AcuteMyocardialInfarctionAcuteMyocardialInfarctionDEFINITION

Acutemyocardialinfarction(MI)isdefinedasdeathornecrosisofmyocardialcells.Itisadiagnosisattheendofthespectrumofmyocardialischemiaoracutecoronarysyndromes.Myocardialinfarctionoccurswhenmyocardialischemiaexceedsacriticalthresholdandoverwhelmsmyocardialcellularrepairmechanismsthataredesignedtomaintainnormaloperatingfunctionandhemostasis.Ischemiaatthiscriticalthresholdlevelforanextendedtimeperiodresultsinirreversiblemyocardialcelldamageordeath.1-3DEFINITIONAcutemyocardialinDEFINITION(Cntd.)Myocardialinfarctioncanbesubcategorizedonthebasisofanatomic,morphologic,anddiagnosticclinicalinformation.Fromananatomicormorphologicstandpoint,thetwotypesofMIaretransmuralandnontransmural.AtransmuralMIischaracterizedbyischemicnecrosisofthefullthicknessoftheaffectedmusclesegment(sInanontransmuralMI,theareaofischemicnecrosisislimitedtoeithertheendocardiumortheendocardiumandmyocardium.ThepresenceorabsenceofQwavesdoesnotdistinguishatransmuralfromanon-transmuralMIasdeterminedbypathology.4DEFINITION(Cntd.)MyocardialiDEFINITION(Cntd.II)AmorecommonclinicaldiagnosticclassificationschemeisalsobasedonECGfindingsasameansofdistinguishingbetweentwotypesofMI—onethatismarkedbySTelevationSTEMIandonethatisnotNSTEMIThedistinctionbetweenanST-elevationMIandanon-ST-elevationMIalsodoesnotdistinguishatransmuralfromanon-transmuralMI.ThepresenceofQwavesorSTsegmentelevationisassociatedwithhigherearlymortalityandmorbidity;DEFINITION(Cntd.II)AmorecoACSTypesACSTypesPREVALENCE

Ingeneral,MIcanoccuratanyage,butitsincidenceriseswithage.Theactualincidenceisdependentuponpredisposingriskfactorsforatherosclerosis,whicharediscussedbelow.Approximately50%ofallMI'sintheUSoccurinpeopleyoungerthan65yearsofage.However,inthefuture,asdemographicsshiftandthemeanageofthepopulationincreases,alargerpercentageofpatientspresentingwithMIwillbeolderthan65yearsPREVALENCEIngeneral,MIcanDIAGNOSIS

