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Atherosclerosis Atherosclerosis&Coronary heart diseasesCoronary heart diseasesZhengzhou University,First affiliated HospitalZhengzhou University,First affiliated HospitalDept.of CardiologyDept.of CardiologyHaiyu Li,M.D.Haiyu Li,M.D.Atherosclerosis Zhengzhou UnivCardiovascular DiseasesCardiovascular DiseasesAtherosclerosisAtherosclerosisAtherosclerosisleading cause of death and disabilityleading cause of death and disabilityCommon location:Common location:Coronary circulation:Proximal left anterior Coronary circulation:Proximal left anterior descendingdescending coronary artery(LAD)coronary artery(LAD)Proximal portion of renal arteriesProximal portion of renal arteriesExtracranialExtracranial circulation to the braincirculation to the brainCarotid bifurcationCarotid bifurcationAtherosclerosisAtherosclerosisleading cause of death and disCoronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia,anoxaemiaanoxaemiaCoronary heart disease,CHDIschemic heart diseaseCoronary heart diseaseatheroscAtherosclerosisAtherosclerosisStable angina pectoris(SAP)Stable angina pectoris(SAP)Acute coronary syndromeAcute coronary syndromeUnstable angina(UAP)and non-STEMIUnstable angina(UAP)and non-STEMI (UA/NSTEMI)(UA/NSTEMI)ST elevation myocardial infarction(STEMI)ST elevation myocardial infarction(STEMI)AtherosclerosisThree fundamental biological Three fundamental biological processes of aprocesses of atherosclerosistherosclerosis1.1.Accumulation of intimal cells:Accumulation of intimal cells:smooth muscle cells smooth muscle cells MacrophagesMacrophagesT-lymphocytesT-lymphocytes2.2.Proliferated connective tissue matrixProliferated connective tissue matrix :collagencollagenelasticelastic fibers fibersproteoglycansproteoglycans3.Accumulation of lipid:3.Accumulation of lipid:cholestercholesterolol esters estersfree cholesterolfree cholesterolThree fundamental biological pPathology and pathophysiologyPathology and pathophysiologyFatty steakFatty steakFibrous plaqueFibrous plaqueComplicated lesionComplicated lesionAtherosclerosisAtherosclerosisPathology and pathophysiologyAInitiation of AtherosclerosisInitiation of AtherosclerosisFatty steak formationFatty steak formationInitiation of AtherosclerosisFInitiation of AtherosclerosisInitiation of AtherosclerosisFatty steak formationFatty steak formation LipoproteinLipoprotein oxidationoxidation Nonenzymatic Nonenzymatic glycationglycationLeukocyte recruitmentLeukocyte recruitmentFoam cell formationFoam cell formationInitiation of AtherosclerosisFAtheroma evolution:fibrous plaqueAtheroma evolution:fibrous plaqueAtheroma evolution and complicationsAtheroma evolution and complicationsVascular remodeling:compensatory enlargementVascular remodeling:compensatory enlargementVascular remodeling:compensatory enlargementVascular remodeling:compensatory enlargementAtheroma evolution:fibrous plAtheroma evolution:Atheroma evolution:Involvement of Involvement of arterial smooth-muscle arterial smooth-muscle cellscellsBlood coagulationBlood coagulationmicrovesselsmicrovesselsAtheroma evolution and complicationsAtheroma evolution and complicationsAtheroma evolution:Atheroma ev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:thrombosisComplicated lesion:thrombosisAtheroma evolution and complicationsAtheroma evolution and complications炎症少量平滑肌激活的巨噬细胞血栓Complicated leAtheroma evolution and complicationsAtheroma evolution and complicationsVulnerable plaque:Vulnerable plaque:Vulnerable plaque:Vulnerable plaque:Thin fibrous capThin fibrous capThin fibrous capThin fibrous capRelatively large lipid coreRelatively large lipid coreRelatively large lipid coreRelatively large lipid coreHigh content of macrophagesHigh content of macrophagesHigh content of macrophagesHigh content of macrophagesInflammatory mediatorsInflammatory mediatorsInflammatory mediatorsInflammatory mediatorsAtheroma evolution and complicIntravascular