冠心病英文版

1、Atherosclerosis 339:229234.,0,5,10,15,20,25,30,35,40,45,50,Events of MI in 7 years,No history of MI OMI No history of MI* OMI,non-diabetics diabetics n = 1373n = 1059,P 0.001,P 0.001,4%,19%,20%,45%,DM: CAD equivalent,5. Cigarette smoking：more thrombogenic 6. Family history：genetic factor 7. Aging：40

2、yrs adults ，4/5 fatal myocardial infarction occured in patiens 65 yrs 8. Male gender/ postmenopausal state： male:female = 2：1, man develop CHD 10-15 yrs earlier than woman 9. alcohol 10. Others: diet,homocysteine, hemostatic factors inflammation/infection,Risk factors and prevention,Drug therapy： an

3、ti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazol Lipid-lowering,Risk factors and prevention,HMG-CoA reductase inhibitors（statins） Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,Simvastatin,Cerivastatin, Rosuvastatin： *elevation of aminopherase, rhabdomyolysis 2. Bil

4、e acid-binding Resins cholestyramine，colestipol 3. Nicotinic Acid： 4. Fibric acid derivatives（fibrates） Gemifibrozil, clofibrate, Fenofibrate 5. Cholesterol absorption inhibitors: ezetimibe 6. Probucol,Lipid-lowering drugs,Prevention of CAD,A: aspirin,ACEI B: blood pressure, -blocker, C: cigarette s

5、moking, Cholesterol D: diet, diabetes E: exercise, education,Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults ATP III (adult treatment panel III) Circulation 2002 17/24: 3144-3373,Atherosclerosi

6、s,Coronary heart disease (CHD),Coronary heart disease (CHD),most common cause: obstruction of atheromatous plaque other causes: spasm arterial thrombi coronary emboli ostial narrowing due to luetic aortitis congenital abnormalities severe LV hypertrophy,Factors effect myocardial oxygen supply and de

7、mand,Oxygen supply,Oxygen demand,Heart rate,Myocardial contractility,Systolic wall stress,oxygen carrying capacity of blood,Coronary blood flow,Vascular resistance,Extravascular compressive forces,autoregulation,Metabolic regulation,Humoral factor,Neural regulation,Duration of diastole,Pressure grad

8、ient,Endothelial control,Coronary heart disease,Type： slient ischemia: delitescence： (ECG change) Angina pectoris： angina, caused by myocardial ischemia myocardial infarction：acute myocardial ischemic necrosis caused by the occlusion of coronary artery Ischemia cardiomyopathy (Heart failure and arrh

9、ythmia)： cardiac enlargement, heart failure, arrhythmia, caused by the myocardial fibrosis as the consequence of chronic mycardial ischemia Sudden death： sudden cardiac arrest caused by ventricular fibrillation/flutter,Coronary heart disease (CHD),Type： slient ischemia: delitescence Angina pectoris：

10、 myocardial infarction： Ischemic cardiomyopathy (Heart failure and arrhythmia) Sudden death,Acute Coronary Syndrome(ACS),Resting ischemia,Non-ST elevation,STelevation,Unstable angina,Non-Q wave AMI,Q wave AMI,*positive serum cardiac markers,*,*,*,*,#,# occasionally variant angina,Stable angina pecto

11、ris (SAP),definition: acute and transient myocardial ischemia and anoxaemia usually caused by coronary insufficiency during exertion or emotional stress Characteristics: paroxysmal precordial squeezing-like chest pain, behind the mid sternum， radiated to left shoulder and upper arm precipitated by s

12、tress or exertion duration:2-5min typically relieved rapidly by rest or nitrates,Stable angina pectoris,Coronary stenosis (others:aortic valve disease, HOCM, MB) + Myocardial oxygen demand（HR X SBP）increased myocardial hypoxia acumulation of metabolic product, stimulate C1-5 nerve to cause the sensa

13、tion of chest pain,Stable angina pectoris,mechanism,in angiography Significant coronary lesion with diameter stenosis 70% in 75% pts No significant stenosis in about 5-10% pts, Ischemia may be related to coronary spasm or microvascular dysfunction.,Pathology,Stable angina pectoris,pathophysiology,1.

