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Coronary Heart Disease 冠心病 张力 [email protected] on behalf of Zhu Jianhua M.D. 朱建华 The First Affiliated Hospital, School of Medicine, Zhejiang University CVD—1st Cause of Death 6% 3% 7% 43% 14% 27% CVD 心脑血管疾病 Cancer 恶性肿瘤 Respiratory dis. 呼吸系统疾病 Accident 意外伤害 Digestive dis. 消化系统疾病 其他Others Number around us In this country,one person died from CVD per 10 seconds 中国冠心病死亡率位列世界第二 俄罗斯:674,881 中国:702,925 印度:1531,543 单位;人 印度、中国和俄罗斯是世界上冠心病死亡人口最多的3个国家 其中,中国的冠心病死亡人口总数列世界第二 急性心肌梗死 ——他们离我们而去的缘由 Coronary arteries--anatomy Lipids • LDL = primary target of therapy • Risk categories - > 20% risk of major coronary event in 10 years = high risk • Known CAD • Diabetes • Known atherosclerotic disease (PVD, carotid disease and abdominal aortic aneurysm) • > 2 risk factors • Consider causes of secondary hyperlipidemia - Diabetes - Hypothyroidism - Obstructive liver disease - Chronic renal failure - Drugs such as progestins, anabolic steroids, corticosteroids Major Risk Factors • Smoking • Hypertension (>=140/90 or on antihypertensive treatment) • HDL < 40* • Family History premature CAD (<55 males, <65 females) • Age (men >=45; women >=55) * HDL >60 is a negative risk factor, its presence removes one risk factor from total count Coronary heart disease atherosclerosis Coronary stenosis coronary spasm Myocardial ischemia, anoxaemia Coronary heart disease, CHD Ischemic heart disease •Atherosclerosis •Stable angina pectoris(SAP) •Acute coronary syndrome Unstable angina(UAP) and non-STEMI (UA/NSTEMI) ST elevation myocardial infarction(STEMI) Atherosclerosis Atherosclerosis •leading cause of death and disability •Common location: Coronary circulation: Proximal left anterior descending coronary artery(LAD) Proximal portion of renal arteries Extracranial circulation to the brain Carotid bifurcation Three fundamental biological processes of atherosclerosis 1. Accumulation of intimal cells: • smooth muscle cells • Macrophages • T-lymphocytes 2. Proliferated connective tissue matrix • Collagen • elastic fibers • proteoglycans 3. Accumulation of lipid: • cholesteryl esters • free cholesterol Evolution of the atherosclerotic plaque Pathophysiology of coronary artery atherosclerosis 1. Fatty streak 2. Fibroatheroma 3. Complicated lesions Atherosclerosis related not only to lipids Less smooth muscle cells Much inflammatory cells Much smooth muscle cells Less inflammatory Thick cells fibrous cap Thin fibrous cap Eroded endothelium Active macrophage Integrated endothelium Unstable plaque Adapted from Libby. Circulation. 1995;91:2844-2850 Foam cells Stable plaque Clinical events related to rupture of unstable plaque Repaired Smooth muscle cell Inflammation Macrophage/T-cell Plaque stable Adapted from Weissberg. Atherosclerosis. 1999;147:S3–S10 Plaque unstable O2 supply O2 demand Normal ECG Normal coronary flow in balance O2 supply Significant stenosis reduce coronary flow Low Demand is in balance with a diminished coronary flow( Under resting condition ) O2 supply Significant stenosis reduce coronary flow O2 demand Normal ECG (CAD Under resting condition) O2 demand (exertion or emotional stress) Ischemia ECG (Angina pectoris) Prevention and Treatment of Athrosclerosis 1.Lifestyle modification 2.Lipid disorders (Dyslipidemia): cholesterol screening in all >20yrs Elevated: cholesterol (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, OGTT Prevention and Treatment of Athrosclerosis 5. Cigarette smoking:more thrombogenic 6. Family history: 7. Aging:>40yrs 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 Prevention and Treatment of Athrosclerosis •Drug therapy: anti-platelet: aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazol Lipid-lowering Prevention and Treatment of Athrosclerosis Lipid-lowering drugs 1. HMG-CoA reductase inhibitors(statins) Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,Sim vastatin,Cerivastatin, Rosuvastatin: *elevation of aminopherase, rhabdomyolysis 2. Bile acid-binding Resins cholestyramine,colestipol 3. Nicotinic Acid: 4. Fibric acid derivatives(fibrates) Gemifibrozil, clofibrate, Fenofibrate 5. Cholesterol absorption inhibitors: ezetimibe 6. Probucol Prevention and Treatment of Athrosclerosis Surgery 1 Surgery : CABG。 