ultrasoundIntravascular ultrasound Intravascular ultrasound Classicification of atherosclerotic Classicification of atherosclerotic lesion using IVUSlesion using IVUSClassicification of atheroscleClinicl stages and classificationClinicl stages and classificationAbsence of symptom or stage of delitescenceAbsence of symptom or stage of delitescenceischemiaischemianecrosis(target organ)necrosis(target organ)fibrosisfibrosisAtherosclerosisAtherosclerosisClinicl stages and classificatGeneral manifestationGeneral manifestationAortic atherosclerosisAortic atherosclerosisCoronary artery atherosclerosisCoronary artery atherosclerosisCerebral atherosclerosisCerebral atherosclerosisMesenteric atherosclerosisMesenteric atherosclerosisPeripheral artery atherosclerosisPeripheral artery atherosclerosisAtherosclerosisAtherosclerosisclinical manifestationclinical manifestationGeneral manifestationAtheroscl laboratory examinationlaboratory examinationLack of sensitive and specific methods for Lack of sensitive and specific methods for early diagnosisearly diagnosisDyslipidemiaDyslipidemia:X-rayX-ray:DSA show severity of stenosisDSA show severity of stenosisDoppler ultrasound:blood flowDoppler ultrasound:blood flowradionuclideradionuclide:detection of ischemiadetection of ischemiaEchocardiogramEchocardiogram:CHDCHDECG and stress test:CHDECG and stress test:CHDNew techniques:intravascular ultrasound,New techniques:intravascular ultrasound,angioscopeangioscopeCT,MRICT,MRIAtherosclerosisAtherosclerosis laboratory examinationAtheroRisk factors and Risk factors and preventionprevention1.Lifestyle modification1.Lifestyle modification2.Lipid disorders(Dyslipidemia):2.Lipid disorders(Dyslipidemia):cholesterol screening in all 20yrs cholesterol screening in all 20yrsElevated:cholesterol(Tc and LDL-c),TG,ApoB/ApoA,Lp(a),Elevated:cholesterol(Tc and LDL-c),TG,ApoB/ApoA,Lp(a),Low:HDL-c Low:HDL-c LDL lowering by HMG-CoA reductase(statins):LDL lowering by HMG-CoA reductase(statins):cardiovascular events 30%cardiovascular events 30%,risk of MI 62%risk of MI 62%3.Hypertension3.Hypertension:4.DM,4.DM,Metabolic syndrome or insulin resistance syndrome:Metabolic syndrome or insulin resistance syndrome:BP,BMI,TG,serum insulin BP,BMI,TG,serum insulin HDL-c HDL-cRisk factors and prevention1.LDiabetes mellitus(DM):Diabetes mellitus(DM):RR 1.9 for male,3.3 for female RR 1.9 for male,3.3 for female more diffuse lesion.more diffuse lesion.CAD equivalentCAD equivalent 75-80%cause of death in adult DM are 75-80%cause of death in adult DM are vascular diseases:vascular diseases:CAD,CAD,cerebrovascular disease,cerebrovascular disease,or peripheral vascular diseaseor peripheral vascular diseaseRisk factors and Risk factors and preventionpreventionRisk factors and prevention7 years incidence of death/non-fatal MI7 years incidence of death/non-fatal MI (East West Study)East West Study)*These patients had no history of myocardial infarction Haffner SM,et al.N Engl J Med.1998;339:229234.0 05 5101015152020252530303535404045455050Events of MI in 7 yearsEvents of MI in 7 yearsNo history of MI OMI No history of MI*No history of MI OMI No history of MI*OMI OMI non-diabetics non-diabetics diabetics diabetics n=1373n=1373n=1059n=1059P P 0.001 0.001P P 0.00140yrs adults 40yrs adults,4/5 fatal myocardial 4/5 fatal myocardial infarction occured in patiens 65 yrsinfarction occured in patiens 65 yrs8.Male gender/postmenopausal state8.Male gender/postmenopausal state:male:female=2male:female=2:1,man develop CHD 10-15 yrs 1,man develop CHD 10-15 yrs earlier than womanearlier than woman9.alcohol9.alcohol10.Others:diet,homocysteine,hemostatic factors10.Others:diet,homocysteine,hemostatic factors inflammation/infection inflammation/infectionRisk factors and Risk factors and preventionprevention5.Cigarette smoking:more thr Drug therapyDrug therapy:anti-plateletanti-platelet:aspirin,clopidogrel,GPIIb/IIIa aspirin,clopidogrel,GPIIb/IIIa