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Dr S.Sadeghian Ischemic Heart Disease. IHD  Imbalance between myocardial oxygen supply and demand.  The most common cause: atherosclerosis  50% stenosis:

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Presentation on theme: "Dr S.Sadeghian Ischemic Heart Disease. IHD  Imbalance between myocardial oxygen supply and demand.  The most common cause: atherosclerosis  50% stenosis:"— Presentation transcript:

1 Dr S.Sadeghian Ischemic Heart Disease

2 IHD  Imbalance between myocardial oxygen supply and demand.  The most common cause: atherosclerosis  50% stenosis: limitation of blood flow on exercise  80%: limitation of blood flow at rest

3 Causes of Myocardial Ischemia  Coronary atherothrombosis  Gradual, progressive   Sudden, ± occlusive   Other causes of  coronary flow  Active spasm   Lack of vasodilatation   Cold  Anemia  Carbon monoxide   High altitude  Cigarette smoking    HR  Exercise, stress  Smoking    LV stress  LVH, HTN   Aortic stenosis, HCM  Cold  Food  Hyperthyroidism Reduced Oxygen Supply Increased Oxygen Demand

4 of CAD: Atherosclerosis Pathophysiology of CAD: Atherosclerosis Foam Cells Fatty Streak Intermediate LesionAtheroma Fibrous Plaque Complicated Lesion/ Rupture From First Decade From Third Decade From Fourth Decade Endothelial Dysfunction

5 Cardiovascular Risks Lipids HTN Diabetes Behavioral Hemostatic Thrombotic InflammatoryGenetic

6 Atherosclerosis is a Diffuse Process  10%: Manifested  Claim  ECG  Other lab data  90%: Hidden  Physician judgment  Careful history taking

7 Myocardial Ischemia Angina & ACS ArrhythmiaBreathlessness Sudden Death Most myocardial ischemia is painless (“silent”) … Transient LV Dysfunction Progressive LV Dysfunction Clinical Manifestations Of IHD

8 Angina Classification  Exertional  Variant  Anginal equivalent syndrome  Prinzmetal’s angina  Syndrome-X  Silent ischemia

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10 Clinical Classification of CP (Chronic Stable Angina) Probability  Definite (typical) angina:  Substernal discomfort, with a characteristic quality and duration and radiation  Provoked by exertion or emotional stress  Relieved by rest or nitroglycerin in less than 10 minutes.  Atypical angina meets 2 of the of characteristics  Noncardiac CP meets  1 of the typical angina characteristics.  “Definitely not” angina: ? CP is unrelated to activity, appears to be clearly non-cardiac origin and is not relieved by nitroglycerin.

11 Grading of Angina of Effort by the Canadian Cardiovascular Society CommentDefinitionCanadian Class Angina only with extraordinary exertion at work or recreation Ordinary physical activity does not cause angina I Angina with walking more that two blocks on a level surface or climbing more that one flight of stairs at a normal pace Slight limitation of ordinary activity II Walking 1-2 blocks on a level surface or climbing 1 flight of stairs at a normal pace Marked limitation of ordinary physical activity III Angina at rest or with minimal activity or stress Inability to carry out any activity without discomfort IV

12 Types of Stressors  Exercise  Treadmill  Bicycle, upright or supine  Pharmacologic  Vasodilators  Dipyridamol  Adenosine  Positive inotropes/chronotropes  Dobutamine

13 Types of Documents  Imaging  Scintigraphy  Echo  CT angio  Angiography  Exercise

14 Anti-ischemic and preventive drugs for IHD  The treatment of angina is aimed at decreasing oxygen demand and/or increasing oxygen supply.  Antiischemic and anti-anginal drugs (most commonly, a combination of these agents is used for management.  A = Anti-platelet (aspirin) and anti-thrombotic therapy and antianginal therapy (nitrates) and ACE inhibitors  B = Beta-blocker and BP  C = Cigarette smoking and Cholesterol lowering agents and Calcium antagonists  D = Diet and Diabetes  E = Education and Exercise

15 Effects of Treatment of Chronic Stable Angina TreatmentAngina ControlImproved Prognosis/ Prevention Of MI NitratesYesNo BBYes CCBs Dihydropyridines: Short acting Long acting Nondihydropyridines: Diltiazem, Verapamil Poor Yes No (prognosis ↓) ? ?No AspirinNoYes Statins?yesYes ACEIs?yesYes PTCAYes? CABGYes

