冠状动脉粥样硬化性心脏病英文-课件

Coronary Atherosclerotic Heart Diseases AffiliatedHospitalofJiningMedicalCollegeDept.ofCardiacCareUnitGuoxiaDCoronaryAtheroscleroticHeart27/10/202428/14/2023ContentsAtherosclerosisStableAnginaPectorisAcuteCoronarySyndromenUAandNSTEMInAMI(STEMI)37/10/2024ContentsAtherosclerosis38/14/2Self-study VariantAnginaCardiacSyndromeXSilentMyocardialIschemiaMyocardialBridging47/10/2024Self-studyVariantAngina48/What Is Atherosclerosis?nAtherosclerosisisthedescriptivetermforthickenedandhardenedlesionsofthemediumandlargemuscularandelasticarteries.57/10/2024WhatIsAtherosclerosis?AtheroWhat Is Coronary Heart Disease?67/10/2024WhatIsCoronaryHeartDiseaseCoronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia,necrosisIschemic heart disease77/10/2024Coronaryheartdiseaseatherosc87/10/202488/14/2023Atherosclerosis97/10/2024Atherosclerosis98/14/2023FoamcellFattysteak atheromatousplaquerupturedplaquesFibrousplaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al.Circulation 1995;92:1355-1374.mediumdamage7/10/202410FoamcellFattysteakatheromWhat damage does atherosclerosis cause?117/10/2024WhatdamagedoesatherosclerosCommon locationnCoronaryHeartDiseasenCarotidArteryDiseasenPeripheralArterialDiseasenChronicKidneyDisease127/10/2024Commonlocation128/14/2023How does atherosclerosis start and progress?137/10/2024HowdoesatherosclerosisstartnElevatedlevelsofcholesterolandtriglyceridesinthebloodnHighbloodpressurenCigarettesmoking147/10/2024ElevatedlevelsofcholesterolBiological processes1.Accumulation of intimal cellssmooth muscle cells MacrophagesT-lymphocytes157/10/2024BiologicalprocessesAccumulatiBiological processes2.Proliferatedconnectivetissuematrixcollagenelasticfibersproteoglycans167/10/2024BiologicalprocessesProliferatBiological processes3.Accumulationoflipid177/10/2024Biologicalprocesses3.AccumulaAtherosclerosis-HypothesisHypothesisoflipoproteininfiltrationAggregationofplateletsandthrombosisClonaltheoryTheresponse-to-injuryhypothesis187/10/2024Atherosclerosis-HypothesisHypnHigh blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance.nPlatelets are activated,adhesion and aggregation of platelets.nLipidoses,growth factor,proliferation of smooth mucle cells,collagen,lipolytic enzyme.Response-to-injury 197/10/2024Highbloodpressure,bacterium,Pathology and pathophysiologyFattysteakFibrousplaqueComplicatedlesion207/10/2024PathologyandpathophysiologyInitiation of AtherosclerosisFatty steak formation217/10/2024InitiationofAtherosclerosisInitiation of Atherosclerosis227/10/2024InitiationofAtherosclerosis2fibrous plaque237/10/2024fibrousplaque238/14/2023247/10/2024248/14/2023257/10/2024258/14/2023Thin CapVulnerable Plaque ThrombusUnstable“Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina“Dormant Volcano”SAPACSpressure or a squeezing pain!267/10/2024ThinCapThickCapSAPACSpressuUnstable and Stable Plaques薄的纤维帽薄的纤维帽薄的纤维帽薄的纤维帽炎性细胞炎性细胞炎性细胞炎性细胞少的平滑少的平滑少的平滑少的平滑肌细胞肌细胞肌细胞肌细胞内皮细胞不完整内皮细胞不完整内皮细胞不完整内皮细胞不完整巨噬细胞巨噬细胞巨噬细胞巨噬细胞较厚的纤维帽较厚的纤维帽较厚的纤维帽较厚的纤维帽没有炎性细胞没有炎性细胞没有炎性细胞没有炎性细胞泡沫细胞泡沫细胞泡沫细胞泡沫细胞完整的内完整的内完整的内完整的内皮细胞皮细胞皮细胞皮细胞 较多平滑较多平滑较多平滑较多平滑肌细胞肌细胞肌细胞肌细胞LibbyP.LibbyP.CirculationCirculation.1995;91:2844-2850.1995;91:2844-2850.unstablestableUnstableandStablePlaques薄的纤7/10/2024288/14/202328AtherosclerosisnClinical stages Absence of symptom or stage of incubationischemianecrosis(target organ)fibrosis297/10/2024AtherosclerosisClinicalstageclinical manifestationuGeneralmanifestationuAorticatherosclerosisuCoronaryarteryatherosclerosisuCerebralatherosclerosisuRAatherosclerosisuMesentericatherosclerosisuPeripheralarteryatherosclerosis307/10/2024clinicalmanifestationGeneralLaboratory