2 PCI: Coronary heart disease (CHD) CHD - Overview • Stable CHD • Unstable CHD - Angina - MI • Pathophysiology • Clinical Features - History/PE • Differential Diagnosis • Diagnostic Testing • Treatment How Does CHD Present? • Chest pain is primary symptom - However, pain not always prominent in patients with CAD; Patients can present with “anginal equivalents” • Dyspnea, faintness, fatigue, exercise intolerance - “Painless” CAD can also present as: • Silent ischemia; CHF; Arrhythmias; Sudden death • Obstruction of coronary artery by athreomatuous plague is most common cause - Other causes of nonatherosclerotic obstruction include • Congenital abnormalities, arteritis, “bridging” • Myocardial Ischemia can occur in absence of obstructive CHD - Aortic stenosis and hypertrophic cardiomyopathy What about physical examination items in CHD? • Physical Examination - Xanthelasma –intracellular lipid deposits near lower lids - Blood pressure - Arterial – decrease peripheral pulses - Cardiac examination The Pathophysiology of Stable CHD • Imbalance between myocardial O2 requirements and supply - Increased requirements in tachycardia, increase wall stress, increased contractility • Physical exertion; heavy meat; fever; thyrotoxicosis; emotional stress (increased catecholamines) - Supply determined by coronary blood flow and coronary arterial O2 content • “Fixed” CHD • Transient vasoconstriction- Coronary “tone” affected by a variety of stimuli What else should we consider in the differential diagnosis? More likely to be confused: • Esophageal problems – reflux; motility disorders; spasm; - Chest pain with normal coronaries commonly due to esophageal abnormalities - Key elements like CHD = characteristics of pain; relieved with nitro - Key elements unlike CHD = pain changes with posture or meals; relieved with antacids (GI cocktail); • Pericarditis - Chest pain not relieved with rest or nitro; pericardia fiction rub and diffuse ST elevations on ECG - Key elements like CHD = retrosternal location, abnormal ECG - Key elements unlike CHD = pain is positional What else should we consider in the differential diagnosis? Less likely to be confused: • Aortic dissection - Severe, sharp, radiates to back, with or without aneurysm - Diagnosis with chest CT or TEE • Severe pulmonary hypertension - From right ventricular ischemia • Pulmonary emboli - From Dyspnea is cardianl symptom; pleuritic chest pain with infarction; pleural friction rub CHD categories : 1、 Absence of symptoms 2、Angina pectoris (AP) 3. Myocardial infarction (MI) 4. Ischemia heart disease 5. sudden death Stable angina pectoris definition: acute and transient myocardial ischemia and anoxaemia usually caused by coronary insufficiency during exertion 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 Stable angina pectoris Pathology in angiography Significant coronary lesion with diameter stenosis > 70% in 75% pts No significant stenosis in about 510% pts, Ischemia may be related to coronary spasm or microvascular dysfunction. Stable angina pectoris Clinical manifestation 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 Stable angina pectoris Clinical manifestation 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: 3-5 mins •pain relief: within several mins after rest or using nitroglycerin What about non-invasive test? • Metabolic abnormalities - Lipids • LDL< 100 mg/dl is optimal - Esp for patients with multiple risk factors, DM and established CAD • HDL<40 mg/dl is an independent risk factor • TG’s > 200 mg/dl should be treated (lifestyle) - Glucose • Impaired fasting glucose= 110-126 mg/dl • DM = FBS > 126 mg/dl - Others – presence increase the risk of future CV events – no consensus on routine measurement • C-reactive protein; homocysteine; lipoprotein Lp(a) What about non-invasive test? • ECG - Resting ECG is normal in 50% patients with stable angina - Most common abnormality with chronic CAD is non-specific ST-T wave changes Non specific changes also seen in electrolyte abnormalities, LVH, antiarrhythmic drugs Stable CHD: Non invasive tests • Exercise ECG ( treadmill test ) - Looking for ST segment depression and symptoms • 1mm (+) typical symptoms = 90% positive predictive value • • • • 2mm (+) typical symptoms= diagnostic 1mm (-) typical symptoms= 70% predictive value 2mm (-) typical symptoms = 90% predictive value Overall sensitivity = 70%; Specificity = 80% - Patients need to get to >85% predicted maximal • Predicted max HR = (220 – age) Stable CHD :Non invasive tests • Radionuclide Perfusion imaging (“Cardiolyte”) - Exercise ECG with images of myocardial blood flow • Compare images at maximal exercise with images at rest - “Defects” with exercise and not with rest = ischemia - “Defects” with both exercise and rest = MI • Sensitivity = 90%; Specificity = 80% • 64 slice MSCT CHD----Diagnosis ECG Treadmill Cardiac Echo ECT Chest X ray Angiograph Coronary stenosis Myocardial ischemia ST segment depression Normal coronary flow Normal Normal ST segment Myocardial infarction Coronary occlusions ST segment elevation Treadmill test Cardiac Echo Cardiac ECT(201TI 或99mTc-MIBI): CHD-- Radionuclide Perfusion imaging 201TI perfusion defects Chest X-ray Soft or ‘Vulnerable’ Plaque Imaging by 64 slice MSCT Stable CHD invasive tests Coronary angiography - golden standard Coronary angiography Left Coronary Angiogram ( LCA) Arterial Anatomy & Projections Left Coronary Artery Right Anterior Oblique RAO 30 Coronary Angiography Stable angina pectoris Prevention and treatment 1. 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 revascularization: percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, LIMA Stable angina pectoris Drug therapy antianginal and anti-ischemic therapy Oxygen supply Oxygen demand a.nitrates b.beta-adrenergic blockers c.Calcium antagonists d.Drugs 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 pectoris Drug therapy b. ß-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 ß1-selective:metoprolol, atenolol, bisoprolol Stable angina pectoris Drug therapy 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: trimethazine(vasorel),selectively inhibit 3-KAT (3-酮酰辅酶A硫解酶),partly inhibit FA Stable angina pectoris Drug therapy prevent MI and death therapy a.antiplatelet angents: ASA,75-325mg/d clopidogrel; ticlopidine: ADP receptor- antagonists: Cilostazol: phosphodiesterase inhititor,50-100mg bid b. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI) Stable angina pectoris stenting Coronary Artery Bypass Graft --CABG Acute Coronary Syndromes • ST segment elevation MI (STEMI) • Unstable angina (UA) • Non ST segment elevation MI (NSTEMI) - Non Q wave MI Plaque rupture/erosion → thrombosis→ coronary completed/incomplete occlusion Acute Coronary Syndromes • Patients presenting to ER with acute chest pain - 15% will be found to have an MI - 30% found to have unstable angina • 50% of deaths from AMI occur within one hour of symptoms onset usually due to arrhythmia (V. fib) • MI’s due to coronary atherosclerosis with superimposed coronary thrombosis – brought on by plaque rupture - This is the cause of almost all acute coronary syndromes leading to either complete occlusion of coronaries leading to Q wave infarction or partial occlusion leading to acute coronary syndrome of unstable angina or non-Q MI ACS—the top of iceberg Coronary Heart Disease Stable plaque Unstable plaque Disrupted plaque From Eugene Braunwald, Heart Disease, A Textbook of Cardiovascular Medicine CHD –Sudden death (arrhythmia) Ventriclar Tachycardia Ventricular flutter Ventricular fibrillation Unstable Angina and Non-ST segment elevation myocardial infarction (NSTEMI) • Caused by non occlusive thrombus • Risk of death and non-fatal cardiac ischemic events can be determined • “High risk” history: • Nature of Symptoms - Accelerating ischemic in past 48 hours and prolonged ongoing (>20 minutes) rest pain • Prior Hx MI • Age • Sex • number of traditional risk factors present Circulation 2000; 102:1193 Unstable Angina and Non-ST segment elevation myocardial infarction (NSTEMI) • “High Risk” PE Findings - Pulmonary edema - S3 gallop - New or worse MR murmur - Hypotension, bradycardia, tachycardia • ECG findings - ST-segment changes of >= 1mm - Sustained V. Tachy - New or presumed new BBB Chest Pain Assessment • ECG most important single source of data in the evaluation of patients with chest pain • ECG findings in patients with acute chest pain - New ST-segment elevation of >=1 mm • Probability of MI = 80% - ST-segment depression or T-wave inversion no know to be old • Sensitivity = 90%; Specificity = 80% Myocardial Infarction • >75% of patients with MI have > 1 coronary artery diseased; - However about 6% of patients with AMI will have angiographically normal coronary arteries • Biochemical markers of necrosis are CK-MB or troponin MI ECG Culprit lesion MI area Total occlu sion Cardiac Biomarkers “enzymes” • Enzymes (cardiac biomarkers) diffuse into the cardiac interstitium after MI and become detectable in the blood within hours. • CK-MB detectable 4 hours after MI and up to about 2 days - Some CK-MB detectable in healthy patients • Troponin I detectable 4 hours after an MI and up to a week afterwards - Therefore, difficult to use to diagnose re-infarction - Troponin I not detectable in healthy patients - “Microinfarctions” can increase troponin I and not increase CK-MB (30% of patients with UA) Time Course of Cardiac Biomarkers after MI Aspects of Diagnosis of Myocardial Infaction by Different Techniques Therapeutics--patients with ACS Anti-ischemic therapy • Nitrates - relieve pain and ischemia, given sublingually or IV acutely • Morphine sulfate - Relieve pain, decreases agitation and decreases preload (decreased venous congestion) • B- Blockers - Decreases myocardial oxygen demand, decreases heart rate, stabilizes membranes thereby decreasing arrhythmia risk Do not use short acting Calcium channel blockers (nifedipine) Therapeutics--patients with ACS Antiplatelet and anticoagulant therapy • Antiplatelets - ASA • Give promptly - Clopridogel • Give promptly • Anticoagulants - Heparin – LMWH or unfractionated RE-vascularization (thrombolytics or PTCA with stent) in patients with STEMI Treatment : myocardial reperfusion PCI: The first choice 经皮冠脉介入治疗(PCI) 无论是否经溶栓治疗,冠状动脉闭 塞或再通后又再堵塞,或虽再通但仍有重 度狭窄者,如禁忌可紧急施行PCI并安置支 架。 目前认为有条件时应首选PCI CAD—Intervention therapy • Percutanouse transluminal coronary angioplasty (PTCA) • Stent • Rotational atherectomy (RA) Acute Myocardial Infarction ischemia ischemic necrosis Reopen the vessels Reduce the area of infarction Rescue the dying myocardium Time = Myocardium! Best time Mild impairment Slightly injury Mild injured Severe injured Moderate impairment Time = Life ! severe impairment Management: onset of STEMI Treatment : myocardial reperfusion Fibrinolysis 原理:起病3~6小时内,使闭塞的冠状动脉再通,心肌得到再灌注, 濒临坏死的心肌可能得以存活,或使坏死范围缩小。 溶栓疗法 常用药物 尿激酶、链激酶、重组组织型纤溶酶原激活 剂(rt-PA) 溶栓成功的判断 间接判断 ST段2小时内回降>50%;胸痛2小时内基本消 失;再灌注性心律失常;CK-MB峰值提前 直接判断 冠状动脉造影 Reperfusion therapy: PCI vs. Fibrinolysis Reperfusion therapy: PCI vs. Fibrinolysis PCI : Time and outcome PCI of STEMI PCI of STEMI Technique revolution → New time 手术要求高 费用昂贵 病人创伤大 并发症多 恢复时间长 创伤小 操作简单 并发症多 病人恢复迅速 创伤小 操作简单 并发症少 病人恢复迅速 Restenosis <5% DES! Restenosis 20%~30% (2002- ) Restenosis ≧50% CABG POBA (1977-1994) BMS (1994- ) One year follow up after PCI before after 4m 1y Therapeutics Acute Coronary Syndromes-Post discharge • A: Antiplatelets / ACE-I • B: β- blockers / Bp control • C: Cholesterol lowering (Statins) / Cigarette quitting • D: Diabetes control / Diet • E: Exercise / Education Potential clinical benefits of Statins in ACS Statins LDL-C↓ VLDL↓, IDL↓, LDL-C↓ • • • • Macrophages lumen Lipid core SMC Endothelium function SMC function Anti-inflammation Thrombosis↓ Take Home Messages Atherosclerosis is the leading cause of death and disability, also the main cause of CHD Risk factors and prevention of atherosclerosis CHD is due to the imbalance between myocardial oxygen supply and demand Two large groups of CHD: chronic(stable angina pectoris) and ACS ACS composed of UAP/NSTEMI and STEMI, resulting from the plaque rupture or erosion, with differing degree of thrombosis and distal embolization, with different obstruction of the coronary artery. reperfusion either by fibrinolysis or primary PCI is the mainstay of therapy of STEMI Thanks!