Cardiogenic-Shock-NT-Cardiovascular-Center：心源性休克-NT心血管中心

CardiogenicShockNickTehrani,MDCardiogenicShockNickTehrani,1Definition<90mmHg<2.2li/min.m2>15mmHgDefinition<90mmHg<2.2li/min.2SHOCKRegistry

JACCSept.2000,Supp.A

SpectrumofClinicalPresentationsMortalityRespiratoryDistressHypotensionHypoperfusion21%22%70%60%5.6%28%65%1.4%SHOCKRegistryJACCSept.20003RiskFactorsforCardiogenicShockDuetoAMI-mediatedLVDysfunction…Age>65FemalegenderLargeinfarctionAnteriorinfarctionPriorinfarctionDMPriorHTNRiskFactorsforCardiogenicS4Post-mortemstudyofShockheartsAtleast40%ofthemyocardiuminfarctedintheaggregate(oldandnewinjury)80%havesignificantLADdisease2/3havesevere3VdzPost-mortemstudyofShockhea5OutcomesofCardiogenicShockHistoricmortality60-80%Morerecentlyreportedmortalitynumbers67%intheSHOCKtrialregistry56%inGUSTO-I(v.s.3%inPts.withoutshock)OutcomesofCardiogenicShockH6OutcomesofCardiogenicShockTheSTpatterninCardiogenicshock:15-30%Non-STelevationMIOlderMortality:77%70-85%STelevationsMI/NewLBBBMortality:53-63%SHOCKregistryfindingsonthispoint…OutcomesofCardiogenicShockT7OutcomesofCardiogenicShockTheSHOCKregistrySimilarmortalityinthetwogroups62.5%innon-STelevation60.4%withSTelevationOutcomesofCardiogenicShockT8PathophysiologyofShockEffectofHypotensionFlowinnormalcoronary:RegulatedbymicrovascularresistanceCoronaryflowmaybepreservedatAOpressuresaslowas50mmHgIncoronaryvesselwithcriticalstenosis:VasodilatorreserveofmicrovascularbedisexhaustedDecreaseinAOpressure=>CoronaryhypoperfusionPathophysiologyofShockEffect9PathophysiologyofShockEffectofHypotension(continued…) Normalheartextracts65%oftheO2presentintheblood

LittleroomforaugmentationofO2extractionPathophysiologyofShockEffect10PathophysiologyofShock

Effectof:

ElevatedLVEDP

oncoronaryflowLVEDP(mmHg)PathophysiologyofShockEffec11PathophysiologyofShock Hypotension+LVEDPandcriticalstenosis

MyocardialHypoperfusionLVdysfunctionSystemiclacticacidosisImpairmentofnon-ischemicmyocardiumworseninghypotension.PathophysiologyofShock Hypot12SchematicLVEDPelevationHypotensionDecreasedcoronaryperfusionIschemiaFurthermyocardialdysfunctionNeurohormonalactivationVasoconstrictionEndorganhypoperfusionSchematicLVEDPelevation13MedicalStabilizationofShockPts.Figureoutthevolumestatus,SwanifindoubtAirwayJudiciousafterloadreductionMaintainAVsynchronyDon’ttolerateAfibDualchamberpacingifA-VblockpresentCorrectAcid-BasedisturbancesMaintainBP(IABPand/orPressors)….MedicalStabilizationofShock14PhysiologicEffectofIABPin-vivoDecreasedafterloadLVO2consumption

Williams,et.al.,Circulation1982

Kern,et.al.,Circulation1993Coronarybloodflowvelocitywasmeasuredusingdoppler-wireinninepatientswithcriticalstenoticlesions.Peakdiastoliccoronaryflowvelocitybeyondthestenosiswasunaffectedbyintra-aorticballoonpumping.TherewasunequivocalIABP-mediatedaugmentationofbothproximalanddistalcoronarybloodflowvelocitiespostPTCA.

PhysiologicEffectofIABPin-15PhysiologicEffectofIABPin-vivoFuchs,et.al.,

Circulation,1983Greatcardiacveinflowwasmeasuredinsevenpatientsreceivingmaximaldrugtherapyandrequiringballoonpumping

forunstableangina.All

patientshadgreaterthan90%stenosisoftheproximalLADcoronaryartery.Increasedgreatcardiacveinflowcorrelatedwithincreasedmeanaortic

diastolicpressureacrosschangesinballoonvolumes(off,20cc,30cc,

and40cc)andchangesinassistratio(off,1:4,1:2,and1:1)(p=.02).

