冠状动脉粥样硬化性心脏病英文课件.ppt

Coronary Atherosclerotic Heart Diseases AffiliatedHospitalofJiningMedicalCollegeDept.ofCardiacCareUnitGuoxiaD25/2/2024ContentsAtherosclerosisStableAnginaPectorisAcuteCoronarySyndromeUAandNSTEMIAMI(STEMI)35/2/2024Self-study VariantAnginaCardiacSyndromeXSilentMyocardialIschemiaMyocardialBridging45/2/2024What Is Atherosclerosis?nAtherosclerosisisthedescriptivetermforthickenedandhardenedlesionsofthemediumandlargemuscularandelasticarteries.55/2/2024What Is Coronary Heart Disease?65/2/2024Coronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia,necrosisIschemic heart disease75/2/202485/2/2024Atherosclerosis95/2/2024FoamcellFattysteak atheromatousplaquerupturedplaquesFibrousplaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al.Circulation 1995;92:1355-1374.mediumdamage5/2/202410What damage does atherosclerosis cause?115/2/2024Common locationnCoronaryHeartDiseasenCarotidArteryDiseasenPeripheralArterialDiseasenChronicKidneyDisease125/2/2024How does atherosclerosis start and progress?135/2/2024nElevatedlevelsofcholesterolandtriglyceridesinthebloodnHighbloodpressurenCigarettesmoking145/2/2024Biological processes1.Accumulation of intimal cellssmooth muscle cells MacrophagesT-lymphocytes155/2/2024Biological processes2.Proliferatedconnectivetissuematrixcollagenelasticfibersproteoglycans165/2/2024Biological processes3.Accumulationoflipid175/2/2024Atherosclerosis-HypothesisHypothesisoflipoproteininfiltrationAggregationofplateletsandthrombosisClonaltheoryTheresponse-to-injuryhypothesis185/2/2024nHigh 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 195/2/2024Pathology and pathophysiologyFattysteakFibrousplaqueComplicatedlesion205/2/2024Initiation of AtherosclerosisFatty steak formation215/2/2024Initiation of Atherosclerosis225/2/2024fibrous plaque235/2/2024245/2/2024255/2/2024Thin CapVulnerable Plaque ThrombusUnstable“Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina“Dormant Volcano”SAPACSpressure or a squeezing pain!265/2/2024Unstable 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.unstablestable5/2/202428AtherosclerosisnClinical stages Absence of symptom or stage of incubationischemianecrosis(target organ)fibrosis295/2/2024clinical manifestationuGeneralmanifestationuAorticatherosclerosisuCoronaryarteryatherosclerosisuCerebralatherosclerosisuRAatherosclerosisuMesentericatherosclerosisuPeripheralarteryatherosclerosis305/2/2024Laboratory ExaminationLackofsensitiveandspecificmethodsforearlydiagnosisDyslipidemiaX-ray：DSAshowseverityofstenosisDopplerultrasound:bloodflow315/2/2024Laboratory Examinationradionuclide：detectionofischemiaEchocardiogram：CHDECGandstresstest:CHDAngiography:themostdirectwayIntravascularultrasound,angioscopeCT,MRI325/2/2024Risk factors n1.Lipid disorders(Dyslipidemia)nIncreasedcholesterol:TcandLDL-c,TG,ApoB,Lp(a)nDecreasedcholesterol:HDL-capoAn2.Hypertension335/2/2024Risk factors n3.DM,Metabolic syndrome or insulin resistance syndrome MorediffuselesionCADequivalent75-80%causeofdeathinadultDMarevasculardiseases:CAD,cerebrovasculardisease,orperipheralvasculardisease345/2/20247 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/infection365/2/2024Drug therapyanti-platelet：aspirin,clopidogrel,GPIIb/IIIa inhitibor,Dipyridamole,cilostazolLipid-loweringHMG-CoAreductaseinhibitors（statins）375/2/2024Doubts of patients nQuest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?385/2/2024Doubts of patients nQuestion2：Myshapeisnotfat,lipidisnothigh,whygivemelipid-loweringdrugs,madeamistake?395/2/2024Doubts of patients nQuestion3：Ihavecoronaryheartdisease,thenshouldIdolessactivitiesinordertoprotecttheheart?405/2/2024Coronary Heart Disease(CHD)5/2/202441Clinical TypenSilentmyocardialischemianAnginapectorisnMyocardialinfarctionnIschemiccardiomyopathynSuddencardiacdeath5/2/202442Silent 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.5/2/202443Ischemic 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.5/2/202444Sudden 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.5/2/202445Acute 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.5/2/202446STABLE ANGINA PECTORIS475/2/2024DefinitionAcute and transient myocardial ischemia and anoxaemia.Usually caused by coronary insufficiency during exertion.485/2/2024Characteristicsparoxysmal precordial squeezing-like chest pain,behind the mid sternumradiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates 495/2/2024 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 mechanism505/2/2024in 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 pectoris515/2/2024pathophysiology1.