冠状动脉疾病

CoronaryArteryDiseaseDr.BenHeMD/PhDRenjiHospital,ShanghaiJiaotongUniversityDeathratefromCHDinsomecountryChangeindeathratefromCHDinsomecountryDifferencebetween1900-1990and1979-1998WomenEpidemiology---AHA2002In1999yr,958,775PtsdiedofCVD2600daily1per33secondsHighBP:50,000,000Heartfailure:4,790,000MyocardialInfarction:7,500,000BigeconomicburdenEpidemiology---ChinaEpidemiology---inChinaDefinitionofCADAnyreasoncausingcoronaryflowdecreaseorobstructionleadingtomyocardialischemiaiscalledCADInmostcircumstance,itiscausedbycoronaryarteryatherosclerosisSo,dependsonthedifferentphaseofASinthecoronaryarterywall,therearevarietiesofmanifestation,fromasymptomatictosuddendeathDiseaseProcessNormalCoronaryArteryCopyright1989.Novartis.ReprintedwithpermissionfromtheAtlasofHumanAnatomy,illustratedbyFrankH.Netter,M.D.Allrightsreserved.DiseaseProcessCopyright1989.Novartis.ReprintedwithpermissionfromtheAtlasofHumanAnatomy,illustratedbyFrankH.Netter,M.D.Allrightsreserved.AtherosclerosisTimelineFoamCellsFattyStreakIntermediateLesionAtheromaFibrousPlaqueComplicatedLesion/RuptureAdaptedfromPepineCJ.AmJCardiol.1998;82(suppl104).FromFirstDecadeFromThirdDecadeFromFourthDecadeEndothelialDysfunctionCausesOfAtherosclerosisHyperlipidemiaHypertensionCigarettehabituationDiabetesmellitusGeneticfactors(Familyhistory)Hyperlipidemia

Hyperlipidemiaisanestablishedriskfactorforatherosclerosis.Convincingevidencethatloweringserumcholesterolreducestheriskofsubsequentcoronaryheartdiseaseeventsandoverallmortalityexists.Elevatedcholesterol,LDLandlipoprotien(a)levelspromoteatherogenesisandthrombosisformation.HyperlipidemiaHypertensionHypertensionisariskfactorforthedevelopmentofatherosclerosis,atheroscleroticcardiovasculardisease,andstroke.Themechanismbywhichhypertensioncausestheseeffectsisnotknown.Hypertensionisassociatedwithmorphologicalterationsofthearterialintimaandfunctionalalterationsoftheendotheliumthataresimilartothechangesobservedinhypercholesterolemiaandestablishedatherosclerosis.CigarettehabituationAmajorandmodifiableriskfactorforatherosclerosisandisassociatedwithanincreasedrelativeriskofdyingfromvasculardisease.Themechanismsarecomplexandlikelymultifactorialandresultinendothelialdysfunctionandarelativelyhypercoagulablestate.

Diabetesmellitus

CADequivalences

Animportantriskfactorforhyperlipidemiaandatherosclerosisandcommonlyassociatedwithhypertension,abnormalitiesofcoagulation,plateletadhesionandaggregation,increasedoxidativestress,andfunctionalandanatomicabnormalitiesoftheendotheliumandendothelialvasomotion.DMisworsethanMIGeneticFactorsSingle-genemutationsinfluencelipidmetabolism.Complexpolygenicdisordersincludehypertension,diabetesmellitus,andhomocysteinemiaalsocontributetoatherogenesis.ObesityHowtodealwithmyabdomenfat?ConceptofMetabolicSyndrome

ATPIII/WHOAbdominalobesity:waistcircumferenceof≥88cminwomenand102cminmenHypertriglyceridemia:≥150mg/dlLowHDL:≤40inmenand≤50inwomenHypertension:≥130/80Highfastingglucose:≥110mg/dlHypertension:≥160/90Hyperlipidemia:Tg≥150mg/dlorHDL≤35(men)or≤39(women)Centralobesity:waist-to-hipratioof≥0.9orof≥0.85inwomenoraBMI≥30kg/m2Microalbuminuria:urinealbuminexcretionrate≥2.0mg/minoralbumin-to-creatinineratioof≥20mg/g≥3criteria≥2criteria+DMorIFGorglucoseIntolenceorInsulinresistenceNostressandAngerNewerRiskFactorsThemechanismsofatherogenesisremainuncertainTheoryoffattyinfiltrationTheoryofplateletaggregationandthrombosisformationTheoryofresponse-to-injuryTheoryofSMCcloningTheresponse-to-injury?theoryismostwidelyaccepted.Endothelialinjurycausesvascularinflammationandafibroproliferativeresponseensues.OxidizedLDLiscapableofawiderangeoftoxiceffectsandcell/vesselwalldysfunctionsthatarecharacteristicallyandconsistentlyassociatedwiththedevelopmentofatherosclerosis.oxLDLProcessofASformationASisawholebodydiseaseDrouetL.CerebrovascDis2002;13(suppl1):1–6CerebralTIAStrokeCVDMIAP（Stable/Unstable）PVD:intermittentclaudication,RestpainExtremitiesnecrosis*Suddendeathdefinedasdeathdocumentedwithin1hourandattributedtocoronaryheartdisease(CHD);†IncludesonlyfatalMIandotherCHDdeath;doesnotincludenon-fatalMI1.KannelWB.JCardiovascRisk1994;1:333–339.2.WilterdinkJI,EastonJD.ArchNeurol1992;49:857–863.