PhysiologicEffectofIABPin-16PhysiologicEffectofIABPin-vivoThus

balloonpumpingincreasedflowtoabedfedbythe

criticalstenosis,orcollateralvesselsPhysiologicEffectofIABPin-17IABPinAcuteMIJACC1985IABPinAcuteMIJACC198518IABPinAcuteMIPre-thrombolyticeraNoLytics,ASA,orLopressor20patientswithAcuteMIand“extensivemyocardiumatriskperbaselineThalium”wereRandomized.Pt.sinShockwereexcludedStd.Rx:O2,MSo4,Lido,HeparinStdRx+IABPPlusIVNTGIABPinAcuteMIPre-thrombolyt19IABPinAcuteMIPatientshadrepeatThaliumscanonDay-4Nodifferenceswereobservedbetweenthetwogroupsregarding: -Thaliumdefectscorecomparingdays1and4 -Theejectionfractioncomparingdays1and4

=> “Unlikelythatamortalitybenefitisconferred

bytheIABP/NTGcombination”

IABPinAcuteMIPatientshadr20UtilityofIABPinShockPts.Observedclinicalbenefits:Improvedacid-basestatusImprovedurineoutputImprovedmentationImprovedoverallhemodynamicsAllthis,however,doesnotadduptoimprovedsurvivalwithoutFlowRestorationUtilityofIABPinShockPts.O21ThrombolysisinCardiogenicShockRatesofReperfusion

Lower,andRatesofReocclusion

Higher Thaninnon-shockptsPossibleReason: Diffusionofthrombolyticagent

intothethrombusmaybePRESSUREDEPENDENT.ThrombolysisinCardiogenicSh22BPEffectonefficacyoflyticsinShockDogdataLADocclusionbythrombusHypotensioninducedbyphlebotomyPrewittJACC1994;23:784BPEffectonefficacyoflytic23AnyRandomizedTrialsof

ThrombolysisinCardiogenicShock????MostthrombolytictrialsspecificallyexcludedpatientsincardiogenicshockTheonlylargeplacebo-controlledthrombolyticstudyspecificallyexaminingPts.presentingwithshockwasGISSI-1Streptokinase=>NoBenefitAnyRandomizedTrialsof

Thro24CombinedIABPandThrombolysisGUSTO-I:IABPin62ofthe310lyticRx’dPts.inshockObservationalData:CombinedIABPandThrombolysis25CombinedIABPandThrombolysisKovack,et.al.,JACC2019Stomel,et.al.,Chest1994 Tworetrospectiveobservationalseriesfromcommunityhospitals:

ImprovedsurvivalfromcombinationRx.CombinedIABPandThrombolysis26CombinedIABPandThrombolysisObservationalDatafromSHOCKRegistery:CombinedIABPandThrombolysis27

CombinedIABPandThrombolysis

-Barron,et.al.,AHJJune2019-NationalRegistryofMI-2,Database

-21,178pts.Presentingwithordevelopingpost-MIshock-32%ReceivedIABPP<0.001P=NSTTTTIABPPPTCAPPTCAIABPTheyoungerpts.,twiceaslikelytogetTT

=>SelectionBias

P<0.001P=NSTTTTIABPPPTCAPPT28CombinedIABPandThrombolysis

AccompanyingEditorialbyMagnusOhman,andJudithHochman:“Although,thereisawealthofphysiologicandoutcomesdatatosupporttheuseofearlyIABPtherapyincardiogenicshock(inconjunctionwithlytics),randomizedtrialsareclearlyneeded….”CombinedIABPandThrombolysis29CombinedIABPandThrombolysisTheonly

randomizedtrialonthesubject:

ThrombolysisandCounterpusiontoImproveCardiogenicShockSurvival(TACTICS):ResultsofaProspectiveRandomizedTrial.