IdentifyingapatientwhoiscurrentlyexperiencingaMIcanbeextremelystraightforward,verydifficult,orsomewhereinbetween.AstraightforwarddiagnosisofMIcanusuallybemadeinpatientswhohaveanumberofatheroscleroticriskfactorsalongwiththepresenceofsymptomsconsistentwithalackofbloodflowtotheheart.PatientswhosuspectthattheyarehavingaMIusuallypresenttoanemergencydepartment.Onceapatient'sclinicalpictureraisesasuspicionofaMI,severalconfirmatorytestscanbeperformedrapidly.ThesetestsincludeECG,bloodtesting,andechocardiography.DIAGNOSISIdentifyingapatienHistoryPRODROMALSYMPTOMS:historyremainsofsubstantialvalueinestablishingadiagnosis.Resemblesclassicanginapectorisbutitoccursatrestorwithlessactivitythanusualandcanthereforebeclassifiedasunstableangina.OfthepatientswithAMIpresentingwithprodromalsymptomsofunstableangina,approximatelyonethirdhavehadsymptomsfrom1to4weeksbeforehospitalization;intheremainingtwothirds,symptomspredatedadmissionby1weekorless,withonethirdofthesepatientshavinghadsymptomsfor24hoursorless.HistoryPRODROMALSYMPTOMS:SIGNSANDSYMPTOMSAcuteMImayhaveuniquepresentationsinindividualpatients.Thedegreeofsymptomsrangesfromnoneatalltosuddencardiacdeath.AnasymptomaticMIisnotnecessarilylessseverethanasymptomaticevent;butpatientswhoexperienceasymptomaticMI'saremorelikelytobediabetic.Chestpaindescribedasapressuresensation,fullness,orsqueezinginthemidportionofthethoraxRadiationofchestpainintothejaw/teeth,shoulder,arm,and/orbackAssociateddyspneaorshortnessofbreathAssociatedepigastricdiscomfortwithorwithoutnauseaandvomitingAssociateddiaphoresisorsweatingSyncopeornear-syncopewithoutothercauseImpairmentofcognitivefunctionwithoutothercauseAMImayoccuratanytimeoftheday,butmostappeartobeclusteredaroundtheearlyhoursofthemorningand/orareassociatedwithdemandingphysicalactivity.Approximately50%ofpatientshavesomewarningsymptoms(anginapectorisorananginalequivalent)priortotheinfarct.4SIGNSANDSYMPTOMSAcuteMImayNatureofPainThepainofAMIisvariableinintensity;inmostpatientsitissevereandinsomeinstancesintolerable.Thepainisprolonged,usuallylastingformorethan30minutesandfrequentlyforanumberofhours.Describedasconstricting,crushing,oppressing,orcompressing;oftenthepatientcomplainsofasensationofaheavyweightorasqueezinginthechest.Althoughthediscomfortistypicallydescribedasachoking,viselike,orheavypain,itmayalsobecharacterizedasastabbing,knifelike,boring,orburningdiscomfort.Thepainisusuallyretrosternalinlocation,spreadingfrequentlytobothsidesoftheanteriorchest,withpredilectionfortheleftside.Oftenthepainradiatesdowntheulnaraspectoftheleftarm,producingatinglingsensationintheleftwrist,hand,andfingers.Somepatientsnoteonlyadullacheornumbnessofthewristsinassociationwithseveresubsternalorprecordialdiscomfort.Insomeinstances,thepainofAMImaybeginintheepigastriumandsimulateavarietyofabdominaldisorders,afactthatoftencauses<MI>tobemisdiagnosedas“indigestionInotherpatientsthediscomfortofAMIradiatestotheshoulders,upperextremities,neck,jaw,andinterscapularregion,againusuallyfavoringtheleftside.Inpatientswithpreexistinganginapectoris,thepainofinfarctionusuallyresemblesthatofanginawithrespecttolocation.However,itisgenerallymuchmoresevere,lastslonger,andisnotrelievedbyrestandnitroglycerin.Insomepatients,particularlytheelderly,AMIismanifestedclinicallynotbychestpainbutratherbysymptomsof<acute>leftventricularfailureandchesttightnessorbymarkedweaknessorfranksyncope.98a,98bThesesymptomsmaybeaccompaniedbydiaphoresis,nausea,andvomiting.Therecognitionthatpainimpliesischemiaandnotinfarctionheightenstheimportanceofseekingwaystorelievetheischemia,forwhichthepainisamarker.ThisfindingsuggeststhattheclinicianshouldnotbecomplacentaboutongoingcardiacpainunderanycircumstancesNatureofPainThepainofAMIOthersymptomsNauseaandvomitingoccurinmorethan50percentofpatientswithtransmural<MI>andseverechestpain,presumablyowingtoactivationofthevagalreflexortostimulationofleftventricularreceptorsaspartoftheBezold-Jarischreflex.Thesesymptomsoccurmorecommonlyinpatientswithinferior<MI>thaninthosewithanterior<MI>.Occasionally,apatientcomplainsofdiarrheaoraviolenturgetoevacuatethebowelsduringthe<acute>phaseof<MI>.Othersymptomsincludefeelingsofprofoundweakness,dizziness,palpitations,coldperspiration,andasenseofimpendingdoom.Onoccasion,symptomsarisingfromanepisodeofcerebralembolismorothersystemicarterialembolismarethefirstsignsofAMI.Theaforementionedsymptomsmayormaynotbeaccompaniedbychestpain.OthersymptomsNauseaandvomitAtypicalpresentationsofAMI(1)congestiveheartfailure—beginningdenovoorworseningofestablishedfailure;(2)classicanginapectoriswithoutaparticularlysevereorprolongedattack;(3)atypicallocationofthepain;(4)centralnervoussystemmanifestations,resemblingthoseofstroke,secondarytoasharpreductionincardiacoutputinapatientwithcerebralarteriosclerosis;(5)apprehensionandnervousness;(6)suddenmaniaorpsychosis;(7)syncope;(8)overwhelmingweakness;(9)<acuteindigestion;and(10)peripheralembolization.AtypicalpresentationsofAMI(SILENT<MI>Populationstudiessuggestthatbetween20and60percentofnonfatal<MIs>areunrecognizedbythepatientandarediscoveredonlyonsubsequentroutineECGorpostmortemexaminations.Oftheseunrecognizedinfarctions,approximatelyhalfaretrulysilent,withthepatientsunabletorecallanysymptomswhatsoever.Theotherhalfofpatientswithso-calledsilentinfarctioncanrecallaneventcharacterizedbysymptomscompatiblewith<acute>infarctionwhenleadingquestionsareposedaftertheECGabnormalitiesarediscovered.Unrecognizedorsilentinfarctionoccursmorecommonlyinpatientswithoutantecedentanginapectorisandinpatientswithdiabetes98aandhypertension.102SILENT<MI>PopulationstudiesDifferentialDiagnosisThepainofAMImaystimulatethepainof<acute>pericarditis(seeChaps.3and50),whichisusuallyassociatedwithsomepleuriticfeatures;thatis,itisaggravatedbyrespiratorymovementsandcoughingandofteninvolvestheshoulder,ridgeofthetrapezius,andneck.Animportantfeaturethatdistinguishespericardialpainfromischemicdiscomfortisthatischemicdiscomfortneverradiatestothetrapeziusridge,Thepaindueto<acute>dissectionoftheaortaisusuallylocalizedinthecenterofthechest,isextremelysevereanddescribedbythepatientasa“ripping”or“tearing”sensation,isatitsmaximalintensityshortlyafteronset,persistsformanyhours,andoftenradiatestothebackorthelowerextremities.Oftenoneormoremajorarterialpulsesareabsent.Painarisingfromthecostochondralandchondrosternalarticulationsmaybeassociatedwithlocalizedswellingandredness;itisusuallysharpand“darting”andischaracterizedbymarkedlocalizedtenderness.EpisodesofretrosternaldiscomfortinducedbyperistalsisinpatientswithincreasedesophagealstiffnessandalsoepisodesofsustainedesophagealcontractioncanmimicthepainofAMI.100,101DifferentialDiagnosisPathophysiologyMechanismsofOcclusion:MostMIsarecausedbyadisruptioninthevascularendotheliumassociatedwithanunstableatheroscleroticplaquethatstimulatestheformationofanintracoronarythrombus,whichresultsincoronaryarterybloodflowocclusion.Ifsuchanocclusionpersistslongenough(20to40min),irreversiblemyocardialcelldamageandcelldeathwilloccur.PathophysiologyMechanismsofOPathophysiology(Cntd.)Thedevelopmentofatheroscleroticplaqueoccursoveraperiodofyearstodecades.Theinitialvascularlesionleadingtothedevelopmentofatheroscleroticplaqueisnotknownwithcertainty.Thetwoprimarycharacteristicsoftheclinicallysymptomaticatheroscleroticplaqueareafibromuscularcapandanunderlyinglipid-richcore.Plaqueerosionmayoccurduetotheactionsofmetalloproteasesandthereleaseofothercollagenasesandproteasesintheplaque,whichresultinthinningoftheoverlyingfibromuscularcap.Hemodynamicforcesappliedtothearterialsegment,canleadtoadisruptionoftheendotheliumandfissuringorruptureofthefibromuscularcap.asiteotherwiseknownastheplaque's"shoulderregion."Pathophysiology(Cntd.)ThedevVulnerablePlaqueVulnerablePlaque急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件PathogenesisOFAMIPathogenesisOFAMI急性心肌梗死AMI診斷和治療進展(英文課件MechanismsofMyocardialDamage:TheseverityofanMIisdependentonthreefactors:Theleveloftheocclusioninthecoronaryartery,ThelengthoftimeoftheocclusionThepresenceorabsenceofcollateralcirculationThedeathofmyocardialcellsfirstoccursintheareaofmyocardiumthatmostdistaltothearterialbloodsupply—thatis,theendocardium.Asthedurationoftheocclusionincreases,theareaofmyocardialcelldeathenlargesMechanismsofMyocardialDamagRiskFactors:

