Myocardial Infarction - Practice Essentials, Background, Definitions

26/4/2016
MyocardialInfarction:PracticeEssentials,Background,Definitions
MyocardialInfarction
Author:AMaziarZafari,MD,PhDChiefEditor:EricHYang,MDmore...
Updated:Mar28,2016
PracticeEssentials
Myocardialinfarction(MI)(ie,heartattack)istheirreversibledeath(necrosis)of
heartmusclesecondarytoprolongedlackofoxygensupply(ischemia).
Approximately1.5millioncasesofMIoccurannuallyintheUnitedStates.Seethe
imagesbelow.
Acutemyocardialinfarction,reperfusiontype.Inthiscase,theinfarctisdiffuselyhemorrhagic.
Thereisarupturetrackthroughthecenterofthisposteriorleftventriculartransmuralinfarct.The
mechanismofdeathwashemopericardium.
Acuteanteriormyocardialinfarction.
SeeAreYouMissingSubtleMICluesonECGs?TestYourSkills,aCriticalImages
slideshow,tohelpidentifyavarietyofelectrocardiographicabnormalities.
Signsandsymptoms
PatientswithtypicalMImayhavethefollowingprodromalsymptomsinthedays
precedingtheevent(althoughtypicalSTEMImayoccursuddenly,withoutwarning):
Fatigue
Chestdiscomfort
Malaise
TypicalchestpaininacuteMIhasthefollowingcharacteristics:
Intenseandunremittingfor3060minutes
Retrosternalandoftenradiatesuptotheneck,shoulder,andjawanddown
totheulnaraspectoftheleftarm
Usuallydescribedasasubsternalpressuresensationthatalsomaybe
characterizedassqueezing,aching,burning,orevensharp
Insomepatients,thesymptomisepigastric,withafeelingofindigestionor
offullnessandgas
ThepatientsvitalsignsmaydemonstratethefollowinginMI:
Thepatientsheartrateisoftenincreasedsecondarytoahigh
http://emedicine.medscape.com/article/155919overview#a2
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sympathoadrenaldischarge
Thepulsemaybeirregularbecauseofventricularectopy,anaccelerated
idioventricularrhythm,ventriculartachycardia,atrialfibrillationorflutter,or
othersupraventriculararrhythmiasbradyarrhythmiasmaybepresent
Ingeneral,thepatient'sbloodpressureisinitiallyelevatedbecauseof
peripheralarterialvasoconstrictionresultingfromanadrenergicresponseto
painandventriculardysfunction
However,withrightventricularMIorsevereleftventriculardysfunction,
hypotensionisseen
Therespiratoryratemaybeincreasedinresponsetopulmonarycongestion
oranxiety
Coughing,wheezing,andtheproductionoffrothysputummayoccur
SeeClinicalPresentationformoredetail.
Diagnosis
Laboratorystudies
LaboratorytestsusedinthediagnosisofMIincludethefollowing:
Cardiacbiomarkers/enzymes:TheAmericanCollegeofCardiology/American
HeartAssociation(ACC/AHA)andtheEuropeanSocietyofCardiology
(ESC)guidelinesrecommendthatcardiacbiomarkersshouldbemeasuredat
presentationinpatientswithsuspectedMI
Troponinlevels:Troponinisacontractileproteinthatnormallyisnotfoundin
serumitisreleasedonlywhenmyocardialnecrosisoccurs
Creatinekinase(CK)levels:CKMBlevelsincreasewithin312hoursofthe
onsetofchestpain,reachpeakvalueswithin24hours,andreturnto
baselineafter4872hours
Myoglobinlevels:Myoglobinisreleasedmorerapidlyfrominfarcted
myocardiumthanistroponinurinemyoglobinlevelsrisewithin14hours
fromtheonsetofchestpain
Completebloodcount
Chemistryprofile
Lipidprofile
Creactiveproteinandotherinflammationmarkers
Electrocardiography
TheECGisthemostimportanttoolintheinitialevaluationandtriageofpatientsin
whomanacutecoronarysyndrome(ACS),suchasMI,issuspected.Itis
confirmatoryofthediagnosisinapproximately80%ofcases.
Cardiacimaging
ForindividualswithhighlyprobableorconfirmedacuteMI,coronaryangiography
canbeusedtodefinitivelydiagnoseorruleoutcoronaryarterydisease.
SeeWorkupformoredetail.
