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1、CoronaryAtheroscleroticHeartDiseases,AffiliatedHospitalofJiningMedicalCollegeDept.ofCardiacCareUnitGuoxiaDongdong.,12/6/2022,2,12/6/2022,3,Contents,AtherosclerosisStable Angina PectorisAcute Coronary Syndrome UA and NSTEMI AMI(STEMI),12/6/2022,4,Self-study,Variant AnginaCardiac Syndrome XSilent Myoc
2、ardial Ischemia Myocardial Bridging,12/6/2022,5,What Is Atherosclerosis?,Atherosclerosis is the descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries.,12/6/2022,6,What Is Coronary Heart Disease?,Coronary heart disease,atherosclerosis,Coronary steno
3、sis,coronary spasm,Myocardial ischemia, necrosis,Ischemic heart disease,12/6/2022,8,12/6/2022,9,Atherosclerosis,12/6/2022,10,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 19
4、95;92:1355-1374.,medium damage,12/6/2022,11,What damage does atherosclerosis cause?,12/6/2022,12,Common locationCoronary Heart DiseaseCarotid Artery DiseasePeripheral Arterial DiseaseChronic Kidney Disease,12/6/2022,13,How does atherosclerosis start and progress?,12/6/2022,14,Elevated levels of chol
5、esterol and triglycerides in the bloodHigh blood pressureCigarette smoking,12/6/2022,15,Biological processes,Accumulation of intimal cellssmooth muscle cells MacrophagesT-lymphocytes,12/6/2022,16,Biological processes,Proliferated connective tissue matrixcollagenelastic fibersproteoglycans,12/6/2022,
6、17,Biological processes,3.Accumulation of lipid,12/6/2022,18,Atherosclerosis-Hypothesis,Hypothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory The response-to-injury hypothesis,12/6/2022,19,High blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive
7、substance.Platelets are activated, adhesion and aggregation of platelets.Lipidoses, growth factor, proliferation of smooth mucle cells, collagen, lipolytic enzyme.,Response-to-injury,12/6/2022,20,Pathology and pathophysiology,Fatty steakFibrous plaqueComplicated lesion,12/6/2022,21,Initiation of Ath
8、erosclerosis,Fatty steak formation,12/6/2022,22,Initiation of Atherosclerosis,12/6/2022,23,fibrous plaque,12/6/2022,24,12/6/2022,25,12/6/2022,26,Thin CapVulnerable Plaque ThrombusUnstable “ Active Volcano”,Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina “ Dormant Volcano ”,SAP,ACS,pressu
9、re or a squeezing pain !,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,12/6/2022,28,12/6/2022,29,Atherosclerosis,Clinical stages Absence of symptom or stage of incubationischemianecrosis(target
10、organ )fibrosis,12/6/2022,30,clinical manifestation,General manifestationAortic atherosclerosisCoronary artery atherosclerosisCerebral atherosclerosisRA atherosclerosisMesenteric atherosclerosisPeripheral artery atherosclerosis,12/6/2022,31,Laboratory Examination,Lack of sensitive and specific metho
11、ds for early diagnosisDyslipidemiaX-ray：DSA show severity of stenosisDoppler ultrasound: blood flow,12/6/2022,32,Laboratory Examination,radionuclide： detection of ischemiaEchocardiogram： CHDECG and stress test: CHDAngiography: the most direct wayIntravascular ultrasound, angioscopeCT, MRI,12/6/2022,
12、33,Risk factors,1.Lipid disorders (Dyslipidemia)Increased cholesterol :Tc and LDL-c, TG, ApoB,Lp(a)Decreased cholesterol: HDL-c apoA2.Hypertension,12/6/2022,34,Risk factors,3.DM,Metabolic syndrome or insulin resistance syndrome More diffuse lesion CAD equivalent 75-80% cause of death in adult DM are
13、 vascular diseases: CAD, cerebrovascular disease, or peripheral vascular disease,12/6/2022,35,7 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
14、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,12/6/2022,36,Risk factors,4. Cigarette smoking：more thrombogenic5. Family history6. Aging：40yrs adults ，4/5 fatal myocardial infarction occured in patie
15、ns 65 yrs7. Male gender/ postmenopausal state：male:female = 2：1, men develop CHD 10-15 yrs earlier than women8. alcohol9. Others: diet,homocysteine, hemostatic factors inflammation/infection,12/6/2022,37,Drug therapy,anti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazol
16、Lipid-lowering HMG-CoA reductase inhibitors（statins）,12/6/2022,38,Doubts of patients,Quest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?,12/6/2022,39,Doubts of patients,Question 2：My shape is not fat, lipid is not high, why give me lipid-lowering drugs, made a mistak