3.AdultTreatmentPanelII.Circulation1994;89:1333–1363.4.CriquiMHetal.NEnglJMed1992;326:381–386.ComparewithnormalMIStroke5–7倍33–4倍12–3倍9倍24倍（仅包括致死性心梗和其他冠心病死亡）42–3倍2缺血性卒中心肌梗死外周动脉疾病Evenrecoverfromfirststrike,PtisstillathighriskPreventionorTreatment?Takesomethingforprevention?ManifestationofCADSilentIschemiaAnginapectorisMyocardialInfarctionIschemiccardiomyopathySuddencardiacdeathAnginaPectorisDefinitionAnginapectorisistheresultofmyocardialischemiacausedbyanimbalancebetweenmyocardialbloodsupplyandoxygendemand.Anginaisacommonpresentingsymptom(typicallychestpain)amongpatientswithcoronaryarterydisease.Pathophysiology(1)

Myocardialischemiadevelopswhencoronarybloodflowbecomesinadequatetomeetmyocardialoxygendemand.Thiscausesmyocardialcellstoswitchfromaerobictoanaerobicmetabolismwithaprogressiveimpairmentofmetabolicfunctions.Pathophysiology(2)

Whypain?Anginapectorisisthemostcommonclinicalmanifestationofmyocardialischemia.Itiscausedbychemicalandmechanicalstimulationofsensoryafferentnerveendingsinthecoronaryvesselsandmyocardium.Pathophysiology(3)

myocardialmetabolicactivityandmyocardialoxygendemandHeartrate,myocardialinotropicstateandmyocardialwalltension3determinantsofO2demandsWalltensionrelatedtoLVsizeandLVcavitypressureConditionsProvokingorExacerbatingIschemiaIncreasedOxygenDemandNon-CardiacHyperthermiaHyperthyroidismSympathomimetictoxicity(cocaineuse)HypertensionAnxietyArteriovenousfistulaCardiacHypertrophiccardiomyopathyAorticstenosisDilatedcardiomyopathyTachycardia ventricular

supraventricularConditionsProvokingorExacerbatingIschemiaDecreasedOxygenSupplyNon-CardiacAnemiaHypoxemia pneumonia,asthma,COPD,

pulmonaryhypertension,

interstitialpulmonaryfibrosis,

obstructivesleepapneaSickle-celldiseaseSympathomimetictoxicityc(cocaineuse)Hyperviscosity polycythemia,leukemia,

thrombocytosis,hypergammaglobulinemiaCardiacAorticstenosisHypertrophiccardiomyopathyHowtomakeadiagnosisofCAD:AssessthePossibilityHowtomakesurethepatient’scomplaintisAnginaPectoris?EvidencesofIschemiaisthepivotalcontributorfordiagnosisofCADClinicalAssessmentofCADPatients

RecommendationsforHistoryandPhysicalHistory:RiskFactorsforCAD

IncreasesthelikelihoodthatCADwillbepresentcigarettesmokinghyperlipidemiadiabeteshypertensionfamilyhistoryofprematureCADHistory:chestdiscomfortQuality-"squeezing,""griplike,""pressurelike,""suffocating"and"heavy”;ora"discomfort"butnot"pain."Anginaisalmostneversharporstabbing,andusuallydoesnotchangewithpositionorrespiration.Duration-anginalepisodeistypicallyminutesinduration.FleetingdiscomfortoradullachelastingforhoursisrarelyanginaLocation-usuallysubsternal,butradiationtotheneck,jaw,epigastrium,orarmsisnotuncommon..Provocation-anginaisgenerallyprecipitatedbyexertionoremotionalstressandcommonlyrelievedbyrest.Sublingualnitroglycerinalsorelievesangina,usuallywithin30secondstoseveralminutes.

