qianjy冠心病英文PPT课件

1、Coronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia, anoxaemiaCoronary heart disease, CHDIschemic heart disease第1页/共116页AtherosclerosisStable angina pectoris(SAP)Acute coronary syndromeUnstable angina(UAP) and non-STEMI (UA/NSTEMI)ST elevation myocardial infarctio

2、n(STEMI)elevation .elivein第2页/共116页Atherosclerosis.rusklirusis第3页/共116页leading cause of death and disabilityCommon location:Coronarykr.neri circulation: Proximalprksiml left anteriorntiri descendingdisendi coronary artery(LAD)Proximal portion of renal arteriesExtracranial.ekstrkreini:lcirculation to

3、 the brainCarotid颈动 krtid bifurcationAtherosclerosis第4页/共116页Three fundamental biological processes of atherosclerosis1. Accumulation of intimalintml cells:smooth muscle cells MacrophagesmkrfeidT-lymphocyteslimfsait2. Proliferatedprlif.reit connective tissue matrixmeitriks 结缔组织基质增生: collagenkldnelas

4、ticilstik fibersproteoglycans.prutiuglaikns3. Accumulation of lipid:cholesteryl estersist free cholesterolklst,rol 第5页/共116页Hypothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory克隆(选择)学说 the response-to-injury hypothesis Atherosclerosis-Hypothesis第6页/共116页Response

5、-to-injury Atherosclerosis: hypothesisHigh blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substanceendothelium damage, metergasis(vasoactive substance, adhesion and aggregation of monocytes-foam cell, platelets)Lipidoses, growth factor, proliferation of smooth mucle cells, coll

6、agen, lipolytic enzyme, atherosclerosis第7页/共116页Pathology and pathophysiologyFatty steakFibrous plaqueComplicated lesionli:nAtherosclerosis第8页/共116页Initiation of AtherosclerosisFatty steak formation第9页/共116页Initiation of AtherosclerosisFatty steak formation Lipoprotein.lippruti:n oxidation Nonenzyma

7、ticnnenzaimtik glycationLeukocyte recruitmentrikru:tmntFoam cell formation第10页/共116页Atheroma evolution: fibrous plaquepl:kAtheroma evolution and complications第11页/共116页Atheroma evolution:Involvement of arterial smooth-muscle cellsBlood coagulationkugjuleinmicrovesselsmaikruveslAtheroma evolution and

8、 complications第12页/共116页Complicated lesionli:n: thrombosisAtheroma evolution and complications第13页/共116页Atheroma evolution and complications第14页/共116页Intravascular ultrasoundltr.saund第15页/共116页Classicification of atherosclerotic lesion using IVUS第16页/共116页Clinicl stages and classificationAbsence of

9、symptom or stage of delitescencedeilitesnsischemianecrosis(targett:git organ )fibrosisAtherosclerosis第17页/共116页General manifestationAortic atherosclerosisCoronary artery atherosclerosisCerebralseribrl atherosclerosisRA atherosclerosisMesentericmesnterik atherosclerosisPeripheralprifrl artery atheros

10、clerosisAtherosclerosisclinical manifestation第18页/共116页 laboratory lbrtri examinationLack of sensitive and specific methods for early diagnosis.daignusisDyslipidemiadislipidemi：X-ray：DSA show severity of stenosisDoppler ultrasound: blood flowradionuclide： detection of ischemiaEchocardiogram： CHDECG

11、and stress test: CHDNew techniques: intravascular ultrasound, angioscopeCT, MRIAtherosclerosis第19页/共116页Risk factors and prevention1.Lifestyle modification2.Lipid disorders (Dyslipidemia): cholesterol screening in all 20yrsElevated: cholesterol (Tc and LDL-c), TG, ApoB/ApoA,Lp(a), Low: HDL-c LDL low

12、ering by HMG-CoA reductase(statins):cardiovascular events 30%，risk of MI 62%3.Hypertension：4.DM,Metabolic syndrome or insulin resistance syndrome: BP, BMI ,TG, serum insulin HDL-c, OGTT第20页/共116页Diabetes mellitus(DM):RR 1.9 for male, 3.3 for female more diffuse lesion.CAD equivalent 75-80% cause of

13、death in adult DM are vascular diseases: CAD, cerebrovascular disease, or peripheral vascular diseaseRisk factors and prevention第21页/共116页7 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