MagnusOhman,et.al.,

CirculationOct.2000Supp.AbstractCombinedIABPandThrombolysis30TACTICSSTelevationMIpatients,presentingwithin12hoursofSx,andCardiogenicshock57PatientswererandomizedThrombolyticTherapyaloneThrombolyticTherapy+IABPTACTICSSTelevationMIpatient31TACTICSTheprimaryendpointof6monthmortalitywasnotstatisticallysignificant,P=0.3Subgroupanalysis:ForKILLIPclassesIIIandIV,P=0.07TACTICSTheprimaryendpointof32PATIENTISINSHOCKw/STelevations,and<12hrsSxonset

IABPPressors

MayincreasetheefficacyofLyticsAdministrationofLyticsshouldnotbedelayed

inanticipationofplacementofIABPdespitelackofrandomizeddataprovingefficay.

IfEARLYREVASCULARIZATION

isnottobepursued:PATIENTISINSHOCKw/STelev33SHOCKTrialWhether

EARLYREVASCULARIZATION

improvessurvivalamong

patientswithcardiogenicshock?SHOCKTrial34SHOCKTrial302Pts.withSTelevation(ornewLBBB)andcardiogenicshockImmediateRevascularization(CABG/PTCA)Laterevascularization(ifindicated)

deferredforatleast54hoursWithin36hrs.ofMIonsetWithin12hrs.ofShockonsetSHOCKTrial302Pts.withSTel35SHOCKTrial:

Primaryendpoint,30daysmortalityDiff.=9%P=0.1147%56%MortalityDiff.=13%P=0.02750%63%52.4%66.4%Diff.=14%P<0.02Revasc.MedRxSHOCKTrial:

Primaryendpoin36SHOCKTrial

Whywasn’tthePrimaryend-pointmet?Lowmortalityintheinitialmedicalmgtgp.HighratesofIABPuse,86%TTuse,63%Delayedrevasculariztion,21%Medianof104hrs postrandomization30daysmortality47%56%SHOCKTrial

Whywasn’tthePri37SHOCKTrial:

Subgroupanalysis,Agelessthan75Revasc.MedRxP=0.02CI<1.0P=0.002CI<1.0Mortality45%65%41%56%66.7%48.4%P<0.02CI<1.0SHOCKTrial:

Subgroupanalysi38SHOCKTrial:

WhattodowithPt.solderthan75Totalno.ofPt.solderthan75y.o.=56(/302)Theearlyrevascularizationgroupshadworseoutcomeat:

30days(CI>>1.0)6months(CI>>1.0)12months,nodifferenceinoutcomeSHOCKTrial:

Whattodowith39WhattodowithPt.solderthan75SHOCKRegistryresultsisincontrasttotheSHOCKTrialfindingsinthissubgroup.Thoseolderthan75y.o.,selectedtoundergoERVhadasurvivaladvantage.Casebycaseassessmentinthispopulation,andnotacrosstheboardexclusioniscalledfor.WhattodowithPt.soldertha40RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockSHOCKTrial:Revascularization(N=152)MedicalTreatment(N=150)IIb/IIIaAntagonist41.7%25%StentPlacement35.7%52.3%RoleofIIb/IIIaInhibitorsan41RoleofIIb/IIIainhibitorsinCardiogenicShock

RetrospectivesubgroupanalysisfromthePURSUITtrial Hassade,et.al.,JACC,2000

RandomizationtoeptifibatidedidnotaffecttheincidenceofshockPatientsrandomizedtoeptifibatidewhodevelopedshockhadasignificantlyreducedincidenceofdeathat30daysApossiblemechanismofbenefitisreliefofmicrovascularobstructionRoleofIIb/IIIainhibitorsin42RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockLong-TermMortalityBenefitWiththeCombinationofStentsandAbciximabforCardiogenicShockComplicatingAcuteMyocardialInfarction[CoronaryArteryDisease]Chan,AlbertW.MD,MS;Chew,DerekP.MBBS;Bhatt,DeepakL.MD;Moliterno,DavidJ.MD;Topol,EricJ.MD;Ellis,StephenG.MD

AJCJan.15,2019RoleofIIb/IIIaInhibitorsan43RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockSinglecenter,non-randomizedDatacollected:Jan.1993andJune2000