inhitibor,inhitibor,Dipyridamole,cilostazol Dipyridamole,cilostazolLipid-lowering Lipid-lowering Risk factors and Risk factors and preventionprevention Risk factors and preven1.1.HMG-CoA reductase inhibitorsHMG-CoA reductase inhibitors(statinsstatins)Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,SiAtorvastatin,Fluvastatin,Lovastatin,Pravastatin,Simvastatin,Cerivastatin,Rosuvastatinmvastatin,Cerivastatin,Rosuvastatin:*elevation of aminopherase,rhabdomyolysiselevation of aminopherase,rhabdomyolysis2.Bile acid-binding Resins2.Bile acid-binding Resins cholestyramine cholestyramine,colestipolcolestipol3.Nicotinic Acid3.Nicotinic Acid:4.Fibric acid derivatives4.Fibric acid derivatives(fibratesfibrates)Gemifibrozil,clofibrate,FenofibrateGemifibrozil,clofibrate,Fenofibrate5.Cholesterol absorption inhibitors:ezetimibe5.Cholesterol absorption inhibitors:ezetimibe6.Probucol6.ProbucolLipid-lowering drugsLipid-lowering drugsHMG-CoA reductase inhibitors(sPrevention of CADPrevention of CADA:aspirin,ACEIB:blood pressure,-blocker,C:cigarette smoking,CholesterolD:diet,diabetesE:exercise,educationPrevention of CADThird Report of the National Cholesterol Third Report of the National Cholesterol Education Program(NCEP)Expert Panel on Education Program(NCEP)Expert Panel on Detection,Evaluation,and Treatment of Detection,Evaluation,and Treatment of High Blood Cholesterol in AdultsHigh Blood Cholesterol in Adults ATP III(adult treatment panel III)ATP III(adult treatment panel III)Circulation 2002 17/24:3144-3373AtherosclerosisAtherosclerosisThird Report of the National CCoronary heart diseaseCoronary heart disease(CHD)(CHD)Coronary heart diseaseCoronary heart disease Coronary heart disease(CHD)(CHD)most common cause:obstruction of most common cause:obstruction of atheromatous plaqueatheromatous plaqueother causes:other causes:spasm spasm arterial thrombi arterial thrombi coronary emboli coronary emboli ostial narrowing due to luetic aortitis ostial narrowing due to luetic aortitis congencongeni ital abnormalities tal abnormalities severe LV hypertrophy severe LV hypertrophy Coronary heart disease(CHD)moFactors effect myocardial oxygen Factors effect myocardial oxygen supply and demandsupply and demandOxygenOxygen supply supplyOxygen Oxygen demanddemandHeart rateHeart rateMyocardial Myocardial contractilitycontractilitySystolic wall stressSystolic wall stressoxygen carryingoxygen carryingcapacity of bloodcapacity of bloodCoronary blood flowCoronary blood flowVascular Vascular resistanceresistanceExtravascularExtravascular compressive forces compressive forcesautoregulationautoregulationMetabolic regulationMetabolic regulationHumoral Humoral factorfactorNeural Neural regulationregulationDuration of diastoleDuration of diastolePressure Pressure gradientgradientEndothelial controlEndothelial controlFactors effect myocardial oxygCoronary heart diseaseCoronary heart disease TypeType:slient ischemia:delitescenceslient ischemia:delitescence:(ECG change)(ECG change)Angina pectorisAngina pectoris:angina,caused by myocardial angina,caused by myocardial ischemiaischemia myocardial infarctionmyocardial infarction:acute myocardial acute myocardial ischemic necrosis caused by the occlusion of ischemic necrosis caused by the occlusion of coronary arterycoronary arteryIschemia cardiomyopathy(Heart failure and Ischemia cardiomyopathy(Heart failure and arrhythmia)arrhythmia):cardiac enlargement,heart failure,cardiac enlargement,heart failure,arrhythmia,caused by the myocardial fibrosis as arrhythmia,caused by the myocardial fibrosis as the consequence of chronic mycardial ischemiathe consequence of chronic mycardial ischemiaSudden deathSudden death:sudden cardiac arrest caused sudden cardiac arrest caused by by ventricular fibrillation/flutterventricular fibrillation/flutterCoronary heart disease Coronary heart disease Coronary heart disease(CHD)(CHD)TypeType:slient ischemia:delitescenceslient ischemia:delitescenceAngina