17、e?,12/6/2022,40,Doubts of patients,Question 3：I have coronary heart disease,then should I do less activities in order to protect the heart?,12/6/2022,41,Coronary Heart Disease (CHD),12/6/2022,42,Clinical Type,Silent myocardial ischemiaAngina pectorisMyocardial infarctionIschemic cardiomyopathySudden
18、 cardiac death,12/6/2022,43,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 (H
19、olter), 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.,12/6/2022,44,Ischemic Cardiomyopathy,Symptoms of heart failure, caused by isc
20、hemic myocardial dysfunction , diffuse fibrosis, and multiple infarction, alone or in combination.Manifestations: ventricles enlargement (dominant left ventricle), heart failure and arrhythmias.,12/6/2022,45,Sudden Cardiac Death,SCD is natural death due to cardiac causes, heralded by abrupt loss of
21、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 arrhythm
22、ias, such as ventricular fibrillation and cardiac arrest.,12/6/2022,46,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.,12/6/2022,47,STABLE ANGINA P
23、ECTORIS,12/6/2022,48,Definition,Acute and transient myocardial ischemia and anoxaemia. Usually caused by coronary insufficiency during exertion.,12/6/2022,49,Characteristics,paroxysmal precordial squeezing-like chest pain, behind the mid sternumradiated to left shoulder and upper armprecipitated by
24、stress or exertionrelieved rapidly by rest or nitrates,12/6/2022,50,hypoxia,Coronary stenosis(others:aortic valve disease, HOCM) + Myocardial oxygen demand（HRXSBP）increased myocardial hypoxiaacumulation of metabolic product, stimulate C1-5 to cause the sensation of chest pain,mechanism,12/6/2022,51,
25、in angiographySignificant coronary lesion with diameter stenosis 70% in 75% ptsNo significant stenosis in about 5-10% pts, Ischemia may be related to coronary spasm or microvascular dysfunction.,Pathology,Stable angina pectoris,12/6/2022,52,pathophysiology,1.Metabolic and electrophysiologyATP reduce
26、d, 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,
27、12/6/2022,53,symptom：chest pain 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,12/6/2022,55,character：tightness, squeezing, burnin
28、g, pressing, choking, bursting,rarely sharpduration：35 minsprecipitating factor exertion or emotional agitationpain relief: within several mins after rest or using nitroglycerin,Clinical manifestation,Stable angina pectoris,12/6/2022,56,Physical examinationincreased HR, elevated BP anxiety cool and
29、sweaty skin occasionally gallop rhythm，transient systolic murmur,Clinical manifestation,Stable angina pectoris,12/6/2022,57,Auxiliary examination,Stable angina pectoris,12/6/2022,58,Stress test,rest,Exerscise,Stable angina pectoris,12/6/2022,59,2.Echocardiography: 3. Scintigraphy assessment: Can det
30、ect filling defect of Infarction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUS,Auxiliary examination,Stable angina pectoris,12/6/2022,60,Coronary Angiography,12/6/2022,61,Stable Angina Pectoris,Diagnosis,Chest painrisk factorsECG evidence of ischemia during chest pain an
31、giography,12/6/2022,62,Cardiovascular causesNoncardiac causes,Stable Angina Pectoris,Differential diagnosis,12/6/2022,63,Cardiovascular cause,Myocardial infarction Pericarditis Aortic dissection Pulmonary embolism Pulmonary hypertension,12/6/2022,64,Noncardiac cause,Pneumonia with pleurisy Spontaneo
32、us pneumothorax Musculoskeletal disordersHerpes zoster Esophageal reflux Peptic ulcer,12/6/2022,65,General treatment：risk factors control2. Drug therapy3. Coronary revascularization:percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, IMAG,Treatment,Stable Angina Pecto
33、ris,12/6/2022,66,Blood and oxygen supply to the heart,Myocardialblood flow,Myocardial oxygenconsumption,4%of totalcardiac outputsupplied to themyocardium,12%of total body oxygen,used at rest bymyocardium,12/6/2022,67,Coronary Reserve,Myocardialblood flowincreases up to4 times ., to meetincreasedmyoc
34、ardial oxygendemand,12/6/2022,68,Myocardial oxygensupply and demand,O2,O2,O2,O2 supply,O2 demand,12/6/2022,69,Aims of medical therapy,Arterial vasodilatation,Reduces arterialresistance,Reduces afterload,Decreasessympathetic drive,Reduce heart rateand contractile force,Reduces cardiac work,LV,RV,Dila