SixprimaryriskfactorshavebeenidentifiedwiththedevelopmentofatheroscleroticcoronaryarterydiseaseandMI:hyperlipidemia,diabetesmellitus,hypertension,Smoking(Tobaccouse),malegender,andfamilyhistoryofatheroscleroticarterialdisease.Thepresenceofanyriskfactorisassociatedwithdoublingtherelativeriskofdevelopingatheroscleroticcoronaryarterydisease.RiskFactors:

SixprimaryriskDIAGNOSIS(Cntd.)Electrocardiography:ThefirsttestistheECG,whichmaydemonstratethataMIisinprogressorhasalreadyoccurred(Figure1).BloodTests:Bloodtestscanbeperformedtodetectevidenceofmyocardialcelldeath.Livingheartcellscontaincertainenzymesandproteins(eg,creatinephosphokinase,troponin,andmyoglobin)withincellmembranesassociatedwithspecializedcellularfunctionssuchascontraction.Whenaheartmuscledies,cellularmembranesloseintegrityandintracellularenzymesandproteinsslowlyleakintothebloodstream.Theseenzymesandproteinscanbedetectedbyabloodsampleanalysis.Theconcentrationofenzymesinabloodsample—andmoreimportantly,thechangesinconcentrationfoundinsamplestakenovertime—correlateswiththeamountofheartmusclethathasdiedDIAGNOSIS(Cntd.)ElectrocardiogAcuteMIAcuteMIDIAGNOSIS(Cntd.)Echocardiography:Anechocardiogrammaybeperformedinordertocompareareasoftheleftventriclethatarecontractingnormallywiththosethatarenot.Oneoftheearliestprotectivemechanismsofmyocardialcellsutilizedduringlimitedbloodflowisto"turnoff"theenergyrequiring"machinery"forcontraction,thismechanismbeginswithinminutesafternormalbloodflowisinterrupted.TheechocardiogramcanbehelpfulinidentifyingwhichportionoftheheartisaffectedbyaMI,andwhichofthecoronaryarteriesismostlikelytobeoccluded.Unfortunately,thepresenceofwallmotionabnormalitiesontheechocardiogrammaybeduetoanacuteMIorprevious(old)MIorothermyopathicprocesses.Thus,theusefulnessofechocardiographyinthediagnosisofMIislimited.DIAGNOSIS(Cntd.)Echocardiograp急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件DIAGNOSIS(Cntd.)NormalValuesofBloodTeststo

DetectMyocardialInfarctionAnalysisNormalRangeTotalcreatinine

phosphokinase(CPK)30-200U/LCPK,MBfraction0.0-8.8ng/mLCPK,MBfractionpercentoftotalCPK0-4%CPK,MB2fraction<1U/LTroponinI0.0-0.4ng/mLTroponinT0.0-0.1ng/mLDIAGNOSIS(Cntd.)NormalValues急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件CK-MB,TROPONINSCRP.

CK-MB,TROPONINSCRP.TimeisMuscleTimeisMuscle急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件THERAPY

ThegoalsoftherapyinAMIaretheexpedientrestorationofnormalcoronarybloodflowandthemaximumsalvageoffunctionalmyocardium.Thesegoalscanbemetbyanumberofmedicalinterventionsandadjunctivetherapies.Theprimaryobstaclestoachievingthesegoalsarethepatient'sfailuretoquicklyrecognizeMIsymptomsandthedelayinseekingmedicalattention.Whenpatientspresenttoahospital,thereareavarietyofinterventionstoachievetreatmentgoals.THERAPYThegoalsoftherapyiCORONARYCAREUNITS

CORONARYCAREUNITS

GeneralTreatmentMeasures

ASPIRINCONTROLOFCARDIACPAINAnalgesicsNITRATESBETA-ADRENOCEPTORBLOCKERSOXYGENLimitationofInfarctSizeGeneralTreatmentMeasures

