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Etiology, mortality, diagnostic and treatment options for cardiogenic shock.
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Controversies in Controversies in TreatingTreatingCardiogenic Cardiogenic ShockShock
Martha Burk, MD, MSMartha Burk, MD, MSBAMC/Wilford Hall/UTHSCSA BAMC/Wilford Hall/UTHSCSA
Combined Pulmonary Fellows Combined Pulmonary Fellows ConferenceConference
Cardiogenic ShockCardiogenic Shock Inadequate perfusion of tissue with Inadequate perfusion of tissue with
relatively decreased cardiac relatively decreased cardiac dysfunctiondysfunction
It is the most common cause of death in It is the most common cause of death in patients hospitalized for AMIpatients hospitalized for AMI
Treatment of AMI complicated by Treatment of AMI complicated by cardiogenic shock remains controversialcardiogenic shock remains controversial
Two Minute Two Minute AssessmenAssessmentt
Cold and DryCold and Dry
No
Warm and Warm and DryDry
Yes
Warm and WetWarm and Wet
Cold and WetCold and Wet
Evidence of Low Perfusion
Narrow pulse pressureNarrow pulse pressure
Pulsus paradoxusPulsus paradoxus
Cool extremitiesCool extremities
Altered mental statusAltered mental status
Drug-related hypotensionDrug-related hypotension
HyponatremiaHyponatremia
Worsening renal functionWorsening renal function
Evidence for CongestionOrthopneaOrthopneaElevated JVPElevated JVPGallopGallopEdemaEdemaAscitesAscitesRalesRalesHepatojugular refluxHepatojugular reflux
Congestion at rest?
LowPerfusionAt Rest?
No
Yes
Nohria, et al JAMA 2002
Causes of Cardiogenic Causes of Cardiogenic ShockShock
Acute MIAcute MI– Pump failurePump failure
Large infarctionLarge infarction Infarct expansionInfarct expansion ReinfarctionReinfarction
Mechanical Mechanical complicationscomplications– Acute MR/papillary Acute MR/papillary
muscle rupturemuscle rupture– Ventricular wall ruptureVentricular wall rupture– Ventricular septal defectVentricular septal defect– Pericardial tamponadePericardial tamponade
End-stage End-stage cardiomyopathycardiomyopathy
MyocarditisMyocarditis Severe septic shockSevere septic shock LV outflow obstructionLV outflow obstruction
– Aortic stenosisAortic stenosis– Hypertrophic LVHypertrophic LV
Valvular diseaseValvular disease– Mitral stenosisMitral stenosis– Left atrial myxomaLeft atrial myxoma
Myocardial contusionMyocardial contusion Hypothyroid stateHypothyroid state Prolonged CABGProlonged CABG
Adapted from UpToDate and Hollenberg, et al Ann Intern Med 1999
EpidemiologyEpidemiology Acute MI is most frequent cause Acute MI is most frequent cause ~10% AMI results in shock~10% AMI results in shock SHOCKSHOCK
– ((ShShould we emergently revascularize ould we emergently revascularize OOccluded ccluded CCoronaries for shocoronaries for shocKK) trial) trialregistryregistry
– 1160 pts with AMI and shock1160 pts with AMI and shock 75% with LV failure75% with LV failure 8% had MR8% had MR 5% had ventricular septal defect5% had ventricular septal defect 3% had RV failure3% had RV failure 2% had tamponade or cardiac rupture2% had tamponade or cardiac rupture 8% had shock for other reasons8% had shock for other reasons
– InfarctionsInfarctions 55% anterior, 46% inferior55% anterior, 46% inferior 21% posterior, 50% multiple21% posterior, 50% multiple Hollenberg, et al Ann Intern Med 1999
Davies QJ Med 2001
MortalityMortality TRACE study TRACE study
– Trandolapril Cardiac Evaluation protocolTrandolapril Cardiac Evaluation protocol– 6676 pts non-invasively managed for AMI6676 pts non-invasively managed for AMI– 59% pts developed shock within 48 hrs59% pts developed shock within 48 hrs– 30 day and 6 year mortality30 day and 6 year mortality
Without shock Without shock 9%/45%9%/45% With shock With shock 62%/88%62%/88%
