冠状动脉粥样硬化性心脏病英文-课件.ppt

1、Coronary Atherosclerotic Heart Diseases Affiliated Hospital of Jining Medical CollegeDept.of Cardiac Care Unit Guoxia Dong 24/29/2023ContentsAtherosclerosisStable Angina PectorisAcute Coronary Syndrome UA and NSTEMI AMI(STEMI)34/29/2023Self-study Variant AnginaCardiac Syndrome XSilent Myocardial Isc

2、hemia Myocardial Bridging44/29/2023What Is Atherosclerosis?nAtherosclerosis is the descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries.54/29/2023What Is Coronary Heart Disease?64/29/2023Coronary heart diseaseatherosclerosisCoronary stenosiscorona

3、ry spasmMyocardial ischemia,necrosisIschemic heart disease74/29/202384/29/2023Atherosclerosis94/29/2023Foam cellFatty steak atheromatous plaqueruptured plaquesFibrous plaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al.Circulation 1995;92:1355-1374.medium damage 4

4、/29/202310What damage does atherosclerosis cause?114/29/2023Common locationnCoronary Heart DiseasenCarotid Artery DiseasenPeripheral Arterial DiseasenChronic Kidney Disease124/29/2023How does atherosclerosis start and progress?134/29/2023nElevated levels of cholesterol and triglycerides in the blood

5、nHigh blood pressurenCigarette smoking144/29/2023Biological processes1.Accumulation of intimal cells smooth muscle cells Macrophages T-lymphocytes154/29/2023Biological processes2.Proliferated connective tissue matrix collagen elastic fibers proteoglycans164/29/2023Biological processes3.Accumulation

6、of lipid174/29/2023Atherosclerosis-HypothesisHypothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory The response-to-injury hypothesis 184/29/2023nHigh blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance.nPlatelets are activated,adhesion

7、and aggregation of platelets.nLipidoses,growth factor,proliferation of smooth mucle cells,collagen,lipolytic enzyme.Response-to-injury 194/29/2023Pathology and pathophysiologyFatty steakFibrous plaqueComplicated lesion204/29/2023Initiation of AtherosclerosisFatty steak formation214/29/2023Initiation

8、 of Atherosclerosis224/29/2023fibrous plaque234/29/2023244/29/2023254/29/2023Thin CapVulnerable Plaque ThrombusUnstable“Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina“Dormant Volcano”SAPACSpressure or a squeezing pain!264/29/2023Unstable and Stable Plaquesunstablestable4/

9、29/202328AtherosclerosisnClinical stages Absence of symptom or stage of incubationischemianecrosis(target organ)fibrosis294/29/2023clinical manifestationuGeneral manifestationuAortic atherosclerosisuCoronary artery atherosclerosisuCerebral atherosclerosisuRA atherosclerosisuMesenteric atherosclerosi

10、suPeripheral artery atherosclerosis304/29/2023Laboratory ExaminationLack of sensitive and specific methods for early diagnosisDyslipidemiaX-ray：DSA show severity of stenosisDoppler ultrasound:blood flow314/29/2023Laboratory Examinationradionuclide：detection of ischemiaEchocardiogram：CHDECG and stres

11、s test:CHDAngiography:the most direct wayIntravascular ultrasound,angioscopeCT,MRI324/29/2023Risk factors n1.Lipid disorders(Dyslipidemia)nIncreased cholesterol:Tc and LDL-c,TG,ApoB,Lp(a)nDecreased cholesterol:HDL-c apoAn2.Hypertension334/29/2023Risk factors n3.DM,Metabolic syndrome or insulin resis

12、tance syndrome More diffuse lesion CAD equivalent 75-80%cause of death in adult DM are vascular diseases:CAD,cerebrovascular disease,or peripheral vascular disease344/29/20237 years incidence of death/non-fatal MI(East West Study)*These patients had no history of myocardial infarction Haffner SM,et

