Complications of Acute Myocardial Infarction, Publish 2014

1/5/2015
ComplicationsofAcuteMyocardialInfarction
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Complicationsof
AcuteMyocardialInfarction
AdamW.Grasso
SorinJ.Brener
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/complicationsofacutemyocardialinfarction/
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Complicationsofacutemyocardialinfarction(MI)includeischemic,mechanical,arrhythmic,embolic,and
inflammatorydisturbances(Table1).Nevertheless,circulatoryfailurefromsevereleftventricular(LV)dysfunction
oroneofthemechanicalcomplicationsofMIaccountformostfatalities.
Table 1:ComplicationsofAcute M yocardialInfarction
ComplicationType Manifestations
Ischemic
Angina,reinfarction,infarctextension
Mechanical
Heartfailure,cardiogenicshock,mitralvalvedysfunction,aneurysms,cardiacrupture
Arrhythmic
Atrialorventriculararrhythmias,sinusoratrioventricularnodedysfunction
Embolic
Centralnervoussystemorperipheralembolization
Inflammatory
Pericarditis
Ischemiccomplications
Ischemiccomplicationscanincludeinfarctextension,recurrentinfarction,andpostinfarctionangina.
Prevalence
Infarctextensionisaprogressiveincreaseintheamountofmyocardialnecrosiswithintheinfarctzoneofthe
originalMI.Thiscanmanifestasaninfarctionthatextendsandinvolvestheadjacentmyocardium,orasa
subendocardialinfarctionthatbecomestransmural.
Followingfibrinolytictherapy,reocclusionoftheinfarctrelatedartery(IRA)occursinapproximately5%to10%
ofpatientsbythetimeofdischarge,andin25%to30%ofpatientsat1year.1Thesepatientsalsotendtohavea
pooreroutcome.2,3ReinfarctionismorecommoninpatientswithdiabetesmellitusorpriorMI.Withtheadventof
primarypercutaneouscoronaryintervention(PCI)andstentplacement,riskofreinfarctionhasdropped
substantially,toapproximately3%duringthefirst90daysafterMI.4
Recurrentinfarctioninaseparateterritorymaybedifficulttodiagnosewithinthefirst24to48hoursaftertheinitial
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event.MultivesselcoronaryarterydiseaseiscommoninpatientswithacuteMI.Infact,angiographicevidenceof
complexorulceratedplaquesinnoninfarctrelatedarteriesispresentinupto40%ofpatientswithacuteMI.
Anginathatoccursfromafewhoursto30daysafteracuteMIisdefinedaspostinfarctionangina.Theincidence
ofpostinfarctionanginaishighestinpatientswithnonSTelevationMI(approximately25%),andinthosetreated
withfibrinolyticsratherthanwithPCI.
Pathophysiology
ReinfarctionoccursmoreoftenwhentheIRAreoccludesthanwhenitremainspatenthowever,reocclusionofthe
IRAdoesnotalwayscausereinfarctionbecauseofabundantcollateralcirculation.Afterfibrinolytictherapy,
reocclusionisfoundonangiogramsof5%to10%ofpatientsandisassociatedwithaworseoutcome.When
primaryPCIisusedforreperfusion,theincidenceofIRAreocclusionismuchlower.Ofparticularconcernisthe
developmentofacutestentthrombosis,usuallywithinthefirstfewhoursafterprimaryPCIin~1%ofpatients.5
Thepathophysiologicmechanismofpostinfarctionanginaissimilartothatofunstableanginaplaquerupture
andshouldbemanagedinasimilarmanner.Patientswithpostinfarctionanginahaveaworseprognosiswithregard
tosuddendeath,reinfarction,andacutecardiacevents,comparedwiththosewithoutsuchsymptoms.
SignsandSymptoms
Patientswithinfarctextensionorpostinfarctionanginausuallyhavecontinuousorintermittentchestpain,with
protractedelevationinthecreatinekinase(CK)levelandoccasionally,newelectrocardiographicchanges.
DiagnosticTesting
Thediagnosisofinfarctexpansion,reinfarction,orpostinfarctionischemiacanbemadewithechocardiographyor
nuclearimaging.Newwallmotionabnormalities,largerinfarctsize,newareaofinfarction,orpersistentreversible
ischemicchangeshelpsubstantiatethediagnosis.CKMBisamoreusefulmarkerfortrackingongoinginfarction
thantroponin,givenitsshorterhalflife.ReelevationandsubsequentdeclineinCKMBlevelssuggestinfarct
expansionorrecurrentinfarction.ElevationsintheCKMBlevelofmorethan50%overapreviousnadirare
diagnosticforreinfarction.
Treatment
Medicaltherapywithaspirin,heparin,nitroglycerin,betablocker,andstatinisindicatedinpatientswhohavehada
MIandareexperiencingongoingischemicsymptoms.6Dependingupontheclinicalsituation,additionalanti
platelettherapy(clopidogrel,prasugrel,ticagrelor)andaglycoproteinIIb/IIIainhibitor(eptifibatide)mayalsobe
given.Anintraaorticballoonpump(IABP)shouldbeinsertedpromptlyinpatientswithhemodynamicinstability
orsevereLVsystolicdysfunction.However,itmustbeborneinmindthatsevereperipheralvasculardiseaseof
theaortoiliacandfemoralarteriesisacontraindicationtoIABPplacement,duetoincreasedriskoflower
extremityischemia.IABPuseisalsocontraindicatedinpatientswithsevereaorticvalveinsufficiency(AI),because
theirAIwillbeworsenedbytheballoonpump.Coronaryangiographyshouldbeperformedinpatientswhoare
stabilizedwithmedicaltherapy,butemergencyangiographyalsomaybeundertakeninunstablepatients,since
restorationofcoronaryarterialbloodflow,eitherbypercutaneousorsurgicalmeans,isassociatedwithan
improvedprognosis.
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MechanicalComplications
MechanicalcomplicationsofacuteMIincludeventricularseptaldefect(VSD),papillarymuscleruptureor
dysfunction,cardiacfreewallrupture(FWR),ventricularaneurysm,LVfailurewithcardiogenicshock,dynamic
LVoutflowtract(LVOT)obstruction,andrightventricular(RV)failure.
VentricularSeptalDefect
IndependentpredictorsofVSDareshowninBox1.