ClinicalClassificationofChestPainTypicalangina(definite)

1)substernalchestdiscomfortwithacharacteristicqualityanddurationthatis...

2)provokedbyexertionoremotionalstressand

3)relievedbyrestornitroglycerinAtypicalangina(probable)

meets2oftheofcharacteristicsNoncardiacchestpain

meets1ofthetypicalanginacharacteristicsJAmCollCardiol.1983;1:574,LetterClassificationOfAnginaPectorisExertionalAnginaPectoris1.Stableanginapectoris2.Initialonsetanginapectoris3.AcceleratedanginapectorisSpontaneousAnginaPectoris1.Anginadecubitus2.Prinzmetalvariantanginapectoris3.Acutecoronaryinsufficiency4.PostinfarctionanginapectorisMixedAnginaPectorisGradingofAnginaofEffort

bytheCanadianCardiovascularSociety

I. “Ordinaryphysicalactivitydoesnotcause…angina,”

suchaswalkingandclimbingstairs.Anginawithstrenuousorrapidorprolongedexertionatworkorrecreation.II. “Slightlimitationofordinaryactivity.”

Walkingorclimbingstairsrapidly,walkinguphill,walkingorstairclimbingaftermeals,orincold,orinwind,orunderemotionalstress,oronlyduringthefewhoursafterawakening.Walkingmorethan2blocksonthelevelandclimbingmorethanoneflightofordinarystairsatanormalpaceandinnormalconditions.III. “Markedlimitationofordinaryphysicalactivity.”

Walkingonetotwoblocksonthelevelandclimbingoneflightofstairsinnormalconditionsandatnormalpace.IV. “Inabilitytocarryonanyphysicalactivitywithoutdiscomfort--anginalsyndromemaybepresentatrest.”

Circulation1976;54:522-523PhysicalexaminationOftennormalSignsofhypertension

ElevatedbloodpressureEnlargedorlaterallydisplacepointofmaximumimpulseS4gallopRetinalvascularchanges5characteristicsinfacePossiblefindingsduringepisodeofangina

S4orS3gallopMitralregurgitationmurmurParadoxicallysplitS2BibasilarcracklesChestwallheaveEvaluationandDiagnosisInpatientspresentingwithchestpaindetailedsymptomhistoryfocusedphysicalexaminationdirectedrisk-factorassessmentEstimatetheprobabilityofsignificantCAD (i.e.,low,intermediate,high)ClinicalAssessment

Recommendationsforroutinenoninvasivetest12leadsElecrocardiogramTransientSTsegmentdeviationsand/orTwaveinversionsoccurcommonly.DynamicshiftsinSTsegmentandTwaveinversionsresolvepartiallywhensymptomsarerelievedandareimportantmarkersofMIanddeath.TransientinvertedUwavesContinuousEKGmonitoringshowedasymptomaticSTdepressionin60%patients.anormalECGdoesnotexcludesevereCAD;Riskstratification:ChestX-Rayoftennormalinpatientwithstableanginapectorisusefulnessasaroutinetestisnotwellestablishedfindingsassociatedwithpoorerlong-termprognosiscardiomegalyLVaneurysmpulmonaryvenouscongestionleftatrialenlargementcalciuminthecoronaryarteriesEchocardiographyRegionalwallmotionabnormalityMyocardialPerfusionImagingEspeciallyimportantwhenECGisnormal,hasnonspecificfindings,obscuredbyLBBBorpacedrhythmSestamibi(Technetium-99m)entersmyocardialcellsproportionaltoregionalbloodflowandthenbindstomitochondriaandthenimagedwithagammacameraPerfusiondefectisthemarkerofischemiaandcanbeassessedbyregionalwall

ClinicalAssessment

RecommendationsforStressTestExerciseStressTests

stepwisestrategy

ExerciseECGsimplicity,lowercostandfamiliaritytheinitialtestinpatientswhoarenottakingdigoxin,haveanormalrestECG,andareabletoexerciseMyocardialPerfusionImagingforpatientswithwidespreadrestSTdepression(>1mm),completeleftbundle-branchblock,ventricularpacedrhythmorpreexcitationDobutamineorExerciseStressechoMarkerofStressECGandEchoComparisonofStressTests

