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Zhu Jianhua M.D. 朱建华
The First Affiliated Hospital,School of Medicine, Zhejiang
University
Coronary Heart Disease
冠心病冠心病张力 [email protected]
on behalf of
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CVD—1st Cause of DeathCVD—1st Cause of DeathCVD—1st Cause of DeathCVD—1st Cause of Death
43%
27%
14%
6%3% 7% 心脑血管疾病
恶性肿瘤呼吸系统疾病意外伤害消化系统疾病其他
CVD
Cancer
Respiratory dis.
Accident
Digestive dis.
Others
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In this country , one person died from CVD per 10 seconds
Number around usNumber around usNumber around usNumber around us
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中国冠心病死亡率位列世界第二
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
俄罗斯: 674 , 881
中国: 702 , 925
印度: 1531 , 543
单位;人
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急性心肌梗死急性心肌梗死————他们离我们而去的缘由他们离我们而去的缘由
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Coronary arteries--anatomyCoronary arteries--anatomy
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LipidsLipids• 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
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Major Risk FactorsMajor 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
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Coronary heart disease
atherosclerosis
Coronary stenosis coronary spasm
Myocardial ischemia, anoxaemia
Coronary heart disease, CHDIschemic heart disease
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•Atherosclerosis
•Stable angina pectoris(SAP)
•Acute coronary syndrome
Unstable angina(UAP) and non-STEMI
(UA/NSTEMI)
ST elevation myocardial infarction(STEMI)
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Atherosclerosis
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•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
Atherosclerosis
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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
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Evolution of the atherosclerotic plaque
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Pathophysiology of coronary Pathophysiology of coronary artery atherosclerosisartery atherosclerosis
1. Fatty streak
2. Fibroatheroma
3. Complicated lesions
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Atherosclerosis related not only to Atherosclerosis related not only to lipidslipids
Thin fibrous cap
Much inflammatory cells
Less smooth muscle cells
Eroded endothelium
Active macrophage
Thick fibrous cap
Foam cells
Integrated endothelium
Much smooth muscle cells
Adapted from Libby. Circulation. 1995;91:2844-2850
Less inflammatory cells
Unstable plaque Stable plaque
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Clinical events related to rupture Clinical events related to rupture of unstable plaqueof unstable plaque
Adapted from Weissberg. Atherosclerosis. 1999;147:S3–S10
Macrophage/T-cellSmooth muscle cell
Plaque unstable
Plaque stable
Repaired Inflammation
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in balance
( exertion or emotional stress )
Low Demand is in balance with a diminished coronary flow ( Under
resting condition )
Normal ECG
Normal ECG
( CAD Under resting condition )
Ischemia ECG
( Angina pectoris )
Normal coronary flow
Significant stenosis reduce coronary flow
OO22 supply supply OO22 demand demand
OO22 supply supply OO22
demanddemand
OO22
demanddemandOO22 supply supply
Significant stenosis reduce coronary flow
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Prevention and Treatment Prevention and Treatment of Athrosclerosisof Athrosclerosis
1.Lifestyle modification2.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
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5. Cigarette smoking : more thrombogenic6. 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 woman9. alcohol10. Others: diet,homocysteine, hemostatic
factors inflammation/infection
Prevention and Treatment of Prevention and Treatment of AthrosclerosisAthrosclerosis
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•Drug therapy:
anti-platelet: aspirin, clopidogrel, GPIIb/IIIa inhitibor,
Dipyridamole, cilostazol
Lipid-lowering
Prevention and Treatment Prevention and Treatment of Athrosclerosisof Athrosclerosis
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1. HMG-CoA reductase inhibitors ( statins ) Atorvastatin,Fluvastatin,Lovastatin,Pravastatin,Simvastatin,Cerivastatin, Rosuvastatin:
*elevation of aminopherase, rhabdomyolysis
2. Bile acid-binding Resins cholestyramine , colestipol3. Nicotinic Acid :4. Fibric acid derivatives ( fibrates ) Gemifibrozil, clofibrate, Fenofibrate5. Cholesterol absorption inhibitors: ezetimibe6. Probucol
Prevention and Treatment of Prevention and Treatment of AthrosclerosisAthrosclerosis Lipid-lowering drugs
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Prevention and Treatment of Prevention and Treatment of AthrosclerosisAthrosclerosis
Surgery 1 Surgery : CABG 。2 PCI:
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Coronary heart disease(CHD)
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CHD - OverviewCHD - Overview• Stable CHD• Unstable CHD - Angina - MI
• Pathophysiology• Clinical Features - History/PE
• Differential Diagnosis• Diagnostic Testing• Treatment
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How Does CHD Present?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
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What about physical What about physical examination items in CHD?examination items in CHD?