Box1:IndependentPredictorsofVentricularSeptalDefect
Olderage
Femalegender
Nonsmokingstatus
Anteriorinfarct
WorseKillipclassonadmission
Increasedheartrateonadmission
Prevalence
VSDformerlyoccurredin1%to2%ofpatientsafteracuteMIinthe
prethrombolyticera(Figures1and2).Theincidencehasdecreased
dramaticallywithreperfusiontherapy.Forexample,theGUSTOI(GlobalUtilizationofStreptokinaseandTissue
plasminogenactivatorforOccludedcoronaryarteries)trialdemonstratedanincidenceofVSDofapproximately
0.2%.7SimilarratesofVSDoccurrencepostMIhavebeenobtainedfromstudiesutilizingprimaryPCI.8VSD
wascommonlyseen3to7daysafterMIintheprefibrinolyticera,butnowisgenerallydiagnosedwithinthefirst
24hoursafterMI.7,8
Pathophysiology
Thedefectusuallyoccursatthejunctionofpreservedandinfarctedmyocardiumintheapicalseptumwithanterior
MI,andinthebasalposteriorseptumwithinferiorMI.VSDalmostalwaysoccursinthesettingofatransmural
MIandismoreoftenseeninanterolateralMIs.Thedefectmightnotalwaysbeasinglelargedefectin30%to
40%ofpatients,ameshworkofserpiginouschannelscanbeidentified.
SignsandSymptoms
Earlyinthediseaseprocess,patientswithVSDmayappearrelativelycomfortable,withnoclinicallysignificant
cardiopulmonarysymptoms.Rapidrecurrenceofangina,togetherwithhypotension,pulmonaryedema,andfrank
cardiogenicshockcandeveloplaterinthecourse.
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Diagnosis
Ruptureoftheventricularseptumisoftenaccompaniedbyanewharshholosystolicmurmurbestheardattheleft
lowersternalborder.Themurmurisaccompaniedbyathrillin50%ofcases.Thissignisgenerallyaccompanied
byaworseninghemodynamicprofileandbiventricularfailure.Therefore,itisimportantthatallpatientswithMI
undergoacareful,welldocumentedcardiacexaminationatpresentationanddailythereafter.
Anelectrocardiogram(ECG)mayshowatrioventricular(AV)nodalorinfranodalconductiondelayabnormalities
inapproximately40%ofpatients.EchocardiographywithcolorflowDopplerimagingisthebestmethodfor
diagnosingVSD.TherearetwotypesofVSD,whichcanbevisualizedbestindifferentechocardiographicplanes.
AposterobasalVSDisbestvisualizedintheparasternallongaxiswithmedialangulation,apicallongaxis,and
subcostallongaxis.AnapicalseptalVSDisbestvisualizedintheapicalfourchamberview.Echocardiography
candefineLVandRVdysfunctionimportantdeterminantsofmortalityaswellasthesizeofthedefectand
degreeoflefttorightshuntbyassessingflowthroughthepulmonaryandaorticvalves.Insomecases,itmaybe
necessarytousetransesophagealechocardiographytoassesstheVSD.
VSDcanalsobediagnosedbydemonstratinganincreaseor"stepup"inoxygensaturationintherightventricle
andpulmonaryartery(PA)onrightheartcatheterization.Thelocationofthestepupissignificant,becausethere
havebeencasereportsofincreasedperipheralPAoxygensaturationduetoacutemitralregurgitation(MR).
Diagnosisinvolvesfluoroscopicallyguidedmeasurementofoxygensaturationinthesuperiorandinferiorvena
cava,rightatrium,rightventricle,andPA.Withalefttorightshuntacrosstheventricularseptum,onewill
generallydetectanincreaseinoxygensaturationofmorethan8%whengoingfromtherightatriumtotheright
ventricleandPA.Ashuntfractioncanbecalculatedasfollows:
where isthepulmonaryflow, isthesystemicflow,SaO2isthearterialoxygensaturation,MvO2isthe

mixedvenousoxygensaturation,PvO2isthepulmonaryvenousoxygensaturation,andPaO2isthepulmonary
arterialoxygensaturation.Acalculated
bythepatient.
>2suggestsalargeshunt,whichisnotlikelytobewelltolerated
Treatment
Earlysurgicalclosureisthetreatmentofchoice,evenifthepatient'sconditionisstable.Initialreportssuggested
thatdelayingsurgerycouldreducesurgicalmortality.9However,theseperceivedbenefitswereprobablytheresult
ofselectionbias,10becausethemortalityrateinpatientswithVSDtreatedmedicallyis24%at72hoursand75%
at3weeks.Therefore,inordertoreducemortality,patientswithpostinfarctionVSDshouldbestrongly
consideredforearlyurgentsurgicalrepair.
Cardiogenicshockandmultisystemfailureareassociatedwithahighsurgicalmortality.Thisfurthersupports
earlieroperativemanagementbeforecomplicationsdevelop.11Mortalityishighestinpatientswithbasalseptal
ruptureassociatedwithinferiorMI(70%,comparedwith30%inpatientswithruptureduetoanteriorinfarction).
Themortalityratewithbasalseptalruptureishigherbecauseofincreasedtechnicaldifficultyandthefrequentneed
formitralvalverepairorreplacementinthepatientswithMR.12RegardlessoftheVSDlocationandthepatient's
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hemodynamiccondition,surgeryshouldalwaysbeconsidered,becauseitisassociatedwithalowermortalityrate
thanconservativemanagement.6
Intensivemedicalmanagementshouldbestartedtosupportthepatientbeforesurgery.Unlessthereissignificant
aorticregurgitation,anIABPshouldbeinsertedurgentlyasabridgetoasurgicalprocedure.TheIABPwill
decreasethesystemicvascularresistance(SVR)andshuntfractionwhileincreasingcoronaryperfusionand
maintainingbloodpressure.AftertheIABPisinserted,vasodilatorscanbeused,withclosehemodynamic
monitoring.VasodilatorscanalsoreducelefttorightshuntingandincreasesystemicflowbyreducingSVR.
CautionshouldbeexercisedtoavoidagreaterdecreaseinpulmonaryvascularresistancethaninSVRanda
consequentincreaseinshunting.Thevasodilatorofchoiceisintravenoussodiumnitroprusside(SNP),whichis
startedat0.5to1.0g/kg/minandtitratedtoameanarterialpressure(MAP)of60to75mmHg.
MitralRegurgitation
Prevalence
MRafteracuteMIportendsapoorprognosis,asdemonstratedinmultipletrials.1316MRofmildtomoderate
severityisfoundin13%to45%ofpatientsfollowingacuteMI.WhereasmostMRistransientindurationand
asymptomatic,MRcausedbypapillarymusclerupture(Figure3)isalifethreateningcomplicationofacuteMI.
Fibrinolyticagentsdecreasetheincidenceofrupturehowever,whenpresent,rupturecanoccurearlierinthe
postMIperiodthanintheabsenceofreperfusion.Althoughpapillarymusclerupturewasreportedtooccur
betweendays2and7intheprefibrinolyticera,theSHOCK(SHouldweemergentlyrevascularizeOccluded
CoronariesincardiogenicshocK?)TrialRegistrydemonstratedamediantimetopapillarymuscleruptureof13
hours.17Papillarymuscleruptureisfoundin7%ofpatientsincardiogenicshockandcontributes5%ofthe
mortalityafteracuteMI.18,19
Pathophysiology
MRcanoccurasaresultofanumberofmechanisms,includingmitralvalveannulardilatationsecondarytoLV
dilatation,papillarymuscledysfunctionwithassociatedischemicregionalwallmotionabnormalityinclose
proximitytotheinsertionoftheposteriorpapillarymuscle,andpartialorcompleteruptureofthechordae
tendineaeorpapillarymuscle.18
PapillarymuscleruptureismostcommonwithaninferiorMI.Theposteromedialpapillarymuscleismostoften
involvedbecauseofitssinglebloodsupplythroughtheposteriordescendingcoronaryartery.20Theanterolateral
papillarymusclehasadualbloodsupply,beingperfusedbytheleftanteriordescending(LAD)andleftcircumflex
coronaryarteries.In50%ofpatientswithpapillarymusclerupture,theinfarctisrelativelysmall.
