冠心病英文版.ppt

Atherosclerosis&Coronary heart diseasesZhengzhouUniversity,FirstaffiliatedHospitalDept.ofCardiologyHaiyuLi,M.D.Cardiovascular DiseasesAtherosclerosisleading cause of death and disabilityCommon location:Coronary circulation:Proximal left anterior descending coronary artery(LAD)Proximal portion of renal arteriesExtracranialcirculation to the brainCarotid bifurcationAtherosclerosisCoronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia,anoxaemiaCoronary heart disease,CHDIschemic heart diseaseAtherosclerosisStable angina pectoris(SAP)Acute coronary syndromeUnstable angina(UAP)and non-STEMI (UA/NSTEMI)ST elevation myocardial infarction(STEMI)Three fundamental biological processes of atherosclerosis1.Accumulationofintimalcells:smoothmusclecellsMacrophagesT-lymphocytes2.Proliferatedconnectivetissuematrix:collagenelastic fibersproteoglycans3.Accumulationoflipid:cholesterolestersfreecholesterolPathologyandpathophysiologyFattysteakFibrousplaqueComplicatedlesionAtherosclerosisAtherosclerosisInitiation of AtherosclerosisFatty steak formationInitiation of AtherosclerosisFatty steak formation Lipoproteinoxidation NonenzymaticglycationLeukocyte recruitmentFoam cell formationAtheroma evolution:fibrous plaqueAtheroma evolution and complicationsVascular remodeling:compensatory enlargementVascular remodeling:compensatory enlargementAtheroma evolution:Involvement of arterial smooth-muscle cellsBlood coagulationmicrovesselsAtheroma evolution and complications炎症炎症细胞细胞少量平滑肌少量平滑肌细胞细胞激活的巨噬细胞激活的巨噬细胞血栓血栓Complicated lesion:thrombosisAtheroma evolution and complicationsAtheroma evolution and complicationsVulnerableplaque:Vulnerableplaque:ThinfibrouscapThinfibrouscapRelativelylargelipidcoreRelativelylargelipidcoreHighcontentofHighcontentofmacrophagesmacrophagesInflammatorymediatorsInflammatorymediatorsIntravascular ultrasound Classicification of atherosclerotic lesion using IVUSCliniclstagesandclassificationAbsenceofsymptomorstageofdelitescenceischemianecrosis(targetorgan)fibrosisAtherosclerosisGeneralmanifestationAorticatherosclerosisCoronaryarteryatherosclerosisCerebralatherosclerosisMesentericatherosclerosisPeripheralarteryatherosclerosisAtherosclerosisclinicalmanifestationlaboratoryexaminationLackofsensitiveandspecificmethodsforearlydiagnosisDyslipidemia：X-ray：DSAshowseverityofstenosisDopplerultrasound:bloodflowradionuclide：detectionofischemiaEchocardiogram：CHDECGandstresstest:CHDNewtechniques:intravascularultrasound,angioscopeCT,MRIAtherosclerosisRisk factors and prevention1.Lifestyle modification2.Lipid disorders(Dyslipidemia):cholesterol screening in all 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-cDiabetes mellitus(DM):RR1.9formale,3.3forfemalemorediffuselesion.CADequivalent75-80%causeofdeathinadultDMarevasculardiseases:CAD,cerebrovasculardisease,orperipheralvasculardiseaseRisk factors and prevention7yearsincidenceofdeath/non-fatalMI(EastWestStudy)*These patients had no history of myocardial infarction Haffner SM,et al.N Engl J Med.1998;339:229234.05101520253035404550EventsofMIin7yearsNohistoryofMIOMINohistoryofMI*OMInon-diabeticsdiabeticsn=1373n=1059P 0.001P 40yrsadults，4/5fatalmyocardialinfarctionoccuredinpatiens65yrs8.Male gender/postmenopausal state：male:female=2：1,mandevelopCHD10-15yrsearlierthanwoman9.alcohol10.Others:diet,homocysteine,hemostaticfactorsinflammation/infectionRisk factors and prevention Drug therapy：anti-platelet：aspirinclopidogrel,GPIIb/IIIa inhitibor,Dipyridamole,cilostazolLipid-lowering Risk factors and