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ComplicationsofMyocardialInfarction

ComplicationsofMyocardialInfarction
Author:AshokKKondur,MDChiefEditor:EricHYang,MDmore...
Updated:Dec18,2014

Overview
Myocardialinfarction(MI)duetocoronaryarterydiseaseisaleadingcauseofdeathintheUnitedStates,where
morethan1millionpeoplehaveacutemyocardialinfarctions(AMIs)eachyear. [1]
Theadventofcoronarycareunitsandearlyreperfusiontherapy(lyticorpercutaneouscoronaryintervention)has
substantiallydecreasedinhospitalmortalityratesandhasimprovedtheoutcomeinsurvivorsoftheacutephaseof
MI.
ComplicationsofMIincludearrhythmic,mechanical,andinflammatory(earlypericarditisandpostMIsyndrome)
sequelae,aswellasleftventricularmuralthrombus(LVMT).Inadditiontothesebroadcategories,rightventricular
(RV)infarctionandcardiogenicshockareotherpossiblecomplicationsofacuteMI.(Seetheimagebelow.)

Modified2dimensional(top)echocardiogramandcolorflow Dopplerimage(bottom).Apical4chamberview sshow abreachinthe

interventricularseptumandfreecommunicationbetw eenventriclesthroughalargeapicalseptumventricularseptaldefectinapatient
w horecentlyhadananteriormyocardialinfarction.

Forotherdiscussionsonmyocardialinfarction,seeMyocardialInfarction,RightVentricularInfarction,Imagingof
AcuteMyocardialInfarcts,andUseofCardiacMarkersintheEmergencyDepartment.

ArrhythmicComplicationsofMI
About90%ofpatientswhohaveanacutemyocardialinfarction(AMI)developsomeformofcardiacarrhythmia
duringorimmediatelyaftertheevent.In25%ofpatients,suchrhythmabnormalitiesmanifestwithinthefirst24
hours.Inthisgroupofpatients,theriskofseriousarrhythmias,suchasventricularfibrillation,isgreatestinthe
firsthouranddeclinesthereafter.TheincidenceofarrhythmiaishigherwithanSTelevationmyocardialinfarction
(STEMI)andlowerwithanonSTelevationmyocardialinfarction(NSTEMI). [2]
Theclinicianmustbeawareofthesearrhythmias,inadditiontoreperfusionstrategies,andmusttreatthosethat
requireinterventiontoavoidexacerbationofischemiaandsubsequenthemodynamiccompromise.Mostperi
infarctarrhythmiasarebenignandselflimited.However,thosethatresultinhypotension,increasemyocardial
oxygenrequirements,and/orpredisposethepatienttodevelopadditionalmalignantventriculararrhythmiasshould
beaggressivelymonitoredandtreated.

Pathophysiologyofarrhythmiccomplications
AMIischaracterizedbygeneralizedautonomicdysfunctionthatresultsinenhancedautomaticityofthe
myocardiumandconductionsystem.Electrolyteimbalances(eg,hypokalemiaandhypomagnesemia)and
hypoxiafurthercontributetothedevelopmentofcardiacarrhythmia.Thedamagedmyocardiumactsassubstrate
forreentrantcircuits,duetochangesintissuerefractoriness.
Enhancedefferentsympatheticactivity,increasedconcentrationsofcirculatingcatecholamines,andlocalrelease
ofcatecholaminesfromnerveendingsintheheartmuscleitselfhavebeenproposedtoplayrolesinthe
developmentofperiinfarctionarrhythmias.Furthermore,transmuralinfarctioncaninterruptafferentandefferent
limbsofthesympatheticnervoussystemthatinnervatesmyocardiumdistaltotheareaofinfarction.Thenetresult
ofthisautonomicimbalanceisthepromotionofarrhythmias.

Classificationofperiinfarctionarrhythmias
Periinfarctionarrhythmiascanbebroadlyclassifiedintothefollowingcategories:
Supraventriculartachyarrhythmias,includingsinustachycardia,prematureatrialcontractions,paroxysmal
supraventriculartachycardia,atrialflutter,andatrialfibrillation
Acceleratedjunctionalrhythms
Bradyarrhythmias,includingsinusbradycardiaandjunctionalbradycardia
Atrioventricular(AV)blocks,includingfirstdegreeAVblock,seconddegreeAVblock,andthirddegreeAV
block

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Intraventricularblocks,includingleftanteriorfascicularblock,rightbundlebranchblock(RBBB),andleft
bundlebranchblock(LBBB)
Ventriculararrhythmias,includingprematureventricularcontractions(PVCs),acceleratedidioventricular
rhythm,ventriculartachycardia,andventricularfibrillation
Reperfusionarrhythmias

ArrhythmicComplications:SupraventricularTachyarrhythmias
Sinustachycardiaisassociatedwithenhancedsympatheticactivityandcanresultintransienthypertensionor
hypotension.Theelevatedheartrateincreasesmyocardialoxygendemand,andadecreasedlengthofdiastole
compromisescoronaryflow,worseningmyocardialischemia.
Causesofpersistentsinustachycardiaincludethefollowing:
Pain
Anxiety
Heartfailure
Hypovolemia
Hypoxia
Anemia
Pericarditis
Pulmonaryembolism
InthesettingofanAMI,sinustachycardiamustbeidentified,andappropriatetreatmentstrategiesmustbe
devised.Treatmentstrategiesincludeadequatepainmedication,diuresistomanageheartfailure,oxygenation,
volumerepletionforhypovolemia,administrationofantiinflammatoryagentstotreatpericarditis,anduseofbeta
blockersand/ornitroglycerintorelieveischemia.

Prematureatrialcontractions
Prematureatrialcontractionsoftenoccurbeforethedevelopmentofparoxysmalsupraventriculartachycardia,atrial
flutter,oratrialfibrillation.Theusualcauseoftheseextraimpulsesisatrialdistentionduetoincreasedleft
ventricular(LV)diastolicpressureorinflammationassociatedwithpericarditis.
Nospecifictherapyisindicated.However,attentionshouldbegiventoidentifyingtheunderlyingdiseaseprocess,
particularlyoccultheartfailure.

Paroxysmalsupraventriculartachycardia
TheincidenceofaparoxysmalsupraventriculartachycardiainthesettingofanAMIislessthan10%.Inthe
absenceofdefinitivedatainthepatientwithAMI,theconsensusisthatadenosinecanbeusedwhenhypotension
isnotpresent.InpatientswithoutclinicallysignificantLVfailure,intravenousdiltiazemorabetablockercanbe
usedinstead.Inpatientswhodevelopsevereheartfailureorhypotension,synchronizedelectricalcardioversionis
required.

Atrialflutter
Atrialflutteroccursinlessthan5%ofpatientswithAMI.Atrialflutterisusuallytransientandresultsfrom
sympatheticoverstimulationoftheatria.
Treatmentstrategiesforpersistentatrialflutteraresimilartothoseforatrialfibrillation,exceptthatventricularrate
controlwithdrugsislesseasilyaccomplishedwithatrialflutterthanwithatrialfibrillation.Therefore,synchronized
electricalcardioversion(beginningwith50J,orthebiphasicequivalent)maybeneededrelativelypromptly
becauseofadecreasecoronarybloodflowand/orhemodynamiccompromise.Forpatientswhoseatrialflutteris
refractorytomedicaltherapy,overdriveatrialpacingmaybeconsidered.