SignsandSymptoms
Completetransectionofbothpapillarymusclesisrareandusuallyresultsinimmediatepulmonaryedema,
cardiogenicshock,anddeath.Physicalexaminationofthepatientwithanterolateralpapillarymusclerupture
usuallydemonstratesanewpansystolicmurmur,whichisaudibleatthecardiacapexandradiatestotheaxillaor
thebaseoftheheart.Ifthereisaposteromedialpapillarymusclerupture,themurmurradiatestotheleftsternal
borderandmaybeconfusedwiththemurmurofVSDoraorticstenosis(intensityofthemurmurdoesnotalways
predicttheseverityofMR).Itisimportanttorememberthatinpatientswithsevereheartfailure,poorcardiac
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output,orelevatedleftatrialpressures,themurmurofsevereMRmaybesoftorabsent.
DiagnosticTesting
TheECGusuallyshowsevidenceofarecentinferiororposteriorMI.Thechestradiographgenerallyshows
pulmonaryedema.Focalpulmonaryedemacanoccurintherightupperlobewhenflowisdirectedattheright
pulmonaryveins.
ThediagnostictestofchoiceistwodimensionalechocardiographywithcolorflowDopplerimaging.Insevere
MR,themitralvalveleafletisusuallyflail.Colorflowimagingcanbeusefulindistinguishingpapillarymuscle
rupturewithsevereMRfromVSD.TransthoracicechocardiographymaynotfullyrevealtheamountofMRin
somepatientswithposteriorlydirectedjets.Intheseindividuals,transesophagealechocardiographycanbe
particularlyuseful.
HemodynamicmonitoringwithaPAcathetercanreveallarge(>50mmHg),earlyvwavesinthepulmonary
capillarywedgepressure(PCWP).PatientswithVSDcanalsohavelargevwavesasaresultofaugmented
pulmonaryvenousreturninaleftatriumofnormalsizeanddecreasedcompliance,buttheyappearlaterinthe
cardiaccycle.Furthercomplicatingthediagnosticpicture,patientswithsevereMRandreflectedvwavesinthe
PAtracingmayhaveanincreaseinoxygensaturationinthePA.21WithSwanGanzcatheterization,MRcanbe
distinguishedfromVSDbytwocharacteristics:First,prominentvwavesinthePCWPtracingprecedingthe
incisuraonthePAtracingarealmostalwayssecondarytosevereMR.Second,inordertoidentifyasignificant
increaseinoxygencontentassociatedwithVSD,bloodforoximetryshouldbeobtainedwithfluoroscopiccontrol
fromthecentralPAratherthanfromitsmoredistalbranches.
Treatment
Patientswithpapillarymuscleruptureshouldberapidlyidentifiedandreceiveaggressivemedicaltreatmentwhile
beingconsideredforsurgery.Medicaltherapyincludesvasodilatortherapy.SNPisusefulinthetreatmentof
patientswithacuteMR.SNPdirectlydecreasesSVR,therebyreducingtheregurgitantfractionandincreasingthe
forwardstrokevolumeandcardiacoutput.SNPcanbestartedat0.5to1.0g/kg/minandtitratedtoaMAPof
60to75mmHg.AnIABPshouldbeinsertedtodecreaseLVafterload,improvecoronaryperfusion,and
increaseforwardcardiacoutput.PatientswithhypotensionmaytoleratevasodilatorsafteranIABPisinserted,but
certainlynotbefore.
Patientswithpapillarymuscleruptureshouldbeconsideredforemergencysurgery,becausetheprognosisis
dismalinmedicallytreatedpatients.Coronaryangiographyshouldbeperformedbeforesurgicalrepair,since
revascularizationduringmitralvalverepairorreplacementisassociatedwithimprovedshorttermandlongterm
mortality.19,22AdditionalsurgicalcandidatesincludepatientswithmoderateMRwhodonotclinicallyimprove
withafterloadreduction.
LeftVentricularFreeWallRupture
Prevalence
WhileLVFWRwasmorecommonbeforetheeraofreperfusion,itnowaffectsonly0.5%ofMIpatients.
However,FWRcarrieswithitasubstantialmortalityrateof20%.8,23Thetimingofcardiacruptureiswithin5
daysofinfarctionin50%ofpatientsandwithin2weeksin90%ofpatients.FWRoccursonlyamongpatients
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withtransmuralMI(Figure4).Riskfactorsincludeadvancedage,femalegender,hypertension,firstMI,andpoor
coronarycollateralization.
Pathophysiology
Comparedwithindividualswhodidnotreceivefibrinolyticagents,MIpatientsadministeredsuchdrugswere
foundtoexperienceFWRearlierintheirclinicalcourse.However,theiroverallriskofFWRwasnot
increased.2325Althoughanywallcanbeinvolved,cardiacrupturemostcommonlyoccursatthelateralwall.
FWRoccursatthreedistinctintervals,withthreedistinctpathologicsubsets.TypeIincreaseswiththeuseof
fibrinolytics,occursearly(withinthefirst24hours)andisafullthicknessrupture.TypeIIruptureoccurs1to3
daysafterMIandisaresultoferosionofthemyocardiumatthesiteofinfarction.TypeIIIruptureoccurslateand
islocatedattheborderzonebetweeninfarctedandnormalmyocardium.
ThereductioninTypeIIIrupturesasaresultoftheadventoffibrinolyticshasresultedinnochangeintheoverall
FWRrate.IthasbeenpostulatedthatTypeIIIrupturesmayoccurasaresultofdynamicLVOTobstructionand
theresultantincreasedwallstress.26
SignsandSymptoms
Suddenonsetofchestpainwithstrainingorcoughingcansuggesttheonsetofmyocardialrupture.Acutely
rupturedpatientsoftenhavepulselesselectricalactivity(electromechanicaldissociation)andsuddencardiacdeath.
Otherpatientsmayhaveamoresubacutecourseasaresultofacontainedrupture,orpseudoaneurysm.Theymay
complainofnausea,painsuggestiveofpericarditis,andareusuallyhypotensive.Inanolderstudyevaluating1,457
patientswithacuteMI,6.2%hadFWR.Approximatelyonethirdofthesepatientspresentedwithasubacute
course.27
Jugularvenousdistention,pulsusparadoxus,diminishedheartsounds,andapericardialrubsuggestsubacute
rupture.Newtoandfromurmursmaybeheardinpatientswithsubacuteruptureorpseudoaneurysm.A
junctionaloridioventricularrhythm,lowvoltagecomplexes,andtallprecordialTwavesmaybeevidentonthe
ECG.Additionally,alargenumberofpatientshavetransientbradycardiajustbeforerupture,aswellasothersigns
orsymptomsofincreasedvagaltone.
