《冠心病英文版》PPT課件

Atherosclerosis Coronaryheartdiseases ZhengzhouUniversity FirstaffiliatedHospitalDept ofCardiologyHaiyuLi M D CardiovascularDiseases Atherosclerosis leadingcauseofdeathanddisabilityCommonlocation Coronarycirculation Proximalleftanteriordescendingcoronaryartery LAD ProximalportionofrenalarteriesExtracranialcirculationtothebrainCarotidbifurcation Atherosclerosis Coronaryheartdisease atherosclerosis Coronarystenosis coronaryspasm Myocardialischemia anoxaemia Coronaryheartdisease CHDIschemicheartdisease AtherosclerosisStableanginapectoris SAP AcutecoronarysyndromeUnstableangina UAP andnon STEMI UA NSTEMI STelevationmyocardialinfarction STEMI Threefundamentalbiologicalprocessesofatherosclerosis Accumulationofintimalcells smoothmusclecellsMacrophagesT lymphocytesProliferatedconnectivetissuematrix collagenelasticfibersproteoglycans3 Accumulationoflipid cholesterolestersfreecholesterol HypothesisoflipoproteininfiltrationAggregationofplateletsandthrombosisClonaltheorytheresponse to injuryhypothesis Atherosclerosis Hypothesis Response to injury Atherosclerosis hypothesis Highbloodpressure bacterium virus toxin ox LDL immunefactor vasoactivesubstanceendotheliumdamageanddysfunction vasoactivesubstance adhesionandaggregationofmonocytes foamcell platelets Lipidosis growthfactor proliferationofsmoothmuclecells collagen lipolyticenzyme atherosclerosis PathologyandpathophysiologyFattysteakFibrousplaqueComplicatedlesion Atherosclerosis InitiationofAtherosclerosis Fattysteakformation InitiationofAtherosclerosis FattysteakformationLipoproteinoxidationNonenzymaticglycationLeukocyterecruitmentFoamcellformation Atheromaevolution fibrousplaque Atheromaevolutionandcomplications Vascularremodeling compensatoryenlargement Atheromaevolution Involvementofarterialsmooth musclecellsBloodcoagulationmicrovessels Atheromaevolutionandcomplications Complicatedlesion thrombosis Atheromaevolutionandcomplications Atheromaevolutionandcomplications Vulnerableplaque ThinfibrouscapRelativelylargelipidcoreHighcontentofmacrophages Inflammatorymediators Intravascularultrasound ClassicificationofatheroscleroticlesionusingIVUS CliniclstagesandclassificationAbsenceofsymptomorstageofdelitescenceischemianecrosis targetorgan fibrosis Atherosclerosis GeneralmanifestationAorticatherosclerosisCoronaryarteryatherosclerosisCerebralatherosclerosisMesentericatherosclerosisPeripheralarteryatherosclerosis Atherosclerosis clinicalmanifestation laboratoryexaminationLackofsensitiveandspecificmethodsforearlydiagnosisDyslipidemia X ray DSAshowseverityofstenosisDopplerultrasound bloodflowradionuclide detectionofischemiaEchocardiogram CHDECGandstresstest CHDNewtechniques intravascularultrasound angioscopeCT MRI Atherosclerosis Riskfactorsandprevention 1 Lifestylemodification2 Lipiddisorders Dyslipidemia cholesterolscreeninginall 20yrsElevated cholesterol TcandLDL c TG ApoB ApoA Lp a Low HDL cLDLloweringbyHMG CoAreductase statins cardiovascularevents30 riskofMI62 3 Hypertension 4 DM Metabolicsyndromeorinsulinresistancesyndrome BP BMI TG seruminsulinHDL c Diabetesmellitus DM RR1 9formale 3 3forfemalemorediffuselesion CADequivalent75 80 causeofdeathinadultDMarevasculardiseases CAD cerebrovasculardisease orperipheralvasculardisease Riskfactorsandprevention 7yearsincidenceofdeath non fatalMI EastWestStudy ThesepatientshadnohistoryofmyocardialinfarctionHaffnerSM etal NEnglJMed 1998 339 229 234 0 5 10 15 20 25 30 35 40 45 50 EventsofMIin7years NohistoryofMIOMINohistoryofMI OMI non diabeticsdiabeticsn 1373n 1059 P 0 001 P 0 001 4 19 20 45 DM CADequivalent 5 Cigarettesmoking morethrombogenic6 