Management
Prehospitalcare
Forpatientswithchestpain,prehospitalcareincludesthefollowing:
Intravenousaccess,supplementaloxygen,pulseoximetry
Immediateadministrationofaspirinenroute
Nitroglycerinforactivechestpain,givensublinguallyorbyspray
TelemetryandprehospitalECG,ifavailable
Emergencydepartmentandinpatientcare
InitialstabilizationofpatientswithsuspectedMIandongoingacutechestpain
shouldincludeadministrationofsublingualnitroglycerinifpatientshaveno
contraindicationstoit.
TheAmericanHeartAssociation(AHA)recommendstheinitiationofbetablockers
toallpatientswithSTEMI(unlessbetablockersarecontraindicated).
IfSTEMIispresent,thedecisionmustbemadequicklyastowhetherthepatient
shouldbetreatedwiththrombolysisorwithprimarypercutaneouscoronary
intervention(PCI). [1,2]
AlthoughpatientspresentingwithnoSTsegmentelevationsarenotcandidatesfor
immediateadministrationofthrombolyticagents,theyshouldreceiveantiischemic
therapyandmaybecandidatesforPCIurgentlyorduringadmission.
CoronarycareunitshavereducedearlymortalityratesfromacuteMIby
approximately50%byprovidingimmediatedefibrillationandbyfacilitatingthe
implementationofbeneficialinterventions.Theseinterventionsincludethe
administrationofintravenous(IV)medicationsandtherapydesignedtodothe
following:
LimittheextentofMI
Salvagejeopardizedischemicmyocardium
Recanalizeinfarctrelatedarteries
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SeeTreatmentandMedicationformoredetail.
Background
Myocardialinfarction(MI)usuallyresultsfromanimbalanceinoxygensupplyand
demand,whichismostoftencausedbyplaquerupturewiththrombusformationin
anepicardialcoronaryartery,resultinginanacutereductionofbloodsupplytoa
portionofthemyocardium.(SeeEtiologyfordetails.)
Theelectrocardiographic(ECG)resultsofanacuteMIareseenbelow.
Acuteinferiormyocardialinfarction.
Althoughtheclinicalpresentationofapatientisakeycomponentintheoverall
evaluationofthepatientwithMI,manyeventsareeither"silent"orarenotclinically
recognizedbypatients,families,andhealthcareproviders.(SeeClinical
Presentation.)Theappearanceofcardiacbiomarkersinthecirculationgenerally
indicatesmyocardialnecrosisandisausefuladjuncttodiagnosis.(SeeWorkup.)
MIisconsideredpartofaspectrumreferredtoasacutecoronarysyndrome(ACS).
TheACScontinuumrepresentingongoingmyocardialischemiaorinjuryconsistsof
unstableangina,nonSTsegmentelevationMI(NSTEMI)collectivelyreferredto
asnonSTsegmentacutecoronarysyndrome(NSTEACS)andSTsegment
elevationMI(STEMI).PatientswithischemicdiscomfortmayormaynothaveST
segmentorTwavechangesdenotedontheelectrocardiogram(ECG).ST
elevationsseenontheECGreflectactiveandongoingtransmuralmyocardialinjury.
Withoutimmediatereperfusiontherapy,mostpatientswithSTEMIdevelopQ
waves,reflectingadeadzoneofmyocardiumthathasundergoneirreversible
damageanddeath.
ThosewithoutSTelevationsarediagnosedeitherwithunstableanginaor
NSTEMIdifferentiatedbythepresenceofcardiacenzymes.Boththeseconditions
mayormaynothavechangesonthesurfaceECG,includingSTsegment
depressionsorTwavemorphologicalchanges.
MImayleadtoimpairmentofsystolicordiastolicfunctionandtoincreased
predispositiontoarrhythmiasandotherlongtermcomplications.
Coronarythrombolysisandmechanicalrevascularizationhaverevolutionizedthe
primarytreatmentofacuteMI,largelybecausetheyallowsalvageofthe
myocardiumwhenimplementedearlyaftertheonsetofischemia.(SeeTreatment
StrategiesandManagement.)
Themodestprognosticbenefitofanopenedinfarctrelatedarterymayberealized
evenwhenrecanalizationisinducedonly6hoursormoreaftertheonsetof
symptomsthatis,whenthesalvageofsubstantialamountsofjeopardizedischemic
myocardiumisnolongerlikely.Theopeningofaninfarctrelatedarterymayimprove
ventricularfunctionandcollateralbloodflowpreventventricularremodeling,aswell
asdecreaseinfarctexpansion,ventricularaneurysmformation,andleftventricular
dilatationandreducelatearrhythmiaassociatedwithventricularaneurysms,and
mortality. [3,4,5]
Evidencesuggestsabenefitfromtheuseofbetablockers,angiotensinconverting
enzyme(ACE)inhibitors,angiotensinIIreceptorblockers,andstatins.