DiagnosticTesting
Althoughthereisgenerallyinsufficienttimeforthoroughdiagnostictestinginthemanagementofpatientswithacute
rupture,transthoracicechocardiographyistheemergenttestofchoice.Echocardiographytypicallydemonstratesa
pericardialeffusionwithfindingsofcardiactamponade.Thesefindingsincluderightatrial(RA)andRVdiastolic
collapse,dilatedinferiorvenacava,andmarkedrespiratoryvariationsinmitralandtricuspidinflow.Additionally,a
SwanGanzPAcathetermayrevealhemodynamicsignsoftamponade,withequalizationoftheRA,RVdiastolic,
andPCWPs.
Treatment
Thegoaloftherapyistodiagnosetheproblemearly,andperformemergencyopenheartsurgerytocorrectthe
rupture.Emergencypericardiocentesismaybeperformedimmediatelyonpatientswithtamponadeandsevere
hemodynamiccompromisewhilearrangementsarebeingmadefortransporttotheoperatingroom.Theprocedure
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carrieswithitconsiderableriskbecauseastheintrapericardialpressureisrelieved,communicationisre
establishedbetweentheintraandextraventricularspaces,oftenleadingtofurtherbleedingintothepericardium.
Medicalmanagementhasnoroleinthetreatmentofthesepatients,exceptfortheuseofvasopressorstomaintain
bloodpressuretemporarilyasthepatientisrushedtotheoperatingroom.
Pseudoaneurysm
Pathophysiology
PseudoaneurysmiscausedbycontainedruptureoftheLVfreewall.Theaneurysmmayremainsmallorundergo
progressiveenlargement.Theouterwallisformedbythepericardiumandmuralthrombus.Thepseudoaneurysm
communicateswiththebodyoftheleftventriclethroughanarrowneckwhosediameterisbydefinitionlessthan
50%ofthediameterofthefundus.
SignsandSymptoms
Somepseudoaneurysmsremainclinicallysilentandarediscoveredduringroutineinvestigations.However,some
patientshaverecurrenttachyarrhythmia,systemicembolization,andheartfailure.Somepatientshavesystolic,
diastolic,ortoandfromurmursrelatedtotheflowofbloodacrosstheneckofthepseudoaneurysmduringLV
systoleanddiastole.Achestradiographmayshowcardiomegaly,withanabnormalbulgeonthecardiacborder.
TheremaybypersistentSTsegmentelevationontheECG.Thediagnosismaybeconfirmedby
echocardiography,magneticresonanceimaging,orcomputedtomography.
Treatment
Spontaneousruptureoccurswithoutwarninginapproximatelyonethirdofpatientswithapseudoaneurysm.
Therefore,surgicalinterventionisrecommendedforallpatients,regardlessofsymptomsorthesizeofthe
aneurysm,topreventsuddendeath.
LeftVentricularFailureandCardiogenicShock
Prevalence
LVdysfunctionistobeexpectedafteranacuteMI.Thedegreeofdysfunctioncorrelateswiththeextentand
locationofmyocardialinjury.Noninfarctedmyocardiumcanalsobecometemporarilyhypokineticorakineticdue
toischemic"stunning."Patientswithsmall,moredistalinfarctionsmayhavediscreteregionalwallmotion
abnormalitieswithpreservedoverallLVfunctionbecauseofcompensatoryhyperkinesisoftheunaffected
segments.28PriorMI,olderage,femalegender,diabetes,andanteriorinfarctionareriskfactorsfordevelopment
ofcardiogenicshock.29,30
Inthelate1960's,KillipandKimball31developedaclassificationschemetocategorizepatients'prognosisbased
ontheirphysicalexamfindings(Table2).Individualswereclassifiedintofoursubsets,from"noevidenceof
congestiveheartfailure"(ClassI)to"cardiogenicshock"(ClassIV).Theauthorsreporteda67%mortalityrate
forClassIVpatients.
Table 2:Incide nce ofHe artFailure inAcute M yocardialInfarction
KillipClass
Characteristics
Patients(%)
30DayMortality(%)
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Noevidenceofcongestiveheartfailure
32
II
Rales,jugularvenousdistention,orS3
38
17
III
Pulmonaryedema
10
38
IV
Cardiogenicshock
19
67
Forresterandcolleagues32,33classifiedpatientsbytheirhemodynamicprofileusingaPAcathetertodefinePCWP
andcardiacindex.Theyreporteda50%mortalityrateinthemostcompromisedsubset(PCWP>18mmHg
cardiacindex<2.2L/min/m2).ResultsoftheGUSTOItrialhaveindicatedthat7%to8%ofacuteMIpatients
developcardiogenicshock.Fibrinolysisdidnotmateriallyaffectmortality,whichremainedhighat58%.34,35In
contrast,intheSHouldweemergentlyrevascularizeOccludedCoronariesforcardiogenicshocK(SHOCK)trial,
urgentpercutaneousorsurgicalrevascularizationmarkedlyreducedearlyandlatemortality,whencomparedwith
continuedmedicaltherapy,includingIABP.36Finally,whenthestudypopulationofGUSTOIwasrestrictedto
thosewithnonSTelevationMI,the30dayriskofmortalityforpooledKillipClassIIIandIVpatientswas
considerablylower,at14%.37
Pathophysiology
PatientscandevelopcardiogenicshockinassociationwithanacuteMIduetomultiplecauses,includinglargeLV
infarction,severeRVinfarction,VSD,FWR,acuteMR,orpharmacologicdepressionofLVfunction(beta
blockersinMIfromaproximalLADlesion).PatientswhohavecardiogenicshockasaresultofacuteMI
typicallyhaveseveremultivesseldisease,withsignificantinvolvementoftheLAD.38,39Generally,atleast40%of
theLVmassisaffectedinpatientswhopresentincardiogenicshockasaresultofafirstMI.40,41Inpatientswith
priorMIandbaselinedepressedLVfunction,asmalleracuteinsultcanresultincardiogenicshock(Figure5).
SignsandSymptoms
PatientswhopresentinKillipClassIIIoftenhaverespiratorydistress,diaphoresis,andcool,clammyextremities
inadditiontothetypicalsignsandsymptomsofacuteMI.PatientsinKillipClassIV(cardiogenicshock)canhave
severeorthopnea,dyspnea,andoliguriaandmayhavealteredmentalstatus,aswellasmultisystemorganfailure
fromhypoperfusion.Itmaybepossibletopalpateanareaofdyskinesiaontheprecordium.AnS3gallop,
pulmonaryrales,andelevatedjugularvenouspressurearecommonfindingsonphysicalexamination.
