1、CoronaryAtheroscleroticHeartDiseasesAffiliatedHospitalofJiningMedicalCollegeDept.ofCardiacCareUnitGuoxiaDongdong.10/12/20222ContentsAtherosclerosisStable Angina PectorisAcute Coronary Syndrome UA and NSTEMI AMI(STEMI) 10/12/20223Self-study Variant AnginaCardiac Syndrome XSilent Myocardial Ischemia M

2、yocardial Bridging10/12/20224What Is Atherosclerosis?Atherosclerosis is the descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries. 10/12/20225What Is Coronary Heart Disease?10/12/20226Coronary heart diseaseatherosclerosisCoronary stenosiscoronary s

3、pasmMyocardial ischemia, necrosisIschemic heart disease10/12/2022710/12/20228Atherosclerosis10/12/20229Foam cellFatty steak atheromatous plaqueruptured plaquesFibrous plaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al. Circulation 1995;92:1355-1374.medium damage

4、10/12/202210What damage does atherosclerosis cause?10/12/202211Common locationCoronary Heart DiseaseCarotid Artery DiseasePeripheral Arterial DiseaseChronic Kidney Disease10/12/202212How does atherosclerosis start and progress?10/12/202213Elevated levels of cholesterol and triglycerides in the blood

5、High blood pressureCigarette smoking10/12/202214Biological processesAccumulation of intimal cellssmooth muscle cells MacrophagesT-lymphocytes10/12/202215Biological processesProliferated connective tissue matrixcollagenelastic fibersproteoglycans 10/12/202216Biological processes3.Accumulation of lipi

6、d10/12/202217Atherosclerosis-HypothesisHypothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory The response-to-injury hypothesis 10/12/202218High blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance.Platelets are activated, adhesion and ag

7、gregation of platelets.Lipidoses, growth factor, proliferation of smooth mucle cells, collagen, lipolytic enzyme.Response-to-injury 10/12/202219Pathology and pathophysiologyFatty steakFibrous plaqueComplicated lesion10/12/202220Initiation of AtherosclerosisFatty steak formation10/12/202221Initiation

8、 of Atherosclerosis10/12/202222fibrous plaque10/12/20222310/12/20222410/12/202225Thin CapVulnerable Plaque ThrombusUnstable “ Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina “ Dormant Volcano ”SAPACSpressure or a squeezing pain !10/12/202226Unstable and Stable Plaques薄的纖維帽

9、炎性細胞少的平滑肌細胞內皮細胞不完整巨噬細胞較厚的纖維帽沒有炎性細胞泡沫細胞完整的內皮細胞 較多平滑肌細胞Libby P. Circulation. 1995;91:2844-2850.unstablestable10/12/202228AtherosclerosisClinical stages Absence of symptom or stage of incubationischemianecrosis(target organ )fibrosis10/12/202229clinical manifestationGeneral manifestationAortic atherosc

10、lerosisCoronary artery atherosclerosisCerebral atherosclerosisRA atherosclerosisMesenteric atherosclerosisPeripheral artery atherosclerosis10/12/202230Laboratory ExaminationLack of sensitive and specific methods for early diagnosisDyslipidemiaX-ray：DSA show severity of stenosisDoppler ultrasound: bl

11、ood flow10/12/202231Laboratory Examinationradionuclide： detection of ischemiaEchocardiogram： CHDECG and stress test: CHDAngiography: the most direct wayIntravascular ultrasound, angioscopeCT, MRI10/12/202232Risk factors 1.Lipid disorders (Dyslipidemia)Increased cholesterol :Tc and LDL-c, TG, ApoB,Lp

12、(a)Decreased cholesterol: HDL-c apoA2.Hypertension10/12/202233Risk 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 disease10/12/2022347 year

13、s 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;339:229234.05101520253035404550Events of MI in 7 yearsNo history of MI OMI No history of MI* OMI non-diabetics diabetics n = 1373n = 1059P 0.001P 40yrs ad

14、ults ，4/5 fatal myocardial infarction occured in patiens 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/infection10/12/202236Drug therapyanti-platelet： aspirin, clopidog

15、rel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazolLipid-lowering HMG-CoA reductase inhibitors（statins） 10/12/202237Doubts of patients Quest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?10/12/202238Doubts of patients Question 2：My shape is not fat, lipid is not high,

16、 why give me lipid-lowering drugs, made a mistake?10/12/202239Doubts of patients Question 3：I have coronary heart disease,then should I do less activities in order to protect the heart?10/12/202240Coronary Heart Disease (CHD) 10/12/202241Clinical TypeSilent myocardial ischemiaAngina pectorisMyocardi

17、al infarctionIschemic cardiomyopathySudden cardiac death 10/12/202242Silent Myocardial IschemiaDefined 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 routi

18、ne 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.10/12/202243Ischemic CardiomyopathySym

19、ptoms 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.10/12/202244Sudden Cardiac DeathSCD is natural death due to cardiac c

20、auses, 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

21、 disease，caused by severe arrhythmias, such as ventricular fibrillation and cardiac arrest.10/12/202245Acute Coronary SyndromeACS represents a spectrum of conditions.Acute plaque change characterized by plaque rupture and exposure of substances that promote platelet activation and thrombin generatio

22、n.10/12/202246STABLE ANGINA PECTORIS10/12/202247DefinitionAcute and transient myocardial ischemia and anoxaemia. Usually caused by coronary insufficiency during exertion.10/12/202248Characteristicsparoxysmal precordial squeezing-like chest pain, behind the mid sternumradiated to left shoulder and up

23、per armprecipitated by stress or exertionrelieved rapidly by rest or nitrates 10/12/202249 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

24、mechanism10/12/202250in 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. PathologyStable angina pectoris10/12/202251pathophysiology1.Metabolic and electrophy

25、siologyATP 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 myocardiumStable

26、angina pectoris10/12/202252symptom：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 neckClinical manifestationStable angina pectoris10/12/202253 character：tightness, squeez

27、ing, burning, pressing, choking, bursting,rarely sharpduration：35 minsprecipitating factor exertion or emotional agitationpain relief: within several mins after rest or using nitroglycerin Clinical manifestationStable angina pectoris10/12/202255Physical examinationincreased HR, elevated BP anxiety c

28、ool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifestationStable angina pectoris10/12/202256Auxiliary examination1.ECG：Resting ECG ECG during chest pain: ST-T change found in 95% ptsHolter: detect of slient ischemiaStress testing :Criteria for positive: ST segment

29、 depression 0.1mV，last 2 minscontraindication：AMI, UAP,myocarditis, Hypertension, heart failure,aortic stenosis, HOCM, sever arrhythmia, aortic aneurysmEnd of the test：ST or 0.2mV，AP attacks，BP220mmHg，BP drop，ventricular arrhythmiaStable angina pectoris10/12/202257Stress testrestExersciseStable angi

30、na pectoris10/12/202258 2.Echocardiography: 3. Scintigraphy assessment: Can detect filling defect of Infarction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUSAuxiliary examinationStable angina pectoris10/12/202259Coronary Angiography10/12/202260Stable Angina PectorisDiagn

31、osisChest painrisk factorsECG evidence of ischemia during chest pain angiography10/12/202261Cardiovascular causesNoncardiac causesStable Angina PectorisDifferential diagnosis10/12/202262Cardiovascular causeMyocardial infarction Pericarditis Aortic dissection Pulmonary embolism Pulmonary hypertension

32、 10/12/202263Noncardiac causePneumonia with pleurisy Spontaneous pneumothorax Musculoskeletal disordersHerpes zoster Esophageal reflux Peptic ulcer 10/12/202264General treatment：risk factors control2. Drug therapy3. Coronary revascularization:percutaneous coronary intervention (PCI) Coronary artery

