1、Coronary Atherosclerotic Heart Diseases 210/31/2022ContentsAtherosclerosisStable Angina PectorisAcute Coronary Syndrome UA and NSTEMI AMI(STEMI)310/31/2022Self-study Variant AnginaCardiac Syndrome XSilent Myocardial Ischemia Myocardial Bridging410/31/2022What Is Atherosclerosis?Atherosclerosis is th
2、e descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries.510/31/2022What Is Coronary Heart Disease?610/31/2022Coronary heart diseaseatherosclerosisCoronary stenosiscoronary spasmMyocardial ischemia,necrosisIschemic heart disease710/31/2022810/31/202
3、2Atherosclerosis910/31/2022Foam cellFatty steak atheromatous plaqueruptured plaquesFibrous plaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al.Circulation 1995;92:1355-1374.medium damage 10/31/202210What damage does atherosclerosis cause?1110/31/2022Common locatio
4、n Coronary Heart Disease Carotid Artery Disease Peripheral Arterial Disease Chronic Kidney Disease1210/31/2022How does atherosclerosis start and progress?1310/31/2022 Elevated levels of cholesterol and triglycerides in the blood High blood pressure Cigarette smoking1410/31/2022Biological processes1.
5、Accumulation of intimal cells smooth muscle cells Macrophages T-lymphocytes1510/31/2022Biological processes2.Proliferated connective tissue matrix collagen elastic fibers proteoglycans1610/31/2022Biological processes3.Accumulation of lipid1710/31/2022Atherosclerosis-HypothesisHypothesis of lipoprote
6、in infiltrationAggregation of platelets and thrombosisClonal theory The response-to-injury hypothesis 1810/31/2022 High blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance.Platelets are activated,adhesion and aggregation of platelets.Lipidoses,growth factor,proliferation o
7、f smooth mucle cells,collagen,lipolytic enzyme.Response-to-injury 1910/31/2022Pathology and pathophysiologyFatty steakFibrous plaqueComplicated lesion2010/31/2022Initiation of AtherosclerosisFatty steak formation2110/31/2022Initiation of Atherosclerosis2210/31/2022fibrous plaque2310/31/20222410/31/2
8、0222510/31/2022Thin CapVulnerable Plaque ThrombusUnstable“Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina“Dormant Volcano”SAPACSpressure or a squeezing pain!2610/31/2022Unstable and Stable Plaquesunstablestable10/31/202228Atherosclerosis Clinical stages Absence of symptom
9、or stage of incubation ischemia necrosis(target organ)fibrosis2910/31/2022clinical manifestationuGeneral manifestationuAortic atherosclerosisuCoronary artery atherosclerosisuCerebral atherosclerosisuRA atherosclerosisuMesenteric atherosclerosisuPeripheral artery atherosclerosis3010/31/2022Laboratory
10、 ExaminationLack of sensitive and specific methods for early diagnosisDyslipidemiaX-ray：DSA show severity of stenosisDoppler ultrasound:blood flow3110/31/2022Laboratory Examinationradionuclide：detection of ischemiaEchocardiogram：CHDECG and stress test:CHDAngiography:the most direct wayIntravascular
11、ultrasound,angioscopeCT,MRI3210/31/2022Risk factors 1.Lipid disorders(Dyslipidemia)Increased cholesterol:Tc and LDL-c,TG,ApoB,Lp(a)Decreased cholesterol:HDL-c apoA 2.Hypertension3310/31/2022Risk factors 3.DM,Metabolic syndrome or insulin resistance syndrome More diffuse lesion CAD equivalent 75-80%c
12、ause of death in adult DM are vascular diseases:CAD,cerebrovascular disease,or peripheral vascular disease3410/31/20227 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;339:229234.05101520253035404550Even
13、ts of MI in 7 yearsNo history of MI OMI No history of MI*OMI non-diabetics diabetics n=1373n=1059P 0.001P 40yrs adults，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,homocy
14、steine,hemostatic factors inflammation/infection3610/31/2022Drug therapyanti-platelet：aspirin,clopidogrel,GPIIb/IIIa inhitibor,Dipyridamole,cilostazolLipid-lowering HMG-CoA reductase inhibitors（statins）3710/31/2022Doubts of patients Quest 1：My blood pressure is only about 100/60 mmHg,Why give me hyp
15、otensor lotensin?3810/31/2022Doubts of patients Question 2：My shape is not fat,lipid is not high,why give me lipid-lowering drugs,made a mistake?3910/31/2022Doubts of patients Question 3：I have coronary heart disease,then should I do less activities in order to protect the heart?4010/31/2022Coronary
16、 Heart Disease(CHD)10/31/202241Clinical Type Silent myocardial ischemia Angina pectoris Myocardial infarction Ischemic cardiomyopathy Sudden cardiac death 10/31/202242Silent Myocardial IschemiaDefined as documented episodes of ischemia not associated with any typical or atypical symptoms that among
17、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
18、chest discomfort and other episodes are asymptomatic.10/31/202243Ischemic 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 a
19、nd arrhythmias.10/31/202244Sudden 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 k
20、ey 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.10/31/202245Acute Coronary Syndrome ACS represents a spectrum of conditions.Acute plaque change characterized by plaque rupture a
21、nd exposure of substances that promote platelet activation and thrombin generation.10/31/202246Stable Angina Pectoris4710/31/2022Definition Acute and transient myocardial ischemia and anoxaemia.Usually caused by coronary insufficiency during exertion.4810/31/2022Characteristics paroxysmal precordial
22、 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 4910/31/2022 hypoxia Coronary stenosis(others:aortic valve disease,HOCM)+Myocardial oxygen demand（HRXSBP）increased myocardial hypoxiaacumu
23、lation of metabolic product,stimulate C1-5 to cause the sensation of chest pain mechanism5010/31/2022in 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
24、Stable angina pectoris5110/31/2022pathophysiology1.Metabolic and electrophysiologyATP 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
25、 decreased LVED pressure and volume Stunning of myocardiumStable angina pectoris5210/31/2022symptom：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 manifestatio
26、nStable angina pectoris5310/31/2022 character：tightness,squeezing,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 pectoris5510/31/20
27、22Physical examinationincreased HR,elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifestationStable angina pectoris5610/31/2022 Auxiliary examination1.ECG：Resting ECG ECG during chest pain:ST-T change found in 95%ptsHolter:detect of slient isc
28、hemiaStress testing:Criteria for positive:ST segment 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 pectoris5
29、710/31/2022Stress testrestExersciseStable angina pectoris5810/31/2022 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 pectoris5910/31/2022Coronary Angiogra
30、phy6010/31/2022Stable Angina PectorisDiagnosisuChest painurisk factorsuECG evidence of ischemia during chest painu angiography6110/31/2022Cardiovascular causesNoncardiac causesStable Angina PectorisDifferential diagnosis6210/31/2022Cardiovascular cause Myocardial infarction Pericarditis Aortic disse
31、ction Pulmonary embolism Pulmonary hypertension 6310/31/2022Noncardiac cause Pneumonia with pleurisy Spontaneous pneumothorax Musculoskeletal disorders Herpes zoster Esophageal reflux Peptic ulcer 6410/31/20221.General treatment：risk factors control2.Drug therapy3.Coronary revascularization:percutan
32、eous coronary intervention(PCI)Coronary artery bypass surgery(CABG)SVG,IMAGTreatmentStable Angina Pectoris6510/31/2022Blood and oxygen supply to the heartMyocardialblood flowMyocardial oxygenconsumption4%of totalcardiac outputsupplied to themyocardium12%of total body oxygen,used at rest bymyocardium
33、10/31/202266Coronary ReserveMyocardialblood flowincreases up to4 times.to meetincreasedmyocardial oxygendemand10/31/202267Myocardial oxygensupply and demandO2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2 supplyO2 demand10/31/202268Aims of medical therapyArterial vasodilatati
34、onReduces arterialresistanceReduces afterloadDecreasessympathetic driveReduce heart rateand contractile forceReduces cardiac workLVRVDilatation ofcoronary arteriesImproves coronarysupplyVenodilatationReducesvenous returnReduces preload10/31/202269antianginal and anti-ischemic therapyDrug therapyOxyg
35、en supplyOxygen demanda.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris7010/31/2022Drug therapya.Nitrateslower oxygen demand:decrease arteriolar and venous tone,reduce preload and afterload increase coronary supply:Coronary dilatationNitroglycerinIsosor
36、bide dinitrateisosorbide 5-mononitrate(long-acting nitrates)Stable Angina Pectoris7110/31/2022Nitrates in anginaReduce preloadthroughvenodilatationReduce afterload bylowering arterialresistanceReduce platelet aggregationIncrease coronary perfusion,includingischaemic areas Reversal of coronary spasm1
37、0/31/202272b.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 failureRelative contraindications:asthma and bronchospastic disease peripheral vascular disease 1-selective
38、：metoprolol,atenolol,bisoprololDrug therapyStable Angina Pectoris7310/31/2022c.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 improvi
39、ng metabolismDrug therapyStable Angina Pectoris7410/31/2022prevent MI and death therapya.antiplatelet angents：ASAclopidogrelCilostazolb.Lipid-lowering angents:statins c.Angiotesin-converting enzyme inhibitor(ACEI)Drug therapyStable Angina Pectoris7510/31/2022stentingStable Angina Pectoris7610/31/202
40、2Unstable Angina(UA)and non-STEMI7710/31/2022ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac markers*#occasionally variant anginaAcute Coronary Syndrome(ACS)7810/31/2022Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0-1%7
41、5%90%Increased 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-STEMI7910/31/2022Occuring at rest(or with mininal exertion):last 20 minssever and of new-onset:withi
42、n 1-2 months,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 features8010/31/2022 Braunwald classification of unstable anginaSeverity：Class I：New-on
43、set,or 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-STEMI8110/31/2022 Braunwald classification of unstable anginaClinical Circums
44、tances 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-STEMI8210/31/2022m
45、echanism：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-STEMI8310/31/2022 ECG:Non-STEMI:ST depression last 12 hrCardiac bi
46、omarkers of myocardium damage:cTnT,cTnICK-MBUAP and non-STEMI8410/31/2022Treatment 1.Genearl management:rest,oxygen,CCU2.Drug therapy A.Anti-ischemic drug:intravenously,orallynitrates-blocker Calcium antagnoist:first choice for variant anginaMorphine sulfateUA and non-STEMI8510/31/2022Treatment 2.Dr
47、ug 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 d
48、rug:bivalirudin,hirudin UA and non-STEMI8610/31/2022Treatment 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 preventionUA and non-STEMI8710/31/2022Treatment 3.Invasive versus conservative strategy earl
49、y 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-STEMI8810/31/202210/31/202289Symptoms Suggestive of ACSDefinite ACSNo ST elevationAlgorithm for th
50、e Evaluation and Managementof Patients Suspected of Having an ACS.ST elevationPossible ACSChronic Stable AnginaNoncardiac DiagnosisTreatment as indicated byalternative diagnosisSee ACC/AHA/ACPGuidelines for ChronicStable AnginaNondiagnostic ECGNormal Initial serumcardiac markersST and/or T wave chan