TheAmericanCollegeofCardiology(ACC)/AmericanHeartAssociation
(AHA)/EuropeanSocietyofCardiology/WorldHeartFederationreleasedthe
ObservationsFromtheTRITONTIMI38Trial(TrialtoAssessImprovementin
TherapeuticOutcomesbyOptimizingPlateletInhibitionWithPrasugrel
ThrombolysisinMyocardialInfarction38),whichbetteroutlinesauniversal
definitionofMI,alongwithaclassificationsystemandriskfactorsforcardiovascular
death. [6]
(SeeTreatmentformoredetails.)
Definitions
Thethirduniversaldefinitionofmyocardialinfarction
Myocardialinfarction(MI),commonlyknownasaheartattack,isdefined
pathologicallyastheirreversibledeathofmyocardialcellscausedbyischemia.
Clinically,MIisasyndromethatcanberecognizedbyasetofsymptoms,chest
painbeingthehallmarkofthesesymptomsinmostcases,supportedby
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biochemicallaboratorychanges,electrocardiographic(ECG)changes,orfindingson
imagingmodalitiesabletodetectmyocardialinjuryandnecrosis.
AccordingtothethirduniversaldefinitionofMI,implementedbyajointtaskforce
fromtheEuropeanSocietyofCardiology(ESC),AmericanCollegeofCardiology
(ACC)Foundation,AmericanHeartAssociation(AHA),andtheWorldHeart
Federation(WHF),MIisdiagnosedwheneitherofthefollowingtwocriteriaare
met. [7]
1.Detectionofanincreaseordecreaseincardiacbiomarkervalues(preferably
usingcardiactroponin[cTn])withatleastonevalueabovethe99thpercentileofthe
upperreferencelimit(URL)andwithatleastoneofthefollowingfindings:
Symptomsofischemia
NeworpresumednewsignificantSTsegmentTwave(STT)changesor
newleftbundlebranchblock(LBBB)
DevelopmentofpathologicQwavesontheECG
Imagingevidenceofnewlossofviablemyocardiumoranewregionalwall
motionabnormality
Identificationofanintracoronarythrombusbyangiographyorautopsy
2.Cardiacdeathwithsymptomssuggestiveofmyocardialischemiaandpresumed
newischemicchangesorinjuryornewBBBonECG,butdeathoccurredbefore
cardiacbiomarkerlevleswereobtained,orbeforecardiacbiomarkervalueswouldbe
increased.
TypesofMI
TheJointESC/ACCF/AHA/WHFTaskForcefurtherclassifiedMIinto5typeson
thebasisoftheunderlyingcause[5]:
Type1(spontaneousMI):Relatedtoatheroscleroticplaquerupture,
ulceration,fissuring,erosion,ordissectionwithintraluminalthrombusinone
ormoreofthecoronaryarteries,leadingtodecreasedmyocardialbloodflow
ordistalplateletemboliandtherebyresultinginmyocytenecrosis.The
patientmayormaynothaveunderlyingobstructivecoronaryarterydisease
(CAD).
Type2(MIsecondarytoanischemicimbalance):MIconsequentto
increasedoxygendemandoradecreasedsupply(eg,coronaryendothelial
dysfunction,coronaryarteryspasm,coronaryartery
embolus,tachyarryhthmias/bradyarrhythmias,anemia,respiratoryfailure,
hypertension,orhypotension).
Type3(MIresultingindeathwhenbiomarkervaluesare
unavailable):Sudden,unexpectedcardiacdeathbeforebloodsamplesfor
biomarkerscouldbedrawnorbeforetheirappearanceinthecirculation.
Type4a(MIrelatedtopercutaneouscoronaryintervention[PCI]):Elevation
ofbiomarkervalues(cTnispreferred)tomorethan5timesthe99
th percentileoftheURLinpatientswithnormalbaselinevalues(<99
th percentileURL)orariseofvaluesover20%ifthebaselinevaluesare
elevatedbutstableorfalling.Inaddition,anyofthefollowingarerequired:
(1)symptomssuggestiveofmyocardialischemia(2)newischemicECG
changesornewBBB(3)angiographiclossofpatencyofamajorcoronary
arteryorasidebranchorpersistentslowflowornofloworembolizationor
(4)demonstrationofthenewlossofviablemyocardiumornewregionalwall
motionabnormalitybycardiacimaging.