33、bypass surgery (CABG) SVG, IMAGTreatmentStable Angina Pectoris10/12/202265Blood and oxygen supply to the heartMyocardialblood flowMyocardial oxygenconsumption4%of totalcardiac outputsupplied to themyocardium12%of total body oxygen,used at rest bymyocardium10/12/202266Coronary ReserveMyocardialblood

34、flowincreases up to4 times . to meetincreasedmyocardial oxygendemand10/12/202267Myocardial oxygensupply and demandO2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2 supplyO2 demand10/12/202268Aims of medical therapyArterial vasodilatationReduces arterialresistanceReduces afterl

35、oadDecreasessympathetic driveReduce heart rateand contractile forceReduces cardiac workLVRVDilatation ofcoronary arteriesImproves coronarysupplyVenodilatationReducesvenous returnReduces preload10/12/202269antianginal and anti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.Nitratesb.Beta blo

36、ckersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris10/12/202270Drug therapya.Nitrateslower oxygen demand: decrease arteriolar and venous tone, reduce preload and afterload increase coronary supply: Coronary dilatationNitroglycerinIsosorbide dinitrateisosorbide 5-mononitrate

37、(long-acting nitrates)Stable Angina Pectoris10/12/202271Nitrates in anginaReduce preloadthroughvenodilatationReduce afterload bylowering arterialresistanceReduce platelet aggregationIncrease coronary perfusion, includingischaemic areas Reversal of coronary spasm10/12/202272b. blockers: reduce myocar

38、dial oxygen: reduce HR, myocardial contractility, BP,the LV wall stress Abslute 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, bisopr

39、ololDrug therapyStable Angina Pectoris10/12/202273c.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 metabolismDrug the

40、rapyStable Angina Pectoris10/12/202274prevent MI and death therapya.antiplatelet angents：ASAclopidogrelCilostazolb. Lipid-lowering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI)Drug therapyStable Angina Pectoris10/12/202275stentingStable Angina Pectoris10/12/202276Unstable Angina(

41、UA) and non-STEMI10/12/202277ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers *# occasionally variant anginaAcute Coronary Syndrome(ACS)10/12/202278Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0-1%75%90%Increased

42、 FPA/TAT0-5%60-80%80-90%Activated platelets0-5%70-80%80-90%Acute coronary occlusion 0-1%10-25%90%mortality 1-2%3-8%6-15%FPA：fibrinopeptide ATAT：thrombin-antithrombin complexesUA and non-STEMI10/12/202279Occuring at rest (or with mininal exertion): last 20 minssever and of new-onset: within 1-2 month

43、s, CCS IIIOccuring with a crescendo pattern: Deterioration of CCS classfication, at least CCS IIIDefinition UA and non-STEMIAngina pectoris or equivalent ischemic discomfort with at least one of the three features10/12/202280 Braunwald classification of unstable anginaSeverity：Class I：New-onset, or

44、accelerated severe anginano rest 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-STEMI10/12/202281 Braunwald classification of unstable anginaClinical Circumst

45、ances Class A：Secondary UAPa 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-STEMI10/12/202

46、282mechanism： 1.plaque rupture and erosion, with nonocclusive thrombus2.dynamic obstruction: Vasoconstruction 3.progressive mechnial obstruction(rapidly advancing or ISR following stenting) 4.secondary UA InflammationThrombogenesisUA and non-STEMI10/12/202283 ECG:Non-STEMI: ST depression last 12 hrC

47、ardiac biomarkers of myocardium damage: cTnT, cTnICK-MBUAP and non-STEMICoronary angiographyAngioscopy and IVUSOther laboratory tests10/12/202284Treatment 1.Genearl management: rest, oxygen, CCU2. Drug therapy A. Anti-ischemic drug: intravenously, orallynitrates -blocker Calcium antagnoist: first ch

48、oice for variant anginaMorphine sulfateUA and non-STEMI10/12/202285Treatment 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. Anticoagulation therapy:HeparinLow molecular weight heparin(LMWH)Direct anti-thrombin drug: bivalirudin, hirudin UA and non-STEMI10/12/202286Treatment 2. Drug therapy: C. other med