Euro-Heart-Survey-ACSEuro-Heart-Survey-ACS– 10,136 patients presenting with ACS10,136 patients presenting with ACS– 549 had cardiogenic shock on presentation549 had cardiogenic shock on presentation– Mortality of pts presenting with/without shock Mortality of pts presenting with/without shock
50%50%/3% with STEMI/3% with STEMI 53%53%/1% with NSTEMI/1% with NSTEMI
Lindholm, et al European Heart Journal 2003Iakobishvili, et al American Heart Journal 2004
Mortality In TRACEMortality In TRACE
Lindholm, et al European Heart Journal 2003
Katayama, et al Circ J 2005
PathophysiologPathophysiologyy
Coronary occlusionCoronary occlusion Impaired coronary flowImpaired coronary flow InfarctInfarct Dysfunction results in Dysfunction results in
hypotensionhypotension Aortic pressures Aortic pressures
<85mmHg<85mmHg Extension of Extension of
infarct/muscle necrosisinfarct/muscle necrosis
Microthrombi developMicrothrombi develop Vasoconstrictors released Vasoconstrictors released
from microthrombifrom microthrombi Vasospasm results in Vasospasm results in
increased flow resistanceincreased flow resistance No reflow phenomenonNo reflow phenomenon
Davies QJ Med 2001
Impaired ThrombolysisImpaired Thrombolysis
Neuroendocrine Neuroendocrine ActivationActivation Neuroendocrine system activatedNeuroendocrine system activated
– Increase cardiac output Increase cardiac output – Include renin, aldosterone, catecholamines, Include renin, aldosterone, catecholamines,
BNP, ANP and adrenomedullinBNP, ANP and adrenomedullin– Adrenomedullin produced unregulated in Adrenomedullin produced unregulated in
ischemia, hypotensionischemia, hypotension Increased demand on myocardiumIncreased demand on myocardium Inadequate coronary flowInadequate coronary flow
– Inability to meet increased oxygen demand Inability to meet increased oxygen demand Increased myonecrosisIncreased myonecrosis
Davies QJ Med 2001Katayama, et al Internal Medicine 2004
Regulation of Regulation of Vascular Smooth Vascular Smooth
Muscle ToneMuscle Tone
Landry NEJM 2001
Neuroendocrine Markers of Neuroendocrine Markers of MortalityMortality
Katayama, et al Internal Medicine 2004
Hollenberg et al, Annals of Internal Medicine 1999
Death
Myocardial DysfunctionSystolic Diastolic
↓ CO↓ SV
↓Systemic Perfusion Hypotension
↓ CoronaryPerfusionPressureVasoconstriction
Fluid retention
IschemiaProgressiveMyocardial Dysfunction
Hollenberg et al, Annals of Internal Medicine 1999
Ischemic myocardium
Cell death
Segments withMyocardialstunning
Segments withStunning andHibernation
Segments withHibernating myocardium
No returnOf function
Return of Myocardial function
Reperfusion Significant residualstenosis
InotropicSupport
Relief ofIschemia
Reperfusion InjuryReperfusion Injury
Free radical productionFree radical production Increased neutrophil adhesionIncreased neutrophil adhesion
– Complement formationComplement formation Free fatty acid metabolism restoredFree fatty acid metabolism restored
– Further decreases intracellular pHFurther decreases intracellular pH– Increased calcium influx due to Na-K exchangeIncreased calcium influx due to Na-K exchange
Result: further myonecrosis during first 2 Result: further myonecrosis during first 2 hours after reperfusionhours after reperfusion
Davies QJ Med 2001
DiagnosisDiagnosis
Diagnosis requires Diagnosis requires – Documentation of myocardial dysfunctionDocumentation of myocardial dysfunction– Exclusion of alternative causesExclusion of alternative causes
HypovolemiaHypovolemia SepsisSepsis PEPE TamponadeTamponade Aortic dissectionAortic dissection Valvular diseaseValvular disease
Severity of Heart Failure in Severity of Heart Failure in AMIAMIKillip ClassificationKillip Classification
– Class IClass I No clinical heart failureNo clinical heart failure < 5% mortality< 5% mortality
– Class IIClass II Rales bilaterally in up to 50% Rales bilaterally in up to 50%
of lung fieldsof lung fields isolated S3isolated S3 good prognosisgood prognosis