14、Metabolic and electrophysiology ATP 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 contractility and speed, systolic BP, stroke volume, cardiac output decreased LVED pressure and v

15、olume,Stunning of myocardium,Stable angina pectoris,symptom：chest pain or oppression location behind or slightly to the left of the mid sternum no definite borderline radiated to the left shoulder and upper arm Atypical location: lower jaw, the back of neck,Clinical manifestation,Stable angina pecto

16、ris,chest pain characteristics： tightness, squeezing, burning, pressing, choking, bursting,rarely sharp, not spasmodic force the patient stop the activity till the symptom relieved precipitation exertion or emotional agitation。 duration： 35 mins pain relief: within several mins after rest or using n

17、itroglycerin,Clinical manifestation,Stable angina pectoris,Physical examination increased HR, elevated BP anxiety sweating occasionally gallop rhythm，transient systolic murmur,Clinical manifestation,Stable angina pectoris,Laboratory,Stable angina pectoris,Stress test,rest,Exerscise,Stable angina pec

18、toris,2.Echocardiography: 3. Radionuclide imaging assessment: TL201，Tc99m-sestamibi myocardial perfusion scintigraphy 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUS、intracoronary Doppler flow 、intracoronary pressure,Laboratory,Stable angina pectoris,Coronary Angiography,1.Card

19、iogenic pain：aortic dissection, HOCM, aortic stenosis 2.Respiratory：PE, pneumothorax, pleuritis 3.Gastrointestinal: gastro-esophageal diseases, Hiatal hernia, cholecystitis, peptic ulceration, pancreatitis 4.Neuromuscular/skeletal ：Tietze Syndrome (Costochondritis), intercostal neuralgia, Herpes zos

20、ter 5.Psychologic: anxiety, depression, panic attacks,Stable angina pectoris,Diagnosis,Chest pain, risk factors, ECG evidence of ischemia during chest pain, angiography,Differentiation,Functional classification of SAP(CCS ) CCS I： no chest pain at ordinary activity. Angina at strenuous or rapid or p

21、rolonged exertion CCS 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 of ordinary activity. Walking 1 to 2 blocks, climbing stairs of 3rd floor

22、 CCS IV：Inability to carry on any activity without discomfort anginal symdrome may be present at rest.,Stable angina pectoris,General consideration： rest，avoid provocative factors , risk factors control 2. Drug therapy: prevent MI and death symptom relief and quality of life improvment 3. Coronary r

23、evascularization: percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, LIMA,Prevention and treatment,Stable angina pectoris,antianginal and anti-ischemic therapy,Drug therapy,Oxygen supply,Oxygen demand,a.nitrates b.beta-adrenergic blockers c.Calcium antagonists d.Drug

24、s improving metabolism,Stable angina pectoris,Drug therapy,a.nitrates lower oxygen demand: decrease arteriolar and venous tone, reduce preload and afterload increase coronary supply: Coronary dilatation Nitroglycerin Isosorbide dinitrate isosorbide 5-mononitrate (long-acting nitrates),Stable angina

25、pectoris,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 Relative contraindications: asthma and bronchospastic disease peripheral vascular disease 1-

26、selective：metoprolol, atenolol, bisoprolol,Drug therapy,Stable angina pectoris,c.Calcium antagonists： Increase oxygen supply: dilate resistance vessels, release spasm, improve microvascular function Decrease oxygen demand: negative inotropic effect, decrease BP Antiplatelet effect,d. Drugs improving

27、 metabolism： trimethazine（vasorel），selectively inhibit 3-KAT（3-酮酰辅酶A硫解酶），partly inhibit FA oxidation,Drug therapy,Stable angina pectoris,prevent MI and death therapy a.antiplatelet angents： ASA，75-325mg/d clopidogrel; ticlopidine: ADP receptor- antagonists: Cilostazol: phosphodiesterase inhititor,50

28、-100mg bid b. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI),Drug therapy,Stable angina pectoris,stenting,Stable angina pectoris,Unstable angina(UAP) and non-STEMI,Resting ischemia,Non-ST elevation,STelevation,Unstable angina,Non-Q wave AMI,Q wave AMI,*positive seru

29、m cardiac markers,*,*,*,*,#,# occasionally variant angina,Acute Coronary Syndrome(ACS),Pathophysiology of ACS,stable angina UAP 284:835-42,TIMI IIB, ESSENCE, PRISM-PLUS,TACTICS-TIMI18,UAP and non-STEMI,Treatment,1.Genearl management: rest, oxygen, CCU 2. Drug therapy A. Anti-ischemic drug: intraveno

30、usly, orally nitrates -blocker Calcium antagnoist: first choice for variant angina Morphine,UAP and non-STEMI,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/d GP IIb/IIIa re

31、ceptor inhibitor: used in pts planned to PCI b. Anticoagulation therapy: Heparin Low molecular weight heparin(LMWH) Direct anti-thrombin drug: bivalirudin, hirudin,UAP and non-STEMI,Treatment,2. Drug therapy: C. other medical therapy a. lipid-lowering drugs: statins, early use(in first 24 hrs) LDL-c