Familyhistory geneticfactor7 Aging 40yrsadults 4 5fatalmyocardialinfarctionoccuredinpatiens 65yrs8 Malegender postmenopausalstate male female 2 1 mandevelopCHD10 15yrsearlierthanwoman9 alcohol10 Others diet homocysteine hemostaticfactorsinflammation infection Riskfactorsandprevention Drugtherapy anti platelet aspirin clopidogrel GPIIb IIIainhitibor Dipyridamole cilostazolLipid lowering Riskfactorsandprevention HMG CoAreductaseinhibitors statins Atorvastatin Fluvastatin Lovastatin Pravastatin Simvastatin Cerivastatin Rosuvastatin elevationofaminopherase rhabdomyolysis2 Bileacid bindingResinscholestyramine colestipol3 NicotinicAcid 4 Fibricacidderivatives fibrates Gemifibrozil clofibrate Fenofibrate5 Cholesterolabsorptioninhibitors ezetimibe6 Probucol Lipid loweringdrugs PreventionofCAD A aspirin ACEIB bloodpressure blocker C cigarettesmoking CholesterolD diet diabetesE exercise education ThirdReportoftheNationalCholesterolEducationProgram NCEP ExpertPanelonDetection Evaluation andTreatmentofHighBloodCholesterolinAdultsATPIII adulttreatmentpanelIII Circulation200217 24 3144 3373 Atherosclerosis Coronaryheartdisease CHD Coronaryheartdisease CHD mostcommoncause obstructionofatheromatousplaqueothercauses spasmarterialthrombicoronaryemboliostialnarrowingduetolueticaortitiscongenitalabnormalitiessevereLVhypertrophy Factorseffectmyocardialoxygensupplyanddemand Oxygensupply Oxygendemand Heartrate Myocardialcontractility Systolicwallstress oxygencarryingcapacityofblood Coronarybloodflow Vascularresistance Extravascularcompressiveforces autoregulation Metabolicregulation Humoralfactor Neuralregulation Durationofdiastole Pressuregradient Endothelialcontrol Coronaryheartdisease Type slientischemia delitescence ECGchange Anginapectoris angina causedbymyocardialischemiamyocardialinfarction acutemyocardialischemicnecrosiscausedbytheocclusionofcoronaryarteryIschemiacardiomyopathy Heartfailureandarrhythmia cardiacenlargement heartfailure arrhythmia causedbythemyocardialfibrosisastheconsequenceofchronicmycardialischemiaSuddendeath suddencardiacarrestcausedbyventricularfibrillation flutter Coronaryheartdisease CHD Type slientischemia delitescenceAnginapectoris myocardialinfarction Ischemiccardiomyopathy Heartfailureandarrhythmia Suddendeath AcuteCoronarySyndrome ACS Restingischemia Non STelevation STelevation Unstableangina Non QwaveAMI QwaveAMI positiveserumcardiacmarkers occasionallyvariantangina Stableanginapectoris SAP definition acuteandtransientmyocardialischemiaandanoxaemiausuallycausedbycoronaryinsufficiencyduringexertionoremotionalstressCharacteristics paroxysmalprecordialsqueezing likechestpain behindthemidsternum radiatedtoleftshoulderandupperarmprecipitatedbystressorexertionduration 2 5mintypicallyrelievedrapidlybyrestornitrates Stableanginapectoris Coronarystenosis others aorticvalvedisease HOCM MB Myocardialoxygendemand HRXSBP increasedmyocardialhypoxiaacumulationofmetabolicproduct stimulateC1 5nervetocausethesensationofchestpain Stableanginapectoris mechanism inangiographySignificantcoronarylesionwithdiameterstenosis 70 in75 ptsNosignificantstenosisinabout5 10 pts Ischemiamayberelatedtocoronaryspasmormicrovasculardysfunction Pathology Stableanginapectoris pathophysiology 1 MetabolicandelectrophysiologyATPreduced accumulationofacidsubstancesDysfunctionofironpump Na K andNa Ca Earlydepolarization STdeviation 2 LVfunctionandhemodynamicsituationLVcontractilityandspeed systolicBP strokevolume cardiacoutputdecreasedLVEDpressureandvolume Stunningofmyocardium Stableanginapectoris symptom