Thirtymonthfollow-upavailable96Pt.sw/CardiogenicShockStent+ReoproN=27StentOnlyN=14PTCA+ReoproN=18PTCAOnlyN=37RoleofIIb/IIIaInhibitorsan44RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockThirtydayMortalityRates(%)Stent+ReoproStentOnlyPTCA+ReoproPTCAOnlyAbsenceofStentuse:HR2.39,95%CI1.22to4.67,p=0.01AbsenceofAbciximabuse:HR1.95,95%CI1.03to3.71,p=0.04OnUnivariateanalysis:EF<=30%

HR3.44,95%CI1.35to8.78,p=0.01RoleofIIb/IIIaInhibitorsan45RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockUseofStents29%Absolutemortalityreduction1additionallifesavedforeach3-4treatedPatients.Abciximab+Stenting10%Absolutemortalityreduction1additionallifesavedforeach10patientstreated.At30monthsRoleofIIb/IIIaInhibitorsan46RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShock

ResultsofPrimaryPercutaneousTransluminalCoronaryAngioplastyPlusAbciximabWithorWithoutStentingforAcuteMyocardialInfarctionComplicatedbyCardiogenicShock[CoronaryArteryDisease]Giri,SatyendraMD,MPH,MRCP;Mitchel,JosephDO;Azar,RabihR.MD,MSc;Kiernan,FrancisJ.MD;Fram,DanielB.MD;McKay,RaymondG.MD;Mennett,RogerMSc;Clive,JonathanPhD;Hirst,JeffreyA.MD,MS AJC,15January2019

.RoleofIIb/IIIaInhibitorsan47RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockThiswasanonrandomized,prospectiveobservationalstudy.113(13.9%)werediagnosedwithcardiogenicshockfrom8/95to8/99.RoleofIIb/IIIaInhibitorsan48RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockNoReoproWithReoproRoleofIIb/IIIaInhibitorsan49RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockMultivariateAnalysisRoleofIIb/IIIaInhibitorsan50RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockSpeculation: GreateruseofAbxicimab,andStentsintheSHOCKTrialmaywellhaveresultedinapositiveprimaryendpoint. Theagecutoffof75mayormaynothaveretaineditssignificancevis-à-visincreasedmortality.RoleofIIb/IIIaInhibitorsan51ReversalofCardiogenicShockbyPercutaneousLeftAtrial-to-FemoralArterialBypassAssistance

Holger,et.al,Circulation.2019;104:2917.VADs

wereimplantedin18consecutivepatientswhohadcardiogenic

shockaftermyocardialinfarctionA21Fvenous

cannulaintotheleftatriumbytransseptalpunctureusingTEEPtsservedastheirowncontrolsAllhemodynamicparametersshowedsignificantimprovement“Theinfluence

ofthisdeviceonlong-termprognosiswarrantsfurtherinvestigation.”ReversalofCardiogenicShock52TakeHomePointsCombiningReoprowithStenting

islikelytoenhancethebenefitofearlyrevascularization.IABPhelpfulinstabilizingthePt.MitigatesclinicalsignsofSHOCKMayimproveoutcomewithconcurrentLyticsNodefinitiveevidence(randomizedtrials)showingimprovedoutcomeswithIABP/Lyticcombinaiton.TakeHomePointsCombiningReop53TakeHomePointsNothingmagicalabouttheagecutoffof75,casebycaseassessmentinthispopulationiscalledfor.Ifpt.isnotacandidateforearlyrevascularization,butiswithin12hrs.ofMIonset,administrationoflytics(subjecttorisk-benefitassessment,age,grafts,…)shouldnotbedelayedinanticipationofplacementofIABP.TakeHomePointsNothingmagica54谢谢！谢谢！55CardiogenicShockNickTehrani,MDCardiogenicShockNickTehrani,56Definition<90mmHg<2.2li/min.m2>15mmHgDefinition<90mmHg<2.2li/min.57SHOCKRegistry