ASPTHERAPY(Cntd.)AntiplateletAgents:Aspirininadoseofatleast160mgandupto325mgshouldbeadministeredimmediatelyonrecognitionofMIsignsandsymptomsandcontinueddailyindefinitely.4Thenidusofanocclusivecoronarythrombusistheadhesionofasmallcollectionofactivatedplateletsatthesiteofintimaldisruptioninan"unstable"atheroscleroticplaque.Aspirininterfereswithfunctionoftheenzymecyclo-oxygenaseandinhibitstheformationofthromboxaneA2.Withinminutes,aspirinpreventsadditionalplateletactivationandinterfereswithplateletOtherantiplateletagents—includingclopidogrel,ticlopidine,anddipyridamole-havenotbeenshowninanylarge-scaletrialtobesuperiortoaspirininMI.Theseotherantiplateletagents(specificallyclopidogrel)maybeusefulforpatientswhohaveatrueallergytoaspirinandforpatientswithknownresistancetoaspirin'seffects.11-13THERAPY(Cntd.)AntiplateletAgTHERAPY(Cntd.)SupplementalOxygen:TherearenopublishedstudiesdemonstratingthatoxygentherapyreducesmortalityormorbidityofaMI.

Nitrates:Beta-blockers:Beta-blockertherapyisrecommendedwithin12hoursofMIsymptomsandiscontinuedindefinitely.Treatmentwithabeta-blockerreducesMImortality—presumablybydecreasingtheincidenceofarrhythmogenicdeath.Betablockadedecreasestherateandforceofmyocardialcontractionanddecreasesoverallmyocardialoxygendemand.InthesettingofreducedoxygensupplyinMI,thereductioninoxygendemandprovidedbybetablockademinimizesmyocardialinjuryanddeath.

THERAPY(Cntd.)SupplementalOxSelectiveBeta-1-blockers

SelectiveBeta-1-blockers急性心肌梗死AMI診斷和治療進展(英文課件Heparin:UnfractionatedHeparin:IntravenousunfractionatedheparinisrecommendedinpatientswithaMIwhoundergopercutaneousrevascularizationorfibrinolytictherapywithalteplase.IntravenousunfractionatedheparinisalsorecommendedinpatientswithaMIwhoreceivefibrinolytictherapywithanon-selectivefibrinolyticagent(urokinase,streptokinase,anistreplase)andareatincreasedriskforsystemicemboli(priorembolicevent,largeoranteriorwallinfarction,knownleftventricularthrombus,oratrialfibrillation).4