Atrialfibrillation
Therateofatrialfibrillationis1015%amongpatientswhohaveAMIs.Theonsetofatrialfibrillationinthefirst
hoursofAMIisusuallycausedbyLVfailure,ischemicinjurytotheatria,orRVinfarction.Pericarditisandall
conditionsleadingtoelevatedleftatrialpressurecanalsoleadtoatrialfibrillationinassociationwithanAMI.The
presenceofatrialfibrillationduringanAMIisassociatedwithanincreasedriskofmortalityandstroke,particularly
inpatientswhohaveanteriorwallMIs.
Immediateelectricalcardioversionisindicatedforthepatientinunstablecondition,suchasonewithnewor
worseningischemicpainand/orhypotension.Synchronizedelectricalcardioversiontotreatatrialfibrillationbegins
with200J(orthebiphasicequivalent).Conscioussedation(preferred)orgeneralanesthesiaisadvisablepriorto
cardioversion.
Forpatientsinstablecondition,controllingtheventricularresponseistheimmediateobjective.Iftheatrial
fibrillationdoesnotrespondtocardioversion,IVamiodarone[3]orIVdigoxin(inpatientswithLVdysfunctionor
heartfailure)canbeusedtoachieveventricularratecontrol.
Forpatientswhodonotdevelophypotension,abetablockercanbeused.Forexample,metoprololmaybegiven
in5mgintravenousbolusesevery510min,withamaximumdoseof15mg.Intravenousdiltiazemisan
alternativeforslowingtheventricularrate,butitshouldbeusedwithcautioninpatientswithmoderatetosevere
heartfailure.Inpatientswithnewonsetsustainedtachycardia(absentbeforeMI),conversiontosinusrhythm
shouldbeconsideredasanoption.
Atrialfibrillationandatrialflutterconferanincreasedriskofthromboembolism(seeDeepVenousThrombosisand
PulmonaryEmbolism).Therefore,anticoagulationwitheitherunfractionatedheparinorlowmolecularweight
heparin(LMWH)shouldbestartedifcontraindicationsareabsent.Itisunclearwhetheranticoagulationisneeded

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incasesoftransientatrialfibrillationandhowlongaftertheonsetofatrialfibrillationshouldtheanticoagulationbe
started.

ArrhythmicComplications:AcceleratedJunctionalRhythm
Anacceleratedjunctionalrhythmresultsfromincreasedautomaticityofthejunctionaltissuethatleadstoaheart
rateof70130bpm.Thistypeofdysrhythmiaismostcommoninpatientswhodevelopinferiormyocardial
infarctions.Treatmentisdirectedatcorrectingtheunderlyingischemia.

ArrhythmicComplications:Bradyarrhythmias
Sinusbradycardia
Sinusbradycardiaisacommonarrhythmiainpatientswithinferiororposterioracutemyocardialinfarctions
(AMIs).Thehighestincidence,40%,isobservedinthefirst12hoursafterAMI.
Thelikelymechanismleadingtobradycardiaandhypotensionisstimulationofcardiacvagalafferentreceptorsthat
resultinefferentcholinergicstimulationoftheheart.IntheearlyphasesofanAMI,resultantsinusbradycardia
mayactuallybeprotective,reducingmyocardialoxygendemand.Clinicallysignificantbradycardiathatdecreases
cardiacoutputandhypotensionmayresultinventriculararrhythmiasandshould,therefore,betreated
aggressively.Isolatedsinusbradycardiaisnotassociatedwithanincreaseintheacutemortalityrisk,andtherapy
istypicallyunnecessarywhenthepatienthasnoadversesignsorsymptoms.
Whenemergencytherapyisindicated(eg,inapatientwithasinusrateof<40bpmwithhypotension),atropine
sulfate0.51mgmaybegivenevery35minutestoamaximumof0.030.04mg/kg.Theinabilitytoreverse
hypotensionwithatropineinpatientswhodevelopsinusbradycardiaandinferiorMIsuggestsvolumedepletion
and/orRVinfarction.
Whenatropineisineffectiveandthepatientissymptomaticorhypotensive,transcutaneousortransvenouspacing
isindicated(seeourmainarticleonExternalPacemakers).Denervate,transplantedheartsdonotrespondto
atropineand,therefore,requirecardiacpacing.
Iftheseinterventionsfail,additionalpharmacologicinterventionmaybeuseful.Examplesaredopamine520
mcg/kg/mingivenintravenously,epinephrine210mcg/min,and/ordobutamine.

Junctionalbradycardia
JunctionalbradycardiaisaprotectiveAVjunctionalescaperhythmatarateof3560bpminpatientswhohavean
inferiorMI.Thisarrhythmiaisnotusuallyassociatedwithhemodynamiccompromise,andtreatmentistypically
notrequired.

ArrhythmicComplications:AVandIntraventricularBlocks
FirstdegreeAVblock
FirstdegreeAVblockischaracterizedbyprolongationofthePRintervaltolongerthan0.20seconds.Thistypeof
blockoccursinapproximately15%ofpatientswhohaveanacutemyocardialinfarction(AMI),mostcommonlyan
inferiorinfarction.AlmostallpatientswhodevelopfirstdegreeAVblockhaveconductiondisturbancesabovethe
Hisbundle.Inthesepatients,theprogressiontocompleteheartblockorventricularasystoleisrare.Nospecific
therapyisindicatedunlessassociatedhemodynamiccompromiseispresent.
CalciumchannelblockersandbetablockersmaycauseorexacerbateafirstdegreeAVblock,buttheyshouldbe
stoppedonlyifhemodynamicimpairmentorahigherdegreeblockoccurs.ForafirstdegreeAVblockassociated
withsinusbradycardiaandhypotension,atropineshouldbeadministered.Continuedcardiacmonitoringis
advisableinviewofpossibleprogressiontohigherdegreesofblock.

SeconddegreeAVblock
MobitztypeI,orWenckebach,AVblockoccursinapproximately10%ofpatientswhohaveanAMIandaccounts
for90%ofallpatientswhohaveanAMIandaseconddegreeAVblock.AseconddegreeAVblockisassociated
withanarrowQRScomplexandismostcommonlyassociatedwithaninferiorMI.Itdoesnotaffectthepatient's
overallprognosis.
AMobitztypeIblockdoesnotnecessarilyrequiretreatment.Iftheheartrateisinadequateforperfusion,
immediatetreatmentwithatropine0.51mgadministeredintravenouslyisindicated.Transcutaneousortemporary
transvenouspacingisrarelyrequired.
AMobitztypeIIAVblockaccountsfor10%ofallseconddegreeAVblocks(overallrateof<1%inthesettingof
AMI).AMobitztypeIIblockischaracterizedbyawideQRScomplex,anditisalmostalwaysassociatedwith
anteriorinfarction.Thistypeofblockoftenprogressessuddenlytoacompleteheartblock.
MobitztypeIIAVblocksareassociatedwithapoorprognosis,asthemortalityrateassociatedwiththeir
progressiontoacompleteheartblockisapproximately80%.Therefore,thistypeofseconddegreeAVblock
shouldbeimmediatelytreatedwithtranscutaneouspacingoratropine.Atropinehelpsinabout50%ofcases,but
itoccasionallyworsenstheblockwithanincreasedheartrate.Atemporarytransvenouspacemaker,andpossibly
apermanentdemandpacemaker,mustultimatelybeplaced.

