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1、ChapterVIDiseasesofCardiovascularSystemCardiovascularsystemHeartBlood vessels“Pump” Moremorbidity&mortality - Approximately half of all death caused by disorders of circulatory system - In US, myocardial infarction alone is responsible for 20-25% of all deathSystemicPathologyEtiology,PathogenesisPat
2、hologicmorphologyClinico-pathologicalcorrelationConsequenceGeneralpathologySystemicpathologyExample: Myocardial infarctionCoagulative necrosis Granulation tissueScarmyocardial rupture ArrhythmiasVentricular aneurysmContractile dysfunction Heart failureshock, deathMorphologyConsequencesCardiovascular
3、diseasesHeartBlood vesselsIschemicheartdiseaseAtherosclerosisHypertensionRheumaticHeartDiseaseValvularheartdisease(InfectiveEndocarditis)MyocarditisCardiomyopathyCongenitalheartdiseaseLarge(Elastic):Aorta&largebranches,pulmonaryarteriesMedial(Muscular):Coronary,renalarteriesSmall(=1.0cmstreaks,oilre
4、dstaining(+)orificesofbranches-Fattystreak:foamcells-MayevolveintoadvancedlesionsordisappearMicroscopy2.AtheroscleroticplaqueGross:whitetoyellow,red-brownwiththrombosisoverthesurface0.31.5cmcancoalescetoformlargermassesThebasicstructureofanatheromatousplaqueMicroscopyMassontrichromestainF:fibrouscap
5、C:acentralnecrotic(lipid)coreL:lumenTheinternalandexternalelasticmembranesaredestroyedThemediaisthinnedunderthemostadvancedplaqueScatteredinflammatorycells,calcification,andneovascularizationatthejunctionofthecapandcore*MinisummaryAtherosclerosisisanintima-basedlesioncomposedofafibrouscapandanathero
6、matous(literally,“gruel-like”)core;theconstituentsoftheplaqueincludeSMCs,ECMs,inflammatorycells,lipids,andnecroticdebris.Naturalhistory,morphologicfeatures&mainpathogeniceventsComplicatedlesionsRupture,ulceration,orerosionthrombusformationHemorrhageintoaplaqueAtheroembolismAneurysmformationCalcifica
7、tionDissectinganeurysmPlaqueruptureAcutecoronarythrombosisonaplaquewithfocalrupture,triggeringfatalmyocardialinfarctionHemorrhageintoplaqueAneurysmAcuteplaquechangeRupture/fissuring Erosion/ulceration Hemorrhage into the atheroma ThinFibrouscapDense LargeLipidcoresSmallDenseInflammationLittle Clinic
8、alconsequencesofatherosclerosis*Atheroscleroticplaquesdevelopandgrowslowlyoverdecades.*Stableplaquescanproducesymptomsrelatedtochronic ischemia bynarrowingvessels,whereasunstableplaquescancausedramaticandpotentiallyfatal ischemic complicationsrelatedtoacuteplaquerupture,thrombosis,orembolization.Aor
9、taAbdominalaorticaneurysmCoronaryA.CoronaryHeartDiseaseCerebralA.Thrombosis,Aneurysm,Hemorrhage,AtrophyRenalA.Infarction,Nephrosclerosis,HypertensionFemoral,Popliteal,TibialA.Claudication,GangreneIschemicHeartDisease(IHD)CoronaryArteryDiseaseNarroworOcclusionofLumenofCoronaryACoronaryperfusionMyocar