ExaminationLackofsensitiveandspecificmethodsforearlydiagnosisDyslipidemiaX-ray：DSAshowseverityofstenosisDopplerultrasound:bloodflow317/10/2024LaboratoryExaminationLackofLaboratory Examinationradionuclide：detectionofischemiaEchocardiogram：CHDECGandstresstest:CHDAngiography:themostdirectwayIntravascularultrasound,angioscopeCT,MRI327/10/2024LaboratoryExaminationradionucRisk factors n1.Lipid disorders(Dyslipidemia)nIncreasedcholesterol:TcandLDL-c,TG,ApoB,Lp(a)nDecreasedcholesterol:HDL-capoAn2.Hypertension337/10/2024Riskfactors1.LipiddisorderRisk factors n3.DM,Metabolic syndrome or insulin resistance syndrome MorediffuselesionCADequivalent75-80%causeofdeathinadultDMarevasculardiseases:CAD,cerebrovasculardisease,orperipheralvasculardisease347/10/2024Riskfactors3.DM,Metabolicsy7 years incidence of death/non-fatal MI(East West Study)*These patients had no history of myocardial infarction Haffner SM,et al.N Engl J Med.1998;339:229234.05101520253035404550Events of MI in 7 yearsNo history of MI OMI No history of MI*OMI non-diabetics diabetics n=1373n=1059P 0.001P 40yrs adults，4/5 fatal myocardial infarction occured in patiens 65 yrs7.Male gender/postmenopausal state：male:female=2：1,men develop CHD 10-15 yrs earlier than women8.alcohol9.Others:diet,homocysteine,hemostatic factors inflammation/infection367/10/2024Riskfactors4.CigarettesmDrug therapyanti-platelet：aspirin,clopidogrel,GPIIb/IIIa inhitibor,Dipyridamole,cilostazolLipid-loweringHMG-CoAreductaseinhibitors（statins）377/10/2024Drugtherapyanti-platelet：37Doubts of patients nQuest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?387/10/2024DoubtsofpatientsQuest1：MyDoubts of patients nQuestion2：Myshapeisnotfat,lipidisnothigh,whygivemelipid-loweringdrugs,madeamistake?397/10/2024DoubtsofpatientsQuestion2：Doubts of patients nQuestion3：Ihavecoronaryheartdisease,thenshouldIdolessactivitiesinordertoprotecttheheart?407/10/2024DoubtsofpatientsQuestion3：Coronary Heart Disease(CHD)7/10/202441CoronaryHeartDisease(CHD)Clinical TypenSilentmyocardialischemianAnginapectorisnMyocardialinfarctionnIschemiccardiomyopathynSuddencardiacdeath7/10/202442ClinicalTypeSilentmyocardialSilent Myocardial IschemiaDefined as documented episodes of ischemia not associated with any typical or atypical symptoms that among patients with obstructive coronary artery disease.Type I:myocardial ischemia is detected on routine ECG,24h ambulatory ECG monitoring(Holter),etc.but not experience angina at any time;Type II:patients are most frequently encountered in clinical practice.Some episodes of ischemia are associated with chest discomfort and other episodes are asymptomatic.7/10/202443SilentMyocardialIschemiaDefiIschemic CardiomyopathynSymptoms of heart failure,caused by ischemic myocardial dysfunction,diffuse fibrosis,and multiple infarction,alone or in combination.nManifestations:ventricles enlargement(dominant left ventricle),heart failure and arrhythmias.7/10/202444IschemicCardiomyopathySymptomSudden Cardiac DeathnSCD is natural death due to cardiac causes,heralded by abrupt loss of consciousness within 1 hour of the onset of acute symptoms.nThe time and mode of death are unexpected.nWHO definition:unexpected death within 6 hours.nThis definition incorporates the key elements of natural,rapid and unexpected.nOne half of SCD due to coronary heart disease，caused by severe arrhythmias,such as ventricular fibrillation and cardiac