ThirddegreeAVblock
AthirddegreeAVblock(ie,acompleteheartblock),occursin515%ofpatientswhohaveanAMIandmayoccur
withanteriororinferiorinfarctions.Inpatientswithinferiorinfarctions,thistypeofblockusuallydevelopsgradually,

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progressingfromfirstdegreeoratypeIseconddegreeblock.Inmostpatients,theleveloftheblockissupranodal
orintranodal,andtheescaperhythmisusuallystablewithanarrowQRSandratesexceeding40bpm.In30%of
patients,theblockisbelowtheHisbundle,whereitresultsinanescaperhythmwitharateslowerthan40bpm
andawideQRScomplex.
CompleteheartblockinpatientswithaninferiorMIusuallyrespondstoatropine.Inmostpatients,itresolves
withinafewdayswithouttheneedforatemporaryorpermanentpacemaker.Themortalityrateforpatientswith
inferiorMIwhodevelopcompleteheartblockisapproximately15%unlessacoexistingRVinfarctionispresent,in
whichcasethemortalityrateishigher.
ImmediatetreatmentwithatropineisindicatedforpatientswiththirddegreeAVblocks.Aswiththerapyfora
MobitztypeIIblock,thistreatmentmaynothelpandmaysometimesworsentheblock.Temporary
transcutaneousortransvenouspacingisindicatedforsymptomaticpatientswhoseconditionisunresponsiveto
atropine.Permanentpacingshouldbeconsideredinpatientswithpersistentsymptomaticbradycardiathat
remainsunresolvedwithlysisorpercutaneouscoronaryintervention.
InpatientswithananteriorMI,anintraventricularblockoraMobitztypeIIAVblockusuallyprecedesathird
degreeAVblock.Thethirddegreeblockoccurssuddenlyandisassociatedwithahighmortalityrate.TheCardiac
ArrhythmiasandRiskStratificationAfterMyocardialInfarction(CARISMA)trialmonitoredpatientswithacute
myocardialinfarctionandreducedleftventricularejectionfractionandfoundthathighdegreeatrioventricularblock
wasthemostpowerfulpredictorofcardiacdeath. [4]Patientswiththeseblockstypicallyhaveunstableescape
rhythmswithwideQRScomplexesandatratesoflessthan40bpm.
Immediatetreatmentwithatropineand/ortranscutaneouspacingisindicated.Thisisfollowedbytemporary
transvenouspacing.PatientswithananteriorMIwhodevelopathirddegreeAVblockandwhosurviveto
hospitalizationoftenreceiveapermanentpacemaker.

Intraventricularblocks
ConductionfromtheHisbundleistransmittedthrough3fascicles:theanteriordivisionoftheleftbundle,the
posteriordivisionoftheleftbundle,andtherightbundle.Anabnormalityofelectricalconductionin1ormoreof
thesefasciclesisnotedinabout15%ofpatientswithAMI.Isolatedleftanteriorfascicularblock(LAFB)occursin
35%ofpatientswithAMIprogressiontocompleteAVblockisuncommon.Isolatedleftposteriorfascicularblock
occursinonly12%ofpatientswhohaveanAMI.Thebloodsupplyoftheposteriorfascicleislargerthanthatof
theanteriorfascicletherefore,ablockhereisassociatedwitharelativelylargeinfarctandhighmortalityrate.
Therightbundlebranchreceivesitsdominantbloodsupplyfromtheleftanteriordescending(LAD)artery.
Therefore,anewRBBB,whichisseeninapproximately2%ofpatientswithAMI,suggestsalargeinfarctterritory.
However,progressiontocompleteheartblockisuncommon.InpatientswhodevelopananteriorMIandanew
RBBB,thesubstantialriskfordeathismostlyfromcardiogenicshock,whichispresumablyduetothelargesize
ofthemyocardialinfarct.
ThecombinationofRBBBwithanLAFBisknownasbifascicularblockandcommonlyoccurswithocclusionof
theproximalLADcoronaryartery.TheriskofdevelopingcompleteAVblockisheightened,butcompleteblockis
stilluncommon.Mortalityismostlyrelatedtotheamountofmuscleloss.Bifascicularblockinthepresenceof
firstdegreeAVblockiscalledatrifascicularblock.In40%ofpatients,atrifascicularblockprogressestoa
completeheartblock.

ArrhythmicComplications:VentricularArrhythmias
Prematureventricularcontractions
Inthepast,frequentprematureventricularcontractions(PVCs)wereconsideredtorepresentwarningarrhythmias
andindicatorsofimpendingmalignantventriculararrhythmias.However,presumedwarningarrhythmiasare
frequentlyobservedinpatientswhohaveanacutemyocardialinfarction(AMI)andwhoneverdevelopventricular
fibrillation.Ontheconverse,primaryventricularfibrillationoftenoccurswithoutantecedentprematureventricular
ectopy.
Forthesereasons,prophylacticsuppressionofPVCswithantiarrhythmicdrugs,suchaslidocaine,isnolonger
recommended.Prophylaxishasbeenassociatedwithanincreasedriskoffatalbradycardiaorasystolebecauseof
thesuppressionofescapepacemakers.
Giventhisevidence,mostclinicianspursueaconservativecoursewhenPVCsareobservedinapatientwithan
AMI,andtheydonotroutinelyadministerprophylacticantiarrhythmics.Instead,attentionshouldbedirected
towardcorrectinganyelectrolyticormetabolicabnormalities,plusidentifyingandtreatingrecurrentischemia.

Acceleratedidioventricularrhythm
Anacceleratedidioventricularrhythmisseeninasmanyas20%ofpatientswhohaveanAMI.Thispatternis
definedasaventricularrhythmcharacterizedbyawideQRScomplexwitharegularescaperatefasterthanthe
atrialrate,butlessthan100bpm.AVdissociationisfrequent.Slow,nonconductedPwavesareseentheseare
unrelatedtothefast,wideQRSrhythm.
Mostepisodesareshortandterminatespontaneously.Theyoccurwithequalfrequencyinanteriorandinferior
infarctions.Themechanismmightinvolve(1)thesinoatrialnodeortheAVnode,whichmaysustainstructural
damageanddepressnodalautomaticity,and/or(2)anabnormalectopicfocusintheventriclethattakesoveras
thedominantpacemaker.
Thepresenceofacceleratedidioventricularrhythmdoesnotaffectthepatient'sprognosisnodefinitiveevidence
hasshownthatanuntreatedoccurrenceincreasestheincidenceofventricularfibrillationordeath.Thisrhythm
occurssomewhatmorefrequentlyinpatientswhodevelopearlyreperfusionthaninothershowever,itisneither
sensitivenorspecificasamarkerofreperfusion.

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Temporarypacingisnotindicatedunlesstherhythmissustainedandresultsinhypotensionorischemic
symptoms.Anacceleratedidioventricularrhythmrepresentsanappropriateescaperhythm.Suppressionofthis
escaperhythmwithanantiarrhythmicdrugcanresultinclinicallysignificantbradycardiaorasystole.Therefore,an
acceleratedidioventricularrhythmshouldbeleftuntreated.