JACCSept.2000,Supp.A

SpectrumofClinicalPresentationsMortalityRespiratoryDistressHypotensionHypoperfusion21%22%70%60%5.6%28%65%1.4%SHOCKRegistryJACCSept.200058RiskFactorsforCardiogenicShockDuetoAMI-mediatedLVDysfunction…Age>65FemalegenderLargeinfarctionAnteriorinfarctionPriorinfarctionDMPriorHTNRiskFactorsforCardiogenicS59Post-mortemstudyofShockheartsAtleast40%ofthemyocardiuminfarctedintheaggregate(oldandnewinjury)80%havesignificantLADdisease2/3havesevere3VdzPost-mortemstudyofShockhea60OutcomesofCardiogenicShockHistoricmortality60-80%Morerecentlyreportedmortalitynumbers67%intheSHOCKtrialregistry56%inGUSTO-I(v.s.3%inPts.withoutshock)OutcomesofCardiogenicShockH61OutcomesofCardiogenicShockTheSTpatterninCardiogenicshock:15-30%Non-STelevationMIOlderMortality:77%70-85%STelevationsMI/NewLBBBMortality:53-63%SHOCKregistryfindingsonthispoint…OutcomesofCardiogenicShockT62OutcomesofCardiogenicShockTheSHOCKregistrySimilarmortalityinthetwogroups62.5%innon-STelevation60.4%withSTelevationOutcomesofCardiogenicShockT63PathophysiologyofShockEffectofHypotensionFlowinnormalcoronary:RegulatedbymicrovascularresistanceCoronaryflowmaybepreservedatAOpressuresaslowas50mmHgIncoronaryvesselwithcriticalstenosis:VasodilatorreserveofmicrovascularbedisexhaustedDecreaseinAOpressure=>CoronaryhypoperfusionPathophysiologyofShockEffect64PathophysiologyofShockEffectofHypotension(continued…) Normalheartextracts65%oftheO2presentintheblood

LittleroomforaugmentationofO2extractionPathophysiologyofShockEffect65PathophysiologyofShock

Effectof:

ElevatedLVEDP

oncoronaryflowLVEDP(mmHg)PathophysiologyofShockEffec66PathophysiologyofShock Hypotension+LVEDPandcriticalstenosis

MyocardialHypoperfusionLVdysfunctionSystemiclacticacidosisImpairmentofnon-ischemicmyocardiumworseninghypotension.PathophysiologyofShock Hypot67SchematicLVEDPelevationHypotensionDecreasedcoronaryperfusionIschemiaFurthermyocardialdysfunctionNeurohormonalactivationVasoconstrictionEndorganhypoperfusionSchematicLVEDPelevation68MedicalStabilizationofShockPts.Figureoutthevolumestatus,SwanifindoubtAirwayJudiciousafterloadreductionMaintainAVsynchronyDon’ttolerateAfibDualchamberpacingifA-VblockpresentCorrectAcid-BasedisturbancesMaintainBP(IABPand/orPressors)….MedicalStabilizationofShock69PhysiologicEffectofIABPin-vivoDecreasedafterloadLVO2consumption

Williams,et.al.,Circulation1982

Kern,et.al.,Circulation1993Coronarybloodflowvelocitywasmeasuredusingdoppler-wireinninepatientswithcriticalstenoticlesions.Peakdiastoliccoronaryflowvelocitybeyondthestenosiswasunaffectedbyintra-aorticballoonpumping.TherewasunequivocalIABP-mediatedaugmentationofbothproximalanddistalcoronarybloodflowvelocitiespostPTCA.

PhysiologicEffectofIABPin-70PhysiologicEffectofIABPin-vivoFuchs,et.al.,

Circulation,1983Greatcardiacveinflowwasmeasuredinsevenpatientsreceivingmaximaldrugtherapyandrequiringballoonpumping

forunstableangina.All

patientshadgreaterthan90%stenosisoftheproximalLADcoronaryartery.Increasedgreatcardiacveinflowcorrelatedwithincreasedmeanaortic

diastolicpressureacrosschangesinballoonvolumes(off,20cc,30cc,

and40cc)andchangesinassistratio(off,1:4,1:2,and1:1)(p=.02).