13、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 1

14、0-15 yrs earlier than women8.alcohol9.Others:diet,homocysteine,hemostatic factors inflammation/infection364/29/2023Drug therapyanti-platelet：aspirin,clopidogrel,GPIIb/IIIa inhitibor,Dipyridamole,cilostazolLipid-lowering HMG-CoA reductase inhibitors（statins）374/29/2023Doubts of patients nQuest 1：My b

15、lood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?384/29/2023Doubts of patients nQuestion 2：My shape is not fat,lipid is not high,why give me lipid-lowering drugs,made a mistake?394/29/2023Doubts of patients nQuestion 3：I have coronary heart disease,then should I do less activi

16、ties in order to protect the heart?404/29/2023Coronary Heart Disease(CHD)4/29/202341Clinical TypenSilent myocardial ischemianAngina pectorisnMyocardial infarctionnIschemic cardiomyopathynSudden cardiac death 4/29/202342Silent Myocardial IschemiaDefined as documented episodes of ischemia not associat

17、ed 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 pra

18、ctice.Some episodes of ischemia are associated with chest discomfort and other episodes are asymptomatic.4/29/202343Ischemic CardiomyopathynSymptoms of heart failure,caused by ischemic myocardial dysfunction,diffuse fibrosis,and multiple infarction,alone or in combination.nManifestations:ventricles

19、enlargement(dominant left ventricle),heart failure and arrhythmias.4/29/202344Sudden 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 de

20、ath 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.4/29/202345Acute Coronary SyndromenACS represents a spectrum of conditions

21、.nAcute plaque change characterized by plaque rupture and exposure of substances that promote platelet activation and thrombin generation.4/29/202346STABLE ANGINA PECTORIS474/29/2023DefinitionAcute and transient myocardial ischemia and anoxaemia.Usually caused by coronary insufficiency during exerti

22、on.484/29/2023Characteristicsparoxysmal precordial squeezing-like chest pain,behind the mid sternumradiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates 494/29/2023 hypoxia Coronary stenosis(others:aortic valve disease,HOCM)+Myocardial oxygen d

23、emand（HRXSBP）increased myocardial hypoxiaacumulation of metabolic product,stimulate C1-5 to cause the sensation of chest pain mechanism504/29/2023in angiographySignificant coronary lesion with diameter stenosis 70%in 75%ptsNo significant stenosis in about 5-10%pts,Ischemia may be related to coronary

24、 spasm or microvascular dysfunction.PathologyStable angina pectoris514/29/2023pathophysiology1.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 contractil

25、ity,systolic BP,stroke volume,cardiac output decreased LVED pressure and volume Stunning of myocardiumStable angina pectoris524/29/2023symptom：chest pain location behind or slightly to the left of the mid sternum no definite borderlineradiated to the left shoulder and upper armAtypical location:lowe

26、r jaw,the back of neckClinical manifestationStable angina pectoris534/29/2023 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 man

27、ifestationStable angina pectoris554/29/2023Physical examinationincreased HR,elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifestationStable angina pectoris564/29/2023 Auxiliary examination1.ECG：Resting ECG ECG during chest pain:ST-T change fo

28、und 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，ventr

29、icular arrhythmiaStable angina pectoris574/29/2023Stress testrestExersciseStable angina pectoris584/29/2023 2.Echocardiography:3.Scintigraphy assessment:Can detect filling defect of Infarction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others:IVUSAuxiliary examinationStable angina

30、 pectoris594/29/2023Coronary Angiography604/29/2023Stable Angina PectorisDiagnosisuChest painurisk factorsuECG evidence of ischemia during chest painu angiography614/29/2023Cardiovascular causesNoncardiac causesStable Angina PectorisDifferential diagnosis624/29/2023Cardiovascular causenMyocardial in