10、dialdemandIschemia,FunctionDisturbance,InfarctionofHeartInthevastmajorityofcases,cardiacischemiaisduetocoronary artery atherosclerosisvasospasm,vasculitis,andembolismarelesscommoncausesEpidemiologyLeadingcauseofmorbidityandmortalityinindustrializednationsAnnually,ahalf-millionAmericansdieofIHDCardia
11、criskfactors:smokingcessationprogramhypertension&diabetictreatmentcholesterol-loweringagentsNormalheart“Pump”Weight:250270g,240260gWallthickness:leftventricle0.91.0cmrightventricle0.30.4cmatrium0.10.2cmValves：asingledirectionofbloodflowMyocardium：nearlyinexhaustibleBloodsupply:coronaryarteriesCorona
12、ryarteriesLesionsofCoronaryAtherosclerosisPlaquechanges,thrombosis,hemorrhage,vasospasmCriticalstenosis:=75%ThefrequenciesofocclusionofvariouscoronaryarteriesandthedistributionoftheresultantinfarctsLeftanteriordescendingcoronaryartery40%50%Anteriorandapicalleftventricle;anteriortwothirdsoftheinterve
13、ntricularseptumRightcoronaryartery30%40%Posteriorwalloftheleftventricle;posterioronethirdoftheinterventricularseptumLeftcircumflexcoronaryartery15%20%lateralwalloftheleftventricleRupture,fissuring,orulcerationrapidthrombosisHemorrhageintothecoreofplaquesVasospasmAcutePlaqueChangeAcutecoronarysyndrom
14、esPalpitations；Pain；Exertionaldyspnea；Diaphoresis；Nausea;DecreasedexercisetolerancePlaqueruptureAcutecoronarythrombosisonaplaquewithfocalrupture,triggeringfatalmyocardialinfarctionMassiveplaquerupturewiththrombus,triggeringafatalmyocardialinfarctionClinicalPresentations1.Anginapectoris2.Myocardialin
15、farction3.Chroniccoronaryheartdisease4.SuddencoronarydeathAnginapectorisAnintermittentchestpaincausedbytransient,reversiblemyocardialischemia(1)Stable-Afixedatheroscleroticnarrowing(usually70%)-Occurinthesettingofincreaseddemands-Relievedbyrest(reducingdemand)orbyadministrationofnitroglycerin(vasodi
16、lator)(2)Unstable-Resultsfromasmallfissureorruptureofatheroscleroticplaquetriggeringplateletaggregation,vasoconstriction,andformationofamuralthrombus-Occurprogressivelyatlesslevelsofexertionorevenatrest(3)Variant-Causedbyvasospasm-OccuratrestAcrushingorsqueezingsubsternalsensation,mayradiatedownthel
17、eftarmMyocardialInfarction(MI，心肌梗死心肌梗死)NecrosisofheartmuscleresultingfromischemiaMostMIsarecausedbyacute coronary artery thrombosisPlaquedisruptionPlateletaggregation&vasospasmThrombosisOccludingthecoronaryarterylumenIschemiaMyocardialResponsetoIschemiaBiochemistry:Withinsecondsaerobicglycolysis,ATP
18、Function&morphology:Withinaminuterapidlossofcontractility,ultrastructuralchangesreversible2040minutescoagulationnecrosisirreversiblePromptinterventionThrombolysisAngioplastyCoronary arterial bypass graftMORPHOLOGYMItypicallybeginsinthesubendocardialregionMIusuallyreachesitsfullsizewithin3to6hoursPat
19、ternsofinfarction Depending on The involved vessel The duration of the occlusion Metabolic demands of the myocardium Extent of collateral supply1.Transmuralinfarctions2.Subendocardialinfarctions3.MicroscopicinfarctsGrossMIslessthan6hoursoldusuallyarenotgrosslyapparentBy12to24hoursafterMI,aninfarctus
