early mortality at 30 days of post-ami heart...

Dr. Elisabet R. UlmeteDr.CosmeArgerichGeneralHospitalofAcuteDiseases

BuenosAires,Argentina

EARLY MORTALITY AT 30 DAYS OF POST-AMI HEART FAILURE

HOWTOINTERPRETITANDHOWTOIMPROVEITSPROGNOSIS

AftercreatingtheCoronaryCareUnitandimplementingefficientantiarrhythmictherapeuticmeasures, heartfailure(HF)constitutesthemostfrequentcomplicationofAMIassociatedtoahighin-hospitalmortalityrate.

Itisdefinedastheinabilityofthehearttomaintainanappropriatebloodflowtosatisfythemetabolic requirementsoftissuesasaconsequenceoflossof functioningmyocardium.

INTRODUCTION

POST-AMIHEARTFAILUREKillip&KimballIndex.

Class Mortality

A: No heart failure 2 - 5 % B: Mild heart failure 10 – 20 % C: Acute pulmonary edema 30% D: Cardiogenic shock 50 – 60 %

INCIDENCEOFPOST-AMIHF Difficultiesofepidemiologicalanalysis

•Thedatacomefromdifferenttypesofstudies(registries,clinicaltrials,epidemiologicalstudies).

•DifferentdefinitionsofHFandinfarctionareused.

•PatientswithcardiogenicshockorwithHFpriortotheanalysisareincludedornot.

•Therearebiasesintheselectionofpatients.

•Differentpopulationsareevaluated(coronaryunits,alladmittancesinahospital,differentagegroups).

INCIDENCEOFPOST-AMIHFDifficultiesofepidemiologicalanalysis

Thecomparisonofclinicaltrialswithregistriesshowsthatpatientsinclinicalstudiesareyounger,withlessproportionofwomenandHFatadmittance,andwithgreaterchancesofreceivingreperfusionprocedures,aspirin,andbetablockers,sotheincidenceinthemisconsiderablylower.

INCIDENCEOFPOST-AMIHF

STUDY TERMOFTHESTUDY HF(%)

Epidemiologicalstudies

WHAS(USA) 2001 39.9

WHAS(USA) 2005 31.5

Registries

NRMI2/3(USA) 1994-2000 29

GRACE(SCA) 1996-2001 13

Clinicalstudies

Meta-analysis 1990-1998 29.4

(GUSTOI;GUSTOIIB;GUSTOIII;ASSENTIII

In-TIMEII 1997-1998 23

VALIANT(Registry) 1991-2001 23.1

Incidenceofpost-AMIHF 25-30

INCIDENCEOFPOST-AMIHFEarlysystolicdysfunctionoftheleftventricle

•Although they are related findings, HF and left ventricular systolic dysfunction (LVSD) are not synonyms.

•A 30-50% of patients with post-AMI HF does not have LVSD and HF is due to mitral dysfunction, arrhythmias, or left ventricular diastolic dysfunction.

•There might be LVSD without clinical signs of HF.

•Specifying the incidence of post-AMI LVSD is even more complex, since it is not evaluated as a routine in several institutions, there are different methods to measure it and the cut point for ejection fraction may vary.

•However, according to literature, a 25-60% of AMI patients will have LVSD, and more than 50% with early LVSD will also present HF.

INCIDENCEOFPOST-AMIHFEarlyleftventricularsystolicdysfunction

STUDY TERM EFVALUE LVSD(%)