• Physical Examination - Xanthelasma –intracellular lipid
deposits near lower lids - Blood pressure - Arterial – decrease peripheral
pulses - Cardiac examination
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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
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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
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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
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CHD categories :
1 、 Absence of symptoms
2 、 Angina pectoris (AP)
3. Myocardial infarction (MI)
4. Ischemia heart disease
5. sudden death
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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 armprecipitated by stress or exertionrelieved rapidly by rest or nitrates
Stable angina pectoris
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in angiographySignificant 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
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symptom : chest pain or oppression•location
behind or slightly to the left of the mid sternum no definite borderlineradiated to the left shoulder and upper armAtypical location: lower jaw, the back of neck
Clinical manifestation
Stable angina
pectoris
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chest pain•characteristics:
tightness, squeezing, burning, pressing, choking, bursting,rarely sharp, not spasmodic force the patient stop the activity till the symptom relieved
•precipitationexertion or emotional agitation。
•duration:3 - 5 mins
•pain relief: within several mins after rest or using nitroglycerin
Clinical manifestation
Stable angina
pectoris
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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)
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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
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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)
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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
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CHD----Diagnosis
ECGECG Chest X rayChest X ray
ECTECT AngiographAngiograph
Cardiac Echo
TreadmillTreadmill
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ST segment depression
ST segment elevation
Normal ST segment
Myocardial ischemia
Myocardial infarction
Normal
Coronary stenosis
Coronary occlusions
Normal coronary flow
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Treadmill testTreadmill test
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Cardiac Echo
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Cardiac ECTCardiac ECT (( 201201TI TI 或或 99m99mTc-MIBTc-MIBII )) ::
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CHD-- Radionuclide CHD-- Radionuclide
Perfusion imagingPerfusion imaging
201TI perfusion defects
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Chest X-ray
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Soft or ‘Vulnerable’Plaque Imaging by 64 slice MSCT
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Stable CHD invasive tests
Coronary angiographyCoronary angiography
- golden standard- golden standard
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Coronary Coronary angiographyangiography
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Left Coronary AngiogramLeft Coronary Angiogram ( ( LCLCAA ) )
Arterial Anatomy & Arterial Anatomy & ProjectionsProjections
Left Coronary ArteryRight Anterior Oblique RAO 30
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Coronary Angiography
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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
Prevention and treatment
Stable angina
pectoris
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antianginal and anti-ischemic therapy
Drug therapy
Oxygen supply
Oxygen demand
a.nitratesb.beta-adrenergic blockersc.Calcium antagonistsd.Drugs improving metabolism
Stable angina
pectoris
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Drug therapy
a.nitrateslower 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
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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
Drug therapy
Stable angina
pectoris
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c.Calcium antagonists:Increase oxygen supply: dilate conduit and resistance vessels, release spasm, improve microvascular functionDecrease 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 oxidation,
Drug therapy
Stable angina
pectoris
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prevent MI and death therapy
a.antiplatelet angents :ASA , 75-325mg/dclopidogrel; ticlopidine: ADP receptor- antagonists:Cilostazol: phosphodiesterase inhititor,50-100mg bid
b. Lipid-lowering angents: statins
c. Angiotesin-converting enzyme inhibitor (ACEI)
Drug therapy
Stable angina
pectoris
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stenting
Stable angina
pectoris
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Coronary Artery Bypass Graft --CABG
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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
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Acute Coronary SyndromesAcute 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
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ACS—the top of icebergACS—the top of iceberg
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Coronary Heart DiseaseCoronary Heart Disease