DiagnosticTesting
PatientswithcardiogenicshockcausedbyacuteMIgenerallyhaveextensiveelectrocardiographicchanges
demonstratingalargeinfarct,diffuseischemia,orpriorinfarcts.Ifthesechangesareabsent,anothercauseof
shocksuchassepsisshouldbeconsidered.Chestradiographyusuallyrevealspulmonaryedema.Laboratorytests
maydemonstratelacticacidemia,renalfailure,andarterialhypoxemia.
ThepatientincardiogenicshockshouldbemonitoredwithaPAcatheterandanarterialline.Thesecanhelp
distinguishbetweenprimaryLVfailureandothermechanicalcausesofcardiogenicshock,asdiscussedabove.
Transthoracicechocardiographyhelpsdeterminetheextentofdysfunctionalmyocardium.Italsohelpsidentify
othermechanicalcomplicationsofMIthatmaybecontributingtocardiogenicshock,suchaspapillarymuscle
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rupture.
Treatment
ApatientincardiogenicshockshouldhaveaLVassistdevice(IABP,Impella,TandemHeart)placed
urgentlytoreduceafterload,improvecardiacoutput,andenhancecoronaryperfusion.Medicaltherapywith
vasodilators(e.g.,nitroglycerinandSNP),angiotensinconvertingenzyme(ACE)inhibitorsandloopdiuretics
shouldbeusedastolerated.Intravenousnitroglycerinisthefirstlinedrugofchoiceamongvasodilatorsbecauseit
islesslikelytoproducecoronarystealthanSNPandhelpsprotectagainstischemia.Thestartingdoseis10to20
g/minanditmaybeincreasedby10g/minevery2to3minutestoagoalMAPof70mmHg.IntravenousSNP
canbeaddediffurtherreductioninafterloadisnecessary.SNPisstartedat0.5to1.0g/kg/minandisalso
titratedtoaMAPofapproximately70mmHg.Patientswhoarehypotensiveonpresentation(MAP<70mmHg)
maynottoleratevasodilatorsorotherbloodpressureloweringagentspriortoplacementofanassistdevice.
ACEinhibitorsimproveLVperformanceanddecreasemyocardialoxygenconsumptionbyreducingthecardiac
afterloadofpatientswithheartfailureandacuteMI.ACEinhibitorscanreduceinfarctexpansionifstartedinthe
first12hoursofanMIifthepatientisnotalreadyincardiogenicshock.Itisrecommendedthatcaptoprilbe
startedearly,at3.125to6.25mgevery8hours,witheachdosesubsequentlydoubledastoleratedtoamaximum
doseof50mgevery8hours.Patientswithmildpulmonaryedemacanbetreatedwithdiureticssuchas
intravenous(IV)furosemide,adjustedforserumcreatinineandhistoryofdiureticuse.
Betaadrenergicagonistssuchasdobutamineordopaminemaybeneededforpatientswithsevereheartfailure
andcardiogenicshock.ThistherapyshouldgenerallybereservedforthosewhohavefailedmechanicalLV
supportandmaximalvasodilatortherapy,orforthosewithaRVinfarct.Phosphodiesteraseinhibitorssuchas
milrinonemaybebeneficialforsomepatients,butcanincreaseventricularectopy.Thebolusmaybeomittedin
patientswithmarginalbloodpressures.Somepatientsmayneednorepinephrinetomaintainarterialpressure.
Norepinephrineisstartedat2g/minandtitratedtomaintaintheMAPatapproximately70mmHg.
PCIandemergencycoronarybypasssurgeryhavebeenassociatedwithimprovedprognosisforpatientsin
cardiogenicshock,reducingthemortalityratefrom80%to50%.EmergencyPCIorsurgicalrevascularizationis
indicatedforpatientswithseveremultivesseldisease.6Substantialleftmaincoronaryarterystenosisisalsoan
indicationforcoronarybypass,asongoingstudiesevaluatetheefficacyofleftmainstentinginthissituation.Other
surgicalmodalitiesthatmaybeconsideredincludeimplantationofLVorbiventricularassistdevicesor
extracorporealmembraneoxygenationasabridgetohearttransplantation.Somepatientsmaybegradually
weanedfromventricularassistdevicesafterthestunnedportionofmyocardiumrecovers,withouttheneedfor
cardiactransplantation.
RightVentricularFailure
Prevalence
MildRVdysfunctioniscommonafterMIoftheinferiororinferoposteriorwall,withanincidenceofapproximately
40%.HemodynamicallysignificantRVimpairmentoccursinonly10%ofpatientswiththesetypesofMI,however
(Figure6).
Pathophysiology
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ThedegreeofRVdysfunctiondependsonthelocationoftherightcoronaryarteryocclusion.Onlyproximal
occlusionsoftherightcoronaryartery(proximaltotheacutemarginalbranch)resultinmarkeddysfunction.42The
degreeofRVinvolvementalsodependsontheamountofcollateralflowfromtheLADandthedegreeofblood
flowthroughthethebesianveins.Becausetherightventricleisthinwalledandhasloweroxygendemand,thereis
coronaryperfusionduringtheentirecardiaccycletherefore,widespreadirreversibleinfarctionisrare.
SignsandSymptoms
Thetriadofhypotension,jugularvenousdistentionwithclearlungs,andabsenceofdyspneahashighspecificity
butlowsensitivityforRVinfarction.43SevereRVfailurecanmanifestwithsignsandsymptomsofalowcardiac
outputstate,includingdiaphoresis,coolclammyextremities,andalteredmentalstatus.Patientsoftenhaveoliguria
andhypotension.OthercausesofseverehypotensioninthesettingofaninferiorMIincludebradyarrhythmia,
acutesevereMR,andVSD.
PatientswithisolatedRVfailurehaveelevatedjugularvenouspressureandrightventricularS3heartsoundinthe
settingofanormallungexamination.Thepresenceofjugularvenouspressuregreaterthan8cmH2Oand
Kussmaul'ssignishighlysensitiveandspecificforsevereRVfailure.Ararebutclinicallyimportantcomplicationof
RVinfarctionisrighttoleftshuntingsecondarytoincreasedpressuresintheRAandRVandopeningofthe
foramenovale.ThisshouldbeconsideredinpatientswithRVinfarctionandpersistenthypoxemia.
Electrocardiographically,patientspresentwithinferiorSTelevationinconjunctionwithSTelevationintheV4R
lead.Thesefindingshaveapositivepredictivevalueof80%forRVinfarction.44Thechestradiographusually
doesnotshowpulmonaryvenoushypertension.
DiagnosticTesting
EchocardiographyisthediagnosticstudyofchoiceforRVinfarction.ItwilldemonstrateRVdilationand
dysfunctionandusuallyLVinferiorwalldysfunctionaswell.Itisalsohelpfulinexcludingcardiactamponade,
whichcanmimicRVinfarctionhemodynamically.ThehemodynamicprofileofacuteRVinfarctioncanalsobedue
toanacutepulmonaryembolismintheabsenceofacardiacischemicevent.
