qianjy冠心病英文ppt课件

1、Atherosclerosis &Coronary heart diseasesFudan University, Zhongshan HospitalDept. of Cardiology, Shanghai Institute of CVDJuying Qian, M.D.qian.juyingzs-hospital.sh2021 Cardiovascular DiseasesCoronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia, anoxaemiaCorona

2、ry heart disease, CHDIschemic heart diseaseAtherosclerosisStable angina pectoris(SAP)Acute coronary syndromeUnstable angina(UAP) and non-STEMI (UA/NSTEMI)ST elevation myocardial infarction(STEMI)elevation .elivein Atherosclerosis.rusklirusisleading cause of death and disabilityCommon location:Corona

3、rykr.neri circulation: Proximalprksiml left anteriorntiri descendingdisendi coronary artery(LAD)Proximal portion of renal arteriesExtracranial.ekstrkreini:l 颅外的颅外的circulation to the brainCarotid颈动颈动 krtid bifurcationAtherosclerosisThree fundamental biological processes of atherosclerosisAccumulation

4、 of intimalintml cells:smooth muscle cells Macrophagesmkrfeid T-lymphocyteslimfsaitProliferatedprlif.reit connective tissue matrixmeitriks 结缔组织基质结缔组织基质增生增生 : collagenkldnelasticilstik fibersproteoglycans.prutiuglaikns蛋白蛋白聚糖聚糖 3. Accumulation of lipid:cholesteryl estersist free cholesterolklst,rol Hy

5、pothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory克隆克隆(选择选择)学说学说 the response-to-injury hypothesis Atherosclerosis-HypothesisResponse-to-injury Atherosclerosis: hypothesisHigh blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substanceendothel

6、ium damage, metergasis(vasoactive substance, adhesion and aggregation of monocytes-foam cell, platelets)Lipidoses, growth factor, proliferation of smooth mucle cells, collagen, lipolytic enzyme, atherosclerosisPathology and pathophysiologyFatty steakFibrous plaqueComplicated lesionli:nAtherosclerosi

7、sAtherosclerosisInitiation of AtherosclerosisFatty steak formationInitiation of AtherosclerosisFatty steak formation Lipoprotein.lippruti:n oxidation Nonenzymaticnnenzaimtik glycationLeukocyte recruitmentrikru:tmnt Foam cell formationAtheroma evolution: fibrous plaquepl:k Atheroma evolution and comp

8、licationsAtheroma evolution:Involvement of arterial smooth-muscle cellsBlood coagulationkugjuleinmicrovesselsmaikruveslAtheroma evolution and complicationsComplicated lesionli:n: thrombosisAtheroma evolution and complicationsAtheroma evolution and complicationsIntravascular ultrasoundltr.saund Class

9、icification of atherosclerotic lesion using IVUSClinicl stages and classificationAbsence of symptom or stage of delitescencedeilitesns埋伏埋伏ischemianecrosis(targett:git organ )fibrosisAtherosclerosisGeneral manifestationAortic atherosclerosisCoronary artery atherosclerosisCerebralseribrl atheroscleros

10、isRA atherosclerosisMesentericmesnterik atherosclerosisPeripheralprifrl artery atherosclerosisAtherosclerosisclinical manifestation laboratory lbrtri examinationLack of sensitive and specific methods for early diagnosis.daignusisDyslipidemiadislipidemi：X-ray：DSA show severity of stenosisDoppler ultr

11、asound: blood flowradionuclide： detection of ischemiaEchocardiogram： CHDECG and stress test: CHDNew techniques: intravascular ultrasound, angioscopeCT, MRIAtherosclerosisRisk factors and prevention1.Lifestyle modification2.Lipid disorders (Dyslipidemia): cholesterol screening in all 20yrsElevated: c

12、holesterol (Tc and LDL-c), TG, ApoB/ApoA,Lp(a), Low: HDL-c LDL lowering 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, OGTTDiabetes mellitus(DM):RR 1.9 for male, 3.3 for fe

