冠狀動脈粥樣硬化性心臟病英文課件

1、Coronary Atherosclerotic Heart Diseases Affiliated Hospital of Jining Medical CollegeDept.of Cardiac Care Unit Guoxia Dong 26/30/2022ContentsAtherosclerosisStable Angina PectorisAcute Coronary Syndrome UA and NSTEMI AMI(STEMI) 36/30/2022Self-study Variant AnginaCardiac Syndrome XSilent Myocardial Is

2、chemia Myocardial Bridging46/30/2022What Is Atherosclerosis?nAtherosclerosis is the descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries. 56/30/2022What Is Coronary Heart Disease?66/30/2022Coronary heart diseaseatherosclerosisCoronary stenosiscoro

3、nary spasmMyocardial ischemia, necrosisIschemic heart disease76/30/202286/30/2022Atherosclerosis96/30/2022Foam cellFatty steak atheromatous plaqueruptured plaquesFibrous plaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al. Circulation 1995;92:1355-1374.medium dama

4、ge 6/30/202210What damage does atherosclerosis cause?116/30/2022Common locationnCoronary Heart DiseasenCarotid Artery DiseasenPeripheral Arterial DiseasenChronic Kidney Disease126/30/2022How does atherosclerosis start and progress?136/30/2022nElevated levels of cholesterol and triglycerides in the b

5、loodnHigh blood pressurenCigarette smoking146/30/2022Biological processes1. Accumulation of intimal cells smooth muscle cells Macrophages T-lymphocytes156/30/2022Biological processes2. Proliferated connective tissue matrix collagen elastic fibers proteoglycans166/30/2022Biological processes3.Accumul

6、ation of lipid176/30/2022Atherosclerosis-HypothesisHypothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory The response-to-injury hypothesis 186/30/2022nHigh blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance.nPlatelets are activated, ad

7、hesion and aggregation of platelets.nLipidoses, growth factor, proliferation of smooth mucle cells, collagen, lipolytic enzyme.Response-to-injury 196/30/2022Pathology and pathophysiologyFatty steakFibrous plaqueComplicated lesion206/30/2022Initiation of AtherosclerosisFatty steak formation216/30/202

8、2Initiation of Atherosclerosis226/30/2022fibrous plaque236/30/2022246/30/2022256/30/2022Thin CapVulnerable Plaque ThrombusUnstable “ Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina “ Dormant Volcano ”SAPACSpressure or a squeezing pain !266/30/2022Unstable and Stable Plaque

9、sunstablestable6/30/202228AtherosclerosisnClinical stages Absence of symptom or stage of incubationischemianecrosis(target organ )fibrosis296/30/2022clinical manifestationuGeneral manifestationuAortic atherosclerosisuCoronary artery atherosclerosisuCerebral atherosclerosisuRA atherosclerosisuMesente

10、ric atherosclerosisuPeripheral artery atherosclerosis306/30/2022Laboratory ExaminationLack of sensitive and specific methods for early diagnosisDyslipidemiaX-ray：DSA show severity of stenosisDoppler ultrasound: blood flow316/30/2022Laboratory Examinationradionuclide： detection of ischemiaEchocardiog

11、ram： CHDECG and stress test: CHDAngiography: the most direct wayIntravascular ultrasound, angioscopeCT, MRI326/30/2022Risk factors n1.Lipid disorders (Dyslipidemia)nIncreased cholesterol :Tc and LDL-c, TG, ApoB,Lp(a)nDecreased cholesterol: HDL-c apoAn2.Hypertension336/30/2022Risk factors n3.DM,Metab

12、olic syndrome or insulin resistance syndrome More diffuse lesion CAD equivalent 75-80% cause of death in adult DM are vascular diseases: CAD, cerebrovascular disease, or peripheral vascular disease346/30/20227 years incidence of death/non-fatal MI (East West Study)* These patients had no history of

13、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/ postmen

14、opausal state：male:female = 2：1, men develop CHD 10-15 yrs earlier than women8. alcohol9. Others: diet,homocysteine, hemostatic factors inflammation/infection366/30/2022Drug therapyanti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazolLipid-lowering HMG-CoA reductase inh

15、ibitors（statins） 376/30/2022Doubts of patients nQuest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?386/30/2022Doubts of patients nQuestion 2：My shape is not fat, lipid is not high, why give me lipid-lowering drugs, made a mistake?396/30/2022Doubts of patients nQuesti

16、on 3：I have coronary heart disease,then should I do less activities in order to protect the heart?406/30/2022Coronary Heart Disease (CHD) 6/30/202241Clinical TypenSilent myocardial ischemianAngina pectorisnMyocardial infarctionnIschemic cardiomyopathynSudden cardiac death 6/30/202242Silent Myocardia

17、l 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

18、 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.6/30/202243Ischemic CardiomyopathynSymptoms of heart failure, caused by ischemic myocardial dysfunction , diffuse fibrosis,

19、 and multiple infarction, alone or in combination.nManifestations: ventricles enlargement (dominant left ventricle), heart failure and arrhythmias.6/30/202244Sudden Cardiac DeathnSCD is natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of acute

20、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 card

21、iac arrest.6/30/202245Acute 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.6/30/202246STABLE ANGINA PECTORIS476/30/2022DefinitionAcute and transient myo

22、cardial ischemia and anoxaemia. Usually caused by coronary insufficiency during exertion.486/30/2022Characteristicsparoxysmal precordial squeezing-like chest pain, behind the mid sternumradiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates 496/

23、30/2022 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 mechanism506/30/2022in angiographySignificant coronary lesion with diameter stenosi