14、.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 yrs8. Male gender/ postmenopausal state：male:female = 2：1, man develop CHD 10-15 yrs earlier tha

15、n woman9. alcohol10. Others: diet,homocysteine, hemostatic factors inflammation/infectionRisk factors and prevention第23页/共116页 Drug therapy：anti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazolLipid-lowering Risk factors and prevention第24页/共116页1. HMG-CoA reductase inhi

16、bitors（statins） Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,Simvastatin,Cerivastatin, Rosuvastatin： *elevation of aminopherase, rhabdomyolysis2. Bile acid-binding Resins cholestyramine，colestipol3. Nicotinic Acid：4. Fibric acid derivatives（fibrates） Gemifibrozil, clofibrate, Fenofibrate5. Choles

17、terol absorption inhibitors: ezetimibe6. ProbucolLipid-lowering drugs第25页/共116页A: aspirin,ACEIB: blood pressure, -blocker, C: cigarette smoking, CholesterolD: diet, diabetesE: exercise, educationPrevention of CAD第26页/共116页Third Report of the National Cholesterol Education Program (NCEP) Expert Panel

18、 on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults ATP III (adult treatment panel III)Circulation 2002 17/24: 3144-3373Atherosclerosis第27页/共116页Coronary heart disease(CHD)第28页/共116页Coronary heart disease (CHD)most common cause: obstruction of atheromatous plaqueother causes

19、: spasm arterial thrombi coronary emboli ostial narrowing due to luetic aortitis congential abnormalitieds severe LV hypertrophy 第29页/共116页Factors effect myocardial oxygen supply and demandOxygen supplyOxygen demandHeart rateMyocardial contractilitySystolic wall stressoxygen carryingcapacity of bloo

20、dCoronary blood flowVascular resistanceExtravascular compressive forcesautoregulationMetabolic regulationHumoral factorNeural regulationDuration of diastolePressure gradientEndothelial control第30页/共116页Coronary heart disease Type： slient ischemia: delitescence： (ECG change)Angina pectoris： angina, c

21、aused by myocardial ischemia myocardial infarction：acute myocardial ischemic necrosis caused by the occlusion of coronary arteryIschemia cardiomyopathy (Heart failure and arrhythmia)： cardiac enlargement, heart failure, arrhythmia, caused by the myocardial fibrosis as the consequence of chronic myca

22、rdial ischemiaSudden death： sudden cardiac arrest caused death第31页/共116页Coronary heart disease (CHD) Type： slient ischemia: delitescenceAngina pectoris： myocardial infarction：Ischemic cardiomyopathy (Heart failure and arrhythmia) Sudden death 第32页/共116页Acute Coronary Syndrome(ACS)Resting ischemiaNon

23、-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers *# occasionally variant angina第33页/共116页Stable angina pectoris(SAP)第34页/共116页definition: acute and transient myocardial ischemia and anoxaemia usually caused by coronary insufficiency during exertionCharac

24、teristics: paroxysmal precordial squeezing-like chest pain, behind the mid sternum，radiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates Stable angina pectoris第35页/共116页Factors effect myocardial oxygen supply and demandOxygen supplyOxygen deman

25、dHeart rateMyocardial contractilitySystolic wall stressoxygen carryingcapacity of bloodCoronary blood flowVascular resistanceExtravascular compressive forcesautoregulationMetabolic regulationHumoral factorNeural regulationDuration of diastolePressure gradientEndothelial control第36页/共116页 hypoxia Cor

26、onary stenosis(others:aortic valve disease, HOCM, MB) +precipitation Myocardial oxygen demand（HRXSBP）increased myocardial hypoxiaacumulation of metabolic product, stimulate C1-5 to cause the sensation of chest pain Stable angina pectorismechanism第37页/共116页in angiographySignificant coronary lesion wi

27、th 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 pectoris第38页/共116页pathophysiology1.Metabolic and electrophysiologyATP reduced, accumulation of acid substances Dysfunction of

28、iron pump (Na+-K+, and Na+-Ca+) Early depolarization (ST deviation) 2.LV function and hemodynamic situation LV contractility and speed, systolic BP, stroke volume, cardiac output decreased LVED pressure and volume Stunning of myocardiumStable angina pectoris第39页/共116页symptom：chest pain or oppression