pectorisAngina pectoris:myocardial infarctionmyocardial infarction:Ischemic cardiomyopathy(Heart Ischemic cardiomyopathy(Heart failure and arrhythmia)failure and arrhythmia)Sudden death Sudden death Coronary heart disease(CHD)Acute Coronary Syndrome(ACS)Acute Coronary Syndrome(ACS)Resting ischemiaResting ischemiaNon-ST elevationNon-ST elevationSTelevationSTelevationUnstable anginaUnstable anginaNon-Q wave AMINon-Q wave AMIQ wave AMIQ wave AMI*positive serum cardiac markers*#occasionally variant anginaAcute Coronary Syndrome(ACS)ReStable angina pectorisStable angina pectoris(SAP)(SAP)Stable angina pectorisdefinition:definition:acute and transient myocardial ischemia and acute and transient myocardial ischemia and anoxaemia anoxaemia usually caused by coronary insufficiency during usually caused by coronary insufficiency during exertionexertion or emotional stress or emotional stressCharacteristics:Characteristics:paroxysmal precordial squeezing-like chest pain,paroxysmal precordial squeezing-like chest pain,behind the mid sternumbehind the mid sternum,radiated to left shoulder and upper armradiated to left shoulder and upper armprecipitated by stress or exertionprecipitated by stress or exertionduration:2-5min duration:2-5min typicallytypically relieved rapidly by rest or nitrates relieved rapidly by rest or nitrates Stable angina pectorisStable angina pectorisdefinition:Stable angina pectCoronary stenosisCoronary stenosis(others:aortic valve disease,HOCM,MB(others:aortic valve disease,HOCM,MB)+Myocardial oxygen demand Myocardial oxygen demand(HRHR X X SBPSBP)increasedincreased myocardial hypoxiamyocardial hypoxiaacumulation of metabolic product,stimulate acumulation of metabolic product,stimulate C1-C1-5 5 nerve nerve to cause the sensation of chest pain to cause the sensation of chest pain Stable angina pectorisStable angina pectorismechanismmechanismCoronary stenosisStable anginain angiographyin angiographySignificant coronary lesion with Significant coronary lesion with diameter stenosis 70%in 75%ptsdiameter stenosis 70%in 75%ptsNo significant stenosis in about 5-No significant stenosis in about 5-10%pts,Ischemia may be related to 10%pts,Ischemia may be related to coronary spasm or microvascular coronary spasm or microvascular dysfunction.dysfunction.PathologyPathologyStable angina pectorisStable angina pectorisin angiographyPathologyStable pathophysiologypathophysiology1.Metabolic and electrophysiology1.Metabolic and electrophysiologyATP reduced,accumulation of acid substances ATP reduced,accumulation of acid substances Dysfunction of iron pump(Na+-K+,and Na+-Ca+)Dysfunction of iron pump(Na+-K+,and Na+-Ca+)Early depolarization(ST deviation)Early depolarization(ST deviation)2.LV function and hemodynamic situation 2.LV function and hemodynamic situation LV contractility and speed,systolic BP,LV contractility and speed,systolic BP,stroke volume,cardiac output decreasedstroke volume,cardiac output decreased LVED pressure and volume LVED pressure and volume Stunning of myocardiumStunning of myocardiumStable angina pectorisStable angina pectorispathophysiology1.Metabolic andsymptomsymptom:chest pain or chest pain or oppressionoppressionlocationlocation behind or slightly to the left behind or slightly to the left of the mid sternum of the mid sternum no definite borderlineno definite borderlineradiated to the left shoulder radiated to the left shoulder and upper armand upper armAtypical location:lower jaw,Atypical location:lower jaw,the back of neckthe back of neckClinical manifestationClinical manifestationStable angina pectorisStable angina pectorissymptom:chest pain or oppressichest painchest paincharacteristicscharacteristics:tightness,squeezing,burning,pressing,choking,tightness,squeezing,burning,pressing,choking,bursting,rarely sharp,not spasmodicbursting,rarely sharp,not spasmodic force the patient stop the activity till the symptom force the patient stop the activity till the symptom relieved relieved precipitationprecipitationexertion or emotional agitationexertion or emotional agitation。