturnisclassifiedasa)STEMI,a
The results of angiographic and angioscopic studies suggest condition for which immediate reperfusion therapy (fibrino-
thatUA/NSTEMIoftenresultsfromthedisruptionorerosion lysisorpercutaneouscoronaryintervention[PCI])shouldbe
of an atherosclerotic plaque and a subsequent cascade of considered, b) NSTEMI, or c) UA (definite, probable, or
pathological processes that decrease coronary blood flow. possible);2)anon-ACScardiovascularcondition(e.g.,acute
MostpatientswhodieduringUA/NSTEMIdosobecauseof pericarditis); 3) a noncardiac condition with another specific
suddendeathorthedevelopment(orrecurrence)ofacuteMI. disease (e.g., chest pain secondary to esophageal spasm); or
The efficient diagnosis and optimal management of these 4) a noncardiac condition that is undefined. In addition, the
patientsmustderivefrominformationreadilyavailableatthe initialevaluationshouldbeusedtodetermineriskandtotreat
time of the initial clinical presentation. The clinical presen- life-threatening events.
tation of patients with a life-threatening ACS often overlaps Intheseguidelines,UAandNSTEMIareconsideredtobe
thatofpatientssubsequentlyfoundnottohaveCAD.More- closely related conditions whose pathogenesis and clinical
over,someformsofMIcannotalwaysbedifferentiatedfrom presentationsaresimilarbutofdifferingseverity;thatis,they
UA at the time of initial presentation. differ primarily in whether the ischemia is severe enough to
“Acute coronary syndrome” has evolved as a useful cause sufficient myocardial damage to release detectable
operational term to refer to any constellation of clinical quantitiesofamarkerofmyocardialinjury,mostcommonly
symptoms that are compatible with acute myocardial isch- troponin I (TnI), troponin T (TnT), or CK-MB. Once it has
emia (Figure 1). It encompasses MI (ST-segment elevation been established that no biomarker of myocardial necrosis
and depression, Q wave and non-Q wave) and UA. These has been released (based on 2 or more samples collected at
guidelinesfocuson2componentsofthissyndrome:UAand least6hapart,withareferencelimitofthe99thpercentileof
NSTEMI. In practice, the term “possible ACS” is often the normal population) (18), the patient with ACS may be
assigned first by ancillary personnel, such as emergency consideredtohaveexperiencedUA,whereasthediagnosisof
medicaltechniciansandtriagenurses,earlyintheevaluation NSTEMI is established if a biomarker has been released.
Markers of myocardial injury can be detected in the blood-
process. A guideline of the National Heart Attack Alert
stream with a delay of up to several hours after the onset of
Program (16) summarizes the clinical information needed to
ischemic chest pain, which then allows the differentiation
make the diagnosis of possible ACS at the earliest phase of
between UA (i.e., no biomarkers in circulation; usually
clinical evaluation (Table 2). The implication of this early
transient, if any, ECG changes of ischemia) and NSTEMI
diagnosis for clinical management is that a patient who is
(i.e.,elevatedbiomarkers).Thus,atthetimeofpresentation,
considered to have an ACS should be placed in an environ-
patientswithUAandNSTEMIcanbeindistinguishableand
ment with continuous ECG monitoring and defibrillation
therefore are considered together in these guidelines.
capability, where a 12-lead ECG can be obtained expedi-
tiously and definitively interpreted, ideally within 10 min of 1.4.2. Pathogenesis of UA/NSTEMI
arrivalintheED.Themosturgentpriorityofearlyevaluation Theseconditionsarecharacterizedbyanimbalancebetween
is to identify patients with ST-elevation MI (STEMI) who myocardial oxygen supply and demand. They are not a
should be considered for immediate reperfusion therapy and specificdisease,suchaspneumococcalpneumonia,butrather
to recognize other potentially catastrophic causes of patient a syndrome, analogous to hypertension. A relatively few
symptoms, such as aortic dissection. nonexclusive causes are recognized (19) (Table 3).
Patients diagnosed as having STEMI are excluded from Themostcommonmechanismsinvolveanimbalancethat
management according to these guidelines and should be is caused primarily by a reduction in oxygen supply to the
managedasindicatedaccordingtotheACC/AHAGuidelines myocardium,whereaswiththefifthmechanismnotedbelow,
for the Management of Patients With ST-Elevation Myocar- the imbalance is principally due to increased myocardial
dialInfarction (8,17). Similarly, management of electrocar- oxygen requirements, usually in the presence of a fixed,
diographic true posterior MI, which can masquerade as restricted oxygen supply:
NSTEMI, is covered in the STEMI guidelines (8). The The most common cause of UA/NSTEMI is reduced
managementofpatientswhoexperienceperiproceduralmyo- myocardial perfusion that results from coronary artery nar-
cardial damage, as reflected in the release of biomarkers of rowing caused by a thrombus that developed on a disrupted
JACCVol.61,No.23,2013 Andersonetal. e187
June11,2013:e179–347 UA/NSTEMIGuideline:2012UpdateIncorporated
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:
XCentral/substernalcompressionorcrushingchestpain
XPressure,tightness,heaviness,cramping,burning,achingsensation
XUnexplainedindigestion,belching,epigastricpain
XRadiatingpaininneck,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.93-3278(6).
