冠状动脉粥样硬化性心脏病英文课件

Coronary Atherosclerotic Heart Diseases,Affiliated Hospital of Jining Medical College Dept.of Cardiac Care Unit Guoxia Dong ,2,5/14/2019,Contents,Atherosclerosis Stable Angina Pectoris Acute Coronary Syndrome UA and NSTEMI AMI(STEMI),3,5/14/2019,Self-study,Variant Angina Cardiac Syndrome X Silent Myocardial Ischemia Myocardial Bridging,4,5/14/2019,What Is Atherosclerosis?,Atherosclerosis is the descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries.,5,5/14/2019,What Is Coronary Heart Disease?,6,5/14/2019,Coronary heart disease,atherosclerosis,Coronary stenosis,coronary spasm,Myocardial ischemia, necrosis,Ischemic heart disease,7,5/14/2019,8,5/14/2019,Atherosclerosis,9,5/14/2019,Foam cell,Fatty steak,atheromatous plaque,ruptured plaques,Fibrous plaque,Endothelial damage,first decade,Third decade,Forth decade,Adapted from Stary HC et al. Circulation 1995;92:1355-1374.,medium damage,5/14/2019,10,What damage does atherosclerosis cause?,11,5/14/2019,Common location Coronary Heart Disease Carotid Artery Disease Peripheral Arterial Disease Chronic Kidney Disease,12,5/14/2019,How does atherosclerosis start and progress?,13,5/14/2019,Elevated levels of cholesterol and triglycerides in the blood High blood pressure Cigarette smoking,14,5/14/2019,Biological processes,Accumulation of intimal cells smooth muscle cells Macrophages T-lymphocytes,15,5/14/2019,Biological processes,Proliferated connective tissue matrix collagen elastic fibers proteoglycans,16,5/14/2019,Biological processes,3.Accumulation of lipid,17,5/14/2019,Atherosclerosis-Hypothesis,Hypothesis of lipoprotein infiltration Aggregation of platelets and thrombosis Clonal theory The response-to-injury hypothesis,18,5/14/2019,High blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance. Platelets are activated, adhesion and aggregation of platelets. Lipidoses, growth factor, proliferation of smooth mucle cells, collagen, lipolytic enzyme.,Response-to-injury,19,5/14/2019,Pathology and pathophysiology,Fatty steak Fibrous plaque Complicated lesion,20,5/14/2019,Initiation of Atherosclerosis,Fatty steak formation,21,5/14/2019,Initiation of Atherosclerosis,22,5/14/2019,fibrous plaque,23,5/14/2019,24,5/14/2019,25,5/14/2019,Thin Cap Vulnerable Plaque Thrombus Unstable “ Active Volcano”,Thick Cap Calcified Plaque Flow-limiting Lesion Stable Angina “ Dormant Volcano ”,SAP,ACS,pressure or a squeezing pain !,26,5/14/2019,Unstable and Stable Plaques,薄的纤维帽,炎性细胞,少的平滑 肌细胞,内皮细胞不完整,巨噬细胞,较厚的纤维帽,没有炎性细胞,泡沫细胞,完整的内 皮细胞,较多平滑 肌细胞,Libby P. Circulation. 1995;91:2844-2850.,unstable,stable,5/14/2019,28,Atherosclerosis,Clinical stages Absence of symptom or stage of incubation ischemia necrosis(target organ ) fibrosis,29,5/14/2019,clinical manifestation,General manifestation Aortic atherosclerosis Coronary artery atherosclerosis Cerebral atherosclerosis RA atherosclerosis Mesenteric atherosclerosis Peripheral artery atherosclerosis,30,5/14/2019,Laboratory Examination,Lack of sensitive and specific methods for early diagnosis Dyslipidemia X-ray：DSA show severity of stenosis Doppler ultrasound: blood flow,31,5/14/2019,Laboratory Examination,radionuclide： detection of ischemia Echocardiogram： CHD ECG and stress test: CHD Angiography: the most direct way Intravascular ultrasound, angioscope CT, MRI,32,5/14/2019,Risk factors,1.Lipid disorders (Dyslipidemia) Increased cholesterol :Tc and LDL-c, TG, ApoB,Lp(a) Decreased cholesterol: HDL-c apoA 2.Hypertension,33,5/14/2019,Risk factors,3.DM,Metabolic 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 disease,34,5/14/2019,7 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.,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 = 1373 n = 1059,P 0.001,P 0.001,4%,19%,20%,45%,DM: CAD equivalent,35,5/14/2019,Risk factors,4. Cigarette smoking：more thrombogenic 5. Family history 6. Aging：40yrs adults ，4/5 fatal myocardial infarction occured in patiens 65 yrs 7. Male gender/ postmenopausal state： male:female = 2：1, men develop CHD 10-15 yrs earlier than women 8. alcohol 9. Others: diet,homocysteine, hemostatic factors inflammation/infection,36,5/14/2019,Drug therapy,anti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazol Lipid-lowering HMG-CoA reductase inhibitors（statins）,37,5/14/2019,Doubts