24、s 70% in 75% ptsNo significant stenosis in about 5-10% pts, Ischemia may be related to coronary spasm or microvascular dysfunction. PathologyStable angina pectoris516/30/2022pathophysiology1.Metabolic and electrophysiologyATP reduced, accumulation of acid substances Dysfunction of ion pump (Na+-K+,

25、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 pectoris526/30/2022symptom：chest pain location behind or slightly to the left

26、of the mid sternum no definite borderlineradiated to the left shoulder and upper armAtypical location: lower jaw, the back of neckClinical manifestationStable angina pectoris536/30/2022 character：tightness, squeezing, burning, pressing, choking, bursting,rarely sharpduration：35 minsprecipitating fac

27、tor exertion or emotional agitationpain relief: within several mins after rest or using nitroglycerin Clinical manifestationStable angina pectoris556/30/2022Physical examinationincreased HR, elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifes

28、tationStable angina pectoris566/30/2022 Auxiliary examination1.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

29、failure,aortic stenosis, HOCM, sever arrhythmia, aortic aneurysmEnd of the test：ST or 0.2mV，AP attacks，BP220mmHg，BP drop，ventricular arrhythmiaStable angina pectoris576/30/2022Stress testrestExersciseStable angina pectoris586/30/2022 2.Echocardiography: 3. Scintigraphy assessment: Can detect filling

30、 defect of Infarction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUSAuxiliary examinationStable angina pectoris596/30/2022Coronary Angiography606/30/2022Stable Angina PectorisDiagnosisuChest painurisk factorsuECG evidence of ischemia during chest painu angiography616/30/2

31、022Cardiovascular causesNoncardiac causesStable Angina PectorisDifferential diagnosis626/30/2022Cardiovascular causenMyocardial infarction nPericarditis nAortic dissection nPulmonary embolism nPulmonary hypertension 636/30/2022Noncardiac causenPneumonia with pleurisy nSpontaneous pneumothorax nMuscu

32、loskeletal disordersnHerpes zoster nEsophageal reflux nPeptic ulcer 646/30/20221. General treatment： risk factors control2. Drug therapy3. Coronary revascularization: percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, IMAGTreatmentStable Angina Pectoris656/30/2022Blo

33、od and oxygen supply to the heartMyocardialblood flowMyocardial oxygenconsumption4%of totalcardiac outputsupplied to themyocardium12%of total body oxygen,used at rest bymyocardium6/30/202266Coronary ReserveMyocardialblood flowincreases up to4 times . to meetincreasedmyocardial oxygendemand6/30/20226

34、7Myocardial oxygensupply and demandO2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2 supplyO2 demand6/30/202268Aims of medical therapyArterial vasodilatationReduces arterialresistanceReduces afterloadDecreasessympathetic driveReduce heart rateand contractile forceReduces cardi

35、ac workLVRVDilatation ofcoronary arteriesImproves coronarysupplyVenodilatationReducesvenous returnReduces preload6/30/202269antianginal and anti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris706/3

36、0/2022Drug 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 Pectoris716/30/2022Nitrates in anginaReduce pr

37、eloadthroughvenodilatationReduce afterload bylowering arterialresistanceReduce platelet aggregationIncrease coronary perfusion, includingischaemic areas Reversal of coronary spasm6/30/202272b. blockers: reduce myocardial oxygen: reduce HR, myocardial contractility, BP,the LV wall stress Abslute cont

38、raindications：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 Pectoris736/30/2022c.Calcium antagonists：Increase oxyg

39、en 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 Pectoris746/30/2022prevent MI and death therapya.antiplatelet angen

40、ts：ASAclopidogrelCilostazolb. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI)Drug therapyStable Angina Pectoris756/30/2022stentingStable Angina Pectoris766/30/2022Unstable Angina(UA) and non-STEMI776/30/2022ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMI

41、Q wave AMI*positive serum cardiac markers *# occasionally variant anginaAcute Coronary Syndrome(ACS)786/30/2022Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0-1%75%90%Increased FPA/TAT0-5%60-80%80-90%Activated platelets0-5%70-80%80-90%Acute coronary occlusion 0-

42、1%10-25%90%mortality 1-2%3-8%6-15%FPA：fibrinopeptide ATAT：thrombin-antithrombin complexesUA and non-STEMI796/30/2022Occuring 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 lea

43、st CCS IIIDefinition UA and non-STEMIAngina pectoris or equivalent ischemic discomfort with at least one of the three features806/30/2022 Braunwald classification of unstable anginaSeverity：Class I：New-onset, or accelerated severe anginano rest pain within 2 monthsClass II：Angina at rest, subacute a

44、ngina 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-STEMI816/30/2022 Braunwald classification of unstable anginaClinical Circumstances Class A：Secondary UAPa clearly identified condition extrinsic to the coronary vascu

45、lar 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-STEMI826/30/2022mechanism： 1.plaque rupture and erosion, with nonocclusive thrombus2.dynamic obstructio

46、n: Vasoconstruction 3.progressive mechnial obstruction(rapidly advancing or ISR following stenting) 4.secondary UA InflammationThrombogenesisUA and non-STEMI836/30/2022 ECG:Non-STEMI: ST depression last 12 hrCardiac biomarkers of myocardium damage: cTnT, cTnICK-MBUAP and non-STEMI846/30/2022Treatmen

47、t 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-STEMI856/30/2022Treatment 2. Drug therapy: B. antithrombotic therapy a. Anti-platelet Aspirin: early, 3

48、00mg 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-STEMI866/30/2022Treatment 2. Drug therapy: C. other medical therapy a.