Registries

FrenchCCU 1995 ≤0.50 52

FrenchUSIC2000 2000 ≤0.50 46

Clinicalstudies

BEAT 1998-1999 <0.40 31.1

VALIANTregistry 1999-2001 ≤0.40 27.2

MAGIC 1999-2002 <0.50 60

EMIAT 1990-1995 ≤0.50 43

DIAMOND-MI 1998 ≤0.35 29

ARGAMI-2 1996 ≤0.40 28

TRACE 1990-1992 ≤0.35 39Robin A.P.Weier y col Am J Cardiol 2006;97 suppl 13F-25F

POST-AMIHEARTFAILUREHFprognosticfactorsatadmittance

HF NOHF p n=1778 n=11929

Age 72.5(63.7-79.5)64.0(54.1-72.9) <0.0001 Men 60.1 69.6 <0.0001 Background Diabetes 29.9 20.9 <0.0001 AMI 32 26.7 <0.0001 TIA/stroke 53.8 59.9 <0.0001 HTN 59.5 55.7 0.0026 Renalfailure 10 6.4 <0.0001

GRACE Registry 2004; 109: 494-499

POST-AMIHEARTFAILUREHFprognosticfactorsatadmittance

OR 95% CI

Advanced age 1.5 1.45 -1.60 High HR 1.23 1.22 -1.28

STEMI 2.1 1.84 - 2.47

NSTEMI 1.6 1.41 - 1.91

Prior use of diuretics 1.5 1.31 – 1.75

LBBB 1.6 1.30 – 2.10

GRACE Registry 2004; 109: 494-499

POST-AMIHEARTFAILURE

0

7,5

15

22,5

3027

15,6

30

15,7

STEMI NSTEMIColumna1

GRACE FRENCH CCU

NS

NS

Robin A.P.Weir y col. Am J Cariol 2006; 97 suppl: 13 F-25F

POST-AMIHEARTFAILUREHFprognosticfactorsatadmittance

%

0

15

30

45

60

CoronaryAngiography PTCA

31,8

54,2

26,00

46,50

WithHF WithoutHF

P<0.0001

POST-AMIHEARTFAILURE

GRACE Registry 2004; 109: 494-499

HFatadmiaance HFduringhospitalizacon

POST-AMIHEARTFAILURE•The analysis of data provided by the NRMI 2 and NRMI 3 reports that those patients wtih smaller infarctions tended to be older with pre-existing morbidity and a high incidence of prior AMI. These patients developed HF at admittance more frequently.

•On the contrary, the group with larger infarctions turned out to be younger, with a lower morbidity and a lower frequency of prior infarction. These patients showed HF more often after admittance.

•Thus, the extent of infarction is an important determinant for the incidence and time of appearance of post-AMI HF.

•Those with morbidity and pre-existing myocardial damage do not tolerate even small infarctions and develop HF early.

0

3

6

9

1212

4

8

2

Death Death/AMIColumna1

POST-AMIHEARTFAILUREMortalityat30days

n= 61041

Inci

denc

e (%

)

NO HF WITH HFHasdai y col. Am Heart J. 2003; 145: 73-79

POST-AMIHEARTFAILUREIn-hospitalmortalityandat6months

GRACE Registry 2004; 109: 494-499

WithHF WithoutHF Columna1%

P< 0.0001

P< 0.0001

POST-AMIHEARTFAILUREMortality

Sur

viva

l

Days

No HF Mild HF Severe HF Shock

n= 15078 P < 0.0001

Kashani y col Eur. Heart J 2004: 25: 1702- 1710

POST-AMIHEARTFAILUREMortality

OR 95% CI

HF at admittance 1.68 1.62 – 1.75

Age 1.58 1.55 – 1.61

Stroke 1.36 1.29 – 1.44

Diabetes 1.21 1.17 – 1.26

Prior HF 0.92 0.88 – 0.97

Am. J. Cardiol 1996; 78: 1124 - 1128

Intrahopitalaria

POST-AMIHEARTFAILUREIn-hospitalmortality

P< 0,001

Circulation. 2002;105:2605-2610.)

HFatadmi]ancePostadmi]anceHFColumna1

POST-AMIHEARTFAILUREMortality

•BothpatientswithHFatadmittancethatfailedtosolveitclinicallyduringhospitalizationandthosewhodevelopedHFonlyafteradmittance,showaworseevolutionthanthosewithHFatadmittanceandsolvedduringhospitalization.