32、 target: 70 mg/dl b. ACEI: long-term secondary prevention,UAP and non-STEMI,Treatment,3. Invasive versus conservative 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, A

33、CEI,aspirin clopidegrel(12m),UAP and non-STEMI,SYMPTOMS SUGGESTIVE OF ACS,Noncardiac Diagnosis,Chronic Stable Angina,Possible ACS,Definite ACS,Treatment as indicated by alternative diagnosis,ACC/AHA Chronic Stable Angina Guidelines,No ST-Elevation,ST-Elevation,Nondiagnostic ECG Normal initial serum

34、cardiac biomarkers,ST and/or T wave changes Ongoing pain Positive cardiac biomarkers Hemodynamic abnormalities,Evaluate for reperfusion therapy,ACC/AHA STEMI Guidelines,Observe 12 h from symptom onset,No recurrent pain; negative follow-up studies,Recurrent ischemic pain or positive follow-up studies

35、 Diagnosis of ACS confirmed,Stress study to provoke ischemia Consider evaluation of LV function if ischemia is present (tests may be performed either prior to discharge or as outpatient),Negative Potential diagnoses: nonischemic discomfort; low-risk ACS,Arrangements for outpatient follow-up,Positive

36、 Diagnosis of ACS confirmed or highly likely,Admit to hospital Manage via acute ischemia pathway,Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1e157, Figure 2.,ST elevation myocardial infarction STEMI,Acute Coronary Syndro

37、me(ACS),Resting ischemia,Non-ST elevation,STelevation,Unstable angina,Non-Q wave AMI,Q wave AMI,*positive serum cardiac markers,*,*,*,*,#,# occasionally variant angina,ischemic necrosis of myocardium results from the prolonged myocardial ischemia precipitated by an occlusive coronary thrombus at the

38、 site of a preexisting atherosclerotic plaque。 With typical and serial ECG changes,Represent the serious situation of coronary artery disease,STEMI,Definition,1.incidence ：in USA, 71 in male between 35-84 yrs, 22 in female, 1 attack in about 20 second 2. mortality： decreased in 30% recent 10 years s

39、till 1/3 of the patients died 50% of the death occured within 1 h after the onset MI most deathes result from ventricular fibrillation,epidemiology,STEMI,Cause of the decreased mortality,new drug therapy -blocker, anti-thrombotic LMWH nitrates ACEI Statins,STEMI,Change of concept 1960-80s: Transmura

40、l, non-transmural or sub-endocardium 1980s: Q wave MI，non-Q wave MI 1990s: STEMI, non-STEMI,STEMI,Possible mechanism of the chronic CAD to ACS,Pathology: Coronary diseases,Occlusion of LAD: anterior wall MI,STEMI,Pathology: myocardium,STEMI,STEMI,Pathology: myocardial diseases,Ventricular remodeling

41、 concept: the changes in LV size, shape, and thickness involving both the infarcted and noninfarcted segments Determinants: the size of infarction Ventricular loading conditions Infarct related artery patency,STEMI,Infarct expansion: an increase in the size of the infarcted segment. “acute dilatatio

42、n and thinning of the area of infaction not explained by additional myocardial necrosis”. . ventricular dilatation： shift of pressure-volume curve of LV to the right larger LV volume at any given diastolic pressure Compensatory mechanisms for maintaining stoke volume Associated with non-uniform repo

43、larization of myocardium, predispose to life-threatening ventricular arrhythmias.,STEMI,Ventricular remodeling,Systolic function: dyssynchrony:dissociation in the time course of contraction of adjacent segment hypokinesis: reduction in the extent of shortening akinesis: cessation of shortening dyski

44、nesis: paradoxical expansion, systolic bulging Diastolic function: reduction in LV compliance: decrease in the peak rate of decline in LV pressure (dP/dt) rise in LV end-diastolic pressure and volume,STEMI,pathophysiology,LV function,Predisposing factor： heavy exercise, mental stress: surgical proce

45、dures fever, tachycardia, respiratory infection, hypoxemia, hypoglycemia Prinzmentals angina Prodromal symptoms： weakness, chest discomfort, restlessness , new onset AP and accelerating AP Circadian periodicity peak incidence:6-12am,STEMI,Clinical manifestation,Symptom Chest pain severe, sometimes i

46、ntolerable, prolonged, usually lasting for 30 mins， less effective of sublingual nitroglycerin, retrosternal in location, sweating, scared, and feeling of impending death in some patients, AMI is manifested by shock and acute LV failure, not by chest pain ( the elderly) alert the epigastrium pain an