prevention1.HMG-CoAreductaseinhibitors（statins）Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,Simvastatin,Cerivastatin,Rosuvastatin：*elevationofaminopherase,rhabdomyolysis2.Bileacid-bindingResinscholestyramine，colestipol3.NicotinicAcid：4.Fibricacidderivatives（fibrates）Gemifibrozil,clofibrate,Fenofibrate5.Cholesterolabsorptioninhibitors:ezetimibe6.ProbucolLipid-lowering drugsPreventionofCADA:aspirin,ACEIB:blood pressure,-blocker,C:cigarette smoking,CholesterolD:diet,diabetesE:exercise,educationThirdReportoftheNationalCholesterolEducationProgram(NCEP)ExpertPanelonDetection,Evaluation,andTreatmentofHighBloodCholesterolinAdults ATPIII(adulttreatmentpanelIII)Circulation 2002 17/24:3144-3373AtherosclerosisCoronary heart disease(CHD)Coronary heart disease(CHD)most common cause:obstruction of atheromatous plaqueother causes:spasm arterial thrombi coronary emboli ostial narrowing due to luetic aortitis congenital abnormalities severe LV hypertrophy Factors effect myocardial oxygen supply and demandOxygensupplyOxygendemandHeartrateMyocardialcontractilitySystolicwallstressoxygencarryingcapacityofbloodCoronarybloodflowVascularresistanceExtravascularcompressiveforcesautoregulationMetabolicregulationHumoralfactorNeuralregulationDurationofdiastolePressuregradientEndothelialcontrolCoronary heart diseaseType：slientischemia:delitescence：(ECGchange)Anginapectoris：angina,causedbymyocardialischemiamyocardialinfarction：acutemyocardialischemicnecrosiscausedbytheocclusionofcoronaryarteryIschemiacardiomyopathy(Heartfailureandarrhythmia)：cardiacenlargement,heartfailure,arrhythmia,causedbythemyocardialfibrosisastheconsequenceofchronicmycardialischemiaSuddendeath：suddencardiacarrestcausedbyventricularfibrillation/flutterCoronary heart disease(CHD)Type：slient ischemia:delitescenceAngina pectoris：myocardial infarction：Ischemic cardiomyopathy(Heart failure and arrhythmia)Sudden death Acute Coronary Syndrome(ACS)RestingischemiaNon-STelevationSTelevationUnstableangina Non-QwaveAMIQwaveAMI*positive serum cardiac markers*#occasionally variant anginaStable angina pectoris(SAP)definition:acute and transient myocardial ischemia and anoxaemia usually caused by coronary insufficiency during exertion or emotional stressCharacteristics:paroxysmal precordial squeezing-like chest pain,behind the mid sternum，radiated to left shoulder and upper armprecipitated by stress or exertionduration:2-5min typicallyrelieved rapidly by rest or nitrates Stable angina pectorisCoronarystenosis(others:aorticvalvedisease,HOCM,MB)+Myocardialoxygendemand（HRXSBP）increasedmyocardialhypoxiaacumulationofmetabolicproduct,stimulateC1-5nervetocausethesensationofchestpainStable angina pectorismechanismin 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 pectorispathophysiology1.MetabolicandelectrophysiologyATPreduced,accumulationofacidsubstancesDysfunctionofironpump(Na+-K+,andNa+-Ca+)Earlydepolarization(STdeviation)2.LVfunctionandhemodynamicsituationLVcontractilityandspeed,systolicBP,strokevolume,cardiacoutputdecreasedLVEDpressureandvolumeStunningofmyocardiumStable angina pectorissymptom：chest pain or oppressionlocation 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 pectorischest paincharacteristics：tightness,squeezing,burning,pressing,choking,bursting,rarely sharp,not spasmodic force the patient stop the activity till the symptom relieved precipitationexertion or emotional agitation。