PhysiologicEffectofIABPin-71PhysiologicEffectofIABPin-vivoThus

balloonpumpingincreasedflowtoabedfedbythe

criticalstenosis,orcollateralvesselsPhysiologicEffectofIABPin-72IABPinAcuteMIJACC1985IABPinAcuteMIJACC198573IABPinAcuteMIPre-thrombolyticeraNoLytics,ASA,orLopressor20patientswithAcuteMIand“extensivemyocardiumatriskperbaselineThalium”wereRandomized.Pt.sinShockwereexcludedStd.Rx:O2,MSo4,Lido,HeparinStdRx+IABPPlusIVNTGIABPinAcuteMIPre-thrombolyt74IABPinAcuteMIPatientshadrepeatThaliumscanonDay-4Nodifferenceswereobservedbetweenthetwogroupsregarding: -Thaliumdefectscorecomparingdays1and4 -Theejectionfractioncomparingdays1and4

=> “Unlikelythatamortalitybenefitisconferred

bytheIABP/NTGcombination”

IABPinAcuteMIPatientshadr75UtilityofIABPinShockPts.Observedclinicalbenefits:Improvedacid-basestatusImprovedurineoutputImprovedmentationImprovedoverallhemodynamicsAllthis,however,doesnotadduptoimprovedsurvivalwithoutFlowRestorationUtilityofIABPinShockPts.O76ThrombolysisinCardiogenicShockRatesofReperfusion

Lower,andRatesofReocclusion

Higher Thaninnon-shockptsPossibleReason: Diffusionofthrombolyticagent

intothethrombusmaybePRESSUREDEPENDENT.ThrombolysisinCardiogenicSh77BPEffectonefficacyoflyticsinShockDogdataLADocclusionbythrombusHypotensioninducedbyphlebotomyPrewittJACC1994;23:784BPEffectonefficacyoflytic78AnyRandomizedTrialsof

ThrombolysisinCardiogenicShock????MostthrombolytictrialsspecificallyexcludedpatientsincardiogenicshockTheonlylargeplacebo-controlledthrombolyticstudyspecificallyexaminingPts.presentingwithshockwasGISSI-1Streptokinase=>NoBenefitAnyRandomizedTrialsof

Thro79CombinedIABPandThrombolysisGUSTO-I:IABPin62ofthe310lyticRx’dPts.inshockObservationalData:CombinedIABPandThrombolysis80CombinedIABPandThrombolysisKovack,et.al.,JACC2019Stomel,et.al.,Chest1994 Tworetrospectiveobservationalseriesfromcommunityhospitals:

ImprovedsurvivalfromcombinationRx.CombinedIABPandThrombolysis81CombinedIABPandThrombolysisObservationalDatafromSHOCKRegistery:CombinedIABPandThrombolysis82

CombinedIABPandThrombolysis

-Barron,et.al.,AHJJune2019-NationalRegistryofMI-2,Database

-21,178pts.Presentingwithordevelopingpost-MIshock-32%ReceivedIABPP<0.001P=NSTTTTIABPPPTCAPPTCAIABPTheyoungerpts.,twiceaslikelytogetTT

=>SelectionBias

P<0.001P=NSTTTTIABPPPTCAPPT83CombinedIABPandThrombolysis

AccompanyingEditorialbyMagnusOhman,andJudithHochman:“Although,thereisawealthofphysiologicandoutcomesdatatosupporttheuseofearlyIABPtherapyincardiogenicshock(inconjunctionwithlytics),randomizedtrialsareclearlyneeded….”CombinedIABPandThrombolysis84CombinedIABPandThrombolysisTheonly

randomizedtrialonthesubject:

ThrombolysisandCounterpusiontoImproveCardiogenicShockSurvival(TACTICS):ResultsofaProspectiveRandomizedTrial.

MagnusOhman,et.al.,

CirculationOct.2000Supp.AbstractCombinedIABPandThrombolysis85TACTICSSTelevationMIpatients,presentingwithin12hoursofSx,andCardiogenicshock57PatientswererandomizedThrombolyticTherapyaloneThrombolyticTherapy+IABPTACTICSSTelevationMIpatient86TACTICSTheprimaryendpointof6monthmortalitywasnotstatisticallysignificant,P=0.3Subgroupanalysis:ForKILLIPclassesIIIandIV,P=0.07TACTICSTheprimaryendpointof87PATIENTISINSHOCKw/STelevations,and<12hrsSxonset

IABPPressors

MayincreasetheefficacyofLyticsAdministrationofLyticsshouldnotbedelayed

inanticipationofplacementofIABPdespitelackofrandomizeddataprovingefficay.