Nonsustainedventriculartachycardia
Nonsustainedventriculartachycardiaisdefinedas3ormoreconsecutiveventricularectopicbeatsatarateof
greaterthan100bpmandlastinglessthan30seconds.Inpatientswhoexperiencemultiplerunsofnonsustained
ventriculartachycardia,theriskforsuddenhemodynamiccollapsemaybesubstantial.
Nonetheless,nonsustainedventriculartachycardiaintheimmediateperiinfarctionperioddoesnotappeartobe
associatedwithanincreasedmortalityrisk,andnoevidencesuggeststhatantiarrhythmictreatmentoffersa
morbidityormortalitybenefit.However,nonsustainedventriculartachycardiaoccurringmorethan48hoursafter
infarctioninpatientswithLVsystolicdysfunction(LVejectionfraction<0.40)posesanincreasedriskforsudden
cardiacdeathelectrophysiologictestingandappropriatetherapyareindicatedinthesepatients.
Multipleepisodesofnonsustainedventriculartachycardiarequireintensifiedmonitoringandattentiontoelectrolyte
imbalances.Serumpotassiumlevelsshouldbemaintainedabove4.5mEq/L,andserummagnesiumlevelsshould
bekeptabove2.0mEq/L.Ongoingischemiashouldaggressivelybesoughtandcorrectediffound.

Sustainedventriculartachycardia
Sustainedventriculartachycardiaisdefinedas3ormoreconsecutiveventricularectopicbeatsatarategreater
than100bpmandlastinglongerthan30secondsorcausinghemodynamiccompromisethatrequiresintervention.
Monomorphicventriculartachycardiaismostlikelytobecausedbyamyocardialscar,whereaspolymorphic
ventriculartachycardiamaybemostresponsivetomeasuresdirectedagainstischemia.Sustainedpolymorphic
ventriculartachycardiaafteranAMIisassociatedwithahospitalmortalityrateof20%.
Emergencytreatmentofsustainedventriculartachycardiaismandatorybecauseofitshemodynamiceffectsand
becauseitfrequentlydeterioratesintoventricularfibrillation.Rapidpolymorphicventriculartachycardia(rate>150
bpm)associatedwithhemodynamicinstabilityshouldbetreatedwithimmediatedirectcurrentunsynchronized
cardioversionof200J(orbiphasicenergyequivalent).Monomorphicventriculartachycardiashouldbetreatedwith
asynchronizeddischargeof100J(orbiphasicenergyequivalent).
Ifsustainedventriculartachycardiaiswelltolerated,antiarrhythmictherapywithamiodarone(drugofchoice)or
procainamidemaybeattemptedbeforeelectricalcardioversion.Precipitatingcauses,suchaselectrolyte
abnormalities,acidbasedisturbances,hypoxia,ormedication,shouldbesoughtandcorrected.Forpersistentor
recurrentventriculartachycardia,overdrivepacingmaybeeffectiveinelectricallyconvertingthepatient'srhythmto
asinusrhythm.

Ventricularfibrillation
Theincidenceofprimaryventricularfibrillationisgreatestinthefirsthouraftertheonsetofinfarct(4.5%)and
declinesrapidlythereafter.Approximately60%ofepisodesoccurwithin4hours,and80%occurwithin12hours.
Secondaryorlateventricularfibrillationoccurringmorethan48hoursafteranMIisusuallyassociatedwithpump
failureandcardiogenicshock.Factorsassociatedwithanincreasedriskofsecondaryventricularfibrillationarea
largeinfarct,anintraventricularconductiondelay,andananteroseptalAMI.Secondaryventricularfibrillationin
conjunctionwithcardiogenicshockisassociatedwithaninhospitalmortalityrateof4060%.
Treatmentforventricularfibrillationisunsynchronizedelectricalcountershockwithatleast200300J(orbiphasic
energyequivalent)administeredasrapidlyaspossible.Eachminuteaftertheonsetofuncorrectedventricular
fibrillationisassociateda10%decreaseinthelikelihoodofsurvival.Restorationofsynchronouscardiacelectrical
activitywithoutthereturnofeffectivecontraction(ie,electromechanicaldissociation,orpulselesselectrical
activity)isgenerallyduetoextensivemyocardialischemiaand/ornecrosisorcardiacrupture.
Antiarrhythmics,suchasintravenousamiodaroneandlidocaine,facilitatesuccessfulelectricaldefibrillationand
helppreventrecurrentorrefractoryepisodes.Afterventricularfibrillationissuccessfullyconverted,antiarrhythmic
therapyisgenerallycontinuedasaconstantintravenousinfusionfor1224hours.
Prophylacticlidocainereducestheincidenceofventricularfibrillation,butitisnotusedbecauseitseemstobe
associatedwithanexcessivemortalityriskowingtobradycardicandasystolicevents. [5]Ontheotherhand,early
useofbetablockersinpatientswithAMIreducestheincidenceofventricularfibrillationaswellasdeath. [6]

ArrhythmicComplications:ReperfusionArrhythmias
Inthepast,thesuddenonsetofrhythmdisturbancesafterthrombolytictherapyinpatientswithAMIwasbelieved
tobeamarkerofsuccessfulcoronaryreperfusion.However,ahighincidenceofidenticalrhythmdisturbancesis
observedinpatientswithAMIinwhomcoronaryreperfusionisunsuccessful.Therefore,thesesocalledreperfusion
arrhythmiasareneithersensitivenorspecificforreperfusionandshouldbetreatedasdiscussedunder
AcceleratedIdioventricularRhythmintheArrhythmicComplications:VentricularArrhythmiassectionabove.

MechanicalComplicationsofMI
The3majormechanicalcomplicationsofAMIareventricularfreewallrupture(VFWR),ventricularseptalrupture
(VSR),andpapillarymusclerupturewithseveremitralregurgitation(MR).Eachofthesecomplicationscanresult
incardiogenicshock.Clinicalissuesrelatedtothesemechanicalproblemsarediscussedbelow.(Seealso
MyocardialRupture.)

Overviewofventricularfreewallrupture
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VFWRisthemostseriouscomplicationofAMI.VFWRisusuallyassociatedwithlargetransmuralinfarctionsand
antecedentinfarctexpansion.Itisthemostcommoncauseofdeath,secondonlytoLVfailure,anditaccountsfor
1530%ofthedeathsassociatedwithAMI.Incontrovertiblythemostcatastrophicofmechanicalcomplications,
VFWRleadstoacutehemopericardiumanddeathfromcardiactamponade.
TheoverallincidenceofVFWRrangesfrom0.86.2%.Theincidenceofthiscomplicationhasdeclinedoverthe
yearswithbetter24hoursystolicbloodpressurecontrolincreaseduseofreperfusiontherapy,betablockers,and
ACEinhibitorsanddecreaseduseofheparin[7].
DatafromtheNationalRegistryofMyocardialInfarction(NRMI)showedanelevatedincidenceofinhospital
mortalityamongpatientswhoreceivedthrombolytictherapy(12.1%)thanamongpatientswhodidnot(6.1%). [8]In
theThrombolysisinMyocardialInfarctionPhaseII(TIMIII)trial,16%ofpatientsdiedfromcardiacrupturewithin18
hoursoftherapy. [9]Patientswhounderwentpercutaneoustransluminalcoronaryangioplasty(PTCA)hadan
incidenceoffreewallrupturelowerthanthatofpatientsreceivingthrombolytictherapy.
RiskfactorsforVFWRincludeadvancedagegreaterthan70years,femalesex,nopreviousMIs,Qwaveson
ECG,hypertensionduringtheinitialphaseofSTEMI,corticosteroidorNSAIDuse,andfibrinolytictherapymore
than14hoursafterSTEMIonset.Patientswithahistoryofanginapectoris,previousAMI,multivesselcoronary
disease,andchronicheartfailurearelesslikelythanotherstodevelopVFWRoftheLVbecausetheydevelop
collateralsandischemicpreconditioning. [8,10,11]