20、uallycanbegrosslyidentifiedbyared-bluediscolorationcausedbystagnated,trappedbloodMap-likeMicroscopyCoagulationnecrosis/inflammationGranulationtissueScar-AcuteMI-Remoteinfarction(Scar)-Rupture(Deathcause)“Irregular”map-like1day-coagulationnecrosisedemawavyfibers3-4daysCompletecoagulationnecrosisofmyo
21、fibersHeavyneutrophilicinfiltrate7-10daysWell-developedphagocytosis3wkCollagenfibersGranulationtissueScar-Richcollagenfibers-ResiduemyofibersReperfusioninjuryRestorationofbloodflowgreaterdamageMitochondrialdysfunction,myocytehypercontracture,freeradicals,leukocyteaggregation,&Plateletandcomplementac
22、tivationcontributingtomicrovascularinjuryClinicalFeaturesThechestpaincannotberelieved“silent”infarctsindiabeticpatients&elderlypersonsRapid&weakpulseDiaphoretic&nauseous,particularlywithposteriorwallMIsElectrocardiographic abnormalitiesQwaves,STsegmentchanges,TwaveinversionslethalArrhythmiasLaborato
23、ry evaluation*MiniSummary1.Myocardialischemialeadstolossofmyocytefunctionwithin1to2minutesbutcausesnecrosisonlyafter20to40minutes.2.Myocardialinfarctionisdiagnosedclinicallyonthebasisofsymptoms,electrocardiographicchanges,andmeasurementofserumCK-MBandtroponins.3.Grossandhistologicchangesofinfarction
24、requirehourstodaystodevelop.4.Infarctioncanbemodifiedbytherapeuticintervention(e.g.,thrombolysisorstenting),whichsalvagesmyocardiumatriskbutmayalsoinducereperfusion-relatedinjury.ComplicationsofMIDependingon-infarctsize-site-fractionalthicknessofthemyocardialwallthatisdamaged1.Contractiledysfunction
25、,cardiogenicshockmassiveMIsinvolving40%oftheleftventricle2.ArrhythmiasMyocardial irritability&conduction disturbancesSuddendeath3.MyocardialruptureMostcommonbetweendays3-7afterMIsThetimewhenlysisofmyocardialtissueismaximalandwhenmuchoftheinfarcthasbeenconvertedtosoft,friablegranulationtissueVentricu
26、larwallfatalhemopericardium&cardiactamponadeMostcommonVentricularseptumleft-to-rightshunting,acuterightheartfailturePapillarymuscleseveremitralregurgitation4.Pericarditis5.Muralthrombusthromboembolism6.Ventricularaneurysm-AlatecomplicationoflargetransmuralMIs-Thebulgingofthenoncontractilefibrousmyoc
27、ardiumduringsystole-Athin-walled,fibrousoutpouchingoftheventricularwall-Oftenwithamuralthrombus7.Progressivelateheartfailure*MiniSummaryComplicationsofinfarctionincludecontractiledysfunction,arrhythmia,myocardialrupture,pericarditis,chamberdilation,muralthrombus,aneurysmformation,andCHF.ChronicIsche
28、micHeartDiseaseThe development of progressive congestive heart failure as a consequence of long-term ischemic myocardial injuryCoronaryarteries:moderatetosevereatherosclerosisHeart:Gross-enlarged,left ventricular dilation and hypertrophy,patchyscars,muralthrombiMicroscopy-myocardialhypertrophy,fibro