13、male more diffuse lesion.CAD equivalent 75-80% cause of death in adult DM are vascular diseases: CAD, cerebrovascular disease, or peripheral vascular diseaseRisk factors and prevention7 years incidence of death/non-fatal MI (East West Study)* These patients had no history of myocardial infarction Ha

14、ffner SM, et al. N Engl J Med. 2019;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 yrs8. Male gender/ postmenopausal state：male:femal

15、e = 2：1, man develop CHD 10-15 yrs earlier than woman9. alcohol10. Others: diet,homocysteine, hemostatic factors inflammation/infectionRisk factors and prevention Drug therapy：anti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazolLipid-lowering Risk factors and preventio

16、nHMG-CoA reductase inhibitorsstatins） Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,Simvastatin,Cerivastatin, Rosuvastatin： *elevation of aminopherase, rhabdomyolysis2. Bile acid-binding Resins cholestyramine，colestipol3. Nicotinic Acid：4. Fibric acid derivativesfibrates） Gemifibrozil, clofibrate,

17、 Fenofibrate5. Cholesterol absorption inhibitors: ezetimibe6. ProbucolLipid-lowering drugsA: aspirin,ACEIB: blood pressure, -blocker, C: cigarette smoking, CholesterolD: diet, diabetesE: exercise, educationPrevention of CADThird Report of the National Cholesterol Education Program (NCEP) Expert Pane

18、l on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults ATP III (adult treatment panel III)Circulation 2019 17/24: 3144-3373AtherosclerosisCoronary heart disease(CHD)Coronary heart disease (CHD)most common cause: obstruction of atheromatous plaqueother causes: spasm arterial th

19、rombi coronary emboli ostial narrowing due to luetic aortitis congential abnormalitieds severe LV hypertrophy Factors effect myocardial oxygen supply and demandOxygen supplyOxygen demandHeart rateMyocardial contractilitySystolic wall stressoxygen carryingcapacity of bloodCoronary blood flowVascular

20、resistanceExtravascular compressive forcesautoregulationMetabolic regulationHumoral factorNeural regulationDuration of diastolePressure gradientEndothelial controlCoronary heart disease Type： slient ischemia: delitescence： (ECG change)Angina pectoris： angina, caused by myocardial ischemia myocardial

21、 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 mycardial ischemiaSudden death： sudden card

22、iac arrest caused deathCoronary heart disease (CHD) Type： slient ischemia: delitescenceAngina pectoris： myocardial infarction：Ischemic cardiomyopathy (Heart failure and arrhythmia) Sudden death Acute Coronary Syndrome(ACS)Resting ischemiaNon-ST elevationSTelevationUnstable angina Non-Q wave AMIQ wav

23、e AMI*positive serum cardiac markers *# occasionally variant anginaStable angina pectoris(SAP)definition: acute and transient myocardial ischemia and anoxaemia usually caused by coronary insufficiency during exertionCharacteristics: paroxysmal precordial squeezing-like chest pain, behind the mid ste

24、rnum，radiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates Stable angina pectorisFactors effect myocardial oxygen supply and demandOxygen supplyOxygen demandHeart rateMyocardial contractilitySystolic wall stressoxygen carryingcapacity of bloodC

25、oronary blood flowVascular resistanceExtravascular compressive forcesautoregulationMetabolic regulationHumoral factorNeural regulationDuration of diastolePressure gradientEndothelial control hypoxia Coronary stenosis(others:aortic valve disease, HOCM, MB) +precipitation Myocardial oxygen demandHRXSB

26、Pincreased myocardial hypoxiaacumulation of metabolic product, stimulate C1-5 to cause the sensation of chest pain Stable angina pectorismechanismin angiographySignificant coronary lesion with diameter stenosis 70% in 75% ptsNo significant stenosis in about 5-10% pts, Ischemia may be related to coro