•Post-AMIHFdoesnotonlyaffectmortalitybutalsomorbidityofpatientsthatpresentit:

withHF withoutHF p

Re-AMI 3.0%2.7% =0.002

Stroke 2.2% 1.4% <0.001

VT/VF 11.2% 9.0% <0.001

Circulation. 2002;105:2605-2610.

POST-AMIHEARTFAILUREPathophysiology

In a setting of AMI, the determinants of heart failure are:

1.- Size of infarcted area

2.- Ventricular distensibility

3.- Functional state of remaining myocardium

4.- Mechanical complications

5.- Rhythm disorders

SIZEOFINFARCTEDAREA

• TheextentofventricularfunctionalterationcausedbyAMIisdirectlyproportionaltotheextentofthenecroticareaandcirculatoryconditionsthatsurroundit.

• Withthelossofanamountenoughofmyocardialmass,thepumpfunctionisdecreased.Theminute-volume,systolicvolume,bloodpressure,anddp/dtmaxdecreaseandtheendsystolicvolumeincreases.Paradoxicalsystolicexpansionoftheinfarctedareadecreasesthesystolicvolumeevenmore.

• Theleftventricle(LV)dilatesduringthefirsthoursanddaysafterAMI,sothatregionalandglobalpressureincreaseaccordingtoLaplace’sLaw.

• ThedegreeofdilationdependsonthesizeoftheAMI,permeabilityoftheinfarctrelatedartery(IRA))andactivationoftherenin-angiotensin-aldosteronesystem(RAAS).

• TheprobabilitytodevelopHFsymptomscorrelatestoventricularfunctionparameters.

• Thefirstalterationisareductionofdiastolicrelaxationthatisobservedininfarctionsthatcompromise8%ofventricularmass.

• With≥15%losses,ejectionfractionreducesandvolumeandendsystolicpressureincrease.

• ThesignsofHFappearwith≥25%lossesofventricularmass.

• Cardiogenicshockaccompaniesa≥40%contractionalteration

SIZE OF INFARCTED AREA

FUNCTIONALSTATEOFREMAININGMYOCARDIUM

• Extensivecoronaryarterydiseasemaycompromiseirrigation,aswellaspriorinfarctionsandfibrosisthatcouldalteritsperformance.

• Themyocardialterritoryinriskconstitutedbyischemiccells,butthatcouldberecovered,isextremelyimportant.ViabilitydependsontheexistenceornotofanappropriateresidualflowafterIRArecanalizationorthepresenceofcollateralcirculationdevelopedbeforeAMI.

• Onthecontrary,thelossofcollateralarteriessecondarytoocclusionoftheresponsiblevessel,aconditionthatwillgenerateremoteischemia,isanotherfactorthatcontributestoventricularfunctionimpairment.

COMPENSATINGMECHANISMS• Thedecreaseofsystolicvolumetriggerscardiacandperipheral

compensatingmechanismstomaintainapropertissueperfusion.However,eachofthemmaylead,inaparadoxicalanddirectorindirectway,anevengreaterimpairmentandthusgenerateaviciouscirclethatwillhavetobeinterruptedwithapropertherapeuticstrategy.

• Duetotheimplicationsintheevolutionofpatientswithpost-AMIHF,amongperipheralmechanismsitistheneurohormonalsystemactivationthatstandsout(sympatheticnervoussystem,RAAS)sinceitdeterminesanincreaseofsystemicvascularresistancethatleadstoagreaterdeclineofventricularfunction,multiorgandysfunction,anddeath

COMPENSATINGMECHANISMS• Intheparticularcaseofcardiogenicshock,thisclassicalparadigmof

peripheralcompensationmaynotbeobservedincertainpatients,butonthecontrary,reducedvascularresistanceisverifiedbythedevelopmentofsystemicinflammatoryresponsesyndrome(SIRS)duetothereleaseofinflammatorymediators(cytokines)thatleadtoanexaggeratedexpressionoftheenzymeinducingnitricoxide(iNOS).