ClinicalpresentationofVFWR
VFWRsaredramatictheypresentacutelyoroccasionallysubacutelyaspseudoaneurysmsandtheymostoften
involvetheanteriororlateralwalloftheLV.MostVFWRsoccurwithinthefirstweekafterAMI.
Beckeretalclassifiedthefollowing3typesofVFWRs [12]:
TypeIanabruptslitliketearthatisfrequentlyassociatedwithanteriorinfarctsandthatoccursearly
(within24h)
TypeIIanerosionofinfarctedmyocardiumattheborderbetweentheinfarctedandviablemyocardium
TypeIIIanearlyaneurysmformationcorrelatedwitholderandseverelyexpandedinfarcts
TypeIIIusuallyoccurslaterthantypeIortypeIIruptures.Thrombolytictherapyacceleratestheoccurrenceof
cardiacruptureinBeckertypeIandtypeIIVFWRs.Inseverelyexpandedinfarctions(typeIII),thrombolytic
therapydecreasestheincidenceofcardiacrupture.
Apseudoaneurysmisformedwhenadjacentpericardiumandhematomasealsoffamyocardialruptureor
perforation.Thewallofapseudoaneurysmismostoftenvisualizedasananeurysmaloutpouchingthat
communicateswiththeLVcavitybymeansofanarrowneck.Thiswalliscomposedofpericardiumandorganized
thrombusand/orhematoma.Itisdevoidofmyocardialelements,whereasatrueaneurysmhasalltheelementsof
theoriginalmyocardialwallandarelativelywidebase.Thepseudoaneurysmmayvaryinsizeandisathighriskof
rupturing.
ClinicalpresentationsofVFWRvarydependingontheacuity,location,andsizeoftherupture.Patientswithacute
VFWRpresentwithseverechestpain,abruptelectromechanicaldissociationorasystole,hemodynamiccollapse,
andpossiblydeath.Inaboutonethirdofthepatients,thecourseissubacute,andtheypresentwithsymptoms
suchassyncope,hypotension,shock,arrhythmia,andprolongedandrecurrentchestpain.

DiagnosisofVFWR
EarlydiagnosisofVFWRsandinterventionarecriticaltopatientsurvival.Ahighindexofsuspicionisrequired
whenpatientswithAMIpresentwithseverechestpain,shockorarrhythmias,andabruptdevelopmentof
electromechanicaldissociation.ECGsignsofimpendingVFWRhavelimitedspecificitybutincludesinus
tachycardia,intraventricularconductiondefect,andpersistentorrecurrentSTsegmentelevation.
Echocardiographyisthediagnostictoolofchoice.Thekeydiagnosticfindingisamoderatetolargepericardial
effusionwithclinicalandechocardiographicsignsofimpendingpericardialtamponade.Inpatientswithcardiac
tamponadeandelectromechanicaldissociation,moderatetoseverepericardialeffusionincreasesthemortality
risk.Thosepatientswithoutinitialcardiactamponade,whileatalowerrateofmortality,shouldstillbefollowed,as
laterupturemaystilloccur. [13]Theabsenceofpericardialeffusiononechocardiographyhashighnegative
predictivevalue.Iftheabilitytoobtaintransthoracicechocardiogramsislimitedinpatientsreceivingmechanical
ventilation,transesophagealechocardiographycanassistinconfirmingVFWR.
MRIprovidessuperiorimagequalityandpermitsidentificationofthesiteandanatomyofaventricular
pseudoaneurysm(ie,rupturedLVrestrainedbythepericardiumwithenclosedclot).However,MRIisoflimiteduse
intheacutesettingbecauseofthetimeinvolvedandnonportabilityofimagingunits.

TreatmentofVFWR
Themostimportantpreventionstrategyisearlyreperfusiontherapy,withpercutaneouscoronaryintervention(PCI)
beingthepreferredmodality.FibrinolytictherapyisassociatedwithoveralldecreasedriskofVFWRhowever,its
usemorethan14hoursafterSTEMIonsetcanincreasetheriskofearlyrupture. [14,15]
ThestandardtreatmentforVFWRisemergencysurgicalrepairafterhemodynamicstabilityisachieved.Patients
mayfirstneedintravenousfluids,inotropicagents,andemergencypericardiocentesis.
Pifarrandassociatesrecommendedthedeploymentofanintraaorticballoonpumptodecreasesystolicafterload
andimprovediastolicmyocardialperfusion. [16]
Severalsurgicaltechniqueshavebeenapplied,includinginfarctectomy,adheringwithbiologicgluepatchesmade
ofpolyethyleneterephthalatepolyesterfiber(DacronDuPont,Wilmington,DE)orpolytetrafluoroethylene
fluoropolymerresin(TeflonDuPont)anduseofpledgetedsutureswithoutinfarctectomy.

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Themortalityrateissignificantlyhighandlargelydependsonthepatient'spreoperativehemodynamicstatus.
Earlydiagnosis,rapidinstitutionofthemeasuresdescribedabovetoachievehemodynamicstability,andprompt
surgicalrepaircanimprovesurvivalrates.AfollowuptotheAcornrandomizedtrialdemonstratedlongterm
improvementinleftventricularstructureandfunctionaftermitralvalvesurgeryforaslongas5years.Thesedata
provideevidencesupportingmitralvalverepairincombinationwiththeAcornCorCapdeviceforpatientswith
nonischemicheartfailurewithsevereleftventriculardysfunctionwhohavebeenmedicallyoptimizedyetremain
symptomaticwithsignificantmitralregurgitation. [17]

