缺血性心脏病教学

北京大学人民医院 心脏中心 孙艺红,Coronary (Ischemic) Heart Disease 冠 心 病 缺血性心脏病,CHD,EpidemiologyPathophysiologyRisk factors and PreventionClinical manifestation,Diagnosis and management,Most common form of heart disease Single most important cause of premature death,Epidemiology,Epidemiology - USA,1/2 deaths (1/2million) 1.5 million MI each year 45% MI under age 65 50-100 billion $ per year,One in 4 men/one in 5 women die from CHD 300 000 people have MI each year 1.7 million people have angina,Epidemiology - UK,The incidence of CHD Eastern Europe Many developing countries China India,Epidemiology,Proportionate Mortality for the Ten Leading Causes of Death in China, 1991-2001,He J 11:1124-34,Pathophysiology,Almost always due to athroma and its complications particularly thrombosis,Occasionally other disorders Congenital anomalies Anomalous origin Fistular/Malformation of a major coronary artery Aortitis Polyarteritis Connective tissue disorders,Pathophysiology,Pathophysiology Atheroma/Atherosclerosis,Diffused disease of the arterial wall Coronary artery at high risk Cerebral / peripheral vascular disease often coexist Radial / Internal mammary artery largely spared,Plaques begin to appear in 2nd and 3rd decade of life The nature/composition of plaques changes,Pathophysiology Plaque Formation 1,Soldiers died in the korean war,77.3% atherosclerosis39% occlusive plaque,ENOS JAMA 1953,300 Cases autopsy (age, 22.1y),Tuzcu Circ 1999,5.07mm2,EEM Area13.2 mm2,Atheroma Area 8.13 mm2,Female,32y,Incidence of atherosclerosis in donor heart,Pathophysiology Plaque Formation 2,Fatty streaks develope migrate into intima take-up oxidised LDL from plasma become lipid-laden foam cells,CirculatingMonocytes,Pathophysiology Plaque Formation 3,Lipid Pool Foam cells die The contents release,Pathophysiology Plaque Formation 4,Early AtheromaSmooth muscle cells migrate into proliferate within Plaque,Pathophysiology Plaque Formation 5,Lesion GrowsEncroaches into lumenErodes media,Pathophysiology Plaque Formation 6,Mature Fibrolipid Plaque Lipid core Surrounded by SMC Fibrous cap,Pathophysiology Plaque Formation 7,Plague Rupture / Fissure Thrombosis + Local spasm Vessel Occlusion ACS,Pathophysiology,Pathophysiology Plaque Rupture,CHDclinical manifestation and pathology,CHD: Risk Factors,Fixed ModifiableAge Lipid disordersMale SmokingFamily history Diabetes mellitus Hypertension Obesity Sedentary lifestyle Dietary deficiencies of fruits and vegetables alchole,IMPORTANT RISK FACTORS FOR CORONARY ARTERY DISEASE,Pathophysiology Atherosclerosis,PREVENTABLE AND CONTROLLABLE DISEASE,Every 10 MI pts，9 PredictableEvery 6 MI pts，5 Preventable,CHD Prevention,CHD Prevention,Primary Prevention Secondary Prevention,Modify Risk Factors Therapeutic Lifestyle Change Evidence-based optimal drug management,CHD Prevention,Population AdviceTLC,Do not smoke Take regular exercise Maintain “ ideal ” body weight Eat a mixed diet rich in fresh fruit and vegetablesAim to get no more than 30% of energy intake from fat Stress control,CHD Prevention,Examples of the benefits of long-term secondary prevention following myocardial infarction,Preventive measure Events prevented per 1000 patient years Smoking cessation 15deaths 46 non-fatal myocardial infarctions(Mls)Aspirin 7 deaths 9 non-fatal Mls 9 non-fatal strokes-adrenoceptor 21 deathsantagonist 21 non-fatal MlsStatins(HMG CoA 7 deathsreductase inhibitors) 12 non-fatal Mls 3 non-fatal strokes 11 revascularisations 4 cases of heart failureN.B. Even in a high-risk rimary prevention (the West of Scotland study), four times as many people needed to be treated with a lipid-lowering agent to prevent a cardiac event compared to secondaryprevention.,Optimal evidence-based drug treatment Anti-hypertension drugs Lipid-lower drugstatins Aspirin- blocker ACEI,CHD Prevention,Clinical ManifestationClassification,Myocardial Ischemia Angina Pectoris Stable Unstable Myocardial Infarction Q- Wave non-Q-Wave Sudden Death,Clinical Manifestation Angina Pectoris,Discomfort due to transient myocardial ischaemia Clinical syndrome rather than a disease Imbalance: O2 supply and demand,Factors Influecing Myocardial O2 Supply and Demand,Oxygen demand Oxygen supplyCardiac work Coronary blood flow*Heart rate Duration of diastoleBlood pressure Coronary perfusion Myocardial contractility pressure (aortic diastolic coronary sinus or right atrial diastolic pressure) Coronary vasomotor tone Oxygenation Haemoglobin Oxygen saturation*N.B. Coronary blood flow occurs mainly in diastole.,Clinical Manifestation Angina Pectoris,Clinical Manifestation Angina Pectoris : Causes,Most Common : Coronary AtheromaOthers : Aortic stenosis Hypertrophic Cardiomyopathy,Case 1,Case discussion 1,Clinical featuresFemale, 40 yAtypical chest painNo history of HTN, dyslipidemia and diabetesECG: normalDiagnosis decision ?,Case discussion 1,Clinical featuresFemale, 40 yAtypical chest painNo history of HTN, dyslipidemia and diabetesECG: normalDiagnosis decision Symptom,Clinical Manifestation Symptom,key factor in Diagnosis making (Stable / Unstable Angina),Clinical Manifestation Symptom: Stable Angina,Location : Central Radiation: neck / jaw / arm Characteristics: Worsening factors: “Start-up angina”,CLINICAL SITUATIONS PRECIPITATING ANGINACommon Physical exertion Cold exposure Heavy meals Intense emotionRare Lying flat (decubitus angina) Vivid dreams (nocturnal angina),Clinical Manifestation Symptom: Stable Angina,Clinical Manifestation Physical Examination,Frequently Negative But: A careful search for - Important Risk Factors - Contributory Disease (obesity, anemia) - LV dysfunction: gallop rhythm, murmur,Case discussion 1,Clinical featuresFemale, 40 yAtypical chest painNo history of HTN, dyslipidemia and diabetesECG: normalDiagnosis decision Symptom Noncardiac chest pain,Angina PectorisDifferential Diagnosis,Acute myocardial infarctionX syndromeCardiac Neurosis,Clinical ManifestationDifferential Diagnosis,Musculoskeletal Pericardial Pain Oesophageal,Angina Pectoris Differential Diagnosis,Musculoskeletal Pain Provoked by special movement rather than walking Background pain often persists at rest Associated chest wall tendernessPain of Pericarditis Provoked by changes in posture or deep inspirationPain Due to oesophagitis with or without hiatus hernia Burning quality Relieved by antacids,Case discussion 1,Clinical featuresFemale, 40 yAtypical chest