duration：35 minspain relief:within several mins after rest or using nitroglycerin Clinical manifestationStable angina pectorisPhysicalexaminationincreasedHR,elevatedBPanxietysweatingoccasionallygalloprhythm，transientsystolicmurmurClinical manifestationStable angina pectorisLaboratory1.ECG：atrestDuringchestpain:ST-Tchangefoundin95%ptsHolter:detectofslientischemiaStresstest:indication：suspectionofCHD,pre-andpost-CABGandPCI,ptswithOMIcontraindication：AMI,UAP,myocarditis,Hypertension,heartfailure,aorticstenosis,HOCM,severarrhythmia,aorticaneurysmEndofthetest：STor0.2mV，APattacks，BP220mmHg，BPdrop，ventriculararrhythmiaCriteriaforpositive:STsegmentdepression 0.1mV，last2minsStable angina pectorisStress testrestExersciseStable angina pectoris2.Echocardiography:3.Radionuclideimagingassessment:TL201，Tc99m-sestamibimyocardialperfusionscintigraphy4.X-rayofheart5.coronaryangiography：finaldiagnose6.others:IVUS、intracoronaryDopplerflow、intracoronarypressureLaboratoryStable angina pectorisCoronary Angiography1.Cardiogenicpain：aorticdissection,HOCM,aorticstenosis2.Respiratory：PE,pneumothorax,pleuritis3.Gastrointestinal:gastro-esophagealdiseases,Hiatalhernia,cholecystitis,pepticulceration,pancreatitis4.Neuromuscular/skeletal：TietzeSyndrome(Costochondritis),intercostalneuralgia,Herpeszoster5.Psychologic:anxiety,depression,panicattacksStable angina pectorisDiagnosisChestpain,riskfactors,ECGevidenceofischemiaduringchestpain,angiographyDifferentiationFunctionalclassificationofSAP(CCS)CCSI：nochestpainatordinaryactivity.AnginaatstrenuousorrapidorprolongedexertionCCSII：Slightlimitationofordinaryactivity.Walkingorclimbingstairsrapidly,aftermeals,incold,inwind.Walkingmorethan2blocks,climbingmorethanstairsof3rdfloor.CCSIII：Markedlimitationofordinaryactivity.Walking1to2blocks,climbingstairsof3rdfloorCCSIV：Inabilitytocarryonanyactivitywithoutdiscomfortanginalsymdromemaybepresentatrest.Stable angina pectoris1.Generalconsideration：rest，avoidprovocativefactors,riskfactorscontrol2.Drugtherapy:preventMIanddeathsymptomreliefandqualityoflifeimprovment3.Coronaryrevascularization:percutaneouscoronaryintervention(PCI)Coronaryarterybypasssurgery(CABG)SVG,LIMAPrevention and treatmentStable angina pectorisantianginalandanti-ischemictherapyDrug therapyOxygensupplyOxygendemanda.nitratesb.beta-adrenergicblockersc.Calciumantagonistsd.DrugsimprovingmetabolismStable angina pectorisDrug therapya.nitratesloweroxygendemand:decreasearteriolarandvenoustone,reducepreloadandafterloadincreasecoronarysupply:CoronarydilatationNitroglycerinIsosorbidedinitrateisosorbide5-mononitrate(long-actingnitrates)Stable angina pectorisb.blockers:reducemyocardialoxygen:reduceHR,myocardialcontractility,BP,theLVwallstressAbslutecontraindications：severbradycardia:high-degreeA-Vblock,SSS,severeunstableLVfailureRelativecontraindications:asthmaandbronchospasticdiseaseperipheralvasculardisease1-selective：metoprolol,atenolol,bisoprololDrug therapyStable angina pectorisc.Calciumantagonists：Increaseoxygensupply:dilateresistancevessels,releasespasm,improvemicrovascularfunctionDecreaseoxygendemand:negativeinotropiceffect,decreaseBPAntiplateleteffectd.Drugsimprovingmetabolism：trimethazine（vasorel），），selectivelyinhibit3-KAT（3-酮酰辅酶酮酰辅酶A硫解酶），硫解酶），partlyinhibitFAoxidationDrug therapyStable angina pectorispreventMIanddeaththerapya.antiplateletangents：ASA，75-325mg/dclopidogrel;ticlopidine:ADPreceptor-antagonists:Cilostazol:phosphodiesteraseinhititor,50-100mgbidb.Lipid-loweringangents:statinsc.Angiotesin-convertingenzymeinhibitor(ACEI)Drug therapyStable angina pectorisstentingStable angina pectorisUnstable angina(UAP)and non-STEMIRestingischemiaNon-STelevationSTelevationUnstableangina Non-QwaveAMIQwaveAMI*positive serum cardiac markers*#occasionally variant anginaAcute Coronary Syndrome(ACS)Occuringatrest(orwithmininalexertion):last20minssevereandofnew-onset:within1-2months,CCSIIIOccuringwithadeteriorativepattern:atleastCCSIIIvariantanginapectoris(Prinzmetalangina):transientSTelevation,causedbythecoronaryspasmDefinitionUAP