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17 Acute Coronary Syndrome

18 ACSs ACS UANSTEMISTEMI

19 What is ACS?  All have sudden ischemia due to sudden occlusion of one or more of the coronary arteries, resulting in decreased oxygen supply to the heart muscle.  Thrombosis with sub-total (UA, NSTMI) or total coronary artery occlusion (STEMI)  Can not be differentiated in the first hours  All have the same initiating events:  Plaque rupture  Thrombus formation  Vasoconstriction

20 Pathophysiology of Acute Coronary Syndromes

21 Unstable Plaque

22 Pathophysiology of Acute Coronary Syndrome  UA  ST depression, T Wave inversion or normal  No enzyme release  NSTEMI  ST depression, T Wave inversion or normal  Usually no Q waves at presentation  CPK, LDH + Troponin release  STEMI  ST elevation  + Q waves at discharge  CPK, LDH + Troponin release

23 Epicardial Coronary Artery Lateral Wall of LV Positive Electrode Septum Left Ventricular Cavity Interior Wall of LV The Three I 1. Ischemia

24 Thrombus Ischemia The Three I 2. Injury

25 Infarcted Area Electrically Silent Thrombus Depolarization Ischemia The Three I 3. Infarction

26 UA Syndromes  New onset angina (1 month)  Crescendo angina  Increased frequency, severity, or duration (prolonged episodes (>10-15min))  Decrease in exertion required to provoke  Acute coronary syndrome (ACS)  Ischemic chest pain >20 minutes  Onset at rest or awakening from sleep  Failure to abate with >2-3 S.L. NTG  Post infarction angina  Prinzmetal’s (variant) angina

27 Unstable Angina  Up to 70% patients sustain MI over the ensuing 3 months  >90% of AMI result from an acute thrombus obstructing a coronary artery with resultant prolonged ischemia and tissue necrosis

28 SYMPTOMS SUGGESTIVE OF ACS Noncardiac DiagnosisChronic Stable Angina Possible ACS Definite ACS Treatment as indicated by alternative diagnosis ACC/AHA Chronic Stable Angina Guidelines No ST-ElevationST-Elevation Nondiagnostic ECG Normal initial serum cardiac biomarkers ST and/or T wave changes Ongoing pain Positive cardiac biomarkers Hemodynamic abnormalities Evaluate for reperfusion therapy ACC/AHA STEMI Guidelines Observe ≥ 12 h from symptom onset No recurrent pain; negative follow-up studies Recurrent ischemic pain or positive follow-up studies Diagnosis of ACS confirmed Stress study to provoke ischemia Consider evaluation of LV function if ischemia is present (tests may be performed either prior to discharge or as outpatient) Negative Potential diagnoses: nonischemic discomfort; low-risk ACS Arrangements for outpatient follow-up Positive Diagnosis of ACS confirmed or highly likely Admit to hospital Manage via acute ischemia pathway Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.

29 Risk Scores TIMIGRACE History Age Hypertension DM Smoking ↑ Cholesterol Family history History of CAD Age Presentation Severe angina Aspirin within 7 days Elevated markers ST-segment deviation  HR  SBP Elevated creatinine Heart failure Cardiac arrest Elevated markers ST-segment deviation Antman EM, et al. JAMA 2000;284:835–42. Eagle KA, et al. JAMA 2004;291:2727–33. GRACE = Global Registry of Acute Coronary Events; TIMI = Thrombolysis in Myocardial Infarction.

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31 Likelihood That S&S Represent an ACS Secondary to CAD LOW LIKELIHOOD INTERMEDIATE LIKELIHOOD HIGH LIKELIHOODFEATURE Absence Of High- Or Intermediate Likelihood Features But May Have: Absence Of High- likelihood Features And Presence Of Any Of The Following: Any Of The Following Probable ischemic symptoms in absence of any of the intermediate-likelihood characteristics Recent cocaine use Chest or left arm pain or discomfort as chief symptom Age >70 years Male sex Diabetes mellitus Chest or left arm pain or discomfort as chief symptom reproducing prior documented angina Known history of CAD, including MI History Chest discomfort reproduced by palpation Extracardiac vascular disease Transient MR murmur, hypotension, diaphoresis, pulmonary edema, or rales Examination T wave flattening or inversion less than 1 mm in leads with dominant R waves Normal ECG Fixed Q waves ST depression 0.5 to 1 mm or T wave inversion greater than 1 mm New, or presumably new, transient ST-segment deviation (≥1 mm) or T wave inversion in multiple precordial leads ECG Normal Elevated cardiac TnI, TnT, or CK-MB Cardiac markers