27、nary spasm or microvascular dysfunction. PathologyStable angina pectorispathophysiology1.Metabolic and electrophysiologyATP reduced, accumulation of acid substances Dysfunction of iron pump (Na+-K+, and Na+-Ca+) Early depolarization (ST deviation) 2.LV function and hemodynamic situation LV contracti

28、lity and speed, systolic BP, stroke volume, cardiac output decreased LVED pressure and volume Stunning of myocardiumStable 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 armAtypic

29、al 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 agitat

30、ion。duration：35 minspain relief: within several mins after rest or using nitroglycerin Clinical manifestationStable angina pectorisPhysical examinationincreased HR, elevated BP anxiety zaiticrymo-skin, sweatingoccasionallykeinli gallop rhythm，transient systolic murmurClinical manifestationStable ang

31、ina pectorisLaboratory1.ECG：at rest During chest pain: ST-T change found in 95% ptsHolter: detect of slient ischemiaStress test:indication：suspection of CHD, pre- and post- CABG and PCI, pts with OMIcontraindication：AMI, UAP,myocarditis, Hypertension, heart failure,aortic stenosis, HOCM, sever arrhy

32、thmia, aortic aneurysmEnd of the test：ST or 0.2mV，AP attacks，BP220mmHg，BP drop，ventricular arrhythmiaCriteria for positive: ST segment depression 0.1mV，last 2 minsStable angina pectorisStress testrestExersciseStable angina pectoris 2.Echocardiography: 3. Scintigraphy assessment: TL201，Tc99m-sestamib

33、i myocardial perfusion scintigraphy 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUS、intracoronary Doppler flow 、intracoronary pressureLaboratoryStable angina pectorisCoronary AngiographyTyping of angina pectoris1.exertional angina：（：（provocated by the increase of myocardial oxy

34、gen demand）stable anginarecent onset anginaprogressive (deteriorative) angina 2.spontaneous angina：（：（not related to the increase of myocardial oxygen demand）angina decubitusvariant angina pectoris(Prinzmetal angina)acute coronary insufficiencypostinfarction angina pectoris3.mixed angina： New typing

35、: stable and unstable angian pectorisAngina Pectoris1.Cardiogenic pain：aortic dissection, HOCM, aortic stenosis2.Throacic- respiratory：PE, pneumothorax, pleuritis 3.Gastrointestinal: gastro-esophageal diseases, Hiatal hernia, cholecystitis, peptic ulceration, pancreatitis4.Neuromuscular/skeletal ：Ti

36、etze Syndrome (Costochondritis), intercostal neuralgia, Herpes zoster5.Psychologic: anxiety, depression, panic attacks Stable angina pectorisDiagnosisChest pain, risk factors, ECG evidence of ischemia during chest pain, angiographyDifferentiationChest pain, risk factors, ECG, angiographyDifferentiat

37、ion: 1.Cardiogenic pain：aortic dissecion, myocarditis, pericarditis, myocardiopathy, severe valvular diseases (aortic stenosis）2.Throacic- respiratory：pulmonary embolism, infarction, pneumothorax, pleuritis, intrathoracic malignancy, pneumonia3.Gastrointestinal:gastroesophageal reflux, esophagitis,

38、esophageal spasm, Hiatal hernia, cholecystitis, gallstones, peptic ulcer disease, Pancreatitis4.Neuromuscular/skeletal ：Tietze Syndrome(Costochondritis),intercostal neuralgia, Cervical or thoracic degenerative arthristis, cardiac causalgia, Herpes zoster5.Psychologic: anxiety, depression, panic atta

39、cks DiagnosisStable angina pectorisFunctional classification of SAP(CCS )CCS 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

40、 blocks,climbing more than stairs of 3rd floor. CCS III： Marked limitation 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 pectorisGeneral consideration：rest，a

41、void provocative factors , risk factors control2. Drug therapy: 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 pectorisantian