Type4b(MIrelatedtostentthrombosis):MIassociatedwithstent
thrombosisasdetectedbycoronaryangiographyorautopsyinthesettingof
myocardialischemiaincombinationwithariseand/orfallofcardiac
biomarkerswithatleastonevalueabovethe99 thpercentileURL.
Type5(MIrelatedtocoronaryarterybypassgrafting[CABG]):Elevationof
cardiacbiomarkervaluesmorethan10timesthe99 thpercentileURLin
patientswithnormalbaselinecTnvalues.Inaddition,either(1)new
pathologicQwavesornewBBB,(2)angiographicdocumentednewgraftor
nativecoronaryarteryocclusion,or(3)evidenceofnewlossofviable
myocardiumornewregionalwallmotionabnormalitybycardiacimagingis
required.
Acutecoronarysyndrome
Theterm"acutecoronarysyndrome"(ACS)referstoaspectrumofconditionsthat
occurduetoacutemyocardialischemiaand/orinfarctionasaresultofanabrupt
reductioninbloodflowthroughthecoronaryarterycirculation.
ACSisdividedintotwomaincategories,nonSTelevation(NSTE)ACSandST
elevationMI(STEMI)
NSTEACS
NSTEACSisfurtherdividedintounstableangina(UA)andnonSTelevation
myocardialinfraction(NSTEMI).Thesetwoconditionsresembleeachothervery
closely.UAisdistinguishedfromNSTEMIbytheabsenceofanelevationofcardiac
biomarkerlevels. [8]
STEMI
ThemajordiscriminatingfeatureofSTEMIisthepresenceofsymptomsof
myocardialischemia/injuryalongwithpersistentECGSTsegmentelevationin
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additiontothepresenceofcardiacbiomarkers. [9]
Pathophysiology
Cellulareffectsofmyocardialinfarction(MI)
Myocardialinjuryandmyocardialcelldeath
Forthenormalhearttocontinuetofunctionandtosteadilypumpbloodefficiently
tomeetthedemandsofthebody,itneedstohaveaconstantsupplyofoxygenand
nutrientsprovidedmainlybythecoronarycirculation.Aconditioncalledmyocardial
ischemiahappensifbloodsupplytothemyocardiumdoesnotmeetthedemand.If
thisimbalancepersists,ittriggersacascadeofcellular,inflammatoryand
biochemicalevents,leadingeventuallytotheirreversibledeathofheartmuscle
cells,resultinginMI.
EvolutionofMIandventricularremodeling
Thespectrumofmyocardialinjurydependsnotonlyontheintensityofimpaired
myocardialperfusionbutalsoonthedurationandthelevelofmetabolicdemandat
thetimeoftheevent.Severelossoftheabilityoftheheartmusclecelltocontract
canbeobservedasearlyaswithin60seconds.Persistenceofoxygendeprivationto
themyocardiumthroughthecessationofbloodsupplywillleadtoirreversible
myocardialinjurywithin20to40minutesanduptoseveralhours,dependingon
severalfactorsincludingtheexistingmetabolicstateofthebodyandpresenceof
coronarycollateralbloodflow. [10]
TypicalMIinitiallymanifestsascoagulationnecrosisthatisultimatelyfollowedbya
healingprocesscharacterizedbyformationofmyocardialscarring,knownas
myocardialfibrosis.Thismechanismallowssignificantarchitecturalchangestothe
composition,shapeandcontractilefunctionofthemyocardium,especiallyintheleft
ventricle,whichisthemajorcontributortothecontractilefunctionoftheheart.
Eventuallytheleftventricledilatesandchangestoamoresphericalshape,ina
processknownasventricularremodeling.Despitebeinganirreversibleprocess,
ventricularremodelingisaregulatedprocess,therefore,specifictreatment
strategiesandagentsshouldbeusedinacuteMImanagementinordertoreduce
theoccurrenceandseverityofventricularremodeling. [11]
Reperfusioninjury
Insomeoccasions,restorationofbloodflowtothedamagedmyocardiumtriggers
furtherischemiccellulardamage,thisparadoxicaleffectisknownasreperfusion
injury.Thisprocessinvolvesacomplexinteractionbetweenoxygenfreeradicalsand
intracellularcalcium,leadingtoaccelerationofmyocardialdamageanddeath,
microvasculardysfunctionandfatalarrhythmias.Theroleofnitricoxide(an
endotheliumderivedrelaxingfactor)asacardioprotectiveagentagainstreperfusion
injury,hasbeendemonstrated,asnitricoxideworkstoinactivateoxygenfree
radicals,therefore,amelioratingtheprocessofreperfusioninjury. [12]Despitethe
improvedunderstandingoftheprocessofreperfusioninjury,therearenospecific
therapiestopreventit.
Stunnedandhibernatingmyocardium
Stunnedmyocardiumisaconditionoftransientleftventriculardysfunctionfollowing
anischemiceventtothemyocardium.Itoccursifcoronarybloodflowwasimpaired
forabriefperiodoftime(5to15minutes).Usually,stunnedmyocardiumpersists
forhoursordaysfollowingthereestablishmentofcoronarybloodflow.
However,prolongedexposureofthemyocardiumtoanischemicstate,resultsinan
impairmentofitscontractilefunction,whichcanbepartialorcomplete,thisis
knownasmyocardialhibernation,andisreversiblewithrevascularization.
Bothmyocardialstunningandhibernationoccurbecauseoflossofessential
metabolitesrequiredfornormalmyocardialcontractility,suchasadenosine,whichis
neededforadenosinetriphosphate(ATP)dependentcontraction. [13]
Plaque
TheatheromatousplaqueresponsibleforacuteMIdevelopsinadynamicprocessin
multiplestages.Startingwitharterialintimalthickening,whichconsistsofvascular
smoothmuscleswithveryminimalornoinflammatorycells,thisprocesscanbe
observedsoonafterbirth.Subsequently,theformationoffibrouscapatheroma
occurs,whichhasalipidrichnecroticcorethatissurroundedbyfibroustissue.
Eventually,athincapfibroatheromadevelops,thisisalsoknownasavulnerable
plaquewhichiscomposedmainlyofalargenecroticcoreseparatedfromthe
vascularlumenbyathinfibrouscapthatisinfiltratedbyinflammatorycellsandis
deficientofsmoothmusclecells,makingitvulnerabletorupture. [14,15]
TheprocessofacutecoronarythrombosisleadingtoACSinvolvesthepathogenic
mechanismofplaquerupture,andlessfrequentlyplaqueerosion.
Etiology
Atherosclerosisisthediseaseprimarilyresponsibleformostacutecoronary
syndrome(ACS)cases.Approximately90%ofmyocardialinfarctions(MIs)result
fromanacutethrombusthatobstructsanatheroscleroticcoronaryartery.Plaque
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ruptureanderosionareconsideredtobethemajortriggersforcoronarythrombosis.
Followingplaqueerosionorrupture,plateletactivationandaggregation,coagulation
pathwayactivation,andendothelialvasoconstrictionoccur,leadingtocoronary
thrombosisandocclusion.
Withinthecoronaryvasculature,flowdynamicsandendothelialshearstressare
implicatedinthepathogenesisofvulnerableplaqueformation. [16]Alargebodyof
evidenceindicatesthatinnumerouscases,culpritlesionsarestenosesoflessthan
70%andarelocatedproximallywithinthecoronarytree. [17,18]Coronary
atherosclerosisisespeciallyprominentnearbranchingpointsofvessels. [19]Culprit
lesionsthatareparticularlypronetoruptureareatheromascontainingabundant
macrophages,alargelipidrichcoresurroundedbyathinnedfibrouscap.
Nonmodifiableriskfactorsforatherosclerosisincludethefollowing:
Age
Sex
Familyhistoryofprematurecoronaryheartdisease
Malepatternbaldness
Modifiableriskfactorsforatherosclerosisincludethefollowing[20]:
Smokingorothertobaccouse
Hypercholesterolemiaandhypertriglyceridemia,includinginheritedlipoprotein
disorders
Dyslipidemia
Diabetesmellitus
Hypertension
Obesity(abdominalobesity)
Psychosocialstress
Sedentarylifestyleand/orlackofexercise
Reducedconsumptionoffruitsandvegetables
Poororalhygiene
TypeApersonality
Elevatedhomocysteinelevels
Presenceofperipheralvasculardisease
MIcanalsooccurforcausesotherthanatherosclerosis.Nonatheroscleroticcauses
ofMIincludethefollowing:
Coronaryocclusionsecondarytovasculitis
Ventricularhypertrophy(eg,leftventricularhypertrophy,hypertrophic
cardiomyopathy)
Coronaryarteryemboli,secondarytocholesterol,air,ortheproductsof
sepsis
Coronarytrauma
Primarycoronaryvasospasm(variantangina)
Druguse(eg,cocaine,amphetamines,ephedrine)
Arteritis
Coronaryanomalies,includinganeurysmsofcoronaryarteries
Factorsthatincreaseoxygenrequirement,suchasheavyexertion,fever,or
hyperthyroidism
Factorsthatdecreaseoxygendelivery,suchashypoxemiaofsevereanemia
Aorticdissection,withretrogradeinvolvementofthecoronaryarteries
Inaddition,MIcanresultfromhypoxiaduetocarbonmonoxidepoisoningoracute
pulmonarydisorders.
Althoughrare,pediatriccoronaryarterydiseasemaybeseenwithMarfan
syndrome,Kawasakidisease,Takayasuarteritis,progeria,andcysticmedial
necrosis.
AcuteMIisrareinchildhoodandadolescence.Althoughadultsacquirecoronary
arterydiseasefromlifelongdepositionofatheromaandplaque,whichcauses
coronaryarteryspasmandthrombosis,childrenwithacuteMIusuallyhaveeitheran
acuteinflammatoryconditionofthecoronaryarteriesorananomalousoriginofthe
leftcoronaryartery.IntrauterineMIalsodoesoccur,ofteninassociationwith
coronaryarterystenosis. [21]
Epidemiology
UnitedStatesstatistics
Coronaryarterydisease(CAD)istheleadingcauseofdeathintheUnitedStates
approximately500,000700,000deathsrelatedtoCADoccureachyear,makingit
thecauseofdeathinanestimatedonethirdofalldeathsinthepopulationfor
thoseolderthan35years.
Approximately1.5millioncasesofmyocardialinfarction(MI)occurannuallyinthe
UnitedStatestheyearlyincidencerateisapproximately600casesper100,000
people.TheproportionofpatientsdiagnosedwithnonSTelevationMI(NSTEMI)
comparedwithSTelevationMI(STEMI)hasprogressivelyincreased.Despitean
impressivedeclineinageadjusteddeathratesattributabletoacuteMIsincethe
mid1970s,thetotalnumberofMIrelateddeathsintheUnitedStateshasnot
declined. [22]
ThedeathraterelatedtoacuteMIisapproximatelythreetimeshigherinmenthan
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inwomen.Itismorefrequentinblackpatientscomparedtowhitepatientss,an
excessthatdisappearsbyage75years.AmongtheHispanicpopulation,coronary
mortalityisnotashighasitisamongblackindividualsandwhitepersons. [23]
Europeanstatistics
CADisalsothenumberonecauseofdeathinEuropeancountries.
IntheEuropeanUnion,deathratesrelatedtoCADdroppedbyalmost30%
betweenthemid1960stothemidandlate1990showever,withinEastern
Europeancountries,therewasanincreaseindeathratesrelatedtoacuteMIinthe
early1990s,followedbyasubsequentdecline.IntheRussianFederation,
cardiovascularmortalityremainedthesame. [24]
Cardiovasculardiseaseinotherdevelopedcountriesandin
developingnations
AnanalysisofdeathcertificatesfromtheWorldHealthOrganization(WHO)
databasedemonstratedthatCADmortalityinJapanwassignificantlylowerthanin
theUnitedStatesandEurope,anditwasfurtherreducedbyabout30%bythemid
1990s. [24]
InChina,therehasbeenasignificantincreaseinmortalityrelatedtoCAD,thisis
mostlikelyattributedtotheincreaseincardiovasculardiseaseriskfactors,
predominantlysmokinganddyslipidemia. [25]
TheincidenceofCADandrelatedmortalityisexpectedtorisedramaticallyinother
developingcountriesincludingIndia,LatinAmerica,theMiddleEastandSub
SaharanAfrica,withanestimated80%increase,fromapproximately9millionin
1990toaprojected20millionby2020. [26,27]
ItisbelievedthattheseinternationaltrendsintheincidenceofCADand
subsequentacuteMIarelargelyrelatedtoconsequencesofsocialandeconomic
changesinthesecountries,resultinginbetterhealthcareaccessandincreasesin
lifeexpectancy,inadditiontoadoptionofwesternizeddiets,reductioninphysical
activity,andhigherratesofsmoking.
AmajorCanadianledglobalstudy(INTERHEARTtrial)in52countriesacross
Africa,Asia,Australia,Europe,theMiddleEast,andNorthandSouthAmerica,has
identified9easilymeasuredriskfactors(smoking,abnormalbloodlipidlevels,
hypertension,diabetes,obesity,diet,physicalactivity,alcoholconsumption,and
psychosocialfactors)thataccountforover90%oftheriskforacuteMI. [20]The
INTERHEARTinvestigatorsfoundthattheseriskfactorsarethesameinalmost
everygeographicregionandeveryracial/ethnicgroupworldwide,andtheyare
consistentinmenandwomen.TheINTERHEARTtrialshowedthatsmoking15
cigarettesdailyincreasedtheriskofanacuteMIby40%,andtheriskincreased
withtheamountoftobaccosmokedperday.Italsoconcludedthatallformsof
tobacco,includingfilteredandnonfilteredcigarettes,pipesandcigars,andchewing
tobacco,areharmful,andthatabdominalobesityisagreaterriskfactorthanbody
massindex(BMI),indicatingthatmeasurementofwaisttohipratiocouldreplace
BMIasanindicatorofobesity. [20,27,28]
Prognosis
Acutemyocardialinfarction(MI)isassociatedwitha30%mortalityrateabout50%
ofthedeathsoccurpriortoarrivalatthehospital.Anadditional510%ofsurvivors
diewithinthefirstyearaftertheirmyocardialinfarction.Approximatelyhalfofall
patientswithanMIarerehospitalizedwithin1yearoftheirindexevent.
Overall,prognosisishighlyvariableanddependslargelyontheextentoftheinfarct,
theresidualleftventricularfunction,andwhetherthepatientunderwent
revascularization.
Betterprognosisisassociatedwiththefollowingfactors:
Successfulearlyreperfusion(STelevationMI[STEMI]goals:patientarrival
tofibrinolysisinfusionwithin30minutesORpatientarrivaltopercutaneous
coronaryintervention[PCI]within90minutes)
Preservedleftventricularfunction
Shorttermandlongtermtreatmentwithbetablockers,aspirin,and
angiotensinconvertingenzyme(ACE)inhibitors
Poorerprognosisisassociatedwiththefollowingfactors:
Advancedage
Diabetesmellitus
Previousvasculardisease(eg,cerebrovasculardiseaseorperipheralvascular
disease)
ElevatedthrombolysisinMI(TIMI)riskscoreforunstableangina/nonST
elevationacutecoronarysyndrome(NSTEACS)(TIMIriskscoreincludes7
factors:age65y,3riskfactorsforcardiacdisease,previouscoronary
disease,STsegmentdeviation0.5mm,2episodesofanginainlast24
hours,aspirinusewithinpriorweek,andelevatedcardiacenzymelevels) [8,
29,30]
Delayedorunsuccessfulreperfusion
Poorlypreservedleftventricularfunction(thestrongestpredictorofoutcome)
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Evidenceofcongestiveheartfailure(KillipclassificationII) [31]orfrank
pulmonaryedema(KillipclassificationIII) [32]
ElevatedBtypenatriureticpeptide(BNP)levels [33,34,35]
ElevatedhighsensitiveCreactiveprotein(hsCRP),anonspecific
inflammatorymarker [36]
Involvementofelectrocardiograph(ECG)leadaVR [37,38]
Depression
Ithasbeenshownthatfivebaselineparametersatpresentationofpatientswith
acuteMIaccountforover90%oftheprognosticpredictorsof30daymortalityfrom
acuteMI.Theseparametersincludeage,systolicbloodpressureonpresentation,
Killipclassification,heartrate,andanatomiclocationoftheMI.
Killipclassification
TheKillipclassificationiswidelyusedinpatientspresentingwithacuteMIforthe
purposeofriskstratification,asfollows[39]:
KillipclassIincludesindividualswithnoclinicalsignsofheartfailure
KillipclassIIincludesindividualswithralesorcracklesinthelungs,anS 3
gallop,andelevatedjugularvenouspressure
KillipclassIIIdescribesindividualswithfrankacutepulmonaryedema
KillipclassIVdescribesindividualsincardiogenicshockorhypotension
(measuredassystolicbloodpressure<90mmHg),andevidenceoflow
cardiacoutput(oliguria,cyanosis,orimpairedmentalstatus).
PatientEducation
Patientswithactivesymptomsofacutecoronarysyndrome(ACS)shouldbe
instructedtocallemergencyservices(eg,911intheUnitedState),andtheyshould
betransportedbyemergencymedicalservicespersonnel,notbythemselves,family,
orfriends.Patientsshouldbeinstructedtogototheemergencydepartment
immediatelyifthesuspectedACSsymptomslastlongerthan20minutesatrestor
areassociatedwithnearsyncope/syncopeorhemodynamicinstability.
IfnitroglycerinisprescribedtoapatientwithsuspectedACS,thepatientshouldbe
instructedtotakeadoseifsymptomsarise.Ifnoreliefisexperienced5minutes
afterthefirstdose,thepatientshouldcontactemergencyservices.Ifreliefis
experiencedwithin5minutesofthefirstnitroglycerindose,repeateddosescanbe
givenevery5minutesforamaximumof3dosestotal.Ifbythenthesymptoms
havenotyetfullyresolved,thepatient,afamilymember,oracaregivershould
contactemergencyservices. [40]
Dietplaysanimportantroleinthedevelopmentofcoronaryarterydisease(CAD).