Overviewofventricularseptalrupture
VSRisaninfrequentbutlifethreateningcomplicationofAMI.Despiteoptimalmedicalandsurgicaltreatment,
patientswithVSRhaveahighinhospitalmortalityrate.Duringtheprethrombolyticera,VSRsoccurredin13%of
individualswithMIs.Theincidencedeclinedwiththrombolytictherapy(to0.20.34%)becauseofimprovementsin
reperfusionandmyocardialsalvage.ThebimodaldistributionofVSRischaracterizedbyahighincidenceinthe
first24hours,withanotherpeakondays35andrarelymorethan2weeksafterAMI.
Inpatientsreceivingthrombolytics,themediantimefromtheonsetofsymptomsofAMItoseptalrupturewas1
dayintheGlobalUtilizationofStreptokinaseandTPA[tissueplasminogenactivator]forOccludedCoronary
Arteries(GUSTOI)trial[18]and16hoursintheShouldWeEmergentlyRevascularizeOccludedCoronariesfor
CardiogenicShock?(SHOCK)trial. [19]
Riskfactorsforseptalruptureincludeadvancedage(>65y),femalesex,singlevesseldisease,extensiveMI,and
poorseptalcollateralcirculation. [20,21]Beforetheadventofthrombolytics,hypertensionandabsenceofahistory
ofanginawereriskfactorsforVSR.ExtensiveinfarctsizeandRVinvolvementareotherknownriskfactorsfor
septalrupture.
InpatientswithAMIwithoutreperfusion,coagulationnecrosisdevelopswithin35daysafterinfarction.Neutrophils
migratetothenecroticzoneandundergoapoptosis,releaselyticenzymes,andhastenthedisintegrationof
necroticmyocardium.Somepatientshaveinfarctswithlargeintramuralhematomas,whichdissectintothetissue
andresultinearlyseptalrupture.Thesizeoftheseptalrupturerangesfromafewmillimeterstoseveral
centimeters.
VSRiscategorizedassimpleorcomplexdependingonitslength,course,andlocation.Insimpleseptalrupture,
theperforationisatthesamelevelonbothsidesoftheseptum,andadirectthroughandthroughcommunication
ispresentacrosstheseptum.Acomplexseptalruptureischaracterizedbyextensivehemorrhagewithirregular,
serpiginoustractsinthenecrotictissue.
SeptalrupturesaremostcommoninpatientswithlargeanteriorMIsduetoocclusionoftheLADarterycausing
extensiveseptalinfarcts.TheseinfarctsareassociatedwithSTsegmentelevationsandQwavesininferiorleads
(II,III,aVF)andtheseECGchangesarethereforemorecommonlyseeninseptalruptures. [22]Theserupturesare
generallyapicalandsimple.
SeptalrupturesinpatientswithinferiorMIoccurrelativelyinfrequently.Theserupturesinvolvethebasal
inferoposteriorseptumandareoftencomplex.

ClinicalpresentationofVSR
SymptomsofVSRcomplicatingAMIincludechestpain,shortnessofbreath,hypotension,biventricularfailure,
andshockwithinhourstodays.Patientsoftenpresentwithanew,loud,andharshholosystolicmurmur.This
murmurisloudestalongthelowerleftsternalborderandisassociatedwithapalpableparasternalsystolicthrill.
RVandLVS3gallopsarecommon.
Inpatientswithcardiogenicshockcomplicatingseptalrupture,themurmurandthrillmaybedifficulttoidentify.In
contrast,patientswithacuteMRoftenhaveasoftsystolicmurmurattheapexwithoutathrill.

DiagnosisofVSR
EchocardiographywithcolorflowDopplerimagingisthediagnostictoolofchoiceforidentifyingaVSR.(Seethe
imagebelow.)Itssensitivityandspecificityhavebeenreportedtobeashighas100%.Inaddition,itcanbeused
forthefollowing:
Definethesiteandsizeofseptalrupture
AssesstheLVandRVfunction
EstimatetheRVsystolicpressure
Quantifythelefttorightshunt
Cardiaccatheterizationisusuallyrequiredtoconfirmthediagnosis,quantitatethedegreeoflefttorightshunt,
differentiateVSRfromotherconditions(eg,mitralregurgitation),plusvisualizethecoronaryarteries.

Modified2dimensional(top)echocardiogramandcolorflow Dopplerimage(bottom).Apical4chamberview sshow abreachinthe

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interventricularseptumandfreecommunicationbetw eenventriclesthroughalargeapicalseptumventricularseptaldefectinapatient
w horecentlyhadananteriormyocardialinfarction.

InpatientswithVSR,rightheartcatheterizationshowsastepupinoxygensaturationfromtherightatriumtothe
RVincontrast,nostepupinoxygensaturationoccursamongpatientswithMR.ThepresenceoflargeVwaves
inthepulmonarycapillarywedgetracingsupportsthediagnosisofsevereacuteMR.
Leftventriculographycanalsobeusedtoidentifythesiteofventricularrupture(seeCardiacCatheterization[Left
Heart]).However,thisstudyisusuallyunnecessaryafteragoodqualityechocardiographicandDoppler
examinationisconducted.

TreatmentofVSR
ThekeytomanagementofVSRispromptdiagnosisandanaggressiveapproachtohemodynamicstabilization,
angiography,andsurgery.Theoptimalapproachincludeshemodynamicstabilizationwiththeadministrationof
oxygenandmechanicalsupportwithuseofanintraaorticballoonpump,aswellastheadministrationof
vasodilators(toreduceafterloadandthusLVpressureandthelefttorightshunt),diuretics,andinotropicagents.
Cardiaccatheterizationisneededtodefinethecoronaryanatomythisisfollowedbyurgentsurgicalrepair.
Medicaltherapyisintendedonlyfortemporarystabilizationbeforesurgery,asmostpatients'conditions
deterioraterapidlyandtheydieintheabsenceofsurgicalintervention.IntheGUSTOItrial,the30daymortality
ratewaslowerinpatientswithVSRwhounderwentsurgicalrepairthaninpatientstreatedmedically(47%vs
94%),aswasthe1yearmortalityrate(53%vs97%). [18]Lemeryetalreporteda30daysurvivalrateof24%in
patientstreatedmedicallycomparedwith47%inthosetreatedsurgically. [23]
CurrentguidelinesoftheAmericanCollegeofCardiology/AmericanHeartAssociationforthetreatmentofpatients
withseptalrupturecomplicatingAMIhighlighturgentsurgicalintervention,regardlessoftheirclinicalstatus. [24]
Surgicalmanagementofseptalruptureincludesthefollowingelements:
Promptestablishmentofhypothermiccardiopulmonarybypass
Anapproachtotheseptalrupturethroughtheinfarctareaandtheexcisionofallnecrotic,friablemarginsof
theseptumandventricularwallstoavoidpostoperativehemorrhage,residualseptaldefect,orboth
Reconstructionoftheseptumandventricularwallsbyusingprostheticmaterialandpreservationofthe
geometricconfigurationoftheventriclesandheartfunction
Percutaneousclosureofseptalruptureisarelativelynewapproach,oneusedinselectpatientsasanalternative
tosurgicalrepairorfortheacutestabilizationofcriticallyillpatients.However,percutaneousclosureiscurrently
unavailableinmanyinstitutions,andnolongtermoutcomedataareavailable.
Severalstudiesfailedtoshowarelationshipbetweenperioperativemortalityandconcomitantcoronary
revascularization(coronaryarterybypassgrafting).Patientswithcardiogenicshockduetoseptalrupturehavethe
poorestoutcome.IntheSHOCKtrial,theinhospitalmortalityratewashigherinpatientswithcardiogenicshock
duetoseptalrupture(87.3%)thaninpatientswithcardiogenicshockfromallothercauses(59.2%withpureLV
failureand55.1%withacuteMR). [19,25]
Inpatientswhosurvivesurgicalrepair,therateofrecurrentorresidualseptaldefectisreportedtobeabout28%,
andtheassociatedmortalityrateishigh.
Repeatsurgicalinterventionisindicatedinpatientswhohaveclinicalheartfailureorapulmonarysystemicfraction
greaterthan2.