arrest.7/10/202445SuddenCardiacDeathSCDisnatAcute Coronary SyndromenACS represents a spectrum of conditions.nAcute plaque change characterized by plaque rupture and exposure of substances that promote platelet activation and thrombin generation.7/10/202446AcuteCoronarySyndrome8/14/20STABLE ANGINA PECTORIS477/10/2024STABLEANGINAPECTORIS478/14/2DefinitionAcute and transient myocardial ischemia and anoxaemia.Usually caused by coronary insufficiency during exertion.487/10/2024DefinitionAcuteandtransientCharacteristicsparoxysmal precordial squeezing-like chest pain,behind the mid sternumradiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates 497/10/2024Characteristicsparoxysmalprec hypoxia Coronary stenosis(others:aortic valve disease,HOCM)+Myocardial oxygen demand（HRXSBP）increased myocardial hypoxiaacumulation of metabolic product,stimulate C1-5 to cause the sensation of chest pain mechanism507/10/2024hypoxiaCoronin angiographySignificant coronary lesion with diameter stenosis 70%in 75%ptsNo significant stenosis in about 5-10%pts,Ischemia may be related to coronary spasm or microvascular dysfunction.PathologyStable angina pectoris517/10/2024inangiographyPathologyStablepathophysiology1.Metabolic and electrophysiologyATP reduced,accumulation of acid substances Dysfunction of ion pump(Na+-K+,and Na+-Ca+)Early depolarization(ST deviation)2.LV function and hemodynamic situation LV contractility,systolic BP,stroke volume,cardiac output decreased LVED pressure and volume Stunning of myocardiumStable angina pectoris527/10/2024pathophysiology1.Metabolicandsymptom：chest pain location behind or slightly to the left of the mid sternum no definite borderlineradiated to the left shoulder and upper armAtypical location:lower jaw,the back of neckClinical manifestationStable angina pectoris537/10/2024symptom：chestpainClinicalma冠状动脉粥样硬化性心脏病英文-课件 character：tightness,squeezing,burning,pressing,choking,bursting,rarely sharpduration：35 minsprecipitating factor exertion or emotional agitationpain relief:within several mins after rest or using nitroglycerin Clinical manifestationStable angina pectoris557/10/2024character：ClinicalmanifestPhysical examinationincreased HR,elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifestationStable angina pectoris567/10/2024PhysicalexaminationClinicalmAuxiliaryexamination1.ECG：Resting ECG ECG during chest pain:ST-T change found in 95%ptsHolter:detect of slient ischemiaStress testing:Criteria for positive:ST segment depression 0.1mV，last 2 minscontraindication：AMI,UAP,myocarditis,Hypertension,heart failure,aortic stenosis,HOCM,sever arrhythmia,aortic aneurysmEnd of the test：ST or 0.2mV，AP attacks，BP220mmHg，BP drop，ventricular arrhythmiaStable angina pectoris577/10/2024Auxiliaryexamination1.ECG：StStress testrestExersciseStable angina pectoris587/10/2024StresstestrestExersciseStable 2.Echocardiography:3.Scintigraphy assessment:Can detect filling defect of Infarction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others:IVUSAuxiliaryexaminationStable angina pectoris597/10/20242.Echocardiography:AuxiliaryCoronary Angiography607/10/2024CoronaryAngiography608/14/202Stable Angina PectorisDiagnosisuChest painurisk factorsuECG evidence of ischemia during chest painu angiography617/10/2024StableAnginaPectorisDiagnosiCardiovascularcausesNoncardiaccausesStable Angina PectorisDifferentialdiagnosis627/10/2024CardiovascularcausesStableAnCardiovascularcausenMyocardialinfarctionnPericarditisnAorticdissectionnPulmonaryembolismnPulmonaryhypertension637/10/2024CardiovascularcauseMyocardiaNoncardiaccausenPneumoniawithpleurisynSpontaneouspneumothoraxnMusculoskeletaldisordersnHerpeszosternEsophagealrefluxnPepticulcer647/10/2024NoncardiaccausePneumoniawi1.General