painNo history of HTN, dyslipidemia and diabetesECG: normalDiagnosis decision Symptom Noncardiac chest painTests,Diagnosis Special Test - ECG,Resting ECG Evidence of OMI Normal in most patients T wave flattening / inversion Non-Specific !,Diagnosis Special Test - ECG,The most convincing Evidence REVERSIBLE ST or with/without T inversion During Chest Pain(Spontaneously or by exercise testing),Diagnosis Special Test - ETT,Treadmill/Bicycle ergometer Confirm/Refute diagnosis Assess Severity of disease Identify high risk patient,Exercise Tolerance Test,Diagnosis Special Test - ETT,Diagnosis Special Test Isotope Scanning,Evaluating Pts with equivocal/uninterpretable ETTPts unable to exercisePredictive accuracy ETT,Technique Scintiscan of Myocardium At rest and during stress (ETT or Dobutamine) After IV radioactive isotope (201TI),Diagnosis Special Test - Isotope Scanning,Isotope Scanning TechniqueThallium - Analogue of potassiumTake-up by viable myocardium,Diagnosis Special Test - Isotope Scanning,Ischemia: during stress Perfusion defect Reversible not at rest Infarction: Perfusion defect Persistent,Diagnosis Special Test - Isotope Scanning,Diagnosis Special Test,Ventricular FunctionRadionuclide blood pool scanningECHO,Diagnosis Special Test - MSCT,Coronary Arteriography,Extent/nature of CAD ?Decide PTCA / CABGDiagnostic - Atypical chest painNon-invasive test failed,Diagnosis Special Test,Case discussion 1,Clinical featuresFemale, 40 yAtypical chest painNo history of HTN, dyslipidemia and diabetesECG: normalDiagnosis decision Symptom Noncardiac chest painTests Stress testAngiography CTA,Rapid worsening angina (Crescendo)Severe angina at restNew-onset anginaPost-infarction anginaWithout evidence of Infarction (ECG / Enzyme),Clinical Manifestation Symptom: Unstable Angina,Clinical Manifestation Risk stratification in Angina,High risk Low riskUnstable angina Predictable exertional anginaPost-infarct anginaPoor effort tolerance Good effort toleranceIschaemia at low workload (ETT) Ischaemia only at high workload (ETT)Left main or three-vessel disease Single-vessel or minor two-vessel diseasePoor LV function Good LV functionN.B. Patients may fall between these categories.,Management Angina Pectoris,Risk factors control Symptoms Control Life expectancy improvement,ADVICE TO PATIENTS WITH ANGINA Do not smoke Aim at ideal body weight Take regular exercise (Exercise up to, but not beyond, the point of chest pain is beneficial and may promote collateral vessels.) Avoid severe unaccustomed exertion, and vigorous exercise after a heavy meal or in very cold weather Take sublingual nitrate before undertaking exertion that may induce angina,Management Angina Pectoris,Anti - anginal Drug Nitrates -blocker CCB anti-platelet Aspirin 75-100mgLipid-lowing Statin ACEI,Management Angina Pectoris,baselinePlaque area 6mm2,Statins for 6monthsPlaque area 6.4mm2,Shinya Okazaki, et al. Circulation. 