Introductionto

CardiovascularPathology

-FredClaytonSystemicPathologyofCongestiveHeartFailurePathologyofMyocarditisPathologyofCardiomyopathyDilatedCardiomyopathyHypertrophicCardiomyopathyRestrictiveCardiomyopathyIntroductionto

Cardiovascula1CongestiveHeartFailureCardiacoutputinsufficientformetabolicrequirementsofthebodySystolicdysfunction–decreasedmyocardialcontractilityDiastolicdysfunction–insufficientexpansionforventricularvolumeProblemsareaccentuatedbyincreaseddemand–highoutputheartfailureCongestiveHeartFailureCardia2CHF–Body’sCompensationTachycardiaFrank-Starling–increasedEndDiastolicVolumeMyocardialhypertrophyRenin-angiotensin-aldosteronesystemCatecholamines–positiveinotropiceffectAdrenergicredistributionofbloodflowIncreaseoxygenextractionfromhemoglobinCHF–Body’sCompensationTachy3【高血壓英文課件】Cardiovascular-Pathology4【高血壓英文課件】Cardiovascular-Pathology5Lungs–PulmonaryedemaDyspnea–breathlessnessOrthopnea–dyspnealyingdownParoxysmalnocturnaldyspnea–extremedyspneaLungs–PulmonaryedemaDyspnea6Lung–PulmonaryEdema–palepinkedemafluidfillingalveoliLung–PulmonaryEdema–pale7Lung–alveolarhemorrhage,heme-filledmacrophages“heartfailurecells”,withironstaintorightLung–alveolarhemorrhage,he8Kidneys–reducedperfusionIschemictubularnecrosis/ATNPrerenalazotemiaKidneys–reducedperfusionIsc9Kidney-ATNKidney-ATN10BraininCHF–cerebralhypoxiaIrritabilityLossofattentionspanRestlessnessStuporComaBraininCHF–cerebralhypoxi11Right-sidedheartfailurePurecorpulmonaleConsequenceofleft-sidedfailureMyocardial–myocarditis,cardiomyopathy,constrictivepericarditisRight-sidedheartfailurePure12【高血壓英文課件】Cardiovascular-Pathology13Rightfailure-systemiceffectsLiver–chronicpassivecongestionSpleen–congestivesplenomegalyKidneys–congestionandhypoxiaSub-Q–peripheraledemaandanasarcaPleuralspace–effusionsBrain–venouscongestionandhypoxiaPortal-ascitesRightfailure-systemiceffec14Liver–chronicpassivecongestion–bloodpoolsnearthecentralveinsLiver–chronicpassiveconges15Liver–chronicpassivecongestionLiver–chronicpassiveconges16Liver–chronicpassivecongestion–bloodpoolsnearthecentralveinsLiver–chronicpassiveconges17Liver–chronicpassivecongestion–redcellpoolingnearcentralveinsandpericentralnecrosisofthehepatocytesLiver–chronicpassiveconges18CHF–finalpathwaytodeathIschemicheartdiseaseHypertensiveheartdiseaseValvularheartdiseaseCardiomyopathyMyocarditisSpecificheartmusclediseasesCHF–finalpathwaytodeathIs19MyocarditisEtiologyViral–CoxsackieA,ECHO,InfluenzaChlamydiaandRickettsia–psittaci&typhiBacteria–diphtheria,TB,StrepFungal&Protozoa–Trypanosomes,ToxoHypersensitivity–SLE,RHD,drugsPhysicalAgents–RadiationIdiopathic–GiantcellmyocarditisMyocarditisEtiologyViral–Co20MyocarditisMorphologyGross–dilated,flabbyheart,palepatcheswithhemorrhageMicroscopic–interstitialinflammatoryinfiltratewithmyocytenecrosis,fibrosisMononuclearcells–idiopathicorviralNeutrophils–bacterialEosinophils–hypersensitivityorprotozoaGranulomatous–TBorsarcoidMyocarditisMorphologyGross–d21Dilated,globoidheartinmyocarditisDilated,globoid22Myocarditis–meetsDallascriteriaofaTlymphocyteinfiltrateandmyocytenecrosisordropout.Thisisusuallyeitherviralorofunknowncause.Myocarditis–meetsDallascri23Diphtheriamyocarditis–duetoatoxinratherthanbacterialinvasion.Thereissomeinflammation,myocytechanges(seethebignucleolus).Myocytenecrosis(notshown)alsohappens.Diphtheriamyocarditis–duet24BacterialcolonyinmyocarditisBacterialcolonyinmyocarditi25ToxoplasmosisToxoplasmosis26ChagasdiseaseChagasdisease27GiantCellMyocarditisMyocytenecrosisMultinucleatedgiantcellsLymphocytes,plasmacells,macrophages,eosinophils,andneutrophilsOftenfulminant,rapidprogressiontodeathDifferentialdiagnosis–cardiacsarcoidosisGiantCellMyocarditisMyocyte28GiantCellMyocarditisGiantCellMyocarditis29GiantCellMyocarditisGiantCellMyocarditis30CardiomyopathiesCardiomyopathies31DilatedCardiomyopathyGross–increasedweight,dilatation,endocardialfibrosis,normalvalvesandcoronaryarteriesMicroscopic–myocytehypertrophy,myofibrillarlossandinterstitialfibrosisEtiology–viral,genetic,toxinsClinicalsignificance–heartfailure&deathDilatedCardiomyopathyGross–32【高血壓英文課件】Cardiovascular-Pathology33DilatedcardiomyopathyDilatedcardiomyopathy34Cardiomyopathy–lossofmyofibrilsCardiomyopathy–lossofmyofi35Cardiomyopathy–trichromestainshowingextensivefibrosis(blue)betweenthemyocytes.Themyocytesalsovaryinsize,andsomehavepartiallossofmyofibrils.Cardiomyopathy–trichromesta36NormalHeart-EMNormalHeart-EM37Lossoffibrilsincardiomyopathy.Themyocyteatlowerleftisaboutnormal;theothershaveanextensivelossofmyofibrils.Lossoffibrilsincardiomyopa38Cardiomyopathy–lossoffibrilsandasmallcontractionbandinthetopcenter.Cardiomyopathy–lossoffibri39【高血壓英文課件】Cardiovascular-Pathology40HypertrophicCardiomyopathyHypertrophyofventricularseptum(95%)Disarrayofmyofibers(100%)Volumereductionofventricles(90%)EndocardialthickeningofLV(75%)Mitralvalveleafletthickening(75%)Dilatedatria(100%)Abnormalintramuralcoronaries(50%)HypertrophicCardiomyopathyHyp41【高血壓英文課件】Cardiovascular-Pathology42HypertrophiccardiomyopathyHypertrophiccardiomyopathy43HypertrophiccardiomyopathyHypertrophiccardiomyopathy44HypertrophiccardiomyopathyHypertrophiccardiomyopathy45Hypertrophiccardiomyopathy–myofiberdysarray–notallfibersarepullingthesamedirection.Thusthecontractionisineffective.However,thecardiacconductionsystemcanhavethesesameproblems,whichmightcausethearrhythmiasandsuddendeaththesepatientstendtodieof.Hypertrophiccardiomyopathy–46HypertrophicCardiomyopathyEtiology–hereditary,mostlyautosomaldominant,canappearsporadicallyClinicalsignificance–syncope,arrhythmiasandsuddendeathwithariskof2-6%peryearCannotequatewithhypertrophyalone!Thereisvariationinheartsizewithoutdisease.Largeheartscorrelatewithendurance(Secretariat,LanceArmstrong).HypertrophicCardiomyopathyEti47【高血壓英文課件】Cardiovascular-Pathology48RestrictiveCardiomyopathyAmyloidosisEndomyocardialfibrosis–subendocardialfibrosisLoeffler’sendocarditis–eosinophilicinfiltrateEndocardialfibroelastosisRestrictiveCardiomyopathyAmyl49Amyloidosis–noticethepinkmaterialbetweenthemyocytes.Amyloidosis–noticethepink50Amyloidosis–CongoRedisvery,verypositive.Amyloidosis–CongoRedisver51Amyloidosis–thisheartisthickened,pale,andhasarubberyconsistencythatinterfereswithcardiacexpansionduringdiastole.Amyloidosis–thisheartisth52Endomyocardialfibrosis–fibrosisundertheendocardiumandinthetheinnerthirdofthemyocardium.Endomyocardialfibrosis–fibr53Endomyocardialfibrosisofaventricularwall.Whenextensive,thiswouldcause

restrictiveheartfailuretoo.Endomyocardialfibrosisofav54Endocardialfibroelastosis–elasticstain(black)isverypositive.Thisdisease,whichoccurredinyoungchildrenandwasonce1:5,000births,nowisalmostneverseen.Etiologyisnotknown(?viralsuchasmumps).Endocardialfibroelastosis–e55EndocardialfibroelastosisEndocardialfibroelastosis56SpecificHeartMuscleDiseasesToxic–alcohol,catecholamines,cocaine,AdriamycinMetabolic–hemochromatosis,hyperthyroidismNeuromuscular–musculardystrophyStoragedisease–glycogen,Fabry’sdiseaseInfiltrative-sarcoidosisSpecificHeartMuscleDiseases57Heart-Becker’smusculardystrophy–lookslikeidiopathicdilatedcardiomyopathy.Heart-Becker’smusculardyst58Notethefibrosisandlossofmyofibrilsinsomecells.Notethefibrosisandlossof59Byelectronmicroscopy,thiswasAdriamycintoxicity.Seetheclearvacuoles(theyaredilatedsarcoplasticreticulum)andseverelossofmyofibrils.Byelectronmicroscopy,thisw60Cocaineheart–necrosiswithcontractionbands.Thiscouldhappenwithanyseverechronicstimulationsuchastoomuchpressorsinafailingheartorapheochromocytoma.Cocaineheart–necrosiswith61CardiacSarcoidosis–welldefinedgranulomawithgiantcells.Dosen’tinfiltrate&destroymyocardiumlikegiantcellmyocarditis.Eosinophilsarelesscommoninsarcoidosisthaningiantcellmyocarditis.CardiacSarcoidosis–welldef62Hemochromatosis-notethebrownperinucleardepositsofhemosiderin.Itis,however,thesolubleiron,notthehemosiderin,thatisconsideredtoxic.Hemochromatosis-notethebro63Hemochromatosis–ironstain(ironisblue).Hemochromatosis–ironstain(64Rheumaticfever–Aschoffbody–Acollectionofcells,oftennearavessel,withafewmultinucleatecellsandsomevesicularnucleiwithbignucleoli(Aschoffcells).Anichkovmyocytes(notshown)aremyocyteswithveryelongatedbignucleoli.Thisisamarkerforrheumaticfever,buttheseriousdamageistothevalves.Rheumaticfever–Aschoffbody65Introductionto

CardiovascularPathology

-FredClaytonSystemicPathologyofCongestiveHeartFailurePathologyofMyocarditisPathologyofCardiomyopathyDilatedCardiomyopathyHypertrophicCardiomyopathyRestrictiveCardiomyopathyIntroductionto

Cardiovascula66CongestiveHeartFailureCardiacoutputinsufficientformetabolicrequirementsofthebodySystolicdysfunction–decreasedmyocardialcontractilityDiastolicdysfunction–insufficientexpansionforventricularvolumeProblemsareaccentuatedbyincreaseddemand–highoutputheartfailureCongestiveHeartFailureCardia67CHF–Body’sCompensationTachycardiaFrank-Starling–increasedEndDiastolicVolumeMyocardialhypertrophyRenin-angiotensin-aldosteronesystemCatecholamines–positiveinotropiceffectAdrenergicredistributionofbloodflowIncreaseoxygenextractionfromhemoglobinCHF–Body’sCompensationTachy68【高血壓英文課件】Cardiovascular-Pathology69【高血壓英文課件】Cardiovascular-Pathology70Lungs–PulmonaryedemaDyspnea–breathlessnessOrthopnea–dyspnealyingdownParoxysmalnocturnaldyspnea–extremedyspneaLungs–PulmonaryedemaDyspnea71Lung–PulmonaryEdema–palepinkedemafluidfillingalveoliLung–PulmonaryEdema–pale72Lung–alveolarhemorrhage,heme-filledmacrophages“heartfailurecells”,withironstaintorightLung–alveolarhemorrhage,he73Kidneys–reducedperfusionIschemictubularnecrosis/ATNPrerenalazotemiaKidneys–reducedperfusionIsc74Kidney-ATNKidney-ATN75BraininCHF–cerebralhypoxiaIrritabilityLossofattentionspanRestlessnessStuporComaBraininCHF–cerebralhypoxi76Right-sidedheartfailurePurecorpulmonaleConsequenceofleft-sidedfailureMyocardial–myocarditis,cardiomyopathy,constrictivepericarditisRight-sidedheartfailurePure77【高血壓英文課件】Cardiovascular-Pathology78Rightfailure-systemiceffectsLiver–chronicpassivecongestionSpleen–congestivesplenomegalyKidneys–congestionandhypoxiaSub-Q–peripheraledemaandanasarcaPleuralspace–effusionsBrain–venouscongestionandhypoxiaPortal-ascitesRightfailure-systemiceffec79Liver–chronicpassivecongestion–bloodpoolsnearthecentralveinsLiver–chronicpassiveconges80Liver–chronicpassivecongestionLiver–chronicpassiveconges81Liver–chronicpassivecongestion–bloodpoolsnearthecentralveinsLiver–chronicpassiveconges82Liver–chronicpassivecongestion–redcellpoolingnearcentralveinsandpericentralnecrosisofthehepatocytesLiver–chronicpassiveconges83CHF–finalpathwaytodeathIschemicheartdiseaseHypertensiveheartdiseaseValvularheartdiseaseCardiomyopathyMyocarditisSpecificheartmusclediseasesCHF–finalpathwaytodeathIs84MyocarditisEtiologyViral–CoxsackieA,ECHO,InfluenzaChlamydiaandRickettsia–psittaci&typhiBacteria–diphtheria,TB,StrepFungal&Protozoa–Trypanosomes,ToxoHypersensitivity–SLE,RHD,drugsPhysicalAgents–RadiationIdiopathic–GiantcellmyocarditisMyocarditisEtiologyViral–Co85MyocarditisMorphologyGross–dilated,flabbyheart,palepatcheswithhemorrhageMicroscopic–interstitialinflammatoryinfiltratewithmyocytenecrosis,fibrosisMononuclearcells–idiopathicorviralNeutrophils–bacterialEosinophils–hypersensitivityorprotozoaGranulomatous–TBorsarcoidMyocarditisMorphologyGross–d86Dilated,globoidheartinmyocarditisDilated,globoid87Myocarditis–meetsDallascriteriaofaTlymphocyteinfiltrateandmyocytenecrosisordropout.Thisisusuallyeitherviralorofunknowncause.Myocarditis–meetsDallascri88Diphtheriamyocarditis–duetoatoxinratherthanbacterialinvasion.Thereissomeinflammation,myocytechanges(seethebignucleolus).Myocytenecrosis(notshown)alsohappens.Diphtheriamyocarditis–duet89BacterialcolonyinmyocarditisBacterialcolonyinmyocarditi90ToxoplasmosisToxoplasmosis91ChagasdiseaseChagasdisease92GiantCellMyocarditisMyocytenecrosisMultinucleatedgiantcellsLymphocytes,plasmacells,macrophages,eosinophils,andneutrophilsOftenfulminant,rapidprogressiontodeathDifferentialdiagnosis–cardiacsarcoidosisGiantCellMyocarditisMyocyte93GiantCellMyocarditisGiantCellMyocarditis94GiantCellMyocarditisGiantCellMyocarditis95CardiomyopathiesCardiomyopathies96DilatedCardiomyopathyGross–increasedweight,dilatation,endocardialfibrosis,normalvalvesandcoronaryarteriesMicroscopic–myocytehypertrophy,myofibrillarlossandinterstitialfibrosisEtiology–viral,genetic,toxinsClinicalsignificance–heartfailure&deathDilatedCardiomyopathyGross–97【高血壓英文課件】Cardiovascular-Pathology98DilatedcardiomyopathyDilatedcardiomyopathy99Cardiomyopathy–lossofmyofibrilsCardiomyopathy–lossofmyofi100Cardiomyopathy–trichromestainshowingextensivefibrosis(blue)betweenthemyocytes.Themyocytesalsovaryinsize,andsomehavepartiallossofmyofibrils.Cardiomyopathy–trichromesta101NormalHeart-EMNormalHeart-EM102Lossoffibrilsincardiomyopathy.Themyocyteatlowerleftisaboutnormal;theothershaveanextensivelossofmyofibrils.Lossoffibrilsincardiomyopa103Cardiomyopathy–lossoffibrilsandasmallcontractionbandinthetopcenter.Cardiomyopathy–lossoffibri104【高血壓英文課件】Cardiovascular-Pathology105HypertrophicCardiomyopathyHypertrophyofventricularseptum(95%)Disarrayofmyofibers(100%)Volumereductionofventricles(90%)EndocardialthickeningofLV(75%)Mitralvalveleafletthickening(75%)Dilatedatria(100%)Abnormalintramuralcoronaries(50%)HypertrophicCardiomyopathyHyp106【高血壓英文課件】Cardiovascular-Pathology107HypertrophiccardiomyopathyHypertrophiccardiomyopathy108HypertrophiccardiomyopathyHypertrophiccardiomyopathy109HypertrophiccardiomyopathyHypertrophiccardiomyopathy110Hypertrophiccardiomyopathy–myofiberdysarray–notallfibersarepullingthesamedirection.Thusthecontractionisineffective.However,thecardiacconductionsystemcanhavethesesameproblems,whichmightcausethearrhythmiasandsuddendeaththesepatientstendtodieof.Hypertrophiccardiomyopathy–111HypertrophicCardiomyopathyEtiology–hereditary,mostlyautosomaldominant,canappearsporadicallyClinicalsignificance–syncope,arrhythmiasandsuddendeathwithariskof2-6%peryearCannotequatewithhypertrophyalone!Thereisvariationinheartsizewithoutdisease.Largeheartscorrelatewithendurance(Secretariat,LanceArmstrong).HypertrophicCardiomyopathyEti112【高血壓英文課件】Cardiovascular-Pathology113RestrictiveCardiomyopathyAmyloidosisEndomyocardialfibrosis–subendocardialfibrosisLoeffler’sendocarditis–eosinophilicinfiltrateEndocardialfibroelastosisRestrictiveCardiomyopathyAmyl114Amyloidosis–noticethepinkmaterialbetweenthemyocytes.Amyloidosis–noticethepink115Amyloidosis–CongoRedisvery,verypositive.Amyloidosis–CongoRedisver116Amyloidosis–thisheartisthickened,pale,andhasarubberyconsistencythatinterfereswithcardiacexpansionduringdiastole.Amyloidosis–thisheartisth117Endomyocardialfibrosis–fibrosisundertheendocardiumandinthetheinnerthirdofthemyocardium.Endomyocardialfibrosis–fibr118Endomyocardialfibrosisofaventricularwall.Whenextensive,thiswouldcause

restrictiveheartfailuretoo.Endomyocardialfibrosisofav119Endocardialfibroelastosis–elasticstain(black)isverypositive.Thisdisease,whichoccurredinyoungchildrenandwasonce1:5,000birt