29、sis,subendocardialmyocytevacuolizationClinicalfeatures:progressiveanginapectoris,MI,arrhythmiasSuddenCardiacDeathUnexpecteddeathfromcardiaccauses,occurringwithin24hoftheonsetofsymptomsCoronaryarterydiseasesinadultsNon-atheroscleroticcausesinyoungervictimsAlethalarrhythmia,eg.VentricularfibrillationH
30、ypertensionAdultbloodpressureGradeSystolicpressure(mmHg)Diastolicpressure(mmHg)Normal=130=140and/or=90Borderline13013985-89ClassificationofHypertensionEssential(idiopathic):9095%Arterioles/smallarteriesBenign:Malignant=9:1Secondary:diseasesofadrenalglands,renaldiseases,renalarterystenosisEssential(P
31、rimary,Idiopathic)HypertensionA chronic disease with spasm & sclerosis of arteriole and small artery causedby different factors and increase of cardiac outputinducesincreaseofbloodpressureandlesionsoforgansPathogenesisTheBPlevelisdeterminedbytheinteractionofmultiplegenetic,environmental,anddemograph
32、icfactorsthatinfluence2hemodynamicvariables:cardiac outputandtotal peripheral resistanceMORPHOLOGYHyalinearteriolosclerosis(benignhypertension)HyperplasticarteriolosclerosisNecrotizingarteriolitis(malignanthypertension)Thickening of the walls with narrowing of the lumenProcessesofbenignhypertensionS
33、tage1:FunctionaldisturbanceSpasmofarterioleandsmallarteriesStage2:ChangesofvascularsystemSmallartery&ArteriolehyalinedegenerationLarge&medialarteryatherosclerosisStage3:LesionsoforgansHeart-HypertensiveheartdiseaseLeftventricularhypertrophyEarlystageConcentrichypertrophyLaterAcentrichypertrophydilat
34、ionofcardiacchambersLM:Myocyteshypertrophy,withprominentnuclearenlargement&hyperchromasiaInterstitialfibrosisKidneyArterionephrosclerosisGrosslysymmetricallyatrophicdiffuse,finegranularityofsurfaceMicroscopicallyhyalinearteriolosclerosisischemicatrophycompensatedhypertrophy&dilationArrangedatinterva
35、ls颗粒性固缩肾颗粒性固缩肾BrainHypertensiveencephalopathyEdema,softening(microinfarct),microaneurysmsHemorrhage:basalganglia基底核（内囊）lenticulostriateartery豆纹动脉MalignanthypertensionNecrotizingarteriolitis:fibrinoidnecrosisHyperplasticarteriolosclerosisonion-skin,concentric,laminatedthickeningofthewallsBenignvsMali
36、gnantHypertensionBenignMalignantIncidencehigh(90%)low(10%)AgemiddleorsenioryoungerormiddleBP140/90mmHg200/120mmHgSymptomlightsevereLesionhyalineofarteriolefibrinoidnecrosisofarteriole&smallarteriesCourse10yr12yrCauseofdeathcerebralhemorrhage,renalfailure,heartfailureuremia(95%)Rheumatism(风湿病）风湿病）Rhe
37、umaticfeverisan acute, immunologically mediated, multisystem inflammatory disease. FollowinganepisodeofgroupA-hemolyticstreptococcalinfections(usuallypharyngitis)afteranintervalofafewweeksOccuringinheart,synovium,joints,bloodvessels,skin,etc.AcuterheumaticcarditisChronicvalvulardeformitiesAfteranini