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.
atheroscleroticplaqueandisusuallynonocclusive.Microem- NSTEMI. Dynamic coronary obstruction can also be caused
bolization of platelet aggregates and components of the by diffuse microvascular dysfunction; for example, due to
disruptedplaquearebelievedtoberesponsiblefortherelease endothelialdysfunctionortheabnormalconstrictionofsmall
of myocardial markers in many of these patients. An occlu- intramural resistance vessels. Coronary spasm also is the
sive thrombus/plaque also can cause this syndrome in the presumed mechanism underlying cocaine-induced UA/
presence of an extensive collateral blood supply. NSTEMI.
The most common underlying molecular and cellular AthirdcauseofUA/NSTEMIisseverenarrowingwithout
pathophysiologyofdisruptedatheroscleroticplaqueisarterial
spasm or thrombus. This occurs in some patients with
inflammation,causedbynoninfectious(e.g.,oxidizedlipids)
progressive atherosclerosis or with restenosis after a PCI.
and, possibly, infectious stimuli, which can lead to plaque
A fourth cause of UA/NSTEMI is coronary artery dissec-
expansionanddestabilization,ruptureorerosion,andthrom-
tion (e.g., as a cause of ACS in peripartal women).
bogenesis. Activated macrophages and T lymphocytes lo-
The fifth mechanism is secondary UA, in which the
cated at the shoulder of a plaque increase the expression of
precipitating condition is extrinsic to the coronary arterial
enzymes such as metalloproteinases that cause thinning and
bed. Patients with secondary UA usually, but not always,
disruption of the plaque, which in turn can lead to UA/
haveunderlyingcoronaryatheroscleroticnarrowingthatlim-
NSTEMI.
its myocardial perfusion, and they often have chronic stable
Alesscommoncauseisdynamicobstruction,whichmaybe
triggered by intense focal spasm of a segment of an epicardial angina. Secondary UA is precipitated by conditions that
coronary artery (Prinzmetal’s angina) (see Section 6.7). This 1) increase myocardial oxygen requirements, such as fever,
local spasm is caused by hypercontractility of vascular tachycardia,orthyrotoxicosis;2)reducecoronarybloodflow,
smooth muscle and/or by endothelial dysfunction. Large- such as hypotension; or 3) reduce myocardial oxygen deliv-
vessel spasm can occur on top of obstructive or destabilized ery, such as anemia or hypoxemia. These causes of UA/
plaque, resulting in angina of “mixed” origin or UA/ NSTEMI are not mutually exclusive.
e188 Andersonetal. JACCVol.61,No.23,2013
UA/NSTEMIGuideline:2012UpdateIncorporated June11,2013:e179–347
Figure1. AcuteCoronarySyndromes.Thetophalfofthefigureillustratesthechronologyoftheinterfacebetweenthepatientandthe
clinicianthroughtheprogressionofplaqueformation,onset,andcomplicationsofUA/NSTEMI,alongwithrelevantmanagementcon-
siderationsateachstage.Thelongitudinalsectionofanarterydepictsthe“timeline”ofatherogenesisfrom1)anormalarteryto2)le-
sioninitiationandaccumulationofextracellularlipidintheintima,to3)theevolutiontothefibrofattystage,to4)lesionprogression
withprocoagulantexpressionandweakeningofthefibrouscap.Anacutecoronarysyndrome(ACS)developswhenthevulnerableor
high-riskplaqueundergoesdisruptionofthefibrouscap(5);disruptionoftheplaqueisthestimulusforthrombogenesis.Thrombusre-
sorptionmaybefollowedbycollagenaccumulationandsmoothmusclecellgrowth(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.*Positiveserumcardiac
marker.ModifiedwithpermissionfromLibbyP.Currentconceptsofthepathogenesisoftheacutecoronarysyndromes.Circulation
2001;104:365(7);©2001Lippincott,Williams&Wilkins;TheLancet,358,HammCW,BertrandM,BraunwaldE.Acutecoronarysyn-
dromewithoutSTelevation:implementationofnewguidelines,1553–8.Copyright2001,withpermissionfromElsevier(8);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.