chestpainoroppressionlocationbehindorslightlytotheleftofthemidsternumnodefiniteborderlineradiatedtotheleftshoulderandupperarmAtypicallocation lowerjaw thebackofneck Clinicalmanifestation Stableanginapectoris chestpaincharacteristics tightness squeezing burning pressing choking bursting rarelysharp notspasmodicforcethepatientstoptheactivitytillthesymptomrelievedprecipitationexertionoremotionalagitation duration 3 5minspainrelief withinseveralminsafterrestorusingnitroglycerin Clinicalmanifestation Stableanginapectoris PhysicalexaminationincreasedHR elevatedBPanxietysweatingoccasionallygalloprhythm transientsystolicmurmur Clinicalmanifestation Stableanginapectoris Laboratory Stableanginapectoris Stresstest rest Exerscise Stableanginapectoris 2 Echocardiography 3 Radionuclideimagingassessment TL201 Tc99m sestamibimyocardialperfusionscintigraphy4 X rayofheart5 coronaryangiography finaldiagnose6 others IVUS intracoronaryDopplerflow intracoronarypressure Laboratory Stableanginapectoris CoronaryAngiography 1 Cardiogenicpain aorticdissection HOCM aorticstenosis2 Respiratory PE pneumothorax pleuritis3 Gastrointestinal gastro esophagealdiseases Hiatalhernia cholecystitis pepticulceration pancreatitis4 Neuromuscular skeletal TietzeSyndrome Costochondritis intercostalneuralgia Herpeszoster5 Psychologic anxiety depression panicattacks Stableanginapectoris Diagnosis Chestpain riskfactors ECGevidenceofischemiaduringchestpain angiography Differentiation FunctionalclassificationofSAP CCS CCSI nochestpainatordinaryactivity AnginaatstrenuousorrapidorprolongedexertionCCSII Slightlimitationofordinaryactivity Walkingorclimbingstairsrapidly aftermeals incold inwind Walkingmorethan2blocks climbingmorethanstairsof3rdfloor CCSIII Markedlimitationofordinaryactivity Walking1to2blocks climbingstairsof3rdfloorCCSIV Inabilitytocarryonanyactivitywithoutdiscomfortanginalsymdromemaybepresentatrest Stableanginapectoris Generalconsideration rest avoidprovocativefactors riskfactorscontrol2 Drugtherapy preventMIanddeathsymptomreliefandqualityoflifeimprovment3 Coronaryrevascularization percutaneouscoronaryintervention PCI Coronaryarterybypasssurgery CABG SVG LIMA Preventionandtreatment Stableanginapectoris antianginalandanti ischemictherapy Drugtherapy Oxygensupply Oxygendemand a nitratesb beta adrenergicblockersc Calciumantagonistsd Drugsimprovingmetabolism Stableanginapectoris Drugtherapy a nitratesloweroxygendemand decreasearteriolarandvenoustone reducepreloadandafterloadincreasecoronarysupply CoronarydilatationNitroglycerinIsosorbidedinitrateisosorbide5 mononitrate long actingnitrates Stableanginapectoris b blockers reducemyocardialoxygen reduceHR myocardialcontractility BP theLVwallstressAbslutecontraindications severbradycardia high degreeA Vblock SSS severeunstableLVfailureRelativecontraindications asthmaandbronchospasticdiseaseperipheralvasculardisease 1 selective metoprolol atenolol bisoprolol Drugtherapy Stableanginapectoris c Calciumantagonists Increaseoxygensupply dilateresistancevessels releasespasm improvemicrovascularfunctionDecreaseoxygendemand negativeinotropiceffect decreaseBPAntiplateleteffect d Drugsimprovingmetabolism trimethazine vasorel selectivelyinhibit3 KAT 3 酮酰輔酶A硫解酶 partlyinhibitFAoxidation Drugtherapy Stableanginapectoris preventMIanddeaththerapya antiplateletangents ASA 75 325mg dclopidogrel ticlopidine ADPreceptor antagonists Cilostazol phosphodiesteraseinhititor 50 100mgbidb Lipid loweringangents statinsc Angiotesin convertingenzymeinhibitor ACEI Drugtherapy Stableanginapectoris stenting Stableanginapectoris Unstableangina UAP andnon STEMI Restingischemia Non STelevation STelevation Unstableangina Non QwaveAMI