HemodynamicmonitoringwithaPAcathetertypicallyrevealshighRApressureswithalowPCWP,becauseRV
failureresultsinunderfillingoftheleftventricleandalowcardiacoutput.ARApressureofhigherthan10mmHg
andaRApressuretoPCWPratioof0.8orgreaterstronglysuggestRVinfarction.45IfsevereLVdysfunctionis
alsopresent,thePCWPcanbehigher.Insomepatients,RVdilatationcanimpairLVperformancebyflatteningor
bowingoftheseptumintotheleftventricle.ThiscanrestrictventricularfillingandelevatethePCWP.
Treatment
VolumeloadingtoincreaseLVpreloadandcardiacoutputiskeytothemanagementofRVinfarction.Some
patientsrequireseverallitersin1hourtoreachatargetcentralvenouspressureof15mmHgandatargetPCWP
of15mmHg.ItisimportanttohavehemodynamicmonitoringwithaPAcatheterinthesepatients,because
overzealousfluidadministrationcanfurtherdecreaseLVoutput.Thisoccursasaresultofseptalshifttowardthe
leftventricleandanintrapericardialpressureshift.Whenvolumeloadingisinsufficienttoimprovecardiacoutput,
inotropesareindicated.AdministrationofdobutaminecanincreasecardiacindexandimproveRVejection
fraction.VasodilatorssuchasnitroglycerinandSNP,whileeffectiveforafterloadreductioninacuteLVinfarction,
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willalmostuniversallycausehypotensionandhemodynamicdecompensationinacuteRVinfarction.43
Patientsmaybenefitfromreperfusiontherapy,becausethosewhoundergosuccessfulreperfusionofRVbranches
haveenhancedRVfunctionandalower30daymortalityrate.46,47PatientswithRVinfarctionand
bradyarrhythmiasorlossofsinusrhythmmayhavesignificantimprovementwithAVsequentialpacing.Optimal
pacersettingstendtoutilizelongerAVdelays(approximately200msec)andaheartrateof80to90beatsper
minute.
AlthoughanIABPactsprimarilyontheLV,therehavebeencasereportsofIABPimprovingthecardiacindex
whenusedincombinationwithdobutamineforacuteRVinfarction.Pericardiectomymaybeconsideredfor
patientswithrefractoryshockbecauseitreversestheseptalimpingementonLVfilling.MostpatientswithRV
infarctionimproveafter48to72hours.AnRVassistdeviceisindicatedforpatientswhoremainincardiogenic
shockinspiteofthesemeasures.
VentricularAneurysm
Prevalence
Patientswhodonotreceivereperfusiontherapyareatgreatestriskfordevelopingthiscomplication(in
10%30%).Amongthevariousinfarctlocations,patientswithapicaltransmuralMIsareatthehighestriskfor
aneurysmformation,followedbythosewithposteriorbasalinfarcts.
Pathophysiology
Theearlyopenarteryhypothesisstatesthatearlyreperfusionshouldresultinimprovedmyocardialsalvageand
preventionofinfarctexpansion.Evenlatereperfusionlimitsinfarctexpansionthroughanumberofmechanisms,
includingimmediatechangeininfarctioncharacteristics,preservationofsmallamountsofresidualmyofibrilsand
interstitialcollagen,acceleratedhealing,thescaffoldeffectofabloodfilledvasculature,andeliminationofischemia
inviablebutdysfunctionalmyocardium.PersistentocclusionoftheIRA,ontheotherhand,canleadtoinfarct
expansionandprogressiveLVdilation.Theaneurysmconsistsofastretchedportionofthemyocardiumwhich
containsallthreetissuelayersandisconnectedtotheventriclebyawideneck(greaterthanhalfthediameterof
thefundus).Thedifferencesbetweenapseudoaneurysm(falseaneurysm)andtrueaneurysmarehighlightedin
Table3.
Table 3:Diffe re nce sBe twe e nTrue Ane urysmsandPse udoane urysms
Parameter
TrueAneurysm
Pseudoaneurysm
Cause
Infarction
Containedrupture
Incidence
1%5%
Rare
Neck
Wide
Narrow
Wall
Allthreelayersscar
Pericardiumandthrombus
Rupture
Veryrare
Common
SignsandSymptoms
AcutedecompensatedheartfailureandevencardiogenicshockcandevelopasaresultofalargeLVaneurysm.
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Becauseacuteaneurysmsexpandduringsystole,contractileenergygeneratedbyanormalmyocardiumiswasted
andputstheentireventricleatamechanicaldisadvantage.Chronicaneurysmspersistformorethan6weeksafter
theacuteevent,arelesscompliantthanacuteaneurysms,andarelesslikelytoexpandduringsystole.Patientswith
chronicaneurysmsmayhaveheartfailure,ventriculararrhythmias,andsystemicembolization,ortheymaybe
asymptomatic.Palpationoftheprecordiumcanrevealadyskineticsegmentoftheventricle.AnS3gallopmaybe
heardinpatientswithpoorventricularfunction.
DiagnosticTesting
TypicalelectrocardiographicfindingsincludeQwavesandSTelevation,whichcanpersistdespiteapplicationof
reperfusiontherapy.Whenelectrocardiographicchanges(STelevation)persistformorethan6weeks,patients
mayhaveachronicventricularaneurysm.Achestradiographmayrevealalocalizedbulgeinthecardiacsilhouette.
Echocardiographyisthegoldstandardforaccurateidentificationoftheaneurysmalsegment.Itmayalso
demonstratethepresenceofamuralthrombus.Additionally,echocardiographyisusefulindifferentiatingtrue
aneurysmsfrompseudoaneurysms.Magneticresonanceimagingmayalsobeusefulanddiagnosticfordelineating
theaneurysmalsection.
Treatment
AcutedecompensatedheartfailurewithacuteaneurysmsismanagedwithIVvasodilators.ACEinhibitorshave
beenshowntoreduceinfarctexpansionandunfavorableLVremodeling.Astoleratedbybloodpressure,ACE
inhibitorsarebeststartedwithinthefirst12to24hoursofonsetofacuteMIbecauseinfarctexpansionstarts
early.Corticosteroidsandnonsteroidalantiinflammatorydrugs(NSAIDs)shouldbeavoidedintheacutesetting
becausetheyhavebeenshowntopromoteinfarctexpansionandaneurysmformationinexperimentalmodels.
ChronicheartfailurewithchronicaneurysmscanbemanagedwithACEinhibitors,betablockers,anddiuretics.
Anticoagulationwithwarfarinisindicatedforpatientswithamuralthrombus.Patientsshouldbetreatedinitially
withIVheparin,withatargetpartialthromboplastintimeof50to70seconds.Warfarinisstartedsimultaneously.