Stable plaque Unstable plaque Disrupted plaque
From Eugene Braunwald, Heart Disease, A Textbook of Cardiovascular Medicine
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CHD –Sudden death (arrhythmia)
Ventriclar TachycardiaVentriclar Tachycardia
Ventricular flutterVentricular flutter
Ventricular fibrillationVentricular fibrillation
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Unstable Angina and Non-ST Unstable Angina and Non-ST segment elevation myocardial segment elevation myocardial
infarction (NSTEMI)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
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Unstable Angina and Non-ST Unstable Angina and Non-ST segment elevation myocardial segment elevation myocardial
infarction (NSTEMI)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
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Chest Pain AssessmentChest 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%
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Myocardial InfarctionMyocardial 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
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MI ECGCulprit lesionCulprit lesion
MI areaMI area
Total Total occluocclusionsion
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Cardiac Biomarkers Cardiac Biomarkers “enzymes”“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)
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Time Course of Cardiac Biomarkers Time Course of Cardiac Biomarkers after MIafter MI
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Aspects of Diagnosis of Aspects of Diagnosis of Myocardial Infaction by Myocardial Infaction by
Different TechniquesDifferent Techniques
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Therapeutics--patients with Therapeutics--patients with ACSACS
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)
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Therapeutics--patients with Therapeutics--patients with ACSACSAntiplatelet 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
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Treatment : myocardial reperfusion
PCI: The first choicePCI: 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
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CAD—Intervention therapy
• Percutanouse transluminal
coronary angioplasty (PTCA)
• Stent
• Rotational atherectomy ( R
A )
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Acute Myocardial Infarction
Reopen the
vesselsReduce the area of infarction
Rescue the dying myocardium
Time = Time =
Myocardium!Myocardium!
Time = Life !Time = Life !
ischemia
ischemic necrosis
Mild impairment
Moderate impairment
severe impairment
Best time
Slightly injury
Mild injured
Severe injured
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Management: onset of STEMI
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Treatment : myocardial reperfusion
FibrinolysisFibrinolysis
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
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Reperfusion therapy : PCI vs. Fibrinolysis
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Reperfusion therapy : PCI vs. Fibrinolysis
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PCI : Time and outcome
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PCI of STEMI
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PCI of STEMI
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Technique revolution → New time
CABGCABG
POBAPOBA(1977-1994)(1977-1994)
BMSBMS(1994- )(1994- )
手术要求高手术要求高费用昂贵费用昂贵
病人创伤大病人创伤大并发症多并发症多
恢复时间长恢复时间长
创伤小创伤小操作简单操作简单并发症多并发症多
病人恢复迅速病人恢复迅速
创伤小创伤小操作简单操作简单并发症少并发症少
病人恢复迅速病人恢复迅速
RestenosisRestenosis ≧50%%
RestenosisRestenosis 20%~30%20%~30%
Restenosis Restenosis <5% <5%
DESDES !!(2002- )(2002- )
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One year follow up after PCI
before before afterafter
4 m4 m 1 y1 y
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TherapeuticsAcute 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
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LDL-C↓
VLDL↓, IDL↓, LDL-C↓
• Endothelium function• SMC function • Anti-inflammation• Thrombosis↓
lumen
Lipid core
Macrophages
SMC
Potential clinical benefits of Statins in ACS
Statins
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Take Home MessagesTake Home MessagesAtherosclerosis is the leading cause of death and Atherosclerosis is the leading cause of death and disability, also the main cause of CHDdisability, also the main cause of CHD
Risk factors and prevention of atherosclerosisRisk factors and prevention of atherosclerosis
CHD is due to the imbalance between myocardial CHD is due to the imbalance between myocardial oxygen supply and demandoxygen supply and demand
Two large groups of CHD: chronic(stable angina Two large groups of CHD: chronic(stable angina pectoris) and ACSpectoris) and ACS
ACS composed of UAP/NSTEMI and STEMI, ACS composed of UAP/NSTEMI and STEMI, resulting from the plaque rupture or erosion, with resulting from the plaque rupture or erosion, with differing degree of thrombosis and distal differing degree of thrombosis and distal embolization, with different obstruction of the embolization, with different obstruction of the coronary artery.coronary artery.
reperfusion either by fibrinolysis or primary PCI reperfusion either by fibrinolysis or primary PCI is the mainstay of therapy of STEMIis the mainstay of therapy of STEMI
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Thanks!