32 ACC/AHA System for Risk Stratification of Patients with UA LOW RISK (30 DAYS DEATH/MI RISK: <3%) INTERMEDIATE RISK (30 DAYS DEATH/MI RISK: 3-8%) HIGH RISK (30 DAYS DEATH/MI RISK: 8-15%) FEATURE No High- Or Intermediate- risk Feature But May Have One Of The Following Features: No High-risk Feature But Must Have One Of The Following: At Least One Of The Following: Prior MI, peripheral or cerebrovascular disease, or CABG; prior aspirin use Accelerating tempo of ischemic symptoms in preceding 48 hr History New-onset or progressive CCS class III or IV angina the past 2 wk without prolonged rest pain but with moderate or high likelihood of CAD Prolonged rest angina, now resolved, with moderate or high likelihood of CAD Rest angina <20 min or relieved with rest or sublingual NTG Prolonged ongoing (>20 min) rest painCharacter of pain Age >70Pulmonary edema, most likely caused by ischemia New or worsening MR murmur S 3 or worsening rales Hypotension, bradycardia, tachycardia Age >75 Clinical findings Normal or unchanged ECG during an episode of chest discomfort T wave inversion >0.2 mV Pathologic Q waves Angina at rest with transient ST- segment changes >0.05 mV BBB, new or presumed new Sustained VT ECG normalSlightly elevatedelevatedCardiac markers

33 Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy InvasiveRecurrent angina/ischemia at rest with low-level activities despite intensive medical therapy Elevated cardiac biomarkers (TnT or TnI) New/presumably new ST-segment depression Signs/symptoms of heart failure or new/worsening mitral regurgitation High-risk findings from noninvasive testing Hemodynamic instability Sustained ventricular tachycardia PCI within 6 months Prior CABG High risk score (e.g., TIMI, GRACE) Reduced left ventricular function (LVEF < 40%) ConservativeLow risk score (e.g., TIMI, GRACE) Patient/physician presence in the absence of high-risk features

34 Angina: Prognosis  LV function  Number of coronary arteries with significant stenosis  Extent of jeoporized myocardium

35 Unstable Angina / NTMI Pharmacologic Therapy  ASA and Heparin beneficial for ACSs (UA, NSTEMI, STEMI)  Decrease MVO2 with nitrates, BBs, CCBs, and ACE inhibitors  consider platelet glycoprotein IIb / IIIa inhibitor and / or LMWH

36 Preparation for Discharge After UA/NSTEMI  Antiplatelet Rx  ASA mg/day  Clopidogrel 75 mg/day  Beta blocker  ACEI/ARB  Especially if DM, HF, EF <40%, HTN  Statin  LDL <100 mg/dL (ideally <70 mg/dL)  Secondary prevention measures (control of RF)

37 Pharmacological Therapy for Musculoskeletal Symptoms With Known CVD or Risk Factors for IHD Acetaminophen, ASA, tramadol, narcotic analgesics (short term) Nonacetylated salicylates Non COX-2 selective NSAIDs NSAIDs with some COX-2 selectivity COX-2 selective NSAIDs  Select pts at low risk of thrombotic events  Prescribe lowest dose required to control symptoms  Add ASA 81 mg and PPI to pts at ↑ risk of thrombotic events*  Regular monitoring for sustained hypertension (or worsening of prior BP control), edema, worsening renal function, or GI bleeding  If these occur, consider reduction of the dose or discontinuation of the offending drug, a different drug, or alternative therapeutic modalities, as dictated by clinical circumstances *Addition of ASA may not be sufficient protection against thrombotic events. Reproduced with permission from Antman EM, et al. Circulation 2007;115:1634–42. PPI = proton-pump inhibitor. New

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39 Myocardial Infarction

40 Definition of MI  Death of part of the heart muscle due to its sudden loss of blood supply.  Often causes chest pain and electrical instability of the heart muscle tissue.