• Theexcessiveproductionofnitricoxideanditsderivativessuchasperoxynitriteproducedeleteriouseffectssuchasinhibitionofcardiaccontractility,systemicvasodilationinduction,suppressionofmitochondrialrespirationofnon-ischemicmyocardiumandavariabledecreaseofadrenergicresponse.

Consideringthesignificanceofthesizeoftheinfarctionasakeydeterminanttodeveloppost-AMIHF,theconceptofthepossibilityofmodifyingithaspromotedthedevelopmentofalargenumberofexperimentalandclinicaltrialsoverthelastfewdecades.Theeffortstolimittheextentoftheinfarctedareahavebeenguidedbydifferentapproachesto:

1. Earlyreperfusion

2. Reductionofmyocardialenergydemand

3. Manipulationofmyocardialenergyproductionsources.

4. Preventionofreperfusioninjury.

POST-AMIHEARTFAILURE Howtoimproveprognosis

POST-AMIHEARTFAILUREReductionofAMIsize

Generalmeasures

Theytendtooptimizeabalancebetweenmyocardialoxygeninputanddemandto savetheischemicareasthatsurroundtheinfarction.

✓Physicalandemotionalrestofthepatienttolowertheheartrate. ✓Oxygenation:kineticsupport,oxygenmask,bronchodilators,noninvasive ventilationorendotrachealintubationformechanicalrespiratoryassistance. ✓Maintainapropersystolicpressure. ✓Managementoftachyarrhythmiaandbradyarrhythmia. ✓Correctionofelectrolyticdisordersandacid-basestate. ✓Managementofassociatedconditions:severeanemia,infectionsaccompanied byfeverandtachycardia.

REDUCTIONOFSIZEOFAMIReperfusion

0

25

50

75

100KILLIP>1 KILLIP1Columna1

TIMI 3 post PTCA BLUSH Solution of ST

p=0.001

p<0.001

p=0.002

Giuseppe De Luca y col. Am. Heart J. 2009; 158: 416-21

%

REPERFUSIONSurvivalinKillipandKimball>1

100

90

80

70

60

50

400 60 120 180 240 300 360

MBG 2 - 3

MBG 0 - 1

p< 0.001

Su

rviv

al (

%)

Days

Giuseppe De Luca y col. Am. Heart J. 2009; 158: 416-21

POST-AMIHEARTFAILUREReperfusion

• Thetwostrategiesofreperfusiondevelopedoverthelastdecades,apharmacologicalonewithfibrinolyticdrugsandprimaryangioplasty(PTCA),achieveanaccelerationoftherecanalizationprocessofIRA,maximizingtheamountofmyocardiumsaved,takingintoaccountasrulethattimeandnotthetypeofreperfusionisthecriticallyrelevantaspect.Thus,arecoveryofLVsystolicfunctionisachieved,aswellasanimprovementinsurvivalintheshortandlongterm.

• PrimaryPTCAproducesasuperiorbenefitinsurvivalcomparedtofibrinolyticagents.ThissuperiorityisdirectlylinkedtoabetterpatencyofIRA(90%vs65%).

POST-AMIHEARTFAILUREReperfusion

•PrimaryPTCAalsoachievesahigherLVEFatdischargeandlowerpercentagesofre-infarction,stroke,andHF.

•However,adelayfromthemomentatwhichthepatientgetsintouchwithmedicalcareuntilperformingtheangioplasty(PTCA),makesthisbenefitnotbealwaysachieved,andinthiscase,fibrinolyticdrugsarearesourcethatmaybeusedmorequickly.

POST-AMIHEARTFAILUREReperfusion

Time of delay (minutes)

1 2 3 4

30

60

90

120

0

Odds Ratio

Am. Heart J. 2002; 144 (3)

p < 0.02

Fibrinolytictreatment

.-Earlypresentation(≤3hsincetheonsetofsymptoms,delayforaninvasivestrategy).