QwaveAMI positiveserumcardiacmarkers occasionallyvariantangina AcuteCoronarySyndrome ACS PathophysiologyofACS stableanginaUAP non Q wAMIQ wAMIAngiographicthrombus0 1 75 90 IncreasedFPA TAT0 5 60 80 80 90 Activatedplatelets0 5 70 80 80 90 Acutecoronaryocclusion0 1 10 25 90 mortality1 2 3 8 6 15 FPA fibrinopeptideATAT thrombin antithrombincomplexes UAPandnon STEMI Occuringatrest orwithmininalexertion last 20minssevereandofnew onset within1 2months CCSIIIOccuringwithadeteriorativepattern atleastCCSIIIvariantanginapectoris Prinzmetalangina transientSTelevation causedbythecoronaryspasm Definition UAPandnon STEMI Anginapectorisorequivalentischemicdiscomfortwithatleastoneofthethreefeatures Braunwaldclassificationofunstableangina Severity ClassI New onset oracceleratedsevereanginanorestpainwithin2monthsClassII Anginaatrest subacuteanginaatrest withintheprecedingmonthbutnotwithin48h ClassIII Anginaatrest acute withinthepreceding48h UAPandnon STEMI Braunwaldclassificationofunstableangina ClinicalCircumstancesClassA SecondaryUAPaclearlyidentifiedconditionextrinsictothecoronaryvascularbedthathasintensifiedmyocardialischemia e g anemia hypotension tachy arrhythmiaClassB PrimaryunstableanginaClassC Post infarctionUAP within2weeksofadocumentedMI UAPandnon STEMI mechanism 1 plaqueruptureanderosion withnonocclusivethrombus2 dynamicobstruction Vasoconstruction3 progressivemechnialobstruction rapidlyadvancingorISRfollowingstenting 4 secondaryUAInflammationThrombogenesis UAPandnon STEMI ECG Non STEMI STdepressionlast 12hr Cardiacbiomarkersofmyocardiumdamage cTnT cTnICK MB UAPandnon STEMI CoronaryangiographyAngioscopyandIVUSOtherlaboratorytests Riskstratification TIMIRiskScoreAge 65yrsMorethan3coronaryriskfactorsPriorangiographiccoronaryobstructionST segmentdeviation 0 5mmMorethan2anginaeventswithin24hoursDevelopmentofUA NSTEMIwhileonaspirinElevatedcardiacmarkers Antaman JAMA2000 284 835 42 TIMIIIB ESSENCE PRISM PLUS TACTICS TIMI18 UAPandnon STEMI Treatment 1 Genearlmanagement rest oxygen CCU2 DrugtherapyA Anti ischemicdrug intravenously orallynitrates blockerCalciumantagnoist firstchoiceforvariantanginaMorphine UAPandnon STEMI Treatment 2 Drugtherapy B antithrombotictherapya Anti plateletAspirin early 300mgloadingdoseADP receptorantagonist clopidogrel300mg 600mgloadingdose 75mg dGPIIb IIIareceptorinhibitor usedinptsplannedtoPCIb Anticoagulationtherapy HeparinLowmolecularweightheparin LMWH Directanti thrombindrug bivalirudin hirudin UAPandnon STEMI Treatment 2 Drugtherapy C othermedicaltherapya lipid loweringdrugs statins earlyuse infirst24hrs LDL ctarget 70mg dlb ACEI long termsecondaryprevention UAPandnon STEMI Treatment 3 Invasiveversusconservativestrategyearlyinvasivestrategyindicatedforhighriskpatients within48 72hrs Followingbycoronaryrevascularization PCIorCABG 4 Long termmanagement blockers Statin ACEI aspirinclopidegrel 12m UAPandnon STEMI SYMPTOMSSUGGESTIVEOFACS NoncardiacDiagnosis ChronicStableAngina PossibleACS DefiniteACS Treatmentasindicatedbyalternativediagnosis ACC AHAChronicStableAnginaGuidelines NoST Elevation ST Elevation NondiagnosticECGNormalinitialserumcardiacbiomarkers STand orTwavechangesOngoingpainPositivecardiacbiomarkersHemodynamicabnormalities Evaluateforreperfusiontherapy ACC AHASTEMIGuidelines Observe 12hfromsymptomonset Norecurrentpain negativefollow upstudies Recurrentischemicpainorpositivefollow upstudiesDiagnosisofACSconfirmed StressstudytoprovokeischemiaConsiderevaluationofLVfunctionifischemiaispresent testsmaybeperformedeitherpriortodischargeorasoutpatient NegativePotentialdiagnoses nonischemicdiscomfort low riskACS