35、tation ofcoronary arteries,Improves coronarysupply,Venodilatation,Reducesvenous return,Reduces preload,12/6/2022,70,antianginal and anti-ischemic therapy,Drug therapy,Oxygen supply,Oxygen demand,a.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolism,Stable Angina Pectoris,12/6/20
36、22,71,Drug therapy,a.Nitrateslower oxygen demand: decrease arteriolar and venous tone, reduce preload and afterload increase coronary supply: Coronary dilatationNitroglycerinIsosorbide dinitrateisosorbide 5-mononitrate (long-acting nitrates),Stable Angina Pectoris,12/6/2022,72,Nitrates in angina,Red
37、uce preloadthroughvenodilatation,Reduce afterload bylowering arterialresistanceReduce platelet aggregation,Increase coronary perfusion, includingischaemic areas Reversal of coronary spasm,12/6/2022,73,b. blockers: reduce myocardial oxygen: reduce HR, myocardial contractility, BP,the LV wall stress A
38、bslute contraindications：sever bradycardia: high-degree A-V block, SSS, severe unstable LV failureRelative contraindications:asthma and bronchospastic disease peripheral vascular disease 1-selective：metoprolol, atenolol, bisoprolol,Drug therapy,Stable Angina Pectoris,12/6/2022,74,c.Calcium antagonis
39、ts：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,Drug therapy,Stable Angina Pectoris,12/6/2022,75,prevent MI and death therap
40、ya.antiplatelet angents：ASAclopidogrelCilostazolb. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI),Drug therapy,Stable Angina Pectoris,12/6/2022,76,stenting,Stable Angina Pectoris,12/6/2022,77,Unstable Angina(UA) and non-STEMI,12/6/2022,78,ACS,Non-ST elevation,STelev
41、ation,Unstable angina,Non-Q wave AMI,Q wave AMI,*positive serum cardiac markers,*,*,*,*,#,# occasionally variant angina,Acute Coronary Syndrome(ACS),12/6/2022,79,Pathophysiology of ACS,stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0-1%75%90%Increased FPA/TAT0-5%60-80%80-90%Activated plate
42、lets0-5%70-80%80-90%Acute coronary occlusion 0-1%10-25%90%mortality 1-2%3-8%6-15%,FPA：fibrinopeptide ATAT：thrombin-antithrombin complexes,UA and non-STEMI,12/6/2022,80,Occuring at rest (or with mininal exertion): last 20 minssever and of new-onset: within 1-2 months, CCS IIIOccuring with a crescendo
43、 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,12/6/2022,81,Braunwald classification of unstable angina,Severity：Class I：New-onset, or accelerated severe anginano res
44、t pain within 2 monthsClass 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,12/6/2022,82,Braunwald classification of unstable angina,Clinical Circumstances Class A：Secondary UAPa
45、clearly identified condition extrinsic to the coronary vascular bed that has intensified myocardial ischemia, e.g. anemia, hypotension, tachy-arrhythmiaClass B：Primary unstable anginaClass C：Post-infarction UAP (within 2 weeks of a documented MI),UA and non-STEMI,12/6/2022,83,mechanism：,1.plaque rup
46、ture and erosion, with nonocclusive thrombus2.dynamic obstruction: Vasoconstruction 3.progressive mechnial obstruction(rapidly advancing or ISR following stenting) 4.secondary UA InflammationThrombogenesis,UA and non-STEMI,12/6/2022,84,ECG:Non-STEMI: ST depression last 12 hr,Cardiac biomarkers of my
47、ocardium damage: cTnT, cTnICK-MB,UAP and non-STEMI,Coronary angiographyAngioscopy and IVUSOther laboratory tests,12/6/2022,85,Treatment,1.Genearl management: rest, oxygen, CCU2. Drug therapy A. Anti-ischemic drug: intravenously, orallynitrates -blocker Calcium antagnoist: first choice for variant an
48、ginaMorphine sulfate,UA and non-STEMI,12/6/2022,86,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/dGP IIb/IIIa receptor inhibitor: used in pts planned to PCI b. Anticoagulat
49、ion therapy:HeparinLow molecular weight heparin(LMWH)Direct anti-thrombin drug: bivalirudin, hirudin,UA and non-STEMI,12/6/2022,87,Treatment,2. Drug therapy: C. other medical therapy a. lipid-lowering drugs: statins, early use(in first 24 hrs) LDL-c target: 100 mg/dl b. ACEI: long-term secondary pre
50、vention,UA and non-STEMI,12/6/2022,88,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, ACEI,aspirin clopidegrel(12m),UA and non