.-PTCAisnotanoptionbecause: -Laboratorynotavailable -Difficultvascularaccess -Difficultiestoobtainaccesstoanexperimentedhemodynamicslab..-Delaysforaninvasivestrategy -Prolongedtransportation -(door-to-balloon)-(door-to-needle)time>1h -Door-to-balloontime>90minutes

POST-AMIHEARTFAILUREChoiceofreperfusiontreatment

ACC/AHA Guidelines 2006

Invasivestrategy

.-Trainedhemodynamicslaboratoryavailable -Door-to-balloontime<90minutes -(door-to-balloon)-(door-to-needle)time<1hour

.-AMIofhighrisk:Cardiogénicshock;Killip≥3

.-Contraindicationsforfibrinolyticdrugs(includingincreasedriskofbleedingandstroke).

.-Delayedpresentation(>3hours).

.-DoubtfuldiagnosisofAMI

Ifadmittanceis<3handthereisnodelayforaninvasivestrategy,therearenopreferencesforanyofthe2modalities.

POST-AMIHEARTFAILUREChoiceofreperfusiontreatment

ACC/AHA Guidelines 2006

POST-AMIHEARTFAILUREChoiceofreperfusionmanagement

• Takingintoaccountthatthebenefitsgrantedbyfibrinolyticagentsoccurwhentheyareadministered,preferablywithinthefirsthouroftheonsetofsymptoms,themodalityofpre-hospitalfibrinolysiswasevaluatedinseveraltrials.

• Comparedwithin-hospitalfibrinolysis,itproduced,inameta-analysisof6434patients,asignificantreductionofmortality.(oddsratio:0.83;95%CI0.70-0.98p=0.03).

• Thecomparisonofpre-hospitalfibrinolysiswithtransfertoacenterforPTCAintheCAPTIMstudy,didnotrevealsignificantdifferencesintermsofmortalityorinthecompositeendpoint(re-infarction,stroke,deathat30days).

POST-AMIHEARTFAILUREPre-hospitalfibrinolyticdrugsvstransferforPTCA

P= 0.058 P< 0.032

CAPTIM Circulation 2003; 108 : 2851- 6

0

1,5

3

4,5

6

Deathat30days Shock

Pre-hospFB PTCAColumna1

POST-AMIHEARTFAILURERescuePTCA

PTCA CONTROL P (%) (%)

Mortality 7.3 10.4 0.09

HF 12.7 17.8 0.05

Re-infarction 6.1 10.7 0.04

Stroke 3.4 0.7 0.04

Bleeding 16.6 3.5 < 0.001

Wijeisundera y col JACC 2007; 49: 422-430

POST-AMIHEARTFAILUREMicrovasculardamage

• Inspiteofrestoringepicardialflow,manypatientsdisplaysuboptimalmyocardialperfusion.Thissuggeststhatpost-AMIHFmayalsodevelopasaconsequenceofextensivenecrosisassociatedtoseveremicrovasculardamage.

• Thehighmortalityratelinkedtoimpairedmyocardialperfusion,makesevidenttheneedtotryhardertoimprovecirculationinsmallvessels,beyondrestoringepicardialflow.

• Althoughseveralfactorsmaycontributetomicrovasculardysfunction,microvascularreperfusioninjuryhasbeenconsideredasthemaindeterminantofthisphenomenon.

POST-AMIHEARTFAILUREMicrovasculardamage

TYPESOFREPERFUSIONINJURY

Stunning:prolongedcontractiledysfunctionofmyocytessavedbyreperfusionbecauseofcellmetabolismalterationsthatreduceenergyproduction.

No-reflowphenomenon:progressivemicrovascularreperfusiondamage.

Arrhythmiasbyreperfusion

Lethalreperfusioninjury:celldeathinducedbycellreperfusion.

POST-AMIHEARTFAILUREMicrovasculardamage

Mediatorsoflethalreperfusioninjuryandevaluatedstrategies

1) Oxidativestress.Antioxidants2) Intracellularcalciumoverload.Diltiazem,cariporide3) RapidrestorationofcellPH.4) Metabolicmodulation.Glucosetherapy,insulin,potassium5) Magnesium6) Inflammation.Pexelizumab;P-selectinantagonist7) Adenosine

POST-AMIHEARTFAILUREMicrovasculardysfunction

• Addedtotheinjurybyreperfusion,anothermechanismlinkedtomicrovasculardysfuncionisthedistalembolizationobservedinahighpercentageinthehighestKillipandKimbalindices.

• Inthisregard,pharmacologicaltherapy(IIb/IIIainhibitors)andmechanicaltherapy(manualaspirationofthrombus)havebeenproposedasstrategiestoprotectthemicrocirculationofthiscomplicationduringPTCA,andthuspreventagreaterdeteriorationofventricularfunction.

• Intheparticularsettingofshock,somestudiessuggestthatthrombusaspirationmayobtainabettersolutionforSTsegmentandasignificantreductionofin-hospitalmortality.

MicrovasculardysfunctionIIb/IIIainhibitorsandPTCAincardiogenicshock

% n= 300

ADMIRAL NEJM 2001 344: 1895-1903

0

4

8

12

16

CEP30days CEP6months

Withabciximab Withoutabciximab Columna1

P= 0.01

P= 0.02

• AlthoughpharmacologicalorinvasiverevascularizationhascausedasignificantdecreaseinthemortalityofAMIpatients,reperfusionisnotalwayseffectivetolimitmyocardialdamageandpreventventricularfunctionimpairment.

• Thisishowaventricularremodelingprocesscoulddevelop,bothintheinfarctedandnon-infarctedsegments,whichinturnprogressivelyworsenssystolicfunction,andsubsequentlytheprognosis.

• Thisprocessiscloselylinkedtoneurohormonalactivationofthesympatheticnervoussystemandtherenin-angiotensin-aldosteronesystem(RAAS),thushavingsignificanttherapeuticimplications.

POST-AMIHEARTFAILURE

POST-AMIHEARTFAILUREMortalityandACEI

StudyDrugFollow-upPlacebo(%)ACEI(%) P

SMILE Zofenopril 42days 6.5 4.9 NS 12mos14.1 10 0.01

SAVE Captopril 42mos2520 0.019

AIRE Ramipril 15mos2317 0.002

TRACE Trandolapril 26mos4235 0.001

ACEI: angiotensin converter enzyme inhibitors

POST-AMI HEART FAILUREMortality and ACEI

P< 0.0001

P< 0.0001

P< 0.0001

P= 0.0057

n= 5966%

Flather y col Lancet 2000: 1575- 1581

0

12,5

25

37,5

50

Mortality Re-hospduetoHF Re-AMI CEP

ACEI Placebo Columna1

• AlthoughACEIareeffectiveinpost-AMIHF,itwasobservedthataldosteroneofRAASisnotcompletelyinhibitedbytheseagents.

• Althoughthemechanismofthisaldosterone“escape”isnotclearlydefinedandtakingintoaccountthesignificantroleofitinpost-AMIHF,acompletehormoneblockadebeyondACEIisessentialtoachieveamoresustainedbenefit.

• Inthisregard,theVALIANTstudyevaluatedtheadditiveeffectsofvalsartan,anantagonistofangiotensinIIreceptors(ARAII)inpatientswithpost-AMIHF.

POST-AMI HEART FAILURE

• ThecombinationofACEIandARAIIdidnotyieldanadditionalclinicaladvantageintermsofmorbidityandmortality.Anyway,thisstudyshowednon-inferiorityofvalsartan,sointhosecasesinwhichACEIisnotwelltolerated(coughing),theycanbereplacedbythistypeofdrug.

• AthirdmodalitytoblockRAASisthroughaldosteroneblockadewithbeneficialeffectsastheRALESstudyshowedinchronicHF.

• Theseobservationshavepromotedtheevaluationofsuchstrategyinpatientswithpost-AMIHF.

POST-AMI HEART FAILURE

POST-AMIHEARTFAILURE Eplerenone

RR (%) p

Total mortality 15 0.008

CV mortality 17 0.005

CEP 13 0.002

Sudden cardiac death 21 <0.03

Hosp due to HF 15 0.03

POST-AMI HEART FAILURE Eplerenone

RR (%) p

Total mortality 31 0.004

CV mortality 32 0.003

Sudden cardiac death 37 0.051

EPHESUS JACC 2005; 46: 425- 431

Follow-up at 30 days

• Initiallyusedorally,inthepre-thrombolyticera,assecondarypreventionfortheirbenefitsonmortalityandre-infarctionincidence,betablockerswereconsideredcontraindicatedinpatientswithpost-AMIHF,withtheideathatablockadeofsympatheticactivitycouldbeharmful.

• ThesuccessofACEIasfirst-linetherapytoimprovetheprognosisofAMIandtheadventofreperfusiontherapieshavemadeofbetablockingbenefitssomethinguncertain.

POST-AMI HEART FAILURE Beta blockers

POST-AMI HEART FAILURE CAPRICORN study

RR (%) p

Total mortality 23 0.031

CV mortality 25 0.024

Non-fatal AMI 40 0.014

Atrial fibrillation 59 0.003

Malignant arrhythmias 76 0.0001

Lancet 2001; 357: 1385- 1390

CONCLUSIONS

• HeartfailureisaveryfrequentcomplicationafterAMIassociatedtosignificantmortalityandmorbidity.

• Themaindeterminantisthelossoffunctioningmyocardiumthatstartsupaseriesofcompensatingmechanismsthatparadoxicallymayinduceagreaterandprogressivedeteriorationofventricularfunction.

• Thus,atimelyreperfusiontakingintoaccounttimeandnotthewaytoimplementit(fibrinolyticagentsorPTCA),appearsasthecriticaldeterminantoftheevolutionofpatientsthatpresentthiscomplication.

• BothIRArecanalizationandtheachievementofanappropriatemyocardialperfusionarekeytorecoverventricularfunctionthroughlimitingthesizeoftheAMI.

• Inthisregard,greatadvancesinreperfusionstrategiesandtechnologyhaveallowedtoobtainanefficientepicardialreperfusion.

CONCLUSIONS (cont’d)

• However,greatresultshavenotbeenachievedyetatmicrovascularlevel,whichstillconstitutesalimitationatthemomentofreducingthesizeofinfarction.

• Theimplementationoftherapiesthatactontheneurohormonalsystemactivation(SNS,RAAS)tendingtoreduceventricularremodelinginthesepatientshasbeenremarkablybeneficialwithasignificantimpactonmortalityandmorbidityintheshortandlongterm.

CONCLUSIONS (cont’d)

• Thecurrenttrendsinpost-AMIHFincidenceandprognosisevaluatedinlargeregistriessuchasGRACE,reportareductionofthiscomplicationovertime(9%decreaseinSTEMIand6.5%inNSTEMIbytheendof2005).

• Likewise,theWHASstudyverifiedadecreaseofin-hospitalmortalitywhencomparingtermssince1975toyear2005.

CONCLUSIONS (cont’d)

• Takingintoaccountthatthesefindingswereobservedinspiteofaprogressivelyolderpopulation,aswellaswithincreasingco-morbidities(diabetes,hypertension,priorHF,etc),thesebettertrendsprobablyreflectimprovementsinreperfusiontechniques,moreeffectiveadjuncttherapies,andincreaseduseoftherapeuticresourcesinthelastfewdecades.

• However,mortalitybypost-AMIHFisstillhighandthesetherapiesarestillunderusedinmanyplaces,soweshouldfocusoureffortsinensuringthateachandeveryelegiblepatientsistreatedappropriatelyaccordingtotheevidencetooptimizetheevolutionofthisseverecomplicationofAMI.

CONCLUSIONS (cont’d)