meta-analysison44articles(publishedbetween1990and1997) Sensitivity Specificity ECG 52% 71% StressTest 85% 77% Scintigraphy 87% 64%notadjustedforreferralbias.JAMA1998;280:913-20NewerNoninvasiveCTscanNewerWeaponsDifferentialDiagnosisAnteriorchestwalldisordersGastrointestionaldisordersPericarditisAcutemyocardialinfarctionAlternativeDiagnosestoAnginaforPatientswithChestPainNon-IschemicCVaorticdissectionpericarditisPulmonarypulmonaryemboluspneumothoraxpneumoniapleuritisChestWallcostochondritisfibrositisribfracturesternoclaviculararthritisherpeszosterGastrointestinalEsophagealesophagitisspasmrefluxBiliarycoliccholecystitischoledocholithiasischolangitisPepticulcerPancreatitisPsychiatricAnxietydisordershyperventilationpanicdisorderprimaryanxietyAffectivedisordersdepressionSomatiformdisordersThoughtdisordersfixedocclusionsCoronaryAngiographyEstablishingthediagnosisDeterminingprognosisPlanningtherapy

1.Medication2.PTCA+STENT3.CABGCoronaryAngiographyCAGestablishthediagnosisofCADCADcanbediagnosedwhentheluminaldiameternarrowingofcoronaryarteryis≥50%TheProcedureTheProcedureCoronaryAngiographyTreatmentRecommendationsforPharmacotherapytoPreventMIandDeathandReduceSymptomsChronicStableAngina

TreatmentObjectivestoreducetheriskofmortalityandmorbideventsreducesymptoms-anginalchestpainorexertionaldyspnea;palpitationsorsyncope;fatigue,edemaororthopnea

MEDICALTHERAPYRiskfactorcontrol

ControlofsymptomsAnti-platelettherapyCoronaryrevascularizationRecommendationsforTreatmentofRiskFactorsTreatmentofhypertension:beta-blocker,CCB,ACEIetalSmokingcessationtherapy.Managementofdiabetes.Exercisetrainingprogram.Lipid-loweringtherapyinpatientswithdocumentedorsuspectedCADandLDLcholesterol>130mg/dL,withatargetLDLof<100mg/dL.Weightreductioninobesepatientsinthepresenceofhypertension,hyperlipidemia,ordiabetesmellitus.ManagementofAnginaManagementofAnginaManagementofAnginaTakehomemessageforstableAPCoffeeBreakTimeAtherosclerosisISCADalumendiseaseoravesselwalldisease?FororAgainst?Mechanismsforabruptblockingflow

Plateletaggregation

Increaseinsympathetictone,hypercholesterolemia,leucocyteactivation,impairedfibrinolysis,increasedlevelsofPAI-1Thrombosis

Suggestedbyincreasedlevelsoffibrinrelatedantigen,D-dimer,tpa,tpainhibitor-1,prothrombinfragmentsetc Intracoronarythrombusatcoronaryangiography.

Coronaryconstriction

Vasomotorhyperactivityintheareaoftheatheromabyendothelin1

&inhibitingthereleaseofEDRFConceptofstable&unstableplaqueConceptofACS1.CannonCP.JThrombThrombolysis1995;2:205–218.AntithrombotictherapyStableanginaUAThrombolysisprimaryPCIMinutes–

hoursDays–weeksSTEMIUA/NSTEMIAtherothrombosisNewtermOldtermUA=不稳定心绞痛;NSTEMI=非ST段抬高心肌梗死;PCI=经皮冠脉介入治疗Non-

Q-waveMIQ-wavePlaque

ruptureWhat’sdifferentbetweenSTEMIandNonSTEMI?RiskstratificationinACSBraunwald’sClassificationforUAPASP+ClopidogrelbetterEvidenceofASP&HepLMWHmoreuserfriendlyGPIIb/IIIainPCIIIb/IIIainACSStrategyforapproachtoACSAcuteMyocardialInfarctionDefinitionMIisischemicnecrosisoftheheart,itisduetocompleteinterruptionofthemyocardialbloodsupply.ItisaseveremanifestationofCHD.