42、ginal and anti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.nitratesb.beta-adrenergic blockersc.Calcium antagonistsd.Drugs improving metabolismStable angina pectorisDrug therapya.nitrateslower oxygen demand: decrease arteriolar and venous tone, reduce preload and afterload increase corona

43、ry supply: Coronary dilatationNitroglycerinIsosorbide dinitrateisosorbide 5-mononitrate (long-acting nitrates)Stable angina pectorisb. blockers: reduce myocardial oxygen: reduce HR, myocardial contractility, BP,the LV wall stress Abslute contraindications：sever bradycardia: high-degree A-V block, SS

44、S, severe unstable LV failureRelative contraindications:asthma and bronchospastic disease peripheral vascular disease 1-selective：metoprolol, atenolol, bisoprololDrug therapyStable angina pectorisc.Calcium antagonists：Increase oxygen supply: dilate conduit and resistance vessels, release spasm, impr

45、ove microvascular functionDecrease oxygen demand: negative inotropic effect, decrease BP Antiplatelet effect d. Drugs improving metabolism：trimethazinevasorel），），selectively inhibit 3-KAT3-酮酰辅酶酮酰辅酶A硫解酶），硫解酶），partly inhibit FA oxidation, Drug therapyStable angina pectorisprevent MI and death therapya

46、.antiplatelet angents：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 pectorisstentingStable angina pectorisUnstable angi

47、na(UAP) and non-STEMIResting ischemiaNon-ST elevationSTelevationUnstable angina Non-Q wave AMIQ wave AMI*positive serum cardiac markers *# occasionally variant anginaAcute Coronary Syndrome(ACS)Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0-1%75%90%Increased FP

48、A/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-STEMIOccuring at rest (or with mininal exertion)ectoris: last 20 minssever and of new-onset: within 1-2 months, CCS II

49、IOccuring 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-STEMIBraunwald classification of unstable anginaSeverity：Class I：New-onset, or a

50、ccelerated 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-STEMIBraunwald classification of unstable anginaClinical Circumstances Class A

51、：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)UAP and non-STEMImechanism： 1.plaque r

52、upture 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: ST depression last 12 hrCardiac biomarkers of myocardium dama

53、ge: cTnT, cTnICK-MBUAP and non-STEMIRisk stratification：TIMI Risk ScoreAge =65yrsMore than 3 coronary risk factorsPrior angiographic coronary obstructionST-segment deviation 0.5 mmMore than 2 angina events within 24 hoursDevelopment of UA/NSTEMI while on aspirinElevated cardiac markersAntaman, JAMA

54、2000; 284:835-42TIMI IIB, ESSENCE, PRISM-PLUS,TACTICS-TIMI18UAP and non-STEMITreatment 1.Genearl management: rest, oxygen, CCU2. Drug therapy A. Anti-ischemic drug: intravenously, orallynitrates -blocker calciumklsim antagnoist: first choice for variant anginaMorphine sulfateUAP and non-STEMITreatme

55、nt 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)Direc

56、t anti-thrombin drug: bivalirudin, hirudin UAP 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 sublingualsbligwl nitroglycerin, retrosternalretrust:nl in location, sweating, scared,

57、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.epigstrim腹上部腹上部 pain and abdominal disordersSTEMIClinical manifestationsymptomsGeneral：fever、HR increase、WBC ，ESR fastingGastrointestinal symptom：

58、nausean:i, vomitingvmiti呕吐呕吐 , arrhythmias：VPs、AV block, atrial arrhythmias occurred more often in patients with HFHeart failure: mainly acute LV failure, may developedivelp RV failure. Initial RV failure occure in patients with RV infarction, associated with hypotensionHypotension and shock：SBP80mm

59、Hg 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 edemai:di:m, rales over 50% of lung fields Class IV: cardiogenic shockClassification based on invasive hemodynamic monitoringClass I：Normal, PCWP 2.2；Class II: Pulmonary congestion, PCWP 18. CI 2.2；Class III: peripheral hypoperfusion, PCWP 18, CI 18, CI 0.2mV in at lea