41 Etiology  Formation of a blood clot on a cholesterol plaque  Occasionally: rupture of the surface of the cholesterol plaque

42 AMI Clinical Features  Typical: intense, oppressive chest pressure radiating to left arm  Atypical – 25% of all AMIs  Pleuritic or sharp/stabbing CP  Palpable CP (10-33% AMI)  Arm pain only  Indigestion  SOB only (40% in elderly)  “Dizziness” (5% AMI)  Nausea  Syncope

43 Diagnosis of AMI: ECG  Defines location, extent, and prognosis of infarction  ST elevation diagnostic of coronary occlusion  Q-waves do NOT signify completed infarction  ST depression or T inversion: unlikely total coronary occlusion  ST elevation in V4R for RV infarction  Observe up to 24 hrs for non-diagnostic ECG  Differentiate from early repolarization

44 Acute Myocardial Infarction  Wavefront phenomenon of ischemic evolution - endocardium to epicardium  If limited area of infarction  homeostasis achieved  If large area of infarction (>20% LV)  congestive heart failure  If larger area of infarction (>40% LV)  hemodynamic collapse

45 AMI - Wavefront Phenomenon

46 Anterolateral Wall MI

47 Inferior Wall MI

48 Inferior + RV MI

49 Posterior Wall MI

50 Lateral Wall MI

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52 Timing of Release of Various Biomarkers After Acute Myocardial Infarction Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3 rd ed. Rochester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.

53 Markers of MI: Troponin I

54 Sample Admitting Orders  IV access: NS or D 5 W to KVO  Vital signs: Q 1/2 hr until stable, then q 4 hr and PRN. Notify if HR 110; BP 150; RR 22.  Pulse oximetry x 24 hrs  Activity: CBR for 12 hrs, with bedside commode and progress as tolerated after 12 hrs  Monitor:  24 hours  Diet: heart-healthy diet  Medications: MONA:  Morphine  Oxygen nasal: 2L/min x 3 hrs  Nitrates: IV NTG for hrs if no  /  HR or  BP  Aspirin: mg QD  β-blocker: IV→po (if no contraindications): metoprolol 12.5 mg po q6  No prophylactic antiarrhythmics  Heparin  IV: large anterior MI, PCI, LV thrombus, alteplase/reteplase use (for ~48 hours)  SQ: for all other MI  Clopidogrel  GP IIb/IIIa inhibitors ( Eptifibatide)  ACEi in all MI if no hypotension: captopril 6.25 mg po q8  Statin: atorvastatin 80 mg po

55 Indications For Reperfusion  ST elevation >0.2 in 2 adjacent chest leads  ST elevation >0.1 in 2 adjacent limb leads  Dominant R waves and ST depression in V1-V3 (posterior infarct)  New LBBB

56 Absolute Contraindications  Patients >75 years may get less overall benefit than younger patients but advanced age is no longer considered a major contraindication for TT  Previous hemorrhagic stroke at any time; other strokes or cerebrovascular events within one year  Known intracranial neoplasm or AVM  Active internal bleeding (does not include menses)  Suspected aortic dissection

57 Relative Contraindications and Cautions for Fibrinolytics in AMI  Severe uncontrolled HTN on presentation (BP >180/110 mm Hg)  History of severe poorly controlled chronic hypertension  History of prior nonhemorrhagic CVA beyond 1 yr or known intra-cerebral pathology not covered in contraindications  Current use of anticoagulants in therapeutic doses (INR  2-3); no bleeding diathesis  Recent trauma (within 2-4 weeks) including head injury  Recent (within 2-4 weeks) internal bleeding  Active peptic ulcer  Known bleeding diathesis (e.g., from significant liver dysfunction, or neoplasm)  Pregnancy  For SK, APSAC, anistreplase: prior exposure (especially within 5 d-2 yrs) or prior allergic reaction  Prior central venous or noncompressible vascular puncture Prolonged cardiopulmonary resuscitation (>10 minutes)  Recent surgery (<2 weeks) excluding intracranial or spinal surgery which may require a longer interval

58 Risks  Bleeding is the primary complication of TT and stroke is the greatest concern (1.8%)  Stroke: 1.4%. Predictors:  Patients with a previous TIA or stroke were at particularly high risk  Older age  SBP >140 mm Hg  DBP >100 mm Hg  Lower body weight  Allergic reactions can be seen in patients treated with SK

59 Extension / Ischemia Complications of AMI AMI Arrhythmia Heart Failure Expansion / Aneurysm RV Infarct Pericarditis Mechanical Mural Thrombus

60 AMI Management Pharmacologic Therapy on Hospital Discharge  Aspirin indefinitely (ticlopidine or clopidogrel for aspirin allergy or intolerance)  Beta blockers for at least 2-3 years  ACE inhibitors for CHF, LVEF <40%, or large infarction (even with preserved LVEF)  Lipid lowering agents  Warfarin for mural thrombus, extensive anterior infarct, DVT, AF

61 Risk Stratification Post-MI Revascularization Strategy Low Risk High Risk*  LV SