冠状动脉粥样硬化性心脏病英文课件.ppt

1、CoronaryAtheroscleroticHeartDiseasesAffiliatedHospitalofJiningMedicalCollegeDept.ofCardiacCareUnitGuoxiaDongdong.7/5/202227/5/20223ContentsAtherosclerosisStable Angina PectorisAcute Coronary Syndrome UA and NSTEMI AMI(STEMI) 7/5/20224Self-study Variant AnginaCardiac Syndrome XSilent Myocardial Ische

2、mia Myocardial Bridging7/5/20225What Is Atherosclerosis?nAtherosclerosis is the descriptive term for thickened and hardened lesions of the medium and large muscular and elastic arteries. 7/5/20226What Is Coronary Heart Disease?7/5/20227Coronary heart diseaseatherosclerosisCoronary stenosiscoronary s

3、pasmMyocardial ischemia, necrosisIschemic heart disease7/5/202287/5/20229Atherosclerosis7/5/202210Foam cellFatty steak atheromatous plaqueruptured plaquesFibrous plaqueEndothelial damagefirst decadeThird decadeForth decadeAdapted from Stary HC et al. Circulation 1995;92:1355-1374.medium damage 7/5/2

4、02211What damage does atherosclerosis cause?7/5/202212Common locationCoronary Heart DiseaseCarotid Artery DiseasePeripheral Arterial DiseaseChronic Kidney Disease7/5/202213How does atherosclerosis start and progress?7/5/202214nElevated levels of cholesterol and triglycerides in the bloodnHigh blood

5、pressurenCigarette smoking7/5/202215Biological processesn Accumulation of intimal cellsn smooth muscle cells n Macrophagesn T-lymphocytes7/5/202216Biological processesn Proliferated connective tissue matrixn collagenn elastic fibersn proteoglycans 7/5/202217Biological processes3.Accumulation of lipi

6、d7/5/202218Atherosclerosis-HypothesisHypothesis of lipoprotein infiltrationAggregation of platelets and thrombosisClonal theory The response-to-injury hypothesis 7/5/202219nHigh blood pressure,bacterium,virus,toxin,ox-LDL,immune factor,vasoactive substance.nPlatelets are activated, adhesion and aggr

7、egation of platelets.nLipidoses, growth factor, proliferation of smooth mucle cells, collagen, lipolytic enzyme.Response-to-injury 7/5/202220Pathology and pathophysiologyFatty steakFibrous plaqueComplicated lesion7/5/202221Initiation of AtherosclerosisFatty steak formation7/5/202222Initiation of Ath

8、erosclerosis7/5/202223fibrous plaque7/5/2022247/5/2022257/5/202226Thin CapVulnerable Plaque ThrombusUnstable “ Active Volcano”Thick Cap Calcified PlaqueFlow-limiting LesionStable Angina “ Dormant Volcano ”SAPACSpressure or a squeezing pain !Unstable and Stable Plaquesunstablestable7/5/2022287/5/2022

9、29AtherosclerosisnClinical stages nAbsence of symptom or stage of incubationnischemiannecrosis(target organ )nfibrosis7/5/202230clinical manifestationuGeneral manifestationuAortic atherosclerosisuCoronary artery atherosclerosisuCerebral atherosclerosisuRA atherosclerosisuMesenteric atherosclerosisuP

10、eripheral artery atherosclerosis7/5/202231Laboratory ExaminationLack of sensitive and specific methods for early diagnosisDyslipidemiaX-ray：DSA show severity of stenosisDoppler ultrasound: blood flow7/5/202232Laboratory Examinationradionuclide： detection of ischemiaEchocardiogram： CHDECG and stress

11、test: CHDAngiography: the most direct wayIntravascular ultrasound, angioscopeCT, MRI7/5/202233Risk factors n1.Lipid disorders (Dyslipidemia)nIncreased cholesterol :Tc and LDL-c, TG, ApoB,Lp(a)nDecreased cholesterol: HDL-c apoAn2.Hypertension7/5/202234Risk factors n3.DM,Metabolic syndrome or insulin

12、resistance syndrome nMore diffuse lesion CAD equivalentn 75-80% cause of death in adult DM are vascular diseases: n CAD, cerebrovascular disease, or peripheral vascular disease7/5/2022357 years incidence of death/non-fatal MI (East West Study)* These patients had no history of myocardial infarction

13、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 adults ，4/5 fatal myocardial infarction occured in patiens 65 yrs7. Male gender/ postmenopausal state：male:fem

14、ale = 2：1, men develop CHD 10-15 yrs earlier than women8. alcohol9. Others: diet,homocysteine, hemostatic factors inflammation/infection7/5/202237Drug therapyanti-platelet： aspirin, clopidogrel, GPIIb/IIIa inhitibor, Dipyridamole, cilostazolLipid-lowering HMG-CoA reductase inhibitors（statins） 7/5/20

15、2238Doubts of patients nQuest 1：My blood pressure is only about 100/60 mmHg,Why give me hypotensor lotensin?7/5/202239Doubts of patients nQuestion 2：My shape is not fat, lipid is not high, why give me lipid-lowering drugs, made a mistake?7/5/202240Doubts of patients nQuestion 3：I have coronary heart

16、 disease,then should I do less activities n in order to protect the heart?7/5/202241Coronary Heart Disease (CHD)Coronary Heart Disease (CHD) 7/5/202242Clinical TypenSilent myocardial ischemianAngina pectorisnMyocardial infarctionnIschemic cardiomyopathynSudden cardiac death 7/5/202243Silent Myocardi

17、al 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 routine ECG, 24h ambulatory ECG monitoring (Holter), etc. but not experience angina at an

18、y 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.7/5/202244Ischemic CardiomyopathynSymptoms of heart failure, caused by ischemic myocardial dysfunction , diffuse fibrosis,

19、 and multiple infarction, alone or in combination.nManifestations: ventricles enlargement (dominant left ventricle), heart failure and arrhythmias.7/5/202245Sudden Cardiac DeathnSCD is natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of acute s

20、ymptoms.nThe time and mode of death are unexpected. nWHO definition: unexpected death within 6 hours.nThis definition incorporates the key elements of natural, rapid and unexpected.nOne half of SCD due to coronary heart disease，caused by severe arrhythmias, such as ventricular fibrillation and cardi

21、ac arrest.7/5/202246Acute Coronary SyndromeACS represents a spectrum of conditions.Acute plaque change characterized by plaque rupture and exposure of substances that promote platelet activation and thrombin generation.7/5/202247STABLE ANGINA PECTORIS7/5/202248DefinitionAcute and transient myocardia

22、l ischemia and anoxaemia. Usually caused by coronary insufficiency during exertion.7/5/202249Characteristicsparoxysmal precordial squeezing-like chest pain, behind the mid sternumradiated to left shoulder and upper armprecipitated by stress or exertionrelieved rapidly by rest or nitrates 7/5/202250

23、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 mechanism7/5/202251in angiographySignificant coronary lesion with diameter stenosis 70% in

24、75% ptsNo significant stenosis in about 5-10% pts, Ischemia may be related to coronary spasm or microvascular dysfunction. PathologyStable angina pectoris7/5/202252pathophysiology1.Metabolic and electrophysiologyATP reduced, accumulation of acid substances Dysfunction of ion pump (Na+-K+, and Na+-Ca

25、+) 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 angina pectoris7/5/202253symptom：chest pain location behind or slightly to the left of the mid

26、sternum no definite borderlineradiated to the left shoulder and upper armAtypical location: lower jaw, the back of neckClinical manifestationStable angina pectoris7/5/202255 character：tightness, squeezing, burning, pressing, choking, bursting,rarely sharpduration：35 minsprecipitating factor exertion

27、 or emotional agitationpain relief: within several mins after rest or using nitroglycerin Clinical manifestationStable angina pectoris7/5/202256Physical examinationincreased HR, elevated BP anxiety cool and sweaty skin occasionally gallop rhythm，transient systolic murmurClinical manifestationStable

28、angina pectoris7/5/202257 Auxiliary 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 depression 0.1mV，last 2 minscontraindication：AMI, UAP,myocarditis, Hypertension, heart failure,aortic

29、 stenosis, HOCM, sever arrhythmia, aortic aneurysmEnd of the test：ST or 0.2mV，AP attacks，BP220mmHg，BP drop，ventricular arrhythmiaStable angina pectoris7/5/202258Stress testrestExersciseStable angina pectoris7/5/202259 2.Echocardiography: 3. Scintigraphy assessment: Can detect filling defect of Infar

30、ction area 4.X-ray of heart 5.coronary angiography：final diagnose 6.others: IVUSAuxiliary examinationStable angina pectoris7/5/202260Coronary Angiography7/5/202261Stable Angina PectorisDiagnosisuChest painurisk factorsuECG evidence of ischemia during chest painu angiography7/5/202262Cardiovascular c

31、ausesNoncardiac causesStable Angina PectorisDifferential diagnosis7/5/202263Cardiovascular causenMyocardial infarction nPericarditis nAortic dissection nPulmonary embolism nPulmonary hypertension 7/5/202264Noncardiac causenPneumonia with pleurisy nSpontaneous pneumothorax nMusculoskeletal disordersn

32、Herpes zoster nEsophageal reflux nPeptic ulcer 7/5/202265General treatment：risk factors control2. Drug therapy3. Coronary revascularization:percutaneous coronary intervention (PCI) Coronary artery bypass surgery (CABG) SVG, IMAGTreatmentStable Angina Pectoris7/5/202266Blood and oxygen supply to the

33、heartMyocardialblood flowMyocardial oxygenconsumption4%of totalcardiac outputsupplied to themyocardium12%of total body oxygen,used at rest bymyocardium7/5/202267Coronary ReserveMyocardialblood flowincreases up to4 times . to meetincreasedmyocardial oxygendemand7/5/202268Myocardial oxygensupply and d

34、emandO2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2O2 supplyO2 demand7/5/202269Aims of medical therapyArterial vasodilatationReduces arterialresistanceReduces afterloadDecreasessympathetic driveReduce heart rateand contractile forceReduces cardiac workLVRVDilatation ofcoronar

35、y arteriesImproves coronarysupplyVenodilatationReducesvenous returnReduces preload7/5/202270antianginal and anti-ischemic therapyDrug therapyOxygen supplyOxygen demanda.Nitratesb.Beta blockersc.Calcium antagonistsd.Drugs improving metabolismStable Angina Pectoris7/5/202271Drug therapya.Nitrateslower

36、 oxygen demand: decrease arteriolar and venous tone, reduce preload and afterload increase coronary supply: Coronary dilatationNitroglycerinIsosorbide dinitrateisosorbide 5-mononitrate (long-acting nitrates)Stable Angina Pectoris7/5/202272Nitrates in anginaReduce preloadthroughvenodilatationReduce a

37、fterload bylowering arterialresistanceReduce platelet aggregationIncrease coronary perfusion, includingischaemic areas Reversal of coronary spasm7/5/202273b. blockers: reduce myocardial oxygen: reduce HR, myocardial contractility, BP,the LV wall stress Abslute contraindications：sever bradycardia: hi

38、gh-degree A-V block, SSS, severe unstable LV failureRelative contraindications:asthma and bronchospastic disease peripheral vascular disease 1-selective：metoprolol, atenolol, bisoprololDrug therapyStable Angina Pectoris7/5/202274c.Calcium antagonists：Increase oxygen supply: dilate conduit and resist

39、ance vessels, release spasm, improve microvascular functionDecrease oxygen demand: negative inotropic effect, decrease BP Antiplatelet effect d. Drugs improving metabolismDrug therapyStable Angina Pectoris7/5/202275prevent MI and death therapya.antiplatelet angents：ASAclopidogrelCilostazolb. Lipid-l

40、owering angents: statins c. Angiotesin-converting enzyme inhibitor (ACEI)Drug therapyStable Angina Pectoris7/5/202276stentingStable Angina Pectoris7/5/202277Unstable Angina(UA) and non-STEMI7/5/202278ACS Non-ST elevationSTelevationUnstable anginaNon-Q wave AMIQ wave AMI*positive serum cardiac marker

41、s *# occasionally variant anginaAcute Coronary Syndrome(ACS)7/5/202279Pathophysiology of ACS stable angina UAP&non-Q-w AMIQ-w AMIAngiographic thrombus0-1%75%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：fibrino

42、peptide ATAT：thrombin-antithrombin complexesUA and non-STEMI7/5/202280Occuring at rest (or with mininal exertion): last 20 minssever and of new-onset: within 1-2 months, CCS IIIOccuring with a crescendo pattern: Deterioration of CCS classfication, at least CCS IIIDefinition UA and non-STEMIAngina pe

43、ctoris or equivalent ischemic discomfort with at least one of the three features7/5/202281 Braunwald classification of unstable anginaSeverity：Class I：New-onset, or accelerated severe anginano rest pain within 2 monthsClass II：Angina at rest, subacute angina at rest (within the preceding month but n

44、ot within 48 h)Class III：Angina at rest, acute ( within the preceding 48 h) UA and non-STEMI7/5/202282 Braunwald classification of unstable anginaClinical Circumstances Class A：Secondary UAPa clearly identified condition extrinsic to the coronary vascular bed that has intensified myocardial ischemia

45、, e.g. anemia, hypotension, tachy-arrhythmiaClass B：Primary unstable anginaClass C：Post-infarction UAP (within 2 weeks of a documented MI)UA and non-STEMI7/5/202283mechanism： 1.plaque rupture and erosion, with nonocclusive thrombus2.dynamic obstruction: Vasoconstruction 3.progressive mechnial obstru

46、ction(rapidly advancing or ISR following stenting) 4.secondary UA InflammationThrombogenesisUA and non-STEMI7/5/202284 ECG:Non-STEMI: ST depression last 12 hrCardiac biomarkers of myocardium damage: cTnT, cTnICK-MBUAP and non-STEMI7/5/202285Treatment 1.Genearl management: rest, oxygen, CCU2. Drug th

47、erapy A. Anti-ischemic drug: intravenously, orallynitrates -blocker Calcium antagnoist: first choice for variant anginaMorphine sulfateUA and non-STEMI7/5/202286Treatment 2. Drug therapy: B. antithrombotic therapy a. Anti-platelet Aspirin: early, 300mg loading dose ADP-receptor antagonist: clopidogr

48、el 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-STEMI7/5/202287Treatment 2. Drug therapy: C. other medical therapy a. lipid-lo

49、wering drugs: statins, early use(in first 24 hrs) LDL-c target: 100 mg/dl b. ACEI: long-term secondary preventionUA and non-STEMI7/5/202288Treatment 3. Invasive versus conservative strategy early invasive strategy indicated for high risk patients: within 48-72 hrs, Following by coronary revasculariz

50、ation(PCI or CABG)4. Long-term management -blockers, Statin, ACEI,aspirin clopidegrel(12m)UA and non-STEMI7/5/202289Symptoms Suggestive of ACSDefinite ACSNo ST elevationAlgorithm for the Evaluation and Managementof Patients Suspected of Having an ACS.ST elevationPossible ACSChronic Stable AnginaNonc