of patients,Quest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?,38,5/14/2019,Doubts of patients,Question 2：My shape is not fat, lipid is not high, why give me lipid-lowering drugs, made a mistake?,39,5/14/2019,Doubts of patients,Question 3：I have coronary heart disease,then should I do less activities in order to protect the heart?,40,5/14/2019,Coronary Heart Disease (CHD),5/14/2019,41,Clinical Type,Silent myocardial ischemia Angina pectoris Myocardial infarction Ischemic cardiomyopathy Sudden cardiac death,5/14/2019,42,Silent Myocardial Ischemia,Defined 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 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.,5/14/2019,43,Ischemic Cardiomyopathy,Symptoms of heart failure, caused by ischemic myocardial dysfunction , diffuse fibrosis, and multiple infarction, alone or in combination. Manifestations: ventricles enlargement (dominant left ventricle), heart failure and arrhythmias.,5/14/2019,44,Sudden Cardiac Death,SCD is natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of acute symptoms. The time and mode of death are unexpected. WHO definition: unexpected death within 6 hours. This definition incorporates the key elements of natural, rapid and unexpected. One half of SCD due to coronary heart disease，caused by severe arrhythmias, such as ventricular fibrillation and cardiac arrest.,5/14/2019,45,Acute Coronary Syndrome,ACS represents a spectrum of conditions. Acute plaque change characterized by plaque rupture and exposure of substances that promote platelet activation and thrombin generation.,5/14/2019,46,Stable Angina Pectoris,47,5/14/2019,Definition,Acute and transient myocardial ischemia and anoxaemia. Usually caused by coronary insufficiency during exertion.,48,5/14/2019,Characteristics,paroxysmal precordial squeezing-like chest pain, behind the mid sternum radiated to left shoulder and upper arm precipitated by stress or exertion relieved rapidly by rest or nitrates,49,5/14/2019,hypoxia,Coronary stenosis (others:aortic valve disease, HOCM) + Myocardial oxygen demand（HRXSBP）increased myocardial hypoxia acumulation of metabolic product, stimulate C1-5 to cause the sensation of chest pain,mechanism,50,5/14/2019,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,51,5/14/2019,pathophysiology,1.Metabolic and electrophysiology ATP reduced, accumulation of acid substances Dysfunction of ion pump (Na+-K+, 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 myocardium,Stable angina pectoris,52,5/14/2019,symptom：chest pain 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 pectoris,53,5/14/2019,character： tightness, squeezing, burning, pressing, choking, bursting,rarely sharp duration： 35 mins precipitating factor exertion or emotional agitation pain relief: within several mins after rest or using nitroglycerin,Clinical manifestation,Stable angina pectoris,55,5/14/2019,Physical examination increased HR, elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmur,Clinical manifestation,Stable angina pectoris,56,5/14/2019,Auxiliary examination,Stable angina pectoris,57,5/14/2019,Stress test,rest,Exerscise,Stable angina pectoris,58,5/14/2019,2.Echocardiography: 3. Scintigraphy assessment: Can detect filling defect of Infarction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUS,Auxiliary examination,Stable angina pectoris,59,5/14/2019,Coronary Angiography,60,5/14/2019,Stable Angina Pectoris,Diagnosis,Chest pain risk factors ECG evidence of ischemia during chest pain angiography,61,5/14/2019,Cardiovascular causes Noncardiac causes,Stable Angina Pectoris,Differential diagnosis,62,5/14/2019,Cardiovascular cause,Myocardial infarction Pericarditis Aortic dissection Pulmonary embolism Pulmonary hypertension,63,5/14/2019,Noncardiac cause,Pneumonia with pleurisy Spontaneous pneumothorax Musculoskeletal disorders Herpes zoster Esophageal reflux Peptic ulcer,64,5/14/2019,General treatment： risk factors control 2. Drug therapy 3. Coronary revascularization: percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, IMAG,Treatment,Stable Angina Pectoris,65,5/14/2019,Blood and oxygen supply to the heart,Myocardial blood flow,Myocardial oxygen consumption,4% of total cardiac output supplied to the