Heparin:Low-molecular-weightHeparin(LMWH)LMWHcanbeadministeredtoMIpatientsnottreatedwithfibrinolytictherapythathavenocontra-indicationtoheparin.4TheLMWHclassofdrugsincludesseveralagentsthathavedistinctlydifferentanticoagulanteffects.Theseeffectscanbecharacterizedbyagivenagent'sratioofactivityagainstfactorsXaandIIa.LMWHshavebeenproventobeeffectiveintreatingacutecoronarysyndromesthatarecharacterizedbyunstableanginaandnon-Q-waveMI.Theirfixeddosesareeasytoadminister,andlaboratorytestingtomeasuretheirtherapeuticeffectisnotnecessary.Low-molecular-weightHeparin(Fibrinolytics:FibrinolytictherapyisindicatedforpatientswithapresentationcompatiblewithMIandSTsegmentelevationgreaterthan0.1mVin2contiguousEKGleads,ornewonsetofabundlebranchblock,whopresentlessthan12hoursbutnotmorethan24hoursaftersymptomonset.4RestorationofcoronarybloodflowinMIcanalsobeaccomplishedpharmacologicallywiththeuseofafibrinolyticagent.Asaclass,theplasminogenactivatorshavebeenshowntorestorecoronarybloodflowin50%to80%ofMIpatients.ThesuccessfuluseoffibrinolyticagentsprovidesadefinitesurvivalbenefitthatismaintainedforyearsAfibrinolyticismosteffectivewhenthe"door-to-needle"timeis30minutesorlessFibrinolytics:急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件PercutaneousCoronaryIntervention:Percutaneouscoronaryinterventionisanalternativetherapytofibrinolysisifperformedbyaskilledoperatorsupportedbyexperiencedpersonnelperformedinawell-equippedcatheterizationlaboratory.PercutaneousCoronaryIntervenPercutaneousCoronaryIntervention:TheperformancestandardforprimarypercutaneousinterventionasaMItherapyisa"door-to-balloon"timeof90minutes(±30minutes).4RestorationofcoronarybloodflowinaMIcanbeaccomplishedmechanicallybypercutaneouscoronaryintervention(PCI).MechanicalrevascularizationbyPCIisusedasaprimarytherapyinmanywell-equippedmedicalcentersandasanalternativetofibrinolysiswhenfibrinolysisisnotclearlyindicatedorcontraindicated.PCIcansuccessfullyrestorecoronarybloodflowin90%to95%ofaMIpatientsPCIprovidesadefinitesurvivaladvantageoverfibrinolysisforMIpatientswhoareincardiogenicshockPercutaneousCoronaryIntervenTIMIgradingsystem:Grade0=completeocclusionoftheinfarct-relatedartery.Grade1=somepenetrationofthecontrastmaterialbeyondthepointofobstructionbutwithoutperfusionofthedistalcoronarybed.Grade2=perfusionoftheentireinfarctvesselintothedistalbedbutwithdelayedflowcomparedwithanormalartery.Grade3=fullperfusionoftheinfarctvesselwithnormalflowTIMIgradingsystem:急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件GlycoproteinIIb/IIIaAntagonists:GlycoproteinIIb/IIIareceptorsonplateletsbindtofibrinogeninthefinalcommonpathwayofplateletaggregation.AntagoniststoglycoproteinIIb/IIIareceptorsarepotentinhibitorsofplateletaggregation.TheuseofintravenousglycoproteinIIb/IIIainhibitorsduringPCIandinpatientswithMIandacutecoronarysyndromeshavebeenshowntoreducethecompositeendpointofdeath,reinfarction,andtheneedfortarget-lesionrevascularizationatfollowupGlycoproteinIIb/IIIaAntagoniSurgicalRevascularization:Emergentorurgentcoronaryarterybypassgraftsurgeryiswarrantedinthesettingoffailedpercutaneousinterventioninpatientswithhemodynamicinstabilityandcoronaryanatomyamenabletosurgicalgrafting.SurgicalrevascularizationisalsoindicatedinthesettingofmechanicalcomplicationsofMIsuchasventricularseptaldefect,freewallrupture,oracutemitralregurgitation.4

Restorationofcoronarybloodflowwithemergencycoronaryarterybypassgrafting(CABG)canlimitmyocardialinjuryandcelldeathifitisperformedwithin2or3hoursofsymptomonsetSurgicalRevascularization:AngiotensinConvertingEnzyme