47、d abdominal disorders,STEMI,Clinical manifestation,symptoms General：fever、HR increase、WBC ，ESR fasting Gastrointestinal symptom：nausea, vomiting , arrhythmias：VPs、AV block, atrial arrhythmias occurred more often in patients with HF Heart failure: mainly acute LV failure, may develope RV failure. Ini

48、tial RV failure occure in patients with RV infarction, associated with hypotension Hypotension and shock：SBP80mmHg after pain release, RV infarction,STEMI,Clinical manifestation,Pump failure Classification based on clinical examination(Killip) Class I：no HF, rales and S3 absent； Class II: mild HF，ra

49、les over 2.2； Class II: Pulmonary congestion, PCWP 18. CI 2.2； Class III: peripheral hypoperfusion, PCWP 18, CI 2.2,STEMI,Clinical manifestation,physical examination General appearance: anxious , distress, cold perspiration, skin pallor Cardiac examination: HR: bradycardia, tachycardia, irregular he

50、art sound: S1 muffled, gallop rhythm cardiac murmurs: systolic pericardial friction rubs BP:previously hypertensive become normotensive others,STEMI,Clinical manifestation,1.rupture of a papillary muscle： rare but fatal complicationcause acute massive mitral regurgitation, pulmonary edema 2.rupture

51、of ventricular wall： occurs most commonly within 1 week free wall rupture; rupture of interventricular septum 3.embolization： LV mural thrombus cause arterial embolization DVT (deep vein thrombus) cause pulmonary embolization 4.cardiac aneurysm： persistant ST elevation cause mural thrombus, heart fa

52、ilure, and arrhythmias 5.post-MI syndrome(Dressler syndrome)： fever, chest pain, repeated pericarditis, pleuritis, pneumonia,STEMI,Clinical manifestation,complications,ECG： Typical： pathological Q wave, ST elevation, inverted T wave Serial ： peaked T wave (hyperacute), ST elevation (acute), Q wave,

53、T wave inversion(old),STEMI,Laboratory test,Anterior AMI,STEMI,Laboratory,Inferior AMI,STEMI,Laboratory,Localization LAD,STEMI,Laboratory,STEMI,Laboratory,Localization LAD,STEMI,Laboratory,Localization LCX,STEMI,Laboratory,Localization RCA,2.vectorcardiography 3.radionuclide angiography： 4.Echocardi

54、ology：distinct region of disordered contraction, LV function, detection complication 5.laboratory examination: blood routine serum cardiac markers,STEMI,Laboratory,Cardiac markers,* Most sensitive and specific marker of myocardial damage,STEMI,Laboratory,Differential diagnosis 1.angina pectoris：ches

55、t pain, complication, general symptoms, elevation of cardia markers, ECG changes 2.acute pericarditis：characteristics of chest pain, time course of chest pain and fever, ECG changes 3.acute pulmonary embolization: chest pain, hemoptysis, dyspnea, increased load of RV (SIQIII),STEMI,Diagnosis,4.Acute

56、 abdominal symptom：acute pancreatitis, cholecystitis, cholelithiasis 5.aortic dissection：sever chest pain with (tearing-like), radiated to back，with aortic regurgitation, CT、UCG、MRI、chest X-ray,Differential diagnosis,STEMI,Diagnosis,Before admission: tranfer, make diagnosis within 10-20min, initiate

57、 reperfusion therapy as soon as possible Monitoring and general treatment: CCU Reperfusion Management of complication others,STEMI,treatment,1.CCU: hemodynamic monitoring, oxygen 2.Pain relief and anti-ischemia: Morphine: 2-4mg IV Nitrates: not use in inferior MI or suspected RV MI with hypotension

58、-blocker: reduce HR, decrease BP, decrease myocardial oxygen consumption, decrease Vf 3. Anti-platelet: aspirin：first dosage 300mg，chewing, 100mg/d forever for patients without contraindication Clopidogrel: 300mg loading, 75mg/d,STEMI,treatment,4.anti-coagulation: anti-thrombin, heparin, LMWH 5.limi

59、tation of infarct size: reperfusion: Fibrinolytic treatment: intravenous，intracoronary rt-PA：100mg，in 90 min, use heprin before infusion Streptokinase (SK)：1500,000U， iv in 60min, allergic reaction Urokinase (UK)：1000.000-1500,000 U，iv fusion in 30min give heprin after intravenous thrombolysis therapy Primary Percutaneous Coronary Intervention(PCI) CABG,STEMI,treatment,AMI,PTCA,Stenting,STEMI,treatment,Primary stenting,Criteria for thrombolysis in STEMI,