IfEARLYREVASCULARIZATION

isnottobepursued:PATIENTISINSHOCKw/STelev88SHOCKTrialWhether

EARLYREVASCULARIZATION

improvessurvivalamong

patientswithcardiogenicshock?SHOCKTrial89SHOCKTrial302Pts.withSTelevation(ornewLBBB)andcardiogenicshockImmediateRevascularization(CABG/PTCA)Laterevascularization(ifindicated)

deferredforatleast54hoursWithin36hrs.ofMIonsetWithin12hrs.ofShockonsetSHOCKTrial302Pts.withSTel90SHOCKTrial:

Primaryendpoint,30daysmortalityDiff.=9%P=0.1147%56%MortalityDiff.=13%P=0.02750%63%52.4%66.4%Diff.=14%P<0.02Revasc.MedRxSHOCKTrial:

Primaryendpoin91SHOCKTrial

Whywasn’tthePrimaryend-pointmet?Lowmortalityintheinitialmedicalmgtgp.HighratesofIABPuse,86%TTuse,63%Delayedrevasculariztion,21%Medianof104hrs postrandomization30daysmortality47%56%SHOCKTrial

Whywasn’tthePri92SHOCKTrial:

Subgroupanalysis,Agelessthan75Revasc.MedRxP=0.02CI<1.0P=0.002CI<1.0Mortality45%65%41%56%66.7%48.4%P<0.02CI<1.0SHOCKTrial:

Subgroupanalysi93SHOCKTrial:

WhattodowithPt.solderthan75Totalno.ofPt.solderthan75y.o.=56(/302)Theearlyrevascularizationgroupshadworseoutcomeat:

30days(CI>>1.0)6months(CI>>1.0)12months,nodifferenceinoutcomeSHOCKTrial:

Whattodowith94WhattodowithPt.solderthan75SHOCKRegistryresultsisincontrasttotheSHOCKTrialfindingsinthissubgroup.Thoseolderthan75y.o.,selectedtoundergoERVhadasurvivaladvantage.Casebycaseassessmentinthispopulation,andnotacrosstheboardexclusioniscalledfor.WhattodowithPt.soldertha95RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockSHOCKTrial:Revascularization(N=152)MedicalTreatment(N=150)IIb/IIIaAntagonist41.7%25%StentPlacement35.7%52.3%RoleofIIb/IIIaInhibitorsan96RoleofIIb/IIIainhibitorsinCardiogenicShock

RetrospectivesubgroupanalysisfromthePURSUITtrial Hassade,et.al.,JACC,2000

RandomizationtoeptifibatidedidnotaffecttheincidenceofshockPatientsrandomizedtoeptifibatidewhodevelopedshockhadasignificantlyreducedincidenceofdeathat30daysApossiblemechanismofbenefitisreliefofmicrovascularobstructionRoleofIIb/IIIainhibitorsin97RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockLong-TermMortalityBenefitWiththeCombinationofStentsandAbciximabforCardiogenicShockComplicatingAcuteMyocardialInfarction[CoronaryArteryDisease]Chan,AlbertW.MD,MS;Chew,DerekP.MBBS;Bhatt,DeepakL.MD;Moliterno,DavidJ.MD;Topol,EricJ.MD;Ellis,StephenG.MD

AJCJan.15,2019RoleofIIb/IIIaInhibitorsan98RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockSinglecenter,non-randomizedDatacollected:Jan.1993andJune2000

Thirtymonthfollow-upavailable96Pt.sw/CardiogenicShockStent+ReoproN=27StentOnlyN=14PTCA+ReoproN=18PTCAOnlyN=37RoleofIIb/IIIaInhibitorsan99RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockThirtydayMortalityRates(%)Stent+ReoproStentOnlyPTCA+ReoproPTCAOnlyAbsenceofStentuse:HR2.39,95%CI1.22to4.67,p=0.01AbsenceofAbciximabuse:HR1.95,95%CI1.03to3.71,p=0.04OnUnivariateanalysis:EF<=30%

HR3.44,95%CI1.35to8.78,p=0.01RoleofIIb/IIIaInhibitorsan100RoleofIIb/IIIaInhibitorsandStentsinCardiogenicShockUseofStents29%