Patientsshouldbetreatedwithwarfarinatatargetinternationalnormalizedratio(INR)of2to3foraperiodof3
to6months.Itiscontroversialwhetherpatientswhohavelargeaneurysmswithoutthrombusshouldreceive
anticoagulants.Manycliniciansprescribeanticoagulantsfor6to12weeksaftertheacutephase.PatientswithLV
aneurysmsandalowglobalejectionfraction(<40%)haveahigherstrokerateandshouldtakeanticoagulantsfor
atleast3monthsaftertheacuteevent.Subsequently,theywillundergoregularsurveillancewithechocardiography
(usuallyeveryyear).Anticoagulationshouldbereinitiatedifanewthrombusdevelops.
Refractoryheartfailureorventriculararrhythmiasinpatientswithaneurysmsareindicationsforsurgicalresection,
alsoreferredtoasLVreconstructivesurgery.Resectionoftheaneurysmmaybefollowedbyconventionalclosure
ornewertechniquestomaintainLVgeometry.Revascularizationisbeneficialforpatientswithalargeamountof
viablemyocardiumaroundtheaneurysmalsegment.
DynamicLeftVentricularOutflowTractObstruction
Prevalence
DynamicLVOTobstructionisanuncommoncomplicationofacuteanteriorMIandwasfirstdescribedinacase
reportbyBartunekandassociates.48
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Pathophysiology
Thiseventisdependentoncompensatoryhyperkinesisofthebasalandmidsegmentsoftheleftventricleinpatients
withdistalLADinfarcts.Predictorsofenhancedregionalwallmotioninnoninfarctzonesaretheabsenceof
multivesseldisease,femalegender,andhigherflowintheinfarctrelatedvessel.Theincreasedcontractileforceof
theseregionsdecreasesthecrosssectionalareaoftheLVOTduringsystole.Theresultingincreasedvelocityof
bloodthroughtheoutflowtractcanproducedecreasedpressurebelowthemitralvalveandcausetheleaflettobe
displacedanteriorlytowardtheseptum(Venturieffect).ThisresultsinfurtherLVOTobstructionresultingfrom
systolicanteriormotion(SAM)oftheanteriormitralvalveleaflet,andinposteriorlydirectedMR.
IthasbeenpostulatedthatdynamicLVOTobstructioncanplayaroleincausingFWR.LVOTobstructionleads
toincreasedendsystolicintraventricularpressure,whichinducesincreasedwallstressoftheweakened,necrotic
infarctzone.Thisfrequentlyfatalcomplicationoccursmostofteninwomen,inolderpatients(olderthan70years),
andinthosewithoutpriorMI.
SignsandSymptoms
Patientsmayhaverespiratorydistress,diaphoresis,andcool,clammyextremitiesinadditiontothetypicalsigns
andsymptomsofacuteMI.PatientswithsevereLVOTobstructionmayappeartobeincardiogenicshockwith
severeorthopnea,dyspnea,andoliguria,andmayhavealteredmentalstatusfromcerebralhypoperfusion.Patients
maypresentwithanewsystolicejectionmurmurheardbestattheleftuppersternalborder,withradiationtothe
neck.Additionally,anewholosystolicmurmurcanbeheardattheapex,withradiationtotheaxillaasaresultof
SAMofthemitralleaflet.AnS3gallop,pulmonaryrales,hypotension,andtachycardiacanalsobepresent.
DiagnosticTesting
Echocardiographyisthediagnostictestofchoiceandcanaccuratelycharacterizethehyperkineticsegment,LVOT
obstruction,andmitralleafletSAM.
Treatment
Treatmentcentersondecreasingmyocardialcontractilityandheartratewhileexpandingintravascularvolumeand
increasingafterload(modestly).Betablockersshouldbeaddedslowlyandwithcarefulmonitoringofheartrate,
bloodpressure,andSvO2.PatientscanreceivegentleIVhydrationwithseveralsmall(250mL)bolusesofsaline
toincreasepreloadanddecreaseLVOTobstructionandSAM.Thepatient'shemodynamicandrespiratorystatus
shouldbemonitoredcloselyduringthistherapeuticinterventionwithaPAcatheter.Vasodilators,inotropes,and
balloonpumpsshouldbeavoidedbecausetheycanincreaseLVOTobstruction.Incontrast,thepureperipheral
vasoconstrictorphenylephrinecanbeuseful,sinceitwillincreaseafterloadanddiminishtheLVOTgradient.
ArrhythmicComplications
VentriculararrhythmiaisacommoncomplicationofacuteMI,occurringinalmostallpatients,evenbefore
monitoringispossible.Itisrelatedtotheformationofreentrycircuitsattheconfluenceofthenecroticandviable
myocardium,aswellastoirritableischemicmyocardium.
Prematureventricularcontractionsoccurinapproximately90%ofpatientswithacuteMI.Attheotherendofthe
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spectrum,theincidenceofventricularfibrillation(VF)isapproximately2%to4%.Althoughlidocainehasbeen
demonstratedtoreducesomewhattherateofprimaryVFinpatientswithMI,thereisnosurvivalbenefitandthere
maybeexcessmortality.Therefore,itisnotrecommendedthatpatientsreceiveprophylacticlidocainetherapy.49
AmiodaronemaybeusedinpatientswithMIwithnonsustainedventriculartachycardia(VT),orafterdefibrillation
forVF.Therecommendeddosingisabolusof150mgandthenadministrationof1mg/minfor6hours,followed
by0.5mg/min.WhenstartingthismedicationforVForpulselessVT,thebolusshouldbeincreasedto300mg
(the150mgboluscanberepeatedin10minutes).Ventriculararrhythmiasnotrespondingtoamiodaronemaybe
treatedwithlidocaine(1mg/kgbolustoamaximumof100mg,followedbya14mg/mindrip),50orwith
procainamide.PolymorphicVTisararecomplicationofacuteMI,usuallyassociatedwithrecurrentischemia.It
canbetreatedwithamiodarone,lidocaine,procainamide,oracombinationofdrugs,asdescribedforthemore
commonlyobservedmonomorphicVT.Acceleratedidioventricularrhythm,sometimesreferredtoas"slowVT,"
oftenoccursduringthereperfusionphaseofPCI,isselflimited,andusuallydoesnotrequiretreatment.
TheimportanceofVFinthesettingofMIhasbeenreevaluatedinthecontextoftheinteractionbetweensevere
systolicdysfunctionandthepotentialforsuddencardiacdeath.Implantablecardioverterdefibrillatorshavebeen
showntoreducemortalityinpostMIpatientswithanejectionfractionlessthanorequalto30%,regardlessof
whetherornotventriculardysrhythmiahasbeenobserved.51
Supraventriculararrhythmiasoccurinlessthan10%ofpatientswithacuteMI,andarenotdirectlyischemicin
origin.Becausepatientswhodevelopthesearrhythmiastendtohavemoresevereventriculardysfunctionthan
thosewhodonot,theywillgenerallyexperienceaworseoutcome.AlthoughisolatedRAinfarctionorsmall
inferiorinfarctsleadingtoatrialarrhythmiasarenotassociatedwithhighermortalityrates,theappearanceofatrial
arrhythmiasusuallyheraldstheonsetofheartfailureinthesettingofacuteanteriorMI.