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 pectoris525/2/2024symptom：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 pectoris535/2/2024 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 pectoris555/2/2024Physical examinationincreased HR,elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifestationStable angina pectoris565/2/2024Auxiliaryexamination1.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 pectoris575/2/2024Stress testrestExersciseStable angina pectoris585/2/2024 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 pectoris595/2/2024Coronary Angiography605/2/2024Stable Angina PectorisDiagnosisuChest painurisk factorsuECG evidence of ischemia during chest painu angiography615/2/2024CardiovascularcausesNoncardiaccausesStable Angina PectorisDifferentialdiagnosis625/2/2024CardiovascularcausenMyocardialinfarctionnPericarditisnAorticdissectionnPulmonaryembolismnPulmonaryhypertension635/2/2024NoncardiaccausenPneumoniawithpleurisynSpontaneouspneumothoraxnMusculoskeletaldisordersnHerpeszosternEsophagealrefluxnPepticulcer645/2/20241.General treatment：risk factors control2.Drug therapy3.Coronary revascularization:percutaneous coronary intervention(PCI)Coronary artery bypass surgery(CABG)SVG,IMAGTreatmentStable Angina Pectoris655/2/2024Blood and oxygen supply to the heartMyocardialbloodflowMyocardial oxygenconsumption4%oftotalcardiacoutputsuppliedtothemyocardium12%oftotalbodyoxygen,usedatrestbymyocardium5/2/202466Coronary ReserveMyocardialbloodflowincreasesupto4times.tomeetincreasedmyocardialoxygendemand5/2/202467Myocardial 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 2supplysupplyO2demand5/2/202468Aims of medical therapyArterialvasodilatationReducesarterialresistanceReducesafterloadDecreasessympatheticdriveReduceheartrateandcontractileforceReducescardiacworkLVRVDilatationofcoronaryarteriesImprovescoronarysupplyVenodilatationReducesvenousreturnReducespreload5/2/202469antianginal and anti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris705/2/2024Drug 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 Pectoris715/2/2024Nitrates in anginaReducepreloadthroughvenodilatationReduceafterloadbyloweringarterialresistanceReduceplateletaggregationIncrease coronary perfusion,includingischaemic areas Reversal of coronary spasm5/2/202472b.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 Pectoris735/2/2024c.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 Pectoris745/2/2024prevent MI and death therapya.antiplatelet angents：ASAclopidogrelCilostazolb.Lipid-lowering angents:statins c.Angiotesin-converting enzyme inhibitor(ACEI)Drug therapyStable Angina Pectoris755/2/2024stentingStable Angina Pectoris765/2/2024Unstable Angina(UA)and non-STEMI775/2/2024ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers*#occasionally variant anginaAcute Coronary Syndrome(ACS)785/2/2024Occuring 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 features805/2/2024 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-STEMI815/2/2024 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-STEMI825/2/2024mechanism：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-STEMI835/2/2024 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 tests845/2/2024Treatment 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-STEMI855/2/2024Treatment 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-STEMI865/2/2024Treatment 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-STEMI875/2/2024Treatment 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-STEMI885/2/20245/2/202489Symptoms 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;E