Overviewofacutemitralregurgitation
MRisacommoncomplicationofAMIthatresultsfromlocalandglobalLVremodelingandthatisanindependent
predictorofheartfailureanddeath.MRtypicallyoccurs710daysafteranAMI,thoughthisonsetmayvary
accordingtothemechanismofMR.PapillarymuscleruptureresultinginMRoccurswithin114days(median,1
d).
MildtomoderateMRisoftenclinicallysilentanddetectedonDopplerechocardiographyperformedduringthe
earlyphaseofAMI.Insuchcases,MRrarelycauseshemodynamiccompromise.
Speckletrackingand3dimensionalechocardiographyprovedtobeimportantimagingtoolsinassessingreverse
LVremodelingafterdegenerativemitralvalveregurgitationsurgery.Subtleregionalpreoperativechangesin
diastolicfunctionoftheseptalandlateralwallcouldbepreoperativelyidentified,aidinginoptimizingthereferral
timingandrecognizingpotentialculpritsasindicatorsofdiseaserecurrenceaftermitralrepair. [26]
SevereacuteMRthatresultsfromtheruptureofpapillarymusclesorchordaetendineaeresultsinabrupt
hemodynamicdeteriorationwithcardiogenicshock.Rapiddiagnosis,hemodynamicstabilization,andprompt
surgicalinterventionareneededbecauseacutesevereMRisassociatedwithahighmortalityrate.
ThereportedincidenceofMRmayvarybecauseofseveralfactors,includingthediagnosticmethodsused,the
presenceorabsenceofheartfailure,thedegreeofMRreported,thetypeoftherapyrendered,andthetimefrom
infarctonsettotesting.
DuringtheGUSTOItrial,theincidenceofMRinpatientsreceivingthrombolytictherapywas1.73%. [18]The
SHOCKtrial,whichincludedMIpatientspresentingwithcardiogenicshock,noteda39.1%incidenceofmoderate
tosevereMR. [27]Kinnetalreportedthatreperfusionwithangioplastyresultedinan82%decreaseintherateof
acuteMR,ascomparedwiththrombolytictherapy(0.31%vs1.73%). [28]
RiskfactorsforMRareadvancedage,femalesex,largeinfarct,previousAMI,recurrentischemia,multivessel
coronaryarterydisease,andheartfailure.
SeveralmechanismscancauseMRafterAMI.Ruptureofthepapillarymuscleisthemostcommonlyreported

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mechanism.
Suchruptureoccursin1%ofpatientswithAMIandfrequentlyinvolvestheposteromedialpapillarymusclerather
thantheanterolateralpapillarymuscle,astheformerhasasinglebloodsupplyversusthedualsupplyforthe
latter.Papillarymusclerupturemayleadtoflailingorprolapseoftheleaflets,resultinginsevereMR.Papillary
muscledysfunctionduetoscarringorrecurrentischemiamayalsoleadtoMRinthesubacuteandchronic
phasesafterMIthisconditioncanresolvespontaneously.
LargeposteriorinfarctionsproduceacuteMRduetoasymmetricannulardilationandalteredfunctionand
geometryofthepapillarymuscle.

ClinicalpresentationofMR
PatientswithfunctionalmildormoderateMRareoftenasymptomatic.Theseverityofsymptomsvariesdepending
onventricularfunction.ClinicalfeaturesofacutesevereMRincludeshortnessofbreath,fatigue,anewapical
holosystolicmurmur,flashpulmonaryedema,andshock.
Thenewsystolicmurmurmaybeonlyearlytomidsystolic,notholosystolic.Itmaybesoftorevenabsent
becauseoftheabruptriseinleftatrialpressure,whichlessensthepressuregradientbetweentheleftatriumand
theLV,ascomparedwithchronicMR.Themurmurisbestheardattheapexratherthanthelowerleftsternal
border,anditisuncommonlyassociatedwithathrill.S3andS4gallopsareexpected.

DiagnosisofMR
ThecliniciancannotrelyonanewholosystolicmurmurtodiagnoseMRorassessitsseveritybecauseofthe
variablehemodynamicstatus.InapatientwithAMIwhopresentswithanewapicalsystolicmurmur,acute
pulmonaryedema,andcardiogenicshock,ahighindexofclinicalsuspicionforsevereMRisthekeytodiagnosis.
Chestradiographymayshowevidenceofpulmonaryedemaintheacutesettingwithoutclinicallysignificant
cardiacenlargement.
EchocardiographywithcolorflowDopplerimagingisthestandarddiagnostictoolfordetectingMR.Transthoracic
echocardiographyisthepreferredinitialscreeningtool,buttransesophagealechocardiographyisinvaluablein
definingtheseverityandexactmechanismofacuteMR,especiallywhensuspicionforpapillarymuscleruptureis
high.Cardiaccatheterizationshouldbeperformedinallpatientstodeterminetheextentandseverityofcoronary
arterydisease.

TreatmentofMR
Determinationofhemodynamicstability,elucidationoftheexactmechanismofacuteMR,andexpedienttherapy
areallnecessaryforafavorableoutcome.Medicalmanagementincludesafterloadreductionwiththeuseof
diuretics,sodiumnitroprusside,andnitratesinpatientswhoarenothypotensive.
Inpatientswhohavehemodynamiccompromise,intraaorticballooncounterpulsationshouldbedeployedrapidly.
Thisinterventionusuallysubstantiallyreducesafterloadandregurgitantvolume,improvingcardiacoutputin
preparationforsurgicalrepair.Withoutsurgicalrepair,medicaltherapyaloneinpatientswithpapillarymuscle
ruptureresultsininadequatehemodynamicimprovementandapoorshorttermprognosis.
Emergencysurgicalinterventionisthetreatmentofchoiceforpapillarymusclerupture.Surgicalapproachesmay
includemitralvalverepairorreplacement.Intheabsenceofpapillarymusclenecrosis,mitralvalverepairimproves
thesurvivalratemorethanmitralvalvereplacementdoes.Thisdifferenceisbecausethesubvalvularapparatusis
usuallypreserved.Mitralvalverepairalsoeliminatescomplicationsrelatedtomalfunctionoftheprosthesis.
Inpatientswithextensivenecrosisofpapillarymuscleand/orventricularfreewall,mitralvalvereplacementisthe
preferredmodality.Coronaryarterybypassgrafting(CABG)performedatthetimeofsurgerywasshowninone
studytoimproveshortandlongtermsurvival. [29]
TheonlysituationinwhichemergencysurgerycansafelybeavoidedisinthecaseofintermittentMRdueto
recurrentischemia.Inthesepatients,successfulmyocardialrevascularizationmaybeeffective.Thisprocedureis
accomplishedbymeansofeitherangioplastyorcoronaryarterybypassgrafting.

LeftVentricularAneurysm
OverviewofLVA
Leftventricularaneurysm(LVA)isdefinedasalocalizedareaofmyocardiumwithabnormaloutwardbulgingand
deformationduringbothsystoleanddiastole.TherateofLVAsafterAMIisapproximately315%.Riskfactorsfor
LVAafterAMIincludefemalesex,totalocclusionoftheLADartery,singlevesseldisease,andabsenceof
previousangina.
Morethan80%ofLVAsaffecttheanterolateralwalltheseareusuallyassociatedwithtotalocclusionoftheLAD.
Theposteriorandinferiorwallsarelesscommonlyaffected.LVAsgenerallyrangefrom18cm.Histologically,
LVAsarecomposedoffibrousscarthatisnotablythinned.Thisscarisclearlydelineatedfromtheadjacent
ventricularmuscleonmicroscopicexamination.
AhistoryofMIandthirdorfourthheartsoundsarecommonfindingsfromthepatient'shistoryandphysical
examination.

