ST Elevation in aVRWord文档格式.docx
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ST Elevation in aVRWord文档格式.docx
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infarctioninthisareacouldtheoreticallyproduceSTelevationinaVR.
STelevationisaVRisthoughttoresultfromtwopossiblemechanisms:
∙Diffusesubendocardialischaemia(producingreciprocalchangeinaVR)
∙Transmuralischaemia/infarctionofthebasalinterventricularseptum(e.g.duetoaproximalocclusionwithintheleftcoronarysystem)
NB.Thebasalseptumissuppliedbythefirstseptalperforatorartery(averyproximalbranchoftheLAD),soischaemia/infarctionofthebasalseptumwouldimplyinvolvementoftheproximalLADorLMCA.
PredictiveValueofSTEinaVR
InthecontextofwidespreadSTdepression+symptomsofmyocardialischaemia:
∙STEinaVR
≥1mmindicatesproximalLAD/LMCAocclusionorsevere3VD
≥1mmpredictstheneedforCABG
≥V1differentiatesLMCAfromproximalLADocclusion
∙AbsenceofSTelevationinaVRalmostentirelyexcludesasignificantLMCAlesion
InthecontextofanteriorSTEMI:
≥1mmishighlyspecificforLADocclusionproximaltothefirstseptalbranch
Inpatientsundergoingexercisestresstesting:
∙STEof
≥1mminaVRduringexercisestresstestingpredictsLMCAorostialLADstenosis
MagnitudeofSTelevationinaVRiscorrelatedwithmortalityinpatientswithacutecoronarysyndromes:
≥0.5mmwasassociatedwitha4-foldincreaseinmortality
≥1mmwasassociatedwitha6-to7-foldincreaseinmortality
≥1.5mmhasbeenassociatedwithmortalitiesrangingfrom20-75%
Foramorein-depthlookattheliteratureonaVR,clickhere
ABriefReviewoftheLiterature
Overthepast18years,multiplestudieshaveexaminedtheutilityofSTelevationinaVRforpredictingseverecoronaryarterydisease(proximalLAD/LMCA/3VD)andmortalityinpatientswithacutecoronarysyndromesandthoseundergoingexercisestresstesting.Someoftheimportantstudiesaresummarisedbelow…
Gorgelsetal.(1993)
Population:
∙113patientswithunstableangina,including20patientswithLMCAstenosisand
24patientswith3VD.
Findings:
∙PatientswithLMCAor3VDfrequentlydemonstratedST-segmentdepressioninmultipleleads(typicallyI,IIandV4-V6)plusST-segmentelevationinleadaVRduringattacksofangina.
Engelenetal.(1999)
∙100patientswithanteriorSTEMI.
∙STEinaVRofanymagnitudewas43%sensitiveand95%specificforLADocclusionproximaltothefirstseptalbranch.
Yamajietal.(2001)
∙16patientswithacuteLMCAocclusion,46patientswithacuteLADocclusionand24patientswithacuteRCAocclusion.
∙STEinaVR(≥0.5mm)
occurredwithasignificantlyhigherincidenceintheLMCAgroup(88%)thanintheLAD(43%)orRCA(8%)groups.
∙MagnitudeofSTEinaVRwassignificantlygreaterintheLMCAgroup(1.6
±
1.3mm)thantheLADgroup(0.4
1.0mm).
∙Incontrast,magnitudeofSTEinV1waslessintheLMCAgroup(0.0
2.1mm)thanintheLADgroup(1.4
1.1mm).
≥V1distinguishedtheLMCAgroupfromtheLADgroupwith
81%sensitivity,80%specificityand81%accuracy.
Barrabesetal.(2003)
∙775patientswithfirstpresentationofacuteNSTEMI.
∙Two-thirdsofpatientswithSTEinaVR≥1mmhadeitherLMCAocclusionorsevere3VD.
∙DegreeofSTEinaVRwasanindependentpredictorofmortality:
STEof≥1mmwasassociatedwithasix-toseven-foldincreaseinin-hospitalmortality(oddsratioofdeath=6.6).
∙MagnitudeofSTEinaVRwasalsocloselyassociatedwithratesofrecurrentischemiceventsandheartfailure.
∙STEinaVRpredictedtheneedforCABG–coronarygraftingwasrequiredin22%ofpatientswithaVRSTE>
1mmcomparedto5%ofthosewithout.
Rostoffetal.(2005)
∙150patientswithacutecoronarysyndromes–46withLMCAobstruction,104withocclusionofadifferentvessel.
∙STEinaVRwastwiceascommoninpatientswithLMCAocclusionasthosewithout(69.6%vs34.6%).
Kosugeetal.(2005)
∙310patientswithnon-ST-elevationacutecoronarysyndromes.
∙STEinaVR
≥
0.5mmwasthestrongestpredictorofLMCAor3VD(78%
sensitivity,86%
specificity,57%
PPVand95%
NPV).
∙STEinaVRwassuperiortothepresenceofSTdepressioninotherleadsforpredictingLMCA/3VD.
Ayguletal.(2008)
∙950patientswithSTEMI(anytype).
∙STEinaVR≥0.5mmpredictedproximalLADorLMCAocclusion(with50%sensitivity,91%specificity,55%PPV,89%NPV).
∙STEinaVR≥0.5mmwasalsoanindependentpredictorofmortality(in-hospitalmortalitywas19%inthosewith≥0.5mmSTEinaVRcomparedtoonly5%inthosewithout).
∙PatientswithSTEinaVRalsohadhigherheartrates,lowersystolicBPs,lowerejectionfractionsandworseKillipclassatthetimeofadmission.
Wongetal.(2011)
∙15,315patientswithSTEMIenrolledintheHERO-2trial
(heparinvsbivalirudinforacuteMI).
∙STE≥1.5mmin
aVRwasassociatedwithatwo-foldincreasein30-daymortalityforbothinferiorandanteriorSTEMI,comparedtothebaselinemortalityrateof10.8%.
Uthamalingametal.(2011)
∙454patientsundergoingbothexercisestresstesting(standardBruceprotocol)andcardiaccatheterizationwithin6months,including75patientswithLMCAorostialLADstenosis.
≥1mminaVRduringstresstestingpredictedLMCAorostialLADstenosiswithsensitivity75%,specificity81%andoverallaccuracy80%.
Kosugeetal.(2011)
∙572patientswithacuteNSTEMI.
∙DegreeofSTEinaVRwasthestrongestindependentpredictorofsevereLMCAocclusion/3VDrequiringCABG(oddsratio29.1),
followedbypositivetroponinTlevel(oddsratio1.27).
∙STE≥
1.0mminaVRidentifiedsevereLMCAocclusion/3VDwith80%sensitivity,93%specificity,56%PPV,and98%NPV.
More
ECGExamples
Example2–LMCAocclusion
AnothertypicalexampleofLMCAocclusion:
∙WidespreadSTdepression,mostprominentinthelateralleads(V4-6,I,aVL)
∙STelevation>
1mminaVR
∙STelevationinaVR≥
V1
Example3–LMCAocclusion
TheECGshows:
∙MarkedSTelevationinaVR>
>
V1
∙STdepressioninmulitpleleads(V2-6,I,II,aVL,aVF),tosomeextentmaskedbya
non-specificinterventricularconductiondelay
ThispatientpresentedtoourEDrecentlywithsevereischaemicchestpain,vomiting,syncope
(duetorunsofVT)andcardiogenicshock.
Hewastakenforemergentangiographyandfoundtohavea
completeostialocclusionofhisleftmaincoronaryartery.
Example4–ProximalLADocclusion
ThisECGshows:
∙STelevationinaVRandV1ofsimilarmagnitude.
∙WidespreadSTdepression(V3-6,I,II,III,aVF)
ThispatienthadasevereostialLADthrombusthatwasclosetotheleftmain.
(ThisECGisreproducedfromDrSmith’sECGBlog–clickheretoseetheECGinitsoriginalcontext)
Example5–SevereMulti-VesselDisease
∙STelevationinaVRandV1,ofsimilarmagnitude
∙STdepressioninmultipleleads(V5-6,I,II,aVL,aVF)
∙EvidenceofanteroseptalSTEMI–STelevationwithQwaveformationinV1-3
ItwouldbereasonabletosuspectaproximalLADocclusionbasedonthisECG.However,thispatientactuallyhadseveremulti-vesseldisease.
Angiographydemonstratedachronictotalocclusionofhiscircumflexartery,withcriticalstenosesofhisproximalLAD,RCAandramusintermedius.Surprisingly,inthiscasetheculpritvesselwasthoughttobetheRCA,whichhadbeencollateralisinghischronicallyoccludedcircumflex.
Implicationsfortherapyinacutecoronarysyndromes
GiventheabilityofSTEinaVR
topredictcriticalcoronarylesionsanddeath,thisECGpatternisincreasinglybeingrecognisedasa
“STEMIequivalent”
that
requiresemergentreperfusiontherapytopreventcardiogenicshockanddeath.
Furthermore,thepresenceorabsenceofSTEinaVRmaypotentiallyinformthedecisiontogivethienopyridineplateletinhibitors(e.g.
clopidogrel,
prasugrel)duringanacutecoronarysyndrome:
∙Clopidogreltreatment≤7daysbeforeCABGisassociatedwithan
increaseinmajorbleeding,haemorrhage-relatedcomplications,andtransfusionrequirements.
∙Prasugrelisassociatedwith
evenmorebleedingthanclopidogrel.
∙IfurgentCABG(within7days)islikely,thenthereisanargumentforomittingthienopyridinesduringtheinitialmanagementofanacutecoronarysyndrome(oratleastusingclopidogrelinsteadofprasugrel).
Intherecentstudyby
1mmwasastrongpredictorofsevereLMCA/3VDrequiringCABG.
∙Conversely,patientswith<
1mm
STelevationinaVRhadanegligibleriskof
severeLMCA/3VDrequiringCABG.
Basedonthisdata:
∙Patientswith<
1mmSTEinaVRmaysafelyreceiveclopidogrel/prasugrelduringtheinitialtreatmentoftheirACSa
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