Educatepostmyocardialinfarction(MI)patientsabouttheroleofalowcholesterol
andlowsaltdiet.Adietitianshouldseeandevaluateallpatientspriortodischarge
fromthehospital.Additionally,emphasisonexercisetrainingshouldbemade,
becausecurrentevidencedemonstratesthatcardiacrehabilitationafterMIresultsin
lowerratesofrecurrentcardiovascularevents. [41]
Allpatientsshouldbeeducatedregardingthecriticalroleofsmokinginthe
developmentofCAD.Smokingcessationclassesshouldbeofferedtohelppatients
avoidsmokingaftertheirMI.
Forpatienteducationresources,seetheHeartHealthCenterandCholesterol
Center,aswellasHighCholesterol,CholesterolCharts(WhattheNumbersMean),
LifestyleCholesterolManagement,ChestPain,CoronaryHeartDisease,Heart
Attack,AnginaPectoris,CholesterolLoweringMedications,andStatinsfor
Cholesterol.
ClinicalPresentation
ContributorInformationandDisclosures
Author
AMaziarZafari,MD,PhDProfessorofMedicine,EmoryUniversitySchoolofMedicineChief,Sectionof
Cardiology,AtlantaVeteransAffairsMedicalCenter
AMaziarZafari,MD,PhDisamemberofthefollowingmedicalsocieties:AmericanAssociationforthe
AdvancementofScience,AmericanCollegeofCardiology,AmericanHeartAssociation,AmericanSocietyof
Echocardiography,AssociationofProfessorsofMedicine
Disclosure:Nothingtodisclose.
Coauthor(s)
MahmoudHAbdou,MDFellow,DivisionofCardiology,EmoryUniversitySchoolofMedicine
MahmoudHAbdou,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofCardiology,
AmericanCollegeofPhysicians,LibyanMedicalAssociation
SpecialtyEditorBoard
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedicalCenterCollege
ofPharmacyEditorinChief,MedscapeDrugReference
8/16
26/4/2016
Disclosure:ReceivedsalaryfromMedscapeforemployment.for:Medscape.
ChiefEditor
EricHYang,MDAssociateProfessorofMedicine,DirectorofCardiacCatherizationLaboratoryand
InterventionalCardiology,MayoClinicArizona
EricHYang,MDisamemberofthefollowingmedicalsocieties:AlphaOmegaAlpha
AdditionalContributors
SamerMGaras,MD,FACCInterventionalCardiologist,AdministrativePhysician,DiagnosticCardiology
Associates,StVincentsHealthcare
SamerMGaras,MD,FACCisamemberofthefollowingmedicalsocieties:AmericanCollegeofCardiology
AhmadMJeroudi,MDFellowinCardiovascularDisease,DivisionofCardiology,EmoryUniversitySchoolof
Medicine
ShilpaVReddy,MDFellowinCardiovascularDisease,DivisionofCardiology,EmoryUniversitySchoolof
Medicine
ShilpaVReddy,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofCardiology
Acknowledgements
DavidFMBrown,MDAssociateProfessor,DivisionofEmergencyMedicine,HarvardMedicalSchoolVice
Chair,DepartmentofEmergencyMedicine,MassachusettsGeneralHospital
DavidFMBrown,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofEmergency
PhysiciansandSocietyforAcademicEmergencyMedicine
DrewEvanFenton,MD,FAAEMPrivatePractice
GarySetnik,MDChair,DepartmentofEmergencyMedicine,MountAuburnHospitalAssistantProfessor,
DivisionofEmergencyMedicine,HarvardMedicalSchool
GarySetnik,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeofEmergencyPhysicians,
NationalAssociationofEMSPhysicians,andSocietyforAcademicEmergencyMedicine
Disclosure:SironaHealthSalaryManagementpositionSouthMiddlesexEMSConsortiumSalaryManagement
positionProceduresConsult.comRoyaltyOther
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedicalCenterCollege
ofPharmacyEditorinChief,MedscapeDrugReference
Disclosure:MedscapeSalaryEmployment
EricVanderbush,MD,FACCChief,DepartmentofInternalMedicine,DivisionofCardiology,HarlemHospital
CenterClinicalAssistantProfessorofCardiology,ColumbiaUniversityCollegeofPhysiciansandSurgeons
EricVanderbush,MD,FACCisamemberofthefollowingmedicalsocieties:AmericanCollegeofCardiologyand
AmericanHeartAssociation
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