DiagnosisofLVA
Thechestradiographmayrevealanenlargedcardiacsilhouette.
ElectrocardiographyischaracterizedbySTelevationthatpersistsseveralweeksafterAMIandthatappearsinthe

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sameleadsasthoseshowingtheacuteinfarct.Echocardiographyis93%sensitiveand94%specificfordetection
ofLVA(seetheimagebelow),butcardiaccatheterizationremainsthestandardforestablishingthediagnosis.

Parasternallongaxisview oftheleftventricledemonstratesalargeinferobasalaneurysm.Notethew ideneckandbaseofthe

aneurysm.

TreatmentofLVA
Patientswithsmallorclinicallyinsignificantaneurysmscanbetreatedconservativelywithclosefollowup.Medical
therapygenerallyconsistsoftheuseofangiotensinconvertingenzyme(ACE)inhibitors,whichreduceafterload,
infarctextension,andLVremodeling.AnticoagulationisrequiredwhenpatientshavesevereLVdysfunctionand/or
thrombusintheLVoraneurysm.
SurgicalresectionoftheLVAisindicatedifsevereheartfailure,ventriculartachyarrhythmiasrefractorytomedical
treatment,orrecurrentthromboembolismispresent.

MiscellaneousComplications
Leftventricularmuralthrombus
LVMTisawellknowncomplicationofAMIandfrequentlydevelopsafteranteriorinfarctsoftheLVwall.The
incidenceofLVMTasacomplicationofAMIrangesfrom2040%andmayreach60%inpatientswithlarge
anteriorwallAMIswhoarenottreatedwithanticoagulanttherapy.LVMTisassociatedwithahighriskofsystemic
embolization.Anticoagulanttherapymaysubstantiallydecreasetherateofemboliceventsby33%comparedwith
noanticoagulation.
FactorscontributingtoLVMTformationincludeLVregionalwallakinesiaordyskinesiawithbloodstasis,injuryto
andinflammationoftheendocardialtissuethatprovidesathrombogenicsurface,andahypercoagulablestate.The
mostcommonclinicalpresentationofpatientswithLVMTcomplicatinganMIisstroke.Mostepisodesoccur
withinthefirst10daysafterAMI.Physicalfindingsdependonthesiteofembolism.
Transthoracicechocardiographyremainstheimagingmodalityofchoiceandis92%sensitiveand88%specificfor
detectingLVMT(seetheimagebelow).ManagementofLVMTincludesheparintreatmentfollowedbyoralwarfarin
therapyfor36months.InpatientswithLVAs,lifelonganticoagulationmaybeappropriateifamuralclotpersists.

Apical2chamberview depictsalargeleftventricularapicalthrombusw ithmobileextensions.

Pericarditis
TheincidenceofearlypericarditisafterMIisapproximately10%,andthiscomplicationusuallydevelopswithin24
96.Pericarditisiscausedbyinflammationofpericardialtissueoverlyinginfarctedmyocardium.Theclinical
presentationmayincludeseverechestpain,usuallypleuritic,andpericardialfrictionrub.
ThekeyECGchangeisdiffuseSTsegmentelevationinallornearlyallofleads.Echocardiographymayreveala
smallpericardialeffusion.Themainstayoftherapyusuallyincludesaspirinandnonsteroidalantiinflammatory
drugs(NSAIDs).Colchicinemaybebeneficialinpatientswithrecurrentpericarditis.

PostMIsyndrome(Dresslersyndrome)
Beforetheeraofreperfusion,theincidenceofpostMIsyndromerangedfrom15%afterAMI,butthisratehas
dramaticallydeclinedwiththeadventofthrombolysisandcoronaryangioplasty.
Althoughtheexactmechanismhasyettobeelucidated,postMIsyndromeisconsideredtobeanautoimmune
process.Clinicalfeaturesincludefever,chestpain,andothersignsandsymptomsofpericarditisoccurring23
weeksafterAMI.Managementinvolveshospitalizationandobservationforanyevidenceofcardiactamponade.
Treatmentcomprisesrest,useofNSAIDs,and/orsteroidsinpatientswithrecurrentpostMIsyndromewith
disablingsymptoms.

"Offhour"MIadmissions
DespitetheperceptionthatpatientswithanacuteMIadmittedduringoffhourshavehigherratesofdeath
comparedtothoseadmittedduringregularhours,amultivariateanalysesofoutcomesdataattheMayoClinicfor
weekends,nights,andholidaysadmissionsofpatientswithacuteMIwhounderwentpercutaneouscoronary
interventionsfoundnosignificantassociationforinpatientmortality,30daymortality,or30dayreadmissions,nor

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werethereanydifferencesinfindingsbetweenthosewithorwithoutSTelevationMI(STEMI,nonSTEMI). [30]
However,theinvestigatorsdidfindasignificantassociationbetweenoffhouradmissionsofthesepatientswith
compositemajorcomplicationsaswellasemergentcoronaryarterybypassgraftsurgery,ventriculararrhythmia,
cerebrovascularevents,andhemorrhage(gastrointestinal,retroperitoneal,intracranial).

ContributorInformationandDisclosures
Author
AshokKKondur,MDClinicalAssistantProfessor,DepartmentofInternalMedicine,DetroitMedicalCenter,
WayneStateUniversity
AshokKKondur,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofPhysiciansand
MichiganStateMedicalSociety
Disclosure:Nothingtodisclose.
Coauthor(s)
PawanHari,MD,MPHResidentPhysician,DepartmentofInternalMedicine,WayneStateUniversitySchool
ofMedicine
Disclosure:Nothingtodisclose.
LuisCAfonso,MDAssistantProfessor,DepartmentofInternalMedicineCardiology,ProgramDirectorof
CardiologyFellowshipProgram,WayneStateUniversityDirectorofEchocardiographyLaboratory,Harper
UniversityHospital
LuisCAfonso,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofCardiology,American
CollegeofPhysicians,AmericanMedicalAssociation,andAmericanSocietyofEchocardiography
Disclosure:Nothingtodisclose.
SpecialtyEditorBoard
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedicalCenter
CollegeofPharmacyEditorinChief,MedscapeDrugReference
Disclosure:MedscapeSalaryEmployment
BrianOlshansky,MDProfessorEmeritusofMedicine,DepartmentofInternalMedicine,UniversityofIowa
CollegeofMedicine
BrianOlshansky,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofCardiology,
AmericanHeartAssociation,CardiacElectrophysiologySociety,andHeartRhythmSociety
Disclosure:Guidant/BostonScientificHonorariaSpeakingandteachingMedtronicHonorariaSpeakingand
teachingGuidant/BostonScientificConsultingfeeConsultingBioControlConsultingfeeConsultingBoehringer
IngelheimConsultingfeeConsultingAmarinConsultingfeeReviewpanelmembershipsanofiaventisReview
panelmembership
ChiefEditor
EricHYang,MDAssociateProfessorofMedicine,DirectorofCardiacCatheterizationLaboratoryand
InterventionalCardiology,MayoClinicArizona
EricHYang,MDisamemberofthefollowingmedicalsocieties:AlphaOmegaAlpha
Disclosure:Nothingtodisclose.
AdditionalContributors
TheauthorsandeditorsofMedscapeReferencegratefullyacknowledgethecontributionsofpreviousauthors
SumanthRDaram,MD,andSrideviRPitta,MD,tothedevelopmentandwritingofthesourcearticle.

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