29、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 pectoris第40页/共116页chest paincharacteristics：tightness, squeezing, burning, pressing, choking,

30、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 pectoris第41页/共116页Physical examinatio

31、nincreased HR, elevated BP anxiety zaiticrymo-skin, sweatingoccasionallykeinli gallop rhythm，transient systolic murmurClinical manifestationStable angina pectoris第42页/共116页Laboratory1.ECG：at rest During chest pain: ST-T change found in 95% ptsHolter: detect of slient ischemiaStress test:indication：s

32、uspection of CHD, pre- and post- CABG and PCI, pts with OMIcontraindication：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 arrhythmiaCriteria for positive: ST segment depre

33、ssion 0.1mV，last 2 minsStable angina pectoris第43页/共116页Stress testrestExersciseStable angina pectoris第44页/共116页 2.Echocardiography: 3. Scintigraphy assessment: TL201，Tc99m-sestamibi myocardial perfusion scintigraphy 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUS、intracoronary

34、Doppler flow 、intracoronary pressureLaboratoryStable angina pectoris第45页/共116页Coronary Angiography第46页/共116页Typing of angina pectoris1.exertional angina：（provocated by the increase of myocardial oxygen demand）stable anginarecent onset anginaprogressive (deteriorative) angina 2.spontaneous angina：（no

35、t related to the increase of myocardial oxygen demand）angina decubitusvariant angina pectoris(Prinzmetal angina)acute coronary insufficiencypostinfarction angina pectoris3.mixed angina： New typing: stable and unstable angian pectorisAngina Pectoris第47页/共116页1.Cardiogenic pain：aortic dissection, HOCM

36、, aortic stenosis2.Throacic- respiratory：PE, pneumothorax, pleuritis 3.Gastrointestinal: gastro-esophageal diseases, Hiatal hernia, cholecystitis, peptic ulceration, pancreatitis4.Neuromuscular/skeletal ：Tietze Syndrome (Costochondritis), intercostal neuralgia, Herpes zoster5.Psychologic: anxiety, d

37、epression, panic attacks Stable angina pectorisDiagnosisChest pain, risk factors, ECG evidence of ischemia during chest pain, angiographyDifferentiation第48页/共116页Chest pain, risk factors, ECG, angiographyDifferentiation: 1.Cardiogenic pain：aortic dissecion, myocarditis, pericarditis, myocardiopathy,

38、 severe valvular diseases (aortic stenosis）2.Throacic- respiratory：pulmonary embolism, infarction, pneumothorax, pleuritis, intrathoracic malignancy, pneumonia3.Gastrointestinal:gastroesophageal reflux, esophagitis, esophageal spasm, Hiatal hernia, cholecystitis, gallstones, peptic ulcer disease, Pa

39、ncreatitis4.Neuromuscular/skeletal ：Tietze Syndrome(Costochondritis),intercostal neuralgia, Cervical or thoracic degenerative arthristis, cardiac causalgia, Herpes zoster5.Psychologic: anxiety, depression, panic attacks DiagnosisStable angina pectoris第49页/共116页Functional classification of SAP(CCS )C

40、CS I： no chest pain at ordinary activity. Angina at strenuous or rapid or prolonged exertionCCS II： Slight limitation of ordinary activity. Walking or climbing stairs rapidly, after meals, in cold, in wind. Walking more than 2 blocks,climbing more than stairs of 3rd floor. CCS III： Marked limitation

41、 of ordinary activity. Walking 1 to 2 blocks, climbing stairs of 3rd floor CCS IV：Inability to carry on any activity without discomfortanginal symdrome may be present at rest. Stable angina pectoris第50页/共116页1. General consideration： rest，avoid provocative factors , risk factors control2. Drug thera

42、py: prevent MI and death symptom relief and quality of life improvment3. Coronary revascularization: percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, LIMAPrevention and treatmentStable angina pectoris第51页/共116页antianginal and anti-ischemic therapyDrug therapyOxygen

43、 supplyOxygen demanda.nitratesb.beta-adrenergic blockersc.Calcium antagonistsd.Drugs improving metabolismStable angina pectoris第52页/共116页Drug therapya.nitrateslower oxygen demand: decrease arteriolar and venous tone, reduce preload and afterload increase coronary supply: Coronary dilatationNitroglyc

44、erinIsosorbide dinitrateisosorbide 5-mononitrate (long-acting nitrates)Stable angina pectoris第53页/共116页b. 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 failure