Arrangementsforoutpatientfollow up PositiveDiagnosisofACSconfirmedorhighlylikely AdmittohospitalManageviaacuteischemiapathway AlgorithmforevaluationandmanagementofpatientssuspectedofhavingACS AndersonJL etal JAmCollCardiol2007 50 e1 e157 Figure2 STelevationmyocardialinfarctionSTEMI AcuteCoronarySyndrome ACS Restingischemia Non STelevation STelevation Unstableangina Non QwaveAMI QwaveAMI positiveserumcardiacmarkers occasionallyvariantangina ischemicnecrosisofmyocardiumresultsfromtheprolongedmyocardialischemiaprecipitatedbyanocclusivecoronarythrombusatthesiteofapreexistingatheroscleroticplaque WithtypicalandserialECGchanges Representtheserioussituationofcoronaryarterydisease STEMI Definition 1 incidence inUSA 71 inmalebetween35 84yrs 22 infemale 1attackinabout20second2 mortality decreasedin30 recent10yearsstill1 3ofthepatientsdied50 ofthedeathoccuredwithin1haftertheonsetMImostdeathesresultfromventricularfibrillation epidemiology STEMI Causeofthedecreasedmortality newdrugtherapy blocker anti thromboticLMWHnitratesACEIStatins STEMI Changeofconcept1960 80s Transmural non transmuralorsub endocardium1980s QwaveMI non QwaveMI1990s STEMI non STEMI STEMI PossiblemechanismofthechronicCADtoACS Pathology Coronarydiseases OcclusionofLAD anteriorwallMI STEMI Pathology myocardium STEMI STEMI Pathology myocardialdiseases Ventricularremodelingconcept thechangesinLVsize shape andthicknessinvolvingboththeinfarctedandnoninfarctedsegmentsDeterminants thesizeofinfarctionVentricularloadingconditionsInfarctrelatedarterypatency STEMI Infarctexpansion anincreaseinthesizeoftheinfarctedsegment acutedilatationandthinningoftheareaofinfactionnotexplainedbyadditionalmyocardialnecrosis ventriculardilatation shiftofpressure volumecurveofLVtotherightlargerLVvolumeatanygivendiastolicpressureCompensatorymechanismsformaintainingstokevolumeAssociatedwithnon uniformrepolarizationofmyocardium predisposetolife threateningventriculararrhythmias STEMI Ventricularremodeling Systolicfunction dyssynchrony dissociationinthetimecourseofcontractionofadjacentsegmenthypokinesis reductionintheextentofshorteningakinesis cessationofshorteningdyskinesis paradoxicalexpansion systolicbulgingDiastolicfunction reductioninLVcompliance decreaseinthepeakrateofdeclineinLVpressure dP dt riseinLVend diastolicpressureandvolume STEMI pathophysiology LVfunction Predisposingfactor heavyexercise mentalstress surgicalproceduresfever tachycardia respiratoryinfection hypoxemia hypoglycemiaPrinzmental sanginaProdromalsymptoms weakness chestdiscomfort restlessness newonsetAPandacceleratingAPCircadianperiodicitypeakincidence 6 12am STEMI Clinicalmanifestation SymptomChestpainsevere sometimesintolerable prolonged usuallylastingfor 30mins lesseffectiveofsublingualnitroglycerin retrosternalinlocation sweating scared andfeelingofimpendingdeathinsomepatients AMIismanifestedbyshockandacuteLVfailure notbychestpain theelderly alerttheepigastriumpainandabdominaldisorders STEMI Clinicalmanifestation symptomsGeneral fever HRincrease WBC ESRfastingGastrointestinalsymptom nausea vomiting arrhythmias VPs AVblock atrialarrhythmiasoccurredmoreofteninpatientswithHFHeartfailure mainlyacuteLVfailure maydevelopeRVfailure InitialRVfailureoccureinpatientswithRVinfarction associatedwithhypotensionHypotensionandshock SBP 80mmHgafterpainrelease RVinfarction STEMI Clinicalmanifestation PumpfailureClassificationbasedonclinicalexamination Killip ClassI noHF ralesandS3absent ClassII mildHF ralesover2 2 ClassII Pulmonarycongestion PCWP 18 CI 2 2 ClassIII peripheralhypoperfusion PCWP18 CI 2 2 STEMI Clinicalmanifestation physicalexaminationGeneralappea