38、tialattack,thereisincreasedvulnerabilitytoreactivationofthedisease.Just like a crazy dog, licking all over the body and finally biting the heartEtiologyandPathogenesisImprovedsocioeconomicconditionsRapiddiagnosisandtreatmentAhypersensitivityreactioninducedbygroupAstreptococci(1)Symptomstypicallydeve
39、lopabout23weeksafterinfection.(2)Streptococciareabsentfromthelesions.AntibodiesdirectedagainsttheMproteinsofgroupAstreptococcicross-reactwithnormalproteinspresentintheheart,joints,andothertissues.TheincidenceandmortalityAnautoimmuneresponseagainstself-antigensGeneticsusceptibilityRheumaticfeveroccur
40、sinonlyabout3%ofpatientswithgroupAstreptococcalpharyngitisMORPHOLOGYBasicpathologicchanges3phases Necrotic&exudativephaseFibrinoidnecrosis,inflammatoryinfiltrates RegenerationRheumaticgranuloma(rheumaticbody,Aschoffbody) Fibrosis“Reoccur”Rheumaticbody(Aschoffbody)-Oftenlieincloseproximitytoasmallves
41、sel-Acentralfocusoffibrinoidnecrosissurroundedbyachronicmononuclearinflammatoryinfiltrate-AschoffcellsRheumaticHeartDisease1.AcutePancarditis(1)RheumaticendocarditisMitral50%Mitral+Aortic50%Edematous,thickened,fibrinoidnecrosis,verrucae(vegetation,mayresolveorprogress)(2)Rheumaticmyocarditis:Aschoff
42、bodies(3)Rheumaticpericarditis:Fibrinousexudate(corvillosum,generallyresolvewithoutsequelae)2.ChronicCharacterizedbyorganizationoftheacuteinflammation&subsequentscarringFibrousscarThemitralvalvesexhibitleafletthickening,commissuralfusionandshortening,andthickeningandfusionofthechordaetendineae.Valvu
43、larstenosis,regurgitationMicroscopy:neovascularization,diffusefibrosisAcutesuperimposedonchronicFishmouthButtonholeTreatment Surgicalreplacementofdiseasedvalves Bioprosthetic valves Mechanical ValvesPathologicChangesinOtherOrgans RheumaticarthritisLarger joints,migratorypolyarthritisWithoutsequelae
44、SkinErythemaannulare,subcutaneousnodules Rheumaticarteritis BrainNeurondegeneration,gliacellproliferationextrapyramidalinvolvedchoreaminorClinicalFeatures AntibodiestooneormorestreptococcalenzymesStreptolysinO SignsPericardialfrictionrubsWeakheartsoundsTachycardiaorotherarrhythmiasCongestiveheartfai
45、lure5%deathMiniSummaryRheumaticheartdiseaseresultsfromantistreptococcalantibodiesthatcross-reactwithcardiactissues.Itmostcommonlyaffectsthemitralvalve.RheumaticgranulomaInfectiveEndocarditisDefinitionInfectionofthecardiacvalvesormuralsurfaceoftheendocardium,resultingintheformationofbulky, friableveg
46、etationCauseAnytypeofmicroorganism,mostbybacteriaAntibiotictherapyblursthedistinction.Aparticularlydifficultinfectiontoeradicatebecauseoftheavascularnatureoftheheartvalves.ClassificationFormsOrganismValvesAcuteHighvirulencePreviouslynormalSubacuteLowvirulencePreviouslyabnormalPathogenesis Conditions
47、thatincreasetherisk(1)Preexistingcardiacabnormalities:rheumaticheartdisease(2)Prostheticheartvalves:nodifferencebetweenmechanicalandbio-prostheticvalves(3)Hostfactors:DM,immunodeficiency,intravenousdrugabuse BacteremiaAninfectionelsewhereApreviousdental,surgicalorotherinterventionalprocedure,e.g.uri
48、narycatheterizationIntravenousdrugabusersMORPHOLOGYThehallmarkisthepresenceofvalvularvegetationscontainingbacteriaorotherorganisms.Aorticandmitralvalvesarethemostcommonsitesofinfection.SBESBE“repair”“repair”ABEABE“damage”“damage” Causativeorganismlowvirulencea-hemolyticstreptococcihighvirulencestaph
49、ylococcusaureusPathogenesisPreexistingabnormalityNativevalvesCommonsitesmitral/aorticvalvesaorticvalvesGrossly Friable , bulky vegetationscontainbacteria,single/multiple,1valveInfluence:typeoforganisms,degreeofhostreaction,previousantibiotictherapyMicroscopicallyPlatelet,fibrin,inflammatoryinfiltrat
50、es,bacteriaGranulation,fibrosis,calcification,chronicinflammatoryinfiltratesdestructionofthevalves&vicinity,ringabscesses(inperivalvulartissue),Sequelaechronicvalvulardisease,regurgitationRupture,suddendeathchronicvalvulardiseaseSBESBE“repair”“repair”ABEABE“damage”“damage”SitesotherthanheartSystemic
51、emboli,anemicinfarcts,GNSystemicemboli,septicinfarcts(suppuration),ConsequenceHealing,chronicvalvulardiseaseDeath,chronicvalvulardiseaseABEofaorticvalveTricuspidvalve,rightatriumOftennotedinintravenousdrugabusersABEofaorticvalve,multipleabscessesEmbolizationviacoronaryarteryComparisonBetweenDiverseV
52、avularVegetationsSmall,warty,inflammatoryvegetations,alongthelinesofvalveclosureIrregular,large,briskdestructionofchordaetendineaeEmboliRheumaticendocarditisInfectiveendocarditisValvularHeartDiseasesAdiversegroupofacquiredorcongenitallesionsStenosis:thick,rigid,adherent,obstructionIncompetence(insuf
53、ficiency):thick,rolling,fusion,retract,regurgitationCombinedvalvulardisease(multivalvulardisease)StenosisandregurgitationcoexistAnatomyofheart&bloodflowMitralStenosisCause:rheumaticheartdiseaseHemodynamicandheartchanges:Earlystage：hypertrophy&dilationofleftatriumLatestage：edemaandcongestionofpulmona
54、ryhypertrophyanddilationoftherightheartrightHeartfailureClinicalfeatures:DiastolicmurmurattheauscultationareaofmitralvalvePinkcoloredfoamysputumMuralthrombus,emboliCongestionofmanyorgans“PyriformHeart”MitralRegurgitation Cause:rheumaticheartdisease Hemodynamicandheartchanges:Hypertrophyanddilationof
55、thefourchambersLeftandRightHeartFailureEdemaandcongestionofpulmonaryPulmonaryarteryhypertensionClinicalfeatures:Systolemurmurattheauscultationareaofmitralvalve“GlobalHeart”AorticStenosis Cause:rheumaticheartdisease Hemodynamicandheartchanges:HypertrophyanddilationofthefourchambersLeftandrightHeartFa
56、ilureEdemaandcongestionofpulmonaryPulmonaryarteryhypertensionClinicalfeatures:SystolemurmurattheauscultationareaofAorticValve;anginapectorisAorticRegurgitation Cause:rheumaticheartdisease,infectiveendocarditis;syphiliticarteritis Hemodynamicandheartchanges:Hypertrophyanddilationofthefourchambers,esp
57、eciallytheleftventricularLeftandRightHeartFailureEdemaandcongestionofpulmonaryPulmonaryarteryhypertensionClinicalfeatures:Diastolicmurmurattheauscultationareaofaorticvalveanginapectoris;widenedpulsepressureBoot-shapedHeartMyocarditis DefinitionAgroupofinflammatoryprocessesprimarilytargetingthemyocar
58、dium Cause:(1)Infections:Chlamydia,rickettsia,bacteria,fungi,etc.(2)Immune-mediatedreactions postviral;postbacteria;systemiclupuserythematosus;drughypersensitivity(e.g.methyldopa,sulfonamides),transplantrejection(3)Unknown:giantcellmyocarditisViralMyocarditisCauseCoxsackievirusesAandBandotherenterov
59、iruses(mostcommon)Direct damage to myocardium Immune-mediated injuryMorphologyGross:Heartisdilated.Myocardiumisflabbyandoftenmottledwithpaleandhemorrhagicareas.Microscopy:EdematousAdiffuselymphocyticinfiltrateMyocytedegenerationand/ornecrosisClinicalfeaturesBroadspectrumFromanasymptomaticstatetoseve
60、recongestiveheartfailureSelf-limited,somemaydevelopdilatedcardiomyopathyCardiomyopathiesHeartdiseasesresultingfromaprimaryabnormalityinthemyocardium “Heart muscle diseases”DilatedHypertrophicRestrictiveDilatedCardiomyopathyProgressivecardiachypertrophy,dilationandcontractile(systolic)dysfunctionCaus
61、eAlargenumberofdifferentmyocardialinsults Genetic; alcohol; peripartum; myocarditis; hemochromatosis; chronic anemia; doxorubicin (adriamycin); sarcoidosis; idiopathic MorphologyGrossEnlargedandflabbywithweightsoftenexceeding900gDilationandhypertrophyofallchambersFragilemuralthrombi&subsequentemboli
62、MicroscopyMyocytehypertrophyInterstitialfibrosisWavyfiberchangeScantymononuclearinflammatoryinfiltrateClinicalFeaturesThemostcommonformofcardiomyopathy(90%)Thefundamentaldefectisineffective contractionejectionfractionfreewalloftheleftventricleAsymmetricseptalhypertrophyassociatedwithobstructiondurin
63、gsystoleMicroscopyMarkedmyocytehypertrophyHaphazardarrangementofhypertrophied,abnormallybranchingmyocytes,InterstitialfibrosisClinicalfeaturesAninabilitytofillahypertrophicleftventricleduringdiastoleEjectionisforcefulbutineffectivelimitationofcardiacoutput,asecondaryincreaseinpulmonaryvenouspressure
64、AharshsystolicejectionmurmurMyocardialischemiaiscommon,andanginalpainisfrequentVentriculararrhythmias,suddendeathInfectiveendocarditisincreased.RestrictivecardiomyopathyAprimarydecreaseinventricularcompliance,resultinginimpaired,ventricularfillingdiastole(diastolic dysfunction)CauseRadiationfibrosis
65、,amyloidosis,sarcoidosis,orproductsofinbornerrorsofmetabolismGrossFirmmyocardiumLMInterstitialfibrosisMiniSummaryCardiomyopathyisintrinsiccardiacmuscledisease;theremaybespecificcauses,oritmaybeidiopathic.Thethreecategoriesaredilated(accountingfor90%ofthecases),hypertrophic,andrestrictive(leastcommon
66、).Dilatedcardiomyopathy)resultsinsystolic(contractile)dysfunction.Hypertrophiccardiomyopathyresultsindiastolic(relaxation)dysfunction.Restrictivecardiomyopathyresultsinastiff, noncompliantmyocardium.Congenitalheartdisease(先天性心脏病先天性心脏病)AbnormalitiesoftheheartorgreatvesselsthatarepresentatbirthArisesf
67、romfaultyembryogenesisduringgestationalweeks3through8Threemajortypes:1,malformationscausingaleft-to-rightshunt2,malformationscausingaright-to-leftshunt3,malformationscausingobstructionAtrialseptaldefect,ASD（房间隔缺损）Ventricularseptaldefect,VSD（室间隔缺损）Patentductusarteriosus,PDA（动脉导管未闭）TetralogyofFallot（法
68、洛四联症）马方综合征非发绀型发绀型左心打开,见房间隔有一个圆形的大孔Atrialseptaldefect,ASD（房间隔缺损）小儿心脏,右心室打开,室间隔上方有一个小孔,房间隔下方动脉导管部位有一个细小裂隙,从背面左心房观察可见裂隙有透光现象Patentductusarteriosus,PDA（动脉导管未闭）Ventricularseptaldefect,VSD（室间隔缺损）心脏标本正面为左心室，见室间隔上部的膜部有一个很大的圆形缺损空洞（红色箭头），缺损口的上方正对着主动脉的开口大部分，而主动脉瓣最里面一个瓣叶内移到右心室（黄色箭头），形成主动脉骑跨，左心室略有扩张，从标本背面观察，可见右心
69、室扩大。TetralogyofFallot（法洛四联症）QuestionsThemorphologiccharacteristicsofmyocardialinfarction?Thepathologicalcharacteristicsofrheumaticheartdisease?病例分析病例分析(A.4937)83岁，男性，死亡后岁，男性，死亡后1天行尸体解剖天行尸体解剖病史病史：24年前有年前有“急性心肌梗塞急性心肌梗塞”史，史，入院前数天有恶心感，突然意识丧失，大汗淋漓，小便失禁半小入院前数天有恶心感，突然意识丧失，大汗淋漓，小便失禁半小时，时，EKG示示S-T段抬高，给予扩血管、溶
70、栓治疗段抬高，给予扩血管、溶栓治疗住院期间出现心源性休克，心动过缓，完全性房室传导阻滞，治住院期间出现心源性休克，心动过缓，完全性房室传导阻滞，治疗后血压、心率、心律恢复正常疗后血压、心率、心律恢复正常住院十天后出现腹胀、下肢浮肿，住院十天后出现腹胀、下肢浮肿，B超示左侧胸水，后突然烦躁、超示左侧胸水，后突然烦躁、大汗、气促而死亡大汗、气促而死亡临床诊断临床诊断：急性（下壁、前侧壁、后壁）心肌梗塞、心源性晕厥、休克、心衰、应激急性（下壁、前侧壁、后壁）心肌梗塞、心源性晕厥、休克、心衰、应激性溃疡、糖尿病性溃疡、糖尿病尸检主要发现尸检主要发现：体表与体腔体表与体腔指甲轻度紫绀，两下肢轻度浮肿，肝
71、剑下指甲轻度紫绀，两下肢轻度浮肿，肝剑下4cm，两，两胸腔淡黄色积液各胸腔淡黄色积液各60ml，心脏膈面有少量纤维蛋白渗，心脏膈面有少量纤维蛋白渗出，颅底动脉硬化，脑萎缩出，颅底动脉硬化，脑萎缩内内脏脏1.心脏心脏520g冠状动脉左前降支狭窄达冠状动脉左前降支狭窄达9598，右冠状动脉距起始右冠状动脉距起始7cm处见附壁血栓。室壁左厚处见附壁血栓。室壁左厚0.81.5cm，右厚，右厚0.6cm。左侧、后壁与右后及后室间隔。左侧、后壁与右后及后室间隔见见9X8X9cm3梗死灶，此处心肌变薄、暗红、灰梗死灶，此处心肌变薄、暗红、灰黄色坏死灶，并波及乳头肌黄色坏死灶，并波及乳头肌2.肝脏肝脏1200
72、g切面红黄相间切面红黄相间诊断：诊断：一、冠状动脉粥样硬化性心脏病：一、冠状动脉粥样硬化性心脏病：1.左前降支及右冠状动脉高度狭窄；左前降支及右冠状动脉高度狭窄；2.右冠状动脉新鲜血栓形成，引起左侧、后、右冠状动脉新鲜血栓形成，引起左侧、后、右后、右后、后间隔急性心肌梗死；后间隔急性心肌梗死；3.纤维素性心外膜炎；纤维素性心外膜炎；二、高血压病累及肾、心、脾等；二、高血压病累及肾、心、脾等；三、两肺灶性炎症伴纤维化，肺淤血、水肿及慢支。三、两肺灶性炎症伴纤维化，肺淤血、水肿及慢支。死因：死因：心律紊乱、左心衰竭心律紊乱、左心衰竭病例分析2（A5988)死者男性，68岁。因“突发中上腹疼痛2小时
73、余”于2010年8月1日14时就诊于急诊，尿常规：RBC10-12/HP，B超显示：胆囊胆固醇结晶，双肾皮质回声稍强。临床以“腹痛待查：肾绞痛？肠绞痛？”收入院，并予以抗菌、解痉治疗。15点45分时，患者仍主诉“疼痛，恶心、呕吐加剧”，临床仍予以抗菌、解痉治疗；15点58分时，患者突然出现意识丧失，血压测不出，实施抢救无效，于当日16时30分死亡。解剖发现：解剖发现：手指甲青紫。大网膜可见2处出血点。于主动脉根部，见外膜有2处裂口，分别长约0.51cm，在距主动脉根部大约10cm处的内膜有一裂口长约3cm，自主动脉根部起的胸主动脉管壁夹层内见血凝块大约200ml。纵隔积血约50ml，心包积血约
74、350ml。病理解剖诊断一、升主动脉及主动脉弓初始段夹层动脉瘤破裂，导致：一、升主动脉及主动脉弓初始段夹层动脉瘤破裂，导致：1.心包积血（心包积血（350ml）；）；2.纵隔积血（纵隔积血（50ml）；）；3.胸主动脉壁夹层血肿（胸主动脉壁夹层血肿（200ml）；）；二、急性肺水肿；二、急性肺水肿；三、胰腺组织内少数钙化灶；三、胰腺组织内少数钙化灶；死亡原因：死亡原因：升主动脉及主动脉弓初始段夹层动脉瘤破裂，导致急性心包填塞升主动脉及主动脉弓初始段夹层动脉瘤破裂，导致急性心包填塞PrinciplesofCardiacDysfunction1.Failureofthepumpitself2.Anobstructiontoflow3.Regurgitantflow4.Disordersofcardiacconduction5.DisruptionofthecontinuityofthecirculatorysystemThanksforyourattention!