ClinicalFeatures1.Chestpain

ThemainclinicalpictureinMIissevere,prolonged(>30min)chestpain,whichisassociatedwithrestlessness,anxietyandafearofimpendingdeath.2.Arrhythmias3.Manifestationofheartfailure4.Manifestationofcardiacshock5.PhysicalfindingsofAMI

HR—,regularorirregularBP—,abnormalapicalimpulse,jugularvenousdistentionS1,S2,S3,S4

pericardialrub,systolicmurmur(ruptureofpapillarymuscle,ruptureofventricularseptum,dysfunctionofpapillarymuscle)ECG

1.Typical,transmuralMI,Q-waveMI

①abnormalQ-wave(duration≥0.04s,amplitude≥1/4R-waveinthesamelead)②STsegmentselevationwithmonophase③Twavehighandpeak(hyperacutephase)inverted

2.Atypical,nontransmuralMI,NQ-waveMI①noQ-wave②STsegmentsdepress③Twavesymmetricallyinverted

3.SerialchangeofECGinMI4.LocationofMI

V1—V3anteriorseptalwallV3—V5anteriorwallV4—V6anteriorlateralwall;V7—V8posteriorwallⅠ,aVLhighlateralwall;Ⅱ,Ⅲ,aVFinferiorwallWideanteriorwallAcuteInferiorWallMI/djenkins/ecghome.html

Copyright1989.Novartis.ReprintedwithpermissionfromtheAtlasofHumanAnatomy,illustratedbyFrankH.Netter,M.D.Allrightsreserved.Laboratorystudy1.WBC(whitebloodcountincrease)ESR(erythrocytesedimentationrateincrease)2.CardiacenzymesincreaseCPK(creatinephosphokinaseincrease)begin3—6hafteronsetofMIpeak12—24hreturntonormal3daysCPK-MB(IsoenzymeCPK)ismorespecificformyocardialcellinjury.SGOT(serumglutamic-oxaloacetictransaminase)begin8—12h

peak18—36h

normal3—4days

LDH(lacticdehydrogenase)

begin24—48h

peak3—6days

normal8—14daysCARDIACPROTEINCHANGESWITHTHROMBOLYSISRELATIVECONCENTRAITONTIMEAFTERINFARCTIONSuccessfulthrombolysisNormalMI,unsuccessfulthrombolysisDiagnosisofAcuteMIHistoryClassicsymptoms:intense,oppressivechestpressureradiatingtoleftarmOthersymptoms:chestheaviness,burningradiationtojaw,neck,shoulder,back,armsnausea,vomitingdiaphoresisdyspnealightheadednessSymptomsmaybemildorsubtleThekillipclassificationKillipclassIincludesindividualswithnoclinicalsignsofheartfailure.KillipclassIIincludesindividualswithralesinthelungs,anS3gallop,andelevatedjugularvenouspressure.2KillipclassIIIdescribesindividualswithfrankpulmonaryedema.KillipclassIVdescribesindividualsincardiogenicshock.Diagnosis

DiagnosisofacuteMIisbasedonatleasttwoofthethreefollowingcriteria:1.Clinicalfindings

Chestpainconsistentwithmyocardialischemia,butitshouldbedifferentiatedfromanginapectoris.2.ECGDevelopmentabnormalnewQwaveandSTsegmentelevationassociatedwithserialchange.

3.CardiacenzymesCharacteristicriseandfallintheserumenzymeactivitieswithoutothercauses.DifferentialDiagnosisofProlongedChestPain

AMIAorticdissectionPericarditisAtypicalanginapain

associatewithhypertrophiccardiomyopathyEsophageal,otheruppergastrointestinal,orbiliarytractdiseasePulmonarydiseasepneumothoraxemboluswithorwithoutinfarctionpleurisy:infectious,malignant,orimmunedisease-relatedHyperventilationsyndromeChestwallskeletalneuropathicPsychogenicComplicationinAMI

1.Ruptureofintraventricularseptum2.Dysfunctionorruptureofpapillarymuscle3.Ruptureoftheheart4.Ventricularofaneurysm5.Embolism6.Postmyocardialinfarctionsyndrome

Treatment1.Generalmanagement

①stayinbedforseveraldays②ECGmonitoring,BPmonitoring(BP),payattentiontothepatient’svitalsigns③Oxygentherapy⑴traditionallyoxygenisgivenroutinelybynasalprongs(2-4L/min)

⑵

patientswithpulmonaryedematointubateandgiveoxygenunderpositivepressure(PEEP).⑶PO2isnormal,Oxygentherapymaybediscontinued.④GIK(glucose-insulin-potassium)

Treatment2.Painreliefmorphine5-10mg(H)extremelyeffectivedolantin50-100mg(H)adversesideeffect:hypotension(BP)bradycardia(HR)inhibitrespiratoryfunction3.Myocardialreperfusion

①thrombolytictherapyThrombosisisthemaincauseofmostAMI.Dissolutionoftheobstructingcoronaryarterialthrombusmayinducereopenofobstructingcoronaryartery.Treatment3.Myocardialreperfusion

①thrombolytictherapy⑴indicationchestpainonset