Inhibitors(ACEI):OralangiotensinconvertingenzymeinhibitorsarerecommendedinMIpatientswithinthefirst24hoursofsymptomonset,ifnocontra-indicationsexist.4Contra-indicationstoACEIuseincludehypotensionanddecliningrenalfunctionwithACEIuse.TheuseofanACEI4to6weeksafterpresentationofMIisrecommendedforpatientswithcongestiveheartfailure,leftventriculardysfunction(ejectionfraction<0.40),hypertension,ordiabetesAngiotensinConvertingEnzyme急性心肌梗死AMI診斷和治療進展(英文課件CalciumAntagonistsGLUCOSE-INSULIN-POTASSIUM.CalciumAntagonists急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件PostMIManagementCardiacStressTesting:Cardiacstresstestingpost-MIhasestablishedvalueinriskstratificationandassessmentoffunctionalcapacityLipidManagement:Allpost-MIpatientsshouldbeonanAmericanHeartAssociationStepIIdiet(<200mgcholesterol/day,<7%oftotalcaloriesfromsaturatedfats).Post-MIpatientswithLDL-cholesterollevels>100mg/dLonaStepIIdietarerecommendedtobeondrugtherapytolowerLDL-cholesterollevels<100mg/dL.Post-MIpatientswithHDL-cholesterollevels<35mg/dLonaStepIIdietarerecommendedtoparticipateinaregularexerciseprogramandondrugtherapydesignedtoincreaseHDL-cholesterollevels.4RecentdataindicatetheallMIpatientsshouldbeonstatintherapy,regardlessoflipidlevelsordietLong-termMedications:MostoralmedicationsinstitutedinthehospitalatthetimeofMIwillbecontinuedlong-term.Therapywithaspirinandbeta-blockadeiscontinuedindefinitelyinallpatients.ACEIiscontinuedindefinitelyinpatientswithcongestiveheartfailure,leftventriculardysfunction(ejectionfraction<0.40),hypertension,ordiabetes.4Alipid-loweringagent,specificallyastatin,inadditiontodietarymodificationiscontinuedindefinitely.PostMIManagementCardiacStrePostMIManagement(Cntd.)ImplantableCardiacDefibrillators:Theresultsofthemulti-centerautomaticdefibrillatorimplantationtrialII(MADITII)haveexpandedtheindicationsforautomaticimplantablecardiacdefibrillators(AICD)inpatientspost-MI.Thetrialdemonstrateda31%relativeriskreductioninall-causemortalitywiththeprophylacticuseofanAICDinpatientspost-MIwithejectionfractionslessthan30%.CardiacRehabilitation:PostMIManagement(Cntd.)Impla急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件急性心肌梗死AMI診斷和治療進展(英文課件ArrhythmiasinAMIMECHANISMOFARRHYTHMIASArrhythmiasoccurringinpatientswithAMIrequireaggressivetreatmentwhentheyimpairhemodynamics;compromisemyocardialviabilitybyaugmentingmyocardialoxygenrequirements;predisposetomalignantventriculararrhythmias,i.e.,ventriculartachycardia,ventricularfibrillation,orasystoleMANAGEMENT.GiventhedecliningincidenceofventricularfibrillationinAMIseeninCCUsoverthelastthreedecades(Fig.37–43AFig.37–43A),thepriorpracticeofprophylacticsuppressionofVPBswithantiarrhythmicdrugsnolongerisnecessaryandmayactuallybeassociatedwithanincreasedriskoffatalbradycardicandasystoliceventsAcceleratedIdioventricularRhythmVentricularTachycardiaLidocaineProcainamidAmiodaroneVentricularFibrillationBRADYARRHYTHMIAS ArrhythmiasinAMIMECHANISMOFPHYSICALEXAMINATION

GENERALAPPEARANCEPatientssufferinganAMIoftenappearanxiousandinconsiderabledistress.Ananguishedfacialexpressioniscommon,and—incontrasttopatientswithsevereanginapectoris,whooftenlie,sit,orstandstill,recognizingthatallformsofactivityincreasethediscomfort—somepatientssufferinganAMImayberestlessandmoveaboutinanefforttofindacomfortableposition.Theyoftenmassageorclutchtheirchestsandfrequentlydescribetheirpainwithaclenchedfistheldagainstthesternum(the“Levine”sign,namedafterDr.SamuelA.Levine).Inpatientswithleftventricularfailureandsympatheticstimulation,coldperspirationandskinpallormaybeevident;theytypicallysitorareproppedupinbed,gaspingforbreath.Betweenbreaths,theymaycomplainofchestdiscomfortorafeelingofsuffocation.Coughproductiveoffrothy,pink,orblood-streakedsputumiscommonHEARTRATE.BLOODPRESSURE.TEMPERATUREANDRESPIRATION.JUGULARVENOUSPULSE.CAROTIDPULSE.THECHEST.PHYSICALEXAMINATION

GENERALCardiacExaminationPALPATIONAUSCULTATION.ThirdandFourthHeartSoundsMurmurs.PericardialFrictionRubs.OTHERFINDINGSFUNDI.ABDOMENEXTREMITIESNEUROPSYCHIATRICFINDINGSCardiacExaminationPALPATIONAntithromboticTherapyEFFECTONMORTALITY.EFFECTONPATENCYOFINFARCTARTERYEFFECTONLEFTVENTRICULARTHROMBUSNEWANTITHROMBOTICAGENTSHIRUDINLOW-MOLECULAR-W