31、farction nPericarditis nAortic dissection nPulmonary embolism nPulmonary hypertension 634/29/2023Noncardiac causenPneumonia with pleurisy nSpontaneous pneumothorax nMusculoskeletal disordersnHerpes zoster nEsophageal reflux nPeptic ulcer 644/29/20231.General treatment：risk factors control2.Drug ther

32、apy3.Coronary revascularization:percutaneous coronary intervention(PCI)Coronary artery bypass surgery(CABG)SVG,IMAGTreatmentStable Angina Pectoris654/29/2023Blood and oxygen supply to the heartMyocardialblood flowMyocardial oxygenconsumption4%of totalcardiac outputsupplied to themyocardium12%of tota

33、l body oxygen,used at rest bymyocardium4/29/202366Coronary ReserveMyocardialblood flowincreases up to4 times.to meetincreasedmyocardial oxygendemand4/29/202367Myocardial oxygensupply and demandO2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2 supplyO2 demand4/29/202368Aims of

34、medical therapyArterial vasodilatationReduces arterialresistanceReduces afterloadDecreasessympathetic driveReduce heart rateand contractile forceReduces cardiac workLVRVDilatation ofcoronary arteriesImproves coronarysupplyVenodilatationReducesvenous returnReduces preload4/29/202369antianginal and an

35、ti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris704/29/2023Drug therapya.Nitrateslower oxygen demand:decrease arteriolar and venous tone,reduce preload and afterload increase coronary supply:Coro

36、nary dilatationNitroglycerinIsosorbide dinitrateisosorbide 5-mononitrate(long-acting nitrates)Stable Angina Pectoris714/29/2023Nitrates in anginaReduce preloadthroughvenodilatationReduce afterload bylowering arterialresistanceReduce platelet aggregationIncrease coronary perfusion,includingischaemic

37、areas Reversal of coronary spasm4/29/202372b.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 periphe

38、ral vascular disease 1-selective：metoprolol,atenolol,bisoprololDrug therapyStable Angina Pectoris734/29/2023c.Calcium antagonists：Increase oxygen supply:dilate conduit and resistance vessels,release spasm,improve microvascular functionDecrease oxygen demand:negative inotropic effect,decrease BP Anti

39、platelet effect d.Drugs improving metabolismDrug therapyStable Angina Pectoris744/29/2023prevent MI and death therapya.antiplatelet angents：ASAclopidogrelCilostazolb.Lipid-lowering angents:statins c.Angiotesin-converting enzyme inhibitor(ACEI)Drug therapyStable Angina Pectoris754/29/2023stentingStab

40、le Angina Pectoris764/29/2023Unstable Angina(UA)and non-STEMI774/29/2023ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers*#occasionally variant anginaAcute Coronary Syndrome(ACS)784/29/2023Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMI

41、Angiographic thrombus0-1%75%90%Increased FPA/TAT0-5%60-80%80-90%Activated platelets0-5%70-80%80-90%Acute coronary occlusion 0-1%10-25%90%mortality 1-2%3-8%6-15%FPA：fibrinopeptide ATAT：thrombin-antithrombin complexesUA and non-STEMI794/29/2023Occuring at rest(or with mininal exertion):last 20 minssev

42、er 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 features804/29/2023 Braunwald classification of unstable angin

43、aSeverity：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-STEMI814/29/2023 Braunwald classification of unstable

44、 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

45、 non-STEMI824/29/2023mechanism：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-STEMI834/29/2023 ECG:Non-STEMI:ST depression

46、 last 12 hrCardiac biomarkers of myocardium damage:cTnT,cTnICK-MBUAP and non-STEMI844/29/2023Treatment 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-STEMI854/29

47、/2023Treatment 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)Dir

48、ect anti-thrombin drug:bivalirudin,hirudin UA and non-STEMI864/29/2023Treatment 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-STEMI874/29/2023Treatment 3.Invasive versus conservat

49、ive 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-STEMI884/29/20234/29/202389Symptoms Suggestive of ACSDefinite ACSNo ST elevationA

50、lgorithm 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