Bradyarrhythmias,includingAVblockandsinusbradycardia,occurmostcommonlywithinferiorMI.Complete
AVblockoccursinapproximately20%ofpatientswithacuteRVinfarction.Infranodalconductiondisturbances
withwidecomplexventricularescaperhythmsoccurmostofteninlargeanteriorinfarctionsandportendavery
poorprognosis.
TemporarytransvenouspacingisindicatedforpatientswhopresentwithMobitztype2seconddegreeAVblock,
completeAVblock,orasystole.Considerationfortransvenouspacingshouldbegiventopatientswithbifascicular
blockor"trifascicularblock"(bifascicularblockwithconcurrentfirstdegreeAVblock)inthesettingofacute
MI.52PacingisnotindicatedforthepatientinsinusbradycardiaorAVdissociationwithaslowsinusrateanda
morerapidventricularescaperhythmaslongasthepatientismaintainingadequatehemodynamics.Ifmild
symptomsexist,theinitialtreatmentfortheserhythmdisturbancesisIVatropine,0.5to1.0mg.Thismaybe
repeatedevery5minutes,toamaximumdoseof2mg.
EmbolicComplications
Prevalence
TheincidenceofclinicallyevidentsystemicembolismafterMIislessthan2%.Theincidenceincreasesinpatients
withanteriorwallMI.TheoverallincidenceofmuralthrombusafterMIisapproximately20%.LargeanteriorMI
maybeassociatedwithmuralthrombusinasmanyas60%ofpatients.53,54
Pathophysiology
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Mostemboliarisefromtheleftventricleasaresultofwallmotionabnormalitiesoraneurysms.Atrialfibrillationin
thesettingofischemiacanalsocontributetosystemicembolization.
SignsandSymptoms
Themostcommonclinicalmanifestationofemboliccomplicationsisstroke,althoughpatientsmayhavelimb
ischemia,renalinfarction,ormesentericischemia.Mostepisodesofsystemicembolioccurwithinthefirst10days
afteracuteMI.Physicalfindingsvarywiththesiteoftheembolism.Focalneurologicdeficitsoccurinpatientswith
centralnervoussystememboli.Limbischemiamanifestswithlimbpaininacold,pulselessextremity.Renal
infarctionmanifestswithflankpain,hematuria,andacuterenalinsufficiency.Mesentericischemiamanifestswith
abdominalpainoutofproportiontophysicalfindings,anorexiaandbloodydiarrhea.
Treatment
Intheabsenceofactivebleeding,IVheparinshouldbestartedimmediatelywithatargetpartialthromboplastin
timeof50to70secondsandcontinueduntilwarfarintreatmenthasbroughttheINRintothetherapeuticrange.
Warfarintherapyshouldbestartedimmediately,withagoalINRof2to3,andcontinuedforatleast3to6
monthsforpatientswithmuralthrombiandforthosewithlargeakineticareasdetectedbyechocardiography.
Pericarditis
Prevalence
TheincidenceofearlypericarditisafteracuteMIisapproximately10%.Thisinflammatoryconditionusually
developsbetween24and96hoursafterMI.55,56Dressler'ssyndrome,orlatepericarditis,occurswithan
incidencebetween1%and3%,typically2to8weeksafterMI.
Pathophysiology
ThepathogenesisofacutepostMIpericarditisisaninflammatoryreactioninresponsetonecrotictissue.Acute
pericarditisthusdevelopsmoreofteninpatientswithtransmuralMI.ThepathogenesisofDressler'ssyndromeis
unknown,butanautoimmunemechanisminvolvingcirculatingmyocardialantigenshasbeensuggested.
SignsandSymptoms
Mostpatientswithearlypericarditisreportnosymptoms.Patientswithsymptomsfromearlyorlatepericarditis
describeprogressive,severechestpainthatlastsforhours.Thesymptomsareposturalworseinthesupine
positionandarealleviatedbysittingupandleaningforward.Thepainispleuriticinnatureandthereforetendsto
beexacerbatedbydeepinspiration,coughing,andswallowing.Radiationofpaintothetrapeziusridgeisalmost
pathognomonicforacutepericarditis.Thepainalsocanradiatetotheneckand,lesscommonly,tothearmor
back.
Apericardialfrictionrubonexaminationisaveryspecificfindingtosupportacutepericarditishowever,itcanbe
ephemeral,andisnotfoundinallpatientswithpericarditis(lowsensitivity).Frequentcardiacphysicalexaminations
willincreasethechanceofhearingtherub.Itisbestheardattheleftlowersternaledgewiththediaphragmofthe
stethoscope.Therubhasthreecomponents:atrialsystole,ventricularsystole,andventriculardiastole.Inabout
30%ofpatientswithrubsitisbiphasic,andin10%itisuniphasic.Apericardialeffusioncancausefluctuationin
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theintensityoftherub.
EvolvingMIchangescanmaskthediagnosisofpericarditis.PericarditisproducesgeneralizedSTsegment
elevation,whichisconcaveupwardsorsaddleshaped.Aspericarditisevolves,Twavesbecomeinvertedafter
theSTsegmentbecomesisoelectric.Conversely,inacuteMI,TwavescanbecomeinvertedwhentheST
segmentisstillelevated.Foursequentialphasesofelectrocardiographicabnormalitieshavebeendescribedin
associationwithpericarditis(Table4).57
Table 4:Ele ctrocardiographicChange sofPe ricarditis
Stage
ElectrocardiographicChange
STelevation,uprightTwaves
II
STelevationresolves,uprighttoflatTwaves
III
STisoelectric,invertedTwaves
IV
STisoelectric,uprightTwaves
Apericardialeffusiononechocardiographystronglysuggestspericarditis,butthelackofaneffusiondoesnotrule
itout.
Treatment
AspirinisthetherapyofchoiceforpostMIpericarditis,650mgevery4to6hours,foratleast4weeks.During
thistime,aprotonpumpinhibitororotherantisecretagogueshouldbecoadministeredforgastricprotection.
NSAIDsandcorticosteroidsshouldbeavoided,astheycaninterferewithmyocardialhealingandcontributeto
expansionoftheinfarct.NSAIDsshouldalsobeavoidedinpatientswithcoronaryarterydisease,duetothe
increasedriskoffurthercardiaceventsonsuchdrugs.Theantiinflammatoryagentcolchicinecanbeusedasinitial
therapy,andisalsothepreferredaddondruginthetreatmentofchronicorrecurrentpostMIpericarditisif
aspirinmonotherapyisineffective.
BacktoTop
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KuttyRS,JonesN,MoorjaniN.Mechanicalcomplicationsofacutemyocardialinfarction[publishedonline
aheadofprintAugust13,2013].CardiolClin201331:519531.doi:10.1016/j.ccl.2013.07.004.
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