2004;110:1061-1068,Regression of Plaque by Statins,Invasive TreatmentRevascularizationPTCA / CABG,Management Angina Pectoris,Management -PCI,A triple coronary artery bypass graft operation,Management coronary artery bypass grafting,PTCA CABGPrincipal use Single-vessel disease; two-vessel Left main stem stenosis;three-vessel disease; unstable angina diseaseMortality 1% 0.2ug/ml Troponin T0.2ug/ml,Myocardial Infarction,冠状动脉破裂斑块,致命性血栓,斑块破裂处,形成血栓的脂质核心,胶原纤维帽,Pathophysiology of Acute Coronary Syndrome,UA,No ST Elevation,ST Elevation,NSTEMI,Unstable Angina,QWMI,NQMI,Myocardial Infarction,Working Dx,ECG,Cardiac Biomarker,Final Dx,The Lancet 2001; 358: 1533-1538 and Heart 2000; 83: 361-366.,Presentation,STEMI 的病理生理和治疗原则,病理生理：,斑块破裂,血栓形成,冠脉急性闭塞,心肌坏死,R.B. Jennings et al., Circulation 68-1 (1983) 25-36,Wavefront Phenomenon of Myocardial Necrosis,PathophysiologyMYOCARDIAL INFARCTION,Diagnosis,Clinical presentationPhysical examinationECGBiochemical markersImaging of the coronary anatomy,Case discussion 2,临床表现男性，65岁，发作性胸痛8小时既往史：吸烟：20支/日，30年；高血压病史10年如何问诊？,Symptoms Prolonged cardiac pain Chest, throat, arms, epigastrium or back Anxiety Fear of impending death Nausea and vomiting Breathlessness Collapse / syncope,Clinical Manifestation MYOCARDIAL INFARCTION,Pallor, sweating, tachycardia Vomiting, bradycardia Hypotension, oliguria, cold peripheries Narrow pulse ressure Raised JVP Third heart sound Quiet first heart sound Diffuse apical impulse Lung crepitations Fever Mitral regurgitation, pericarditis,Signs of sympathetic activation Signs of vagal activationSigns of impaired myocardial functionSigns of tissue damage Signs of complications,Physical signs,Clinical Manifestation MYOCARDIAL INFARCTION,Differential Diagnosis,Case discussion 2,临床表现男性，65岁，发作性胸痛8小时既往史：吸烟：20支/日，30年；高血压病史10年需要哪些辅助检查？,辅助检查结果,血液学：血常规、生化、凝血分析心肌酶学标志物心电图运动平板冠脉CT冠状动脉造影超声心动图,1000,100,10,1,0,Relative Marker Increase,Hours After Chest Pain Onset,Upper Reference Interval,Antman EM. In: Braunwald E, ed. Heart Disease: A Textbook in Cardiovascular Medicine, 5th ed. Philadelphia, Pa: WB Saunders; 1997.,DiagnosisCardiac Biomarkers in STEMI,心电图,ECG,特征性改变高尖T波ST段抬高异常Q波或QS波T波改变分期和动态演变超级期急性期演变期陈旧期,冠状动脉造影,Case discussion 2,临床表现男性，65岁，发作性胸痛8小时既往史：吸烟：20支/日，30年；高血压病史10年辅助检查心电图：V2-V5 st段抬高心肌标志物：TNI:7.8ng/ml如何治疗？,治疗原则,冠状动脉血运重建治疗恢复心肌血流和再灌注溶栓PCI CABG,STEMI - Management,Anti-ischemic agents Anticoagulants Provide facilities for defib Antiplatelet agents Coronary revascularization ( Reperfusion Strategy-Reopen IRA) Detect and Treat complications early Long-term management,A triple coronary artery bypass graft operation,Management coronary artery bypass grafting,确诊ST段抬高心肌梗死,一般治疗（抗血小板、抗凝、 B阻断剂）,治疗原则,12小时以内,12小时以上,再灌注治疗,溶栓治疗,冠脉介入治疗,是,否,是,保守治疗,Management -PCI,Case discussion 2,临床表现男性，65岁发作性胸痛8小时既往史：吸烟：20支/日，30年；高血压病史10年辅助检查心电图：V2-V5 st段抬高心肌标志物：TNI:7.8ng/ml治疗直接PCI二级预防药物,STEMI Complications,Electronic Arrhythmias Mechanical,COMMON ARRHYTHMIAS IN ACUTE MYOGARDIALINFARCTION Ventricular fibrillation Ventricular tachycardia Accelerated idioventricular rhythm Ventricular ectopics Atrial fibrillation Atrial tachycardia Sinus bradycardia(particularly after inferior MI) Heart block,STEMI Complications,STEMI Complications Mechanical,Pump failure Cardiogenic Shock Papillary muscle damage Rupture of ventricular septum Rupture of free wall,Ventricular Septal Rupture,Mitral Regurgitation(Pap. M. dysfunction),Incidence1-2% 1-6%1-2%Timing3-5 d p MI 3-6 d p MI3-5 d p MIPhy Exammurmur 90% JVD, EMDmurmur 50%ThrillC