myocardium,12% of total body oxygen, used at rest by myocardium,5/14/2019,66,Coronary Reserve,Myocardial blood flow increases up to 4 times ., to meet increased myocardial oxygen demand,5/14/2019,67,Myocardial oxygen supply and demand,O2,O2,O2,O2 supply,O2 demand,5/14/2019,68,Aims of medical therapy,Arterial vasodilatation,Reduces arterial resistance,Reduces afterload,Decreases sympathetic drive,Reduce heart rate and contractile force,Reduces cardiac work,LV,RV,Dilatation of coronary arteries,Improves coronary supply,Venodilatation,Reduces venous return,Reduces preload,5/14/2019,69,antianginal and anti-ischemic therapy,Drug therapy,Oxygen supply,Oxygen demand,a.Nitrates b.Beta blockers c.Calcium antagonists d.Drugs improving metabolism,Stable Angina Pectoris,70,5/14/2019,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 Pectoris,71,5/14/2019,Nitrates in angina,Reduce preload through venodilatation,Reduce afterload by lowering arterial resistance Reduce platelet aggregation,Increase coronary perfusion, including ischaemic areas Reversal of coronary spasm,5/14/2019,72,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-selective：metoprolol, atenolol, bisoprolol,Drug therapy,Stable Angina Pectoris,73,5/14/2019,c.Calcium antagonists： Increase oxygen supply: dilate conduit and resistance vessels, release spasm, improve microvascular function Decrease oxygen demand: negative inotropic effect, decrease BP Antiplatelet effect,d. Drugs improving metabolism,Drug therapy,Stable Angina Pectoris,74,5/14/2019,prevent MI and death therapy a.antiplatelet angents： ASA clopidogrel Cilostazol b. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI),Drug therapy,Stable Angina Pectoris,75,5/14/2019,stenting,Stable Angina Pectoris,76,5/14/2019,Unstable Angina(UA) and non-STEMI,77,5/14/2019,ACS,Non-ST elevation,STelevation,Unstable angina,Non-Q wave AMI,Q wave AMI,*positive serum cardiac markers,*,*,*,*,#,# occasionally variant angina,Acute Coronary Syndrome(ACS),78,5/14/2019,Pathophysiology of ACS,stable angina UAP&non-Q-w AMI Q-w AMI Angiographic thrombus 0-1% 75% 90% Increased FPA/TAT 0-5% 60-80% 80-90% Activated platelets 0-5% 70-80% 80-90% Acute coronary occlusion 0-1% 10-25% 90% mortality 1-2% 3-8% 6-15%,FPA：fibrinopeptide A TAT：thrombin-antithrombin complexes,UA and non-STEMI,79,5/14/2019,Occuring at rest (or with mininal exertion): last 20 mins sever and of new-onset: within 1-2 months, CCS III Occuring with a crescendo pattern: Deterioration of CCS classfication, at least CCS III,Definition,UA and non-STEMI,Angina pectoris or equivalent ischemic discomfort with at least one of the three features,80,5/14/2019,Braunwald classification of unstable angina,Severity： Class I： New-onset, or accelerated severe angina no rest pain within 2 months Class 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),UA and non-STEMI,81,5/14/2019,Braunwald classification of unstable angina,Clinical Circumstances Class A：Secondary UAP a clearly identified condition extrinsic to the coronary vascular bed that has intensified myocardial ischemia, e.g. anemia, hypotension, tachy-arrhythmia Class B：Primary unstable angina Class C：Post-infarction UAP (within 2 weeks of a documented MI),UA and non-STEMI,82,5/14/2019,mechanism：,1.plaque rupture and erosion, with nonocclusive thrombus 2.dynamic obstruction: Vasoconstruction 3.progressive mechnial obstruction(rapidly advancing or ISR following stenting) 4.secondary UA Inflammation Thrombogenesis,UA and non-STEMI,83,5/14/2019,ECG: Non-STEMI: ST depression last 12 hr,Cardiac biomarkers of myocardium damage: cTnT, cTnI CK-MB,UAP and non-STEMI,Coronary angiography Angioscopy and IVUS Other laboratory tests,84,5/14/2019,Treatment,1.Genearl management: rest, oxygen, CCU 2. Drug therapy A. Anti-ischemic drug: intravenously, orally nitrates -blocker Calcium antagnoist: first choice for variant angina Morphine sulfate,UA and non-STEMI,85,5/14/2019,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 receptor inhibitor: used in pts planned to PCI b. Anticoagulation therapy: Heparin Low molecular weight heparin(LMWH) Direct anti-thrombin drug: bivalirudin, hirudin,UA and non-STEMI,86,5/14/2019,Treatment,2. Drug therapy: C. other medical therapy a. lipid-lowering drugs