durationduration:3 35 mins5 minspain relief:within several mins after rest or using pain relief:within several mins after rest or using nitroglycerin nitroglycerin Clinical manifestationClinical manifestationStable angina pectorisStable angina pectorischest painClinical manifestatiPhysical examinationPhysical examinationincreased HR,elevated BP increased HR,elevated BP anxiety anxiety sweatingsweatingoccasionally gallop rhythmoccasionally gallop rhythm,transient transient systolic murmursystolic murmurClinical Clinical manifestationmanifestationStable angina pectorisStable angina pectorisPhysical examinationClinical mLaboratoryLaboratory1.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 pectorisStable angina pectorisLaboratory1.ECG:Stable angina Stress testStress testrestrestExersciseExersciseStable angina pectorisStable angina pectorisStress testrestExersciseStable 2.Echocardiography:2.Echocardiography:3.3.Radionuclide imagingRadionuclide imaging assessment assessment:TLTL201201,TcTc99m99m-sestamibi myocardial perfusion-sestamibi myocardial perfusion scintigraphy scintigraphy 4.X-ray of heart 4.X-ray of heart 5.coronary angiography 5.coronary angiography:final diagnosefinal diagnose 6.others:6.others:IVUSIVUS、intracoronary Doppler flow intracoronary Doppler flow、intracoronary pressureintracoronary pressureLaboratoryLaboratoryStable angina pectorisStable angina pectoris 2.Echocardiography:LaboratorCoronary AngiographyCoronary AngiographyCoronary Angiography1.Cardiogenic pain1.Cardiogenic pain:aortic dissection,HOCM,aortic stenosisaortic dissection,HOCM,aortic stenosis2.2.R Respiratoryespiratory:PE,pneumothorax,pleuritisPE,pneumothorax,pleuritis 3.Gastrointestinal:3.Gastrointestinal:gastro-esophageal diseases,Hiatal hernia,gastro-esophageal diseases,Hiatal hernia,cholecystitis,peptic ulceration,pancreatitischolecystitis,peptic ulceration,pancreatitis4.Neuromuscular/skeletal 4.Neuromuscular/skeletal:Tietze Syndrome(Costochondritis),Tietze Syndrome(Costochondritis),intercostal neuralgia,Herpes zosterintercostal neuralgia,Herpes zoster5.Psychologic:5.Psychologic:anxiety,depression,panic attacksanxiety,depression,panic attacks Stable angina pectorisStable angina pectorisDiagnosisDiagnosisChest pain,risk factors,ECG evidence of Chest pain,risk factors,ECG evidence of ischemia during chest pain,angiographyischemia during chest pain,angiographyDifferentiationDifferentiation1.Cardiogenic pain:aortic dissFunctional classification of SAP(CCS)Functional classification of SAP(CCS)CCS ICCS I:no chest pain at ordinary activity.no chest pain at ordinary activity.Angina at strenuous or rapid or prolonged exertion Angina at strenuous or rapid or prolonged exertionCCS IICCS II:Slight limitation of ordinary activity.Slight limitation of ordinary activity.Walking or climbing stairs rapidly,after meals,in Walking or climbing stairs rapidly,after meals,in cold,in wind.cold,in wind.Walking more than 2 blocks,climbing more than stairs Walking more than 2 blocks,climbing more than stairs of 3rd floor.of 3rd floor.CCS IIICCS III:Marked limitation of ordinary activity.Marked limitation of ordinary activity.Walking 1 to 2 blocks,climbing stairs of 3rd floor Walking 1 to 2 blocks,climbing stairs of 3rd floor CCS IVCCS IV:Inability to carry on any activity without discomfortInability to carry on any activity without discomfortanginal symdrome may be present at rest.anginal symdrome may be present at rest.Stable angina pectorisStable angina pectorisFunctional classification of S1.1.General considerationGeneral consideration:restrest,avoid provocative factors,risk factors avoid provocative factors,risk factors controlcontrol2.Drug therapy:2.Drug therapy:prevent MI and death prevent MI and death symptom relief and quality of life
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