and non-STEMIAnginapectorisorequivalentischemicdiscomfortAnginapectorisorequivalentischemicdiscomfortwithatleastoneofthethreefeatureswithatleastoneofthethreefeaturesBraunwaldclassificationofunstableanginaSeverity：ClassI：New-onset,oracceleratedsevereanginanorestpainwithin2monthsClassII：Anginaatrest,subacuteanginaatrest(withintheprecedingmonthbutnotwithin48h)ClassIII：Anginaatrest,acute(withinthepreceding48h)UAP and non-STEMIBraunwaldclassificationofunstableanginaClinicalCircumstancesClassA：SecondaryUAPaclearlyidentifiedconditionextrinsictothecoronaryvascularbedthathasintensifiedmyocardialischemia,e.g.anemia,hypotension,tachy-arrhythmiaClassB：PrimaryunstableanginaClassC：Post-infarctionUAP(within2weeksofadocumentedMI)UAP and non-STEMImechanism：1.plaque rupture and erosion,with nonocclusive thrombus2.dynamic obstruction:Vasoconstruction 3.progressive mechnial obstruction(rapidly advancing or ISR following stenting)4.secondary UA InflammationThrombogenesisUAP and non-STEMIECG:Non-STEMI:STdepressionlast12hrCardiacbiomarkersofmyocardiumdamage:cTnT,cTnICK-MBUAP and non-STEMICoronaryangiographyCoronaryangiographyAngioscopyandIVUSAngioscopyandIVUSOtherlaboratorytestsOtherlaboratorytestsRiskstratification：TIMIRiskScoreAge=65yrsMorethan3coronaryriskfactorsPriorangiographiccoronaryobstructionST-segmentdeviation 0.5mmMorethan2anginaeventswithin24hoursDevelopmentofUA/NSTEMIwhileonaspirinElevatedcardiacmarkersAntaman,JAMA2000;284:835-42TIMIIIB,ESSENCE,PRISM-PLUS,TACTICS-TIMI18UAP and non-STEMITreatment 1.Genearlmanagement:rest,oxygen,CCU2.DrugtherapyA.Anti-ischemicdrug:intravenously,orallynitrates-blockerCalciumantagnoist:firstchoiceforvariantanginaMorphineUAP and non-STEMITreatment 2.Drugtherapy:B.antithrombotictherapya.Anti-plateletAspirin:early,300mgloadingdoseADP-receptorantagonist:clopidogrel300mg-600mgloadingdose,75mg/dGPIIb/IIIareceptorinhibitor:usedinptsplannedtoPCIb.Anticoagulationtherapy:HeparinLowmolecularweightheparin(LMWH)Directanti-thrombindrug:bivalirudin,hirudinUAP and non-STEMITreatment 2.Drug therapy:C.other medical therapy a.lipid-lowering drugs:statins,early use(in first 24 hrs)LDL-c target:30 mins，less effective of sublingual nitroglycerin,retrosternal in location,sweating,scared,and feeling of impending deathin some patients,AMI is manifested by shock and acute LV failure,not by chest pain(the elderly)alert the epigastrium pain and abdominal disordersSTEMIClinical manifestationsymptomsGeneral：fever、HR increase、WBC ，ESR fastingGastrointestinal symptom：nausea,vomiting,arrhythmias：VPs、AV block,atrial arrhythmias occurred more often in patients with HFHeart failure:mainly acute LV failure,may develope RV failure.Initial RV failure occure in patients with RV infarction,associated with hypotensionHypotension and shock：SBP80mmHg after pain release,RV infarctionSTEMIClinical manifestationPump failureClassification based on clinical examination(Killip)Class I：no HF,rales and S3 absent；Class II:mild HF，rales over 50%of lung,with or without s3；Class III:acute pulmonary edemarales over 50%of lung fields Class IV:cardiogenic shockClassification based on invasive hemodynamic monitoringClass I：Normal,PCWP pulmonary capillary wedge pressure 2.2；Class II:Pulmonary congestion,PCWP 18.CI 2.2；Class III:peripheral hypoperfusion,PCWP 18,CI 18,CI 0.2mV in at least two contiguous leads;new or presumably new LBBB3.Time from onset of symptoms 12hrs：diminishing benefits but may still be useful in selected patinets 4.age 180/110mmHg on at least two reading2.History of chronic,severe hypertension with or without drug therapy3.active peptic ulcer4.History of cerebrovascular accide