45、Relative contraindications:asthma and bronchospastic disease peripheral vascular disease 1-selective：metoprolol, atenolol, bisoprololDrug therapyStable angina pectoris第54页/共116页c.Calcium antagonists：Increase oxygen supply: dilate conduit and resistance vessels, release spasm, improve microvascular f

46、unctionDecrease oxygen demand: negative inotropic effect, decrease BP Antiplatelet effect d. Drugs improving metabolism：trimethazine（vasorel），selectively inhibit 3-KAT（3-酮酰辅酶A硫解酶），partly inhibit FA oxidation, Drug therapyStable angina pectoris第55页/共116页prevent MI and death therapya.antiplatelet ange

47、nts：ASA，75-325mg/dclopidogrel; ticlopidine: ADP receptor- antagonists:Cilostazol: phosphodiesterase inhititor,50-100mg bidb. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI)Drug therapyStable angina pectoris第56页/共116页stentingStable angina pectoris第57页/共116页Unstable an

48、gina(UAP) and non-STEMI第58页/共116页Resting ischemiaNon-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers *# occasionally variant anginaAcute Coronary Syndrome(ACS)第59页/共116页Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0

49、-1%75%90%Increased FPA/TAT0-5%60-80%80-90%Activated platelets0-5%70-80%80-90%Acute coronary occlusion0-1%10-25%90%mortality1-2%3-8%6-15%FPA：fibrinopeptide ATAT：thrombin-antithrombin complexesUAP and non-STEMI第60页/共116页Occuring at rest (or with mininal exertion)ectoris: last 20 minssever and of new-o

50、nset: within 1-2 months, CCS IIIOccuring with a crescendo pattern: Deterioration of CCS classfication, at least CCS IIIvariant angina pectoris (Prinzmetal angina): transient ST elevation, caused by the coronary spasm Definition (main type)UAP and non-STEMI第61页/共116页Braunwald classification of unstab

51、le 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) UAP and non-STEMI第62页/共116页Braunwald classificati

52、on 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 d

53、ocumented MI)UAP and non-STEMI第63页/共116页mechanism： 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-STEMI第64页/共116页ECG:N

54、on-STEMI: ST depression last 12 hrCardiac biomarkers of myocardium damage: cTnT, cTnICK-MBUAP and non-STEMI第65页/共116页Risk stratification：TIMI Risk ScoreAge =65yrsMore than 3 coronary risk factorsPrior angiographic coronary obstructionST-segment deviation 0.5 mmMore than 2 angina events within 24 hou

55、rsDevelopment of UA/NSTEMI while on aspirinElevated cardiac markersAntaman, JAMA 2000; 284:835-42TIMI IIB, ESSENCE, PRISM-PLUS,TACTICS-TIMI18UAP and non-STEMI第66页/共116页Treatment 1.Genearl management: rest, oxygen, CCU2. Drug therapy A. Anti-ischemic drug: intravenously, orallynitrates -blocker calci

56、umklsim antagnoist: first choice for variant anginaMorphine sulfateUAP and non-STEMI第67页/共116页Treatment 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:

57、 used in pts planned to PCI b. Anticoagulation therapy:HeparinLow molecular weight heparin(LMWH)Direct anti-thrombin drug: bivalirudin, hirudin UAP and non-STEMI第68页/共116页Treatment 2. Drug therapy: C. other medical therapy a. lipid-lowering drugs: statins, early use(in first 24 hrs) LDL-c target: 30

58、 mins，less effective of sublingualsbligwl nitroglycerin, retrosternalretrust:nl 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)alertl:t the epigastrium.epigstrimpain and abdominal disorde

59、rsSTEMIClinical manifestation第86页/共116页symptomsGeneral：fever、HR increase、WBC ，ESR fastingGastrointestinal symptom：nausean:i, vomitingvmiti, arrhythmias：VPs、AV block, atrial arrhythmias occurred more often in patients with HFHeart failure: mainly acute LV failure, may developedivelp RV failure. Initi

60、al RV failure occure in patients with RV infarction, associated with hypotensionHypotension and shock：SBP80mmHg after pain release, RV infarctionSTEMIClinical manifestation第87页/共116页Pump failureClassification based on clinical examination(Killip)Class I：no HF, rales and S3 absent；Class II: mild HF，rales