– Class IIIClass III Rales in all lung fieldsRales in all lung fields acute mitral regurgitationacute mitral regurgitation aggressive management aggressive management
requiredrequired
– Class IVClass IV Cardiogenic shockCardiogenic shock StuporousStuporous systolic BP < 90systolic BP < 90 decreased urine decreased urine
outputoutput pulmonary edema pulmonary edema
and cold clammy and cold clammy skinskin
mortality near 80%mortality near 80%
www.ahcpub.com
Pfisterer Lancet 2003
Management GoalsManagement Goals Early recognitionEarly recognition Early reperfusionEarly reperfusion Maintenance of adequate preloadMaintenance of adequate preload Decreased afterloadDecreased afterload
Initial Diagnostic and Therapeutic Initial Diagnostic and Therapeutic StepsSteps
History and ExamECGECHOLabsCXRPAC
Oxygenate/VentilateVenous accessECGPain controlHemodynamic support
Tissue perfusionRemains inadequate Inotropes IABP
Adequate perfusionWithout congestion
Adequate perfusionWith pulmonary congestion
Reperfusion
Card cath available No card cath available
Cardiac cath
Angioplasty CABG Continued shock
Clinical management
Thrombolytics and IABP
Hollenberg, et al Ann Intern Med 1999
Menon and Hochman Heart 2002
Utility of ECHOUtility of ECHO EvaluateEvaluate
– LV function and myocardium at riskLV function and myocardium at risk– Screen for ventricular septal Screen for ventricular septal
rupturerupture– Screen for severe mitral Screen for severe mitral
regurgitationregurgitation– Look for tamponade/ruptureLook for tamponade/rupture– Assess right ventricular functionAssess right ventricular function– Look for aortic dissectionLook for aortic dissection
Echo Survival and Response Echo Survival and Response Predictors in Cardiogenic ShockPredictors in Cardiogenic Shock 169 pts with MI randomized w/in 12 hrs of 169 pts with MI randomized w/in 12 hrs of
diagnosis of shock to receive diagnosis of shock to receive – early emergency revascularization early emergency revascularization
PTCA or CABG was performed w/in 6 hrsPTCA or CABG was performed w/in 6 hrs IABP was recommendedIABP was recommended
– initial medical stabilizationinitial medical stabilization– Echo performed w/in 24 hrs of randomization, and Echo performed w/in 24 hrs of randomization, and
7 days later7 days later– Study designed and powered to detect 20% Study designed and powered to detect 20%
difference in overall 30 day mortalitydifference in overall 30 day mortality LVEF >/= 28% and Grade 0/1 MR were LVEF >/= 28% and Grade 0/1 MR were
associated with improved survivalassociated with improved survival– Odds Ratio 4 and 3, respectivelyOdds Ratio 4 and 3, respectively
Picard, et al Circulation 2003
Pulmonary Artery Pulmonary Artery CathetersCatheters
UpToDate
Importance of PositionImportance of Position
UpToDate
Respiratory Variation With Respiratory Variation With PEEPPEEP
0 PEEP
15 PEEP
20 PEEP
UpToDate
UpToDate
PAWP is a reliable indicator of LVEDP only when ventricular compliance is stable
PACs in High PACs in High Risk Surgical Risk Surgical
PatientsPatients 1994 pts 1994 pts
– ≥≥60 years old60 years old– Deemed ASA class III or IV riskDeemed ASA class III or IV risk– Undergoing elective or urgent Undergoing elective or urgent
major abdominal, thoracic, major abdominal, thoracic, vascular or hip frax surgery vascular or hip frax surgery and requiring intensive careand requiring intensive care
– Randomized to receive Randomized to receive treatment w/ or w/o PAC treatment w/ or w/o PAC guidanceguidance
ConclusionConclusion– No benefit to therapy directed No benefit to therapy directed
by PAC versus standard careby PAC versus standard care
NEJM 2003
Class III = Severe disease, but not incapacitatingClass IV = Severe disease that is a constant threat to life
Complications of PACComplications of PAC PneumothoraxPneumothorax HemothoraxHemothorax HematomaHematoma ArrhythmiasArrhythmias Heart blockHeart block Arterial lacerationArterial laceration Pulmonary artery Pulmonary artery
perforationperforation Valvular damageValvular damage
Catheter site Catheter site infectioninfection
ThrombosisThrombosis InfarctionInfarction EndocarditisEndocarditis ThrombocytopeniaThrombocytopenia
Layon Chest 1999
Perioperative Use in Cardiac Perioperative Use in Cardiac SurgerySurgery
Differentiation between causes of low CODifferentiation between causes of low CO– Hypovolemia v ventricular dysfunctionHypovolemia v ventricular dysfunction– Echo is inconclusiveEcho is inconclusive
Differentiation between L v R heart failure Differentiation between L v R heart failure and pericardial tamponadeand pericardial tamponade– Echo is inconclusiveEcho is inconclusive
Guidance of management of low CO stateGuidance of management of low CO state Diagnosis and management of PAH in Diagnosis and management of PAH in
patients with systemic hypotension and patients with systemic hypotension and impaired organ perfusionimpaired organ perfusion
Conditions in which there is general agreement that RHC is warranted
J American College Cardiology 1998
Conditions In Which Conditions In Which Reasonable Differences of Reasonable Differences of
Opinion ExistOpinion Exist Guidance of inotropic and/or vasopressor Guidance of inotropic and/or vasopressor
therapy after patients with significant therapy after patients with significant cardiac dysfunction have achieved cardiac dysfunction have achieved hemodynamic stabilityhemodynamic stability
Guidance of management of hypotension Guidance of management of hypotension and evidence of inadequate organ and evidence of inadequate organ perfusion when a therapeutic trial of perfusion when a therapeutic trial of intravascular volume expansion and/or intravascular volume expansion and/or vasoactive agents is associated with vasoactive agents is associated with moderate riskmoderate risk
J American College Cardiology 1998
Intra-Aortic Balloon Intra-Aortic Balloon PumpPump Reduces systolic afterloadReduces systolic afterload Augments diastolic perfusion Augments diastolic perfusion
pressurespressures Increases cardiac outputIncreases cardiac output Improves coronary artery perfusionImproves coronary artery perfusion
– Not true for critically stenosed vesselsNot true for critically stenosed vessels
Decreases reocclusion and cardiac Decreases reocclusion and cardiac events after emergency angioplasty events after emergency angioplasty for AMIfor AMI
No increase in myocardial oxygen No increase in myocardial oxygen demanddemand
No clear survival benefit No clear survival benefit
IABPIABP Initially improves hemodynamic statusInitially improves hemodynamic status
– Impact temporaryImpact temporary 80% mortality in patients with CS treated with80% mortality in patients with CS treated with
– IABP placement, CCU monitoring and vasopressorIABP placement, CCU monitoring and vasopressor Fornaro, et al retrospectively studied 15 patients Fornaro, et al retrospectively studied 15 patients
admitted for AMI with cardiogenic shockadmitted for AMI with cardiogenic shock– All pts underwent IABP, angiography followed by PTCA, All pts underwent IABP, angiography followed by PTCA,
CABG and cardiac surgery or medical treatmentCABG and cardiac surgery or medical treatment– 5 pts (33%) died5 pts (33%) died
~18% patients in Euro-Heart-Survey in CS had ~18% patients in Euro-Heart-Survey in CS had IABPIABP
IABP is useful with early revascularizationIABP is useful with early revascularizationFornaro, et al G Ital Cardiol 1996Iakobishvili, et al Am Heart J 2005
Benchmark Counterpulsation Benchmark Counterpulsation Outcomes RegistryOutcomes Registry
Prospective registry of all Prospective registry of all patients who receive IABPs patients who receive IABPs at participating centers at participating centers 1996-20011996-2001
22,663 patients22,663 patients– 185 US sites, 65 non-US 185 US sites, 65 non-US
sitessites– 4314 had cardiogenic 4314 had cardiogenic
shockshock– Primary endpointsPrimary endpoints
Major limb ischemiaMajor limb ischemia Severe bleedingSevere bleeding IABP failureIABP failure All cause in-hospital All cause in-hospital
mortality mortality
21% all cause mortality21% all cause mortality
12% mortality/balloon in 12% mortality/balloon in placeplace
0.05% IABP-related 0.05% IABP-related mortalitymortality
1% major limb ischemia1% major limb ischemia
1% severe bleeding1% severe bleeding
4% balloon failure/leak4% balloon failure/leak
Cohen, et al European Heart Journal 2003
Risks of IABPRisks of IABP ArterialArterial
– PerforationPerforation– ThrombosisThrombosis– Embolization Embolization – Limb ischemiaLimb ischemia– Visceral ischemiaVisceral ischemia
BalloonBalloon– RuptureRupture– Incorrect positioningIncorrect positioning– Gas embolizationGas embolization
MiscellaneousMiscellaneous– HemorrhageHemorrhage– InfectionInfection– EntrapmentEntrapment
Overwalder The Internet Journal of Thoracic and Cardiovascular Surgery 1999
ACC/AHA GuidelinesACC/AHA Guidelines
Class I recommendationsClass I recommendations STEMI patients with BP <90STEMI patients with BP <90
– Or 30mm Hg below baselineOr 30mm Hg below baseline– No response to other interventionsNo response to other interventions
STEMI patients with low output statesSTEMI patients with low output states As a stabilizing measure for angiography and As a stabilizing measure for angiography and
revascularizationrevascularizationClass II recommendationsClass II recommendations STEMI patients with refractory pulmonary STEMI patients with refractory pulmonary
congestioncongestion
Level B Evidence
Level C Evidence
Antman, et al JACC 2004
Reestablishing Reestablishing PerfusionPerfusion
NEJM 2002
Benefits of Thrombolysis in Benefits of Thrombolysis in AMIAMI
Absolute Reduction in Mortality
TIMI 0 absence of any antegrade flow beyond a coronary occlusion.TIMI 1 faint antegrade coronary flow beyond the occlusion although filling of the distal coronary bed is incomplete.TIMI 2 delayed or sluggish antegrade flow with complete filling of the distal territory.TIMI 3 normal flow which fills the distal coronary bed completely.
Impact of Blood Flow on Survival
UpToDate
Occlusion Penetration Slow Flow Normal Flow
TIMI 0 TIMI 1 TIMI 2 TIMI 3
% M
ort
alit
y
9.3%
6.1%
3.7%
p<0.0001 vs TIMI 0/1p<0.0001 vs TIMI 2
P=0.003 vs TIMI 0/1
Tea
m 2
Tea
m 2
Tea
m 2
Ger
ma
n
Ger
ma
n
Ger
ma
n
GU
ST
O 1
GU
ST
O 1
GU
ST
O 1
TA
M I
1-7
TA
M I
1-7
TA
M I
1-7
TIM
I 1
,45,
10B
TIM
I 1
,45,
10B
TIM
I 1
,45,
10B
Gibson 1998
Sample Size of Pooled Analysis: 5,498
0
2
4
6
8
10
12
10 16 33 34 44 2784 13 19 9 15 18 29 34
Both Culprit and Non-Culprit Flow are Both Culprit and Non-Culprit Flow are Abnormal in Acute MIAbnormal in Acute MI
0
5
10
15
20
25
30
35
40
Culprit Culprit postPTCA
Non-Culprit Normal
CTF
C
Even PTCA of the culprit artery residual stenosis restores flow only to that observed in the non-culprit (30 frames) and not to normal flow (21 frames)
The difference between culprit & non-culprit flow is only 6 frames; the difference between non-culprit and normal flow is 9 frames
36.8 + 22.3
n =1,322
30.6 + 14.6
n = 232 n =1,589
30.6 + 13.4
21.0 + 3.1
n = 78
6 frames
9 frames
Gibson et al, JACC 1999; 34: 974-82
In 25% of cases, flow is slower in the non-culprit than culpritIn 33% of cases, flow is abnormal following stent placement
Thrombolytic Therapy in Thrombolytic Therapy in CSCS Less benefit once cardiogenic shock occursLess benefit once cardiogenic shock occurs Mortality unaffected by type of thrombolyticMortality unaffected by type of thrombolytic
– GISSI trial 30 day mortality 70% for each groupGISSI trial 30 day mortality 70% for each group Increased risk of significant bleeding with Increased risk of significant bleeding with
streptokinase versus alteplasestreptokinase versus alteplase
– International Study Group International Study Group Streptokinase v recombinant Tissue Plasminogen ActivatorStreptokinase v recombinant Tissue Plasminogen Activator 65% mortality with SK v 78% with rTPA65% mortality with SK v 78% with rTPA
– GUSTO GUSTO 56% with SK v 59% with rTPA56% with SK v 59% with rTPA
Lancet 1990
Risks of ThrombolysisRisks of Thrombolysis
BleedingBleedingBleedingBleedingBleedingBleeding
Thrombolytic Thrombolytic TherapyTherapy Not beneficial in NSTEMINot beneficial in NSTEMI
– Coronary arteries not usually occludedCoronary arteries not usually occluded
Useful in STEMIUseful in STEMI– IF PTCA not available within 2 hoursIF PTCA not available within 2 hours
ACC/AHA recommends thrombolyticsACC/AHA recommends thrombolytics– Patients w/o contraindicationsPatients w/o contraindications– Present w/in 12 hours of symptom onsetPresent w/in 12 hours of symptom onset– Greatest benefit if given w/in 2 hours of symptomsGreatest benefit if given w/in 2 hours of symptoms
Approximately 50% will achieve Approximately 50% will achieve normalized return of blood flow (TIMI normalized return of blood flow (TIMI grade 3)grade 3)– 90% of patients undergoing PCI achieve TIMI grade 3 90% of patients undergoing PCI achieve TIMI grade 3
flowflowUpToDate
30 Day Mortality of Early v Late 30 Day Mortality of Early v Late PTCAPTCA
GUSTO-1 TrialGUSTO-1 Trial
Berger, et al Circulation 1997
Markers of TIMI 2/3 FlowMarkers of TIMI 2/3 Flow Decrease in chest Decrease in chest
painpain– TAMI studyTAMI study
PPV 57% PPV 57% TIMI 3TIMI 3 NPV 86% NPV 86% TIMI 3TIMI 3
ECG changesECG changes– >50% decrease in ST >50% decrease in ST
elevation elevation in the lead with the most in the lead with the most
elevationelevation– PPV 66%PPV 66%– NPV 86%NPV 86%
<50% decrease in ST<50% decrease in ST– AND absence of arrhythmias AND absence of arrhythmias
at 2 hours after at 2 hours after thrombolyticsthrombolytics
– Predicted LACK of TIMI 3 Predicted LACK of TIMI 3 flowflow Sens 81%Sens 81% Spec 88%Spec 88% PPV 87%PPV 87% NPV 83%NPV 83%
Mb, CK-Mb, Troponin Mb, CK-Mb, Troponin – Ratio of baseline/60minute Ratio of baseline/60minute
myoglobin ≥4 predicts 90% myoglobin ≥4 predicts 90% probability of TIMI 3 flowprobability of TIMI 3 flow
Oldroyd Heart 2000
Is Thrombolysis Is Thrombolysis Obsolete?Obsolete? Nearly all patients with AMIs are Nearly all patients with AMIs are
eligible for cardiac catheterizationeligible for cardiac catheterization PCI identifies anatomy involvedPCI identifies anatomy involved Acts as a triage for CT surgeryActs as a triage for CT surgery IABPs can be placed in the cath labIABPs can be placed in the cath lab 90% pts achieve TIMI 3 flow with PCI90% pts achieve TIMI 3 flow with PCI
Grines, et al Circulation 2003
RevascularizationRevascularization SHOCK trialSHOCK trial
– 302 pts with cardiogenic shock (largely due to LV 302 pts with cardiogenic shock (largely due to LV dysfunction) randomized to early revascularization within 6 dysfunction) randomized to early revascularization within 6 hours, or initial medical stabilizationhours, or initial medical stabilization
– Primary end point was 30 day mortalityPrimary end point was 30 day mortality No survival difference at 30 days (53% v 44%)No survival difference at 30 days (53% v 44%) 6 month survival 6 month survival 50% v 37%50% v 37% (p = 0.027) (p = 0.027)
– Early revascularization v initial medical stabilizationEarly revascularization v initial medical stabilization 12 month survival 47% v 34% (p = 0.025)12 month survival 47% v 34% (p = 0.025) At 1 year, 62% survived if TIMI flow grade 3 was achievedAt 1 year, 62% survived if TIMI flow grade 3 was achieved
v 19% survival if PTCA was unsuccessfulv 19% survival if PTCA was unsuccessful– Conclusion: Rapid revascularization is a survival predictorConclusion: Rapid revascularization is a survival predictor
American College of Cardiology, American Heart American College of Cardiology, American Heart Association guidelines recommend emergency Association guidelines recommend emergency revascularization for pts ≤ 75 years with AMI revascularization for pts ≤ 75 years with AMI complicated by cardiogenic shockcomplicated by cardiogenic shock Menon Congest Heart Fail
2003Webb, et al J Am Coll Cardiol 2003Grines, et al Circulation 2003
Menon and Hochman Heart 2002
Barbash et al, Heart 2001
Outcome Outcome Predictors After Predictors After PCIPCI
Retrospective Retrospective review of 113 pts review of 113 pts who underwent PCI who underwent PCI for AMI complicated for AMI complicated by shockby shock– PCI occurred w/in 12 PCI occurred w/in 12
hours of sx onsethours of sx onset Factors w/o impact Factors w/o impact
on survivalon survival– GenderGender– Smoking statusSmoking status– DiabetesDiabetes– Time to interventionTime to intervention
6, 6-12, or >12 6, 6-12, or >12 hourshours
FactorFactor In In Hospital Hospital Mortality Mortality
%%
pp
Prior MIPrior MI
No or YesNo or Yes 41 v 7741 v 77 < 0.001< 0.001
Age (years)Age (years)
<70 or ≥70<70 or ≥70
46 v 7246 v 72 0.020.02
Failed Failed ReperfusionReperfusion
No or YesNo or Yes 36 v 7236 v 72 <0.001<0.001
DiseaseDisease
Single/Single/MultivesselMultivessel
29 v 5729 v 57 0.010.01Sutton, et al Heart 2005
OR 5
OR 4
OR 4
Another Look at Outcomes, Another Look at Outcomes, PCIPCI
Patients with AMI and cardiogenic shockPatients with AMI and cardiogenic shock– 152 underwent emergency revascularization152 underwent emergency revascularization– 150 underwent medical stabilization150 underwent medical stabilization– Primary endpoint was 30 day mortalityPrimary endpoint was 30 day mortality– Secondary endpoint was 6 month survivalSecondary endpoint was 6 month survival
Median time from AMI to shock was 5.6 hoursMedian time from AMI to shock was 5.6 hours Mean age of patients was 66 yearsMean age of patients was 66 years 32% patients were female32% patients were female
30 day mortality (revascularization v medical 30 day mortality (revascularization v medical treatment)treatment)– Not statistically significant (47 v 56%)Not statistically significant (47 v 56%)
6 month mortality6 month mortality– 50 v 63%50 v 63% ( p = 0.027) ( p = 0.027)
Hochman, et al NEJM 1999
Ohman, et al NEJM 1996
Predictive Value Troponin Predictive Value Troponin TT
2004 ACC/AHA Guidelines on 2004 ACC/AHA Guidelines on CABGCABG
Class I RecommendationClass I Recommendation– STEMISTEMI
Pts who fail angioplasty and remain hemodynamically Pts who fail angioplasty and remain hemodynamically unstable (Level B evidence)unstable (Level B evidence)
At time of surgical repair of ventricular septal wall At time of surgical repair of ventricular septal wall rupture or mitral valve insufficiencyrupture or mitral valve insufficiency
CS pts <75 with ST elevation or LBBB (Level B) or CS pts <75 with ST elevation or LBBB (Level B) or posterior MI who develop shock w/in 36 hrs (Level A)posterior MI who develop shock w/in 36 hrs (Level A)
– LV dysfunctionLV dysfunction Significant left main stenosis (Level B)Significant left main stenosis (Level B) Left main equivalent stenosis (Level B)Left main equivalent stenosis (Level B) Proximal LAD with 2 or 3 vessel disease Proximal LAD with 2 or 3 vessel disease
Novel Potential Novel Potential TherapiesTherapies
Nitric Oxide Synthase Nitric Oxide Synthase InhibitionInhibition
Nitric oxide is a strong vasodilatorNitric oxide is a strong vasodilator Positive inotropic effect at low levelsPositive inotropic effect at low levels Negative inotropic effect at high Negative inotropic effect at high
levelslevels Large MIs are associated with NO Large MIs are associated with NO
overproductionoverproduction Could NO inhibition improve the Could NO inhibition improve the
hemodynamic status of patients with hemodynamic status of patients with cardiogenic shock?cardiogenic shock?
Nitric Oxide Synthase Nitric Oxide Synthase InhibitorInhibitor 30 patients with AMI and shock30 patients with AMI and shock
– All received IABP, IVFs, pressors, and were immediately referred for All received IABP, IVFs, pressors, and were immediately referred for coronary catheterizationcoronary catheterization
– Revascularization performed only by PCIRevascularization performed only by PCI– Swan-Ganz catheters used after revascularizaitonSwan-Ganz catheters used after revascularizaiton
Pts in the treatment arm received L-NAME at 1 Pts in the treatment arm received L-NAME at 1 mg/kg/h x 5 hmg/kg/h x 5 h
Primary end pointPrimary end point– All cause 30 day mortalityAll cause 30 day mortality
Secondary end pointsSecondary end points– All cause mortality at 1 wk and 4 mosAll cause mortality at 1 wk and 4 mos– Time on mechanical ventilationTime on mechanical ventilation– Time on IABPTime on IABP– Urine output at 24 hoursUrine output at 24 hours– Change in cardiac indexChange in cardiac index
1 month Survival 73% v 33%1 week survival 80% v 40%4 month survival 73% v 33%MAP improved by 25mm HgUrine output 210 v 110cc/hTime on IABP 59h v 103hVentilation time 77 v 140h
Cotter, et al European Heart Journal 2003
Other Novel TherapiesOther Novel Therapies Monoclonal antibodies to CD11/CD18Monoclonal antibodies to CD11/CD18
– Inhibit neutrophil adhesionInhibit neutrophil adhesion– HALT-MIHALT-MI– AMI pts from ER to cath labAMI pts from ER to cath lab
Randomized by TIMI 0/1 flow to receive drug or Randomized by TIMI 0/1 flow to receive drug or placeboplacebo
Primary end point: size of infarct by SPECT 5-9 days Primary end point: size of infarct by SPECT 5-9 days after MI and angioplastyafter MI and angioplasty
No significant differenceNo significant difference
Na-H inhibitionNa-H inhibition– -Guardian trial showed no benefit-Guardian trial showed no benefit
www.acc.org
Menon and Hochman Heart 2002
Assess volume statusTreat sustained arrhythmias
Mechanical ventilation as neededInotropic/vasopressor support
Acute massive ST elevationExtensive Q waves
Or new LBBB
Cath lab Immediately available
Cath lab
Rapid IABP
Coronary angioPulmonary artery cath
No ST elevationLimited ST, Q changes
Pump failureRV, LV, both
Emergency ECHO with Color flow doppler
Acute severe MRVSR
Critical AS/MS
OR
Aortic dissectionTamponade
ST elevation -> LysisNo ST elevation -> GP IIbIIIa
Aspirin, Heparin
Cardiac surgeryCABG for severe 3v dz or L main
Correct mechanical lesions
No
Yes
Yes No
PTCA for 1, 2, or mod 3 v CADGP IIb/IIIa antagCoronary stent
Treasures Treasures of of San San
AntonioAntonio