treatment：risk factors control2.Drug therapy3.Coronary revascularization:percutaneous coronary intervention(PCI)Coronary artery bypass surgery(CABG)SVG,IMAGTreatmentStable Angina Pectoris657/10/2024Generaltreatment：TreatmentStaBlood and oxygen supply to the heartMyocardialbloodflowMyocardial oxygenconsumption4%oftotalcardiacoutputsuppliedtothemyocardium12%oftotalbodyoxygen,usedatrestbymyocardium7/10/202466BloodandoxygensupplytotheCoronary ReserveMyocardialbloodflowincreasesupto4times.tomeetincreasedmyocardialoxygendemand7/10/202467CoronaryReserveMyocardialbloMyocardial oxygensupply and demandOO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2OO2 2supplysupplyO2demand7/10/202468MyocardialoxygensupplyanddAims of medical therapyArterialvasodilatationReducesarterialresistanceReducesafterloadDecreasessympatheticdriveReduceheartrateandcontractileforceReducescardiacworkLVRVDilatationofcoronaryarteriesImprovescoronarysupplyVenodilatationReducesvenousreturnReducespreload7/10/202469AimsofmedicaltherapyArteriaantianginal and anti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris707/10/2024antianginalandanti-ischemicDrug therapya.Nitrateslower oxygen demand:decrease arteriolar and venous tone,reduce preload and afterload increase coronary supply:Coronary dilatationNitroglycerinIsosorbide dinitrateisosorbide 5-mononitrate(long-acting nitrates)Stable Angina Pectoris717/10/2024Drugtherapya.NitratesStableANitrates in anginaReducepreloadthroughvenodilatationReduceafterloadbyloweringarterialresistanceReduceplateletaggregationIncrease coronary perfusion,includingischaemic areas Reversal of coronary spasm7/10/202472NitratesinanginaReduceprelob.blockers:reduce myocardial oxygen:reduce HR,myocardial contractility,BP,the LV wall stress Abslute contraindications：sever bradycardia:high-degree A-V block,SSS,severe unstable LV failureRelative contraindications:asthma and bronchospastic disease peripheral vascular disease 1-selective：metoprolol,atenolol,bisoprololDrug therapyStable Angina Pectoris737/10/2024b.blockers:DrugtherapyStac.Calcium antagonists：Increase oxygen supply:dilate conduit and resistance vessels,release spasm,improve microvascular functionDecrease oxygen demand:negative inotropic effect,decrease BP Antiplatelet effect d.Drugs improving metabolismDrug therapyStable Angina Pectoris747/10/2024c.Calciumantagonists：d.Drugsprevent MI and death therapya.antiplatelet angents：ASAclopidogrelCilostazolb.Lipid-lowering angents:statins c.Angiotesin-converting enzyme inhibitor(ACEI)Drug therapyStable Angina Pectoris757/10/2024preventMIanddeaththerapyDrstentingStable Angina Pectoris767/10/2024stentingStableAnginaPectorisUnstable Angina(UA)and non-STEMI777/10/2024UnstableAngina(UA)778/14/202ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers*#occasionally variant anginaAcute Coronary Syndrome(ACS)787/10/2024ACSNon-STelevationSTelevatioOccuring at rest(or with mininal exertion):last 20 minssever and of new-onset:within 1-2 months,CCS IIIOccuring with a crescendo pattern:Deterioration of CCS classfication,at least CCS IIIDefinition UA and non-STEMIAngina pectoris or equivalent ischemic discomfort with at least one of the three features807/10/2024Occuringatrest(orwithmini Braunwald classification of unstable anginaSeverity：Class I：New-onset,or accelerated severe anginano rest pain within 2 monthsClass II：Angina at rest,subacute angina at rest(within the preceding month but not within 48 h)Class III：Angina at rest,acute(within the preceding 48 h)UA and non-STEMI817/10/2024Braunwaldclassificatio Braunwald classification of unstable anginaClinical Circumstances Class A：Secondary UAPa clearly identified condition extrinsic to the coronary vascular bed that has intensified myocardial ischemia,e.g.anemia,hypotension,tachy-arrhythmiaClass B：Primary unstable anginaClass C：Post-infarction UAP(within 2 weeks of a documented MI)UA and non-STEMI827/10/2024Braunwaldclassificationmechanism：1.plaque rupture and erosion,with nonocclusive thrombus2.dynamic obstruction:Vasoconstruction 3.progressive mechnial obstruction(rapidly advancing or ISR following stenting)4.secondary UA InflammationThrombogenesisUA and non-STEMI837/10/2024mechanism：1.plaquerupturea ECG:Non-STEMI:ST depression last 12 hrCardiac biomarkers of myocardium damage:cTnT,cTnICK-MBUAP and non-STEMICoronary angiographyCoronary angiographyAngioscopy and IVUSAngioscopy and IVUSOther laboratory testsOther laboratory tests847/10/2024ECG:CardiacbiomarkerTreatment 1.Genearl management:rest,oxygen,CCU2.Drug therapy A.Anti-ischemic drug:intravenously,orallynitrates-blocker Calcium antagnoist:first choice for variant anginaMorphine sulfateUA and non-STEMI857/10/2024Treatment1.GenearlmanagementTreatment 2.Drug therapy:B.antithrombotic therapy a.Anti-platelet Aspirin:early,300mg loading dose ADP-receptor antagonist:clopidogrel 300mg-600mg loading dose,75 mg/dGP IIb/IIIa receptor inhibitor:used in pts planned to PCI b.Anticoagulation therapy:HeparinLow molecular weight heparin(LMWH)Direct anti-thrombin drug:bivalirudin,hirudin UA and non-STEMI867/10/2024Treatment2.Drugtherapy:UAaTreatment 2.Drug therapy:C.other medical therapy a.lipid-lowering drugs:statins,early use(in first 24 hrs)LDL-c target:100 mg/dl b.ACEI:long-term secondary preventionUA and non-STEMI877/10/2024Treatment2.Drugtherapy:UAaTreatment 3.Invasive versus conservative strategy early invasive strategy indicated for high risk patients:within 48-72 hrs,Following by coronary revascularization(PCI or CABG)4.Long-term management -blockers,Statin,ACEI,aspirin clopidegrel(12m)UA and non-STEMI887/10/2024Treatment3.Invasiveversusc7/10/202489Symptoms Suggestive of ACSDefinite ACSNo ST elevationAlgorithm for the Evaluation and Managementof Patients Suspected of Having an ACS.ST elevationPossible ACSChronic Stable AnginaNoncardiac DiagnosisTreatment as indicated byalternative diagnosisSee ACC/AHA/ACPGuidelines for ChronicStable AnginaNondiagnostic ECGNormal Initial serumcardiac markersST and/or T wave changesOngoing painPositive cardiac markersHemodynamic abnormalitiesObserveFollow-up at 4-8 hours;ECG,cardiac markersEvaluation forreperfusion therapySee ACC/AHA Guidelines forAcute MINo recurrent pain;Negative follow-up studiesRecurrent ischemic painor positive follow-up studiesDiagnosis of ACS confirmedAdmit to hospitalManage via acute ischemia pathwayStress study to provoke ischemiaConsider evaluation of LV function if ischemia present(Test may be performed prior to discharge or as outpatient)Negative:Potential diagnoses:nonischemic discomfortlow-risk ACSPositive:Diagnosis of ACSconfirmedArrangement for outpatientfollow-up8/14/202389SymptomsSuggestivePrevention of CADnA:aspirin,ACEInB:bloodpressure,-blocker,nC:cigarettesmoking,CholesterolnD:diet,controldiabetesnE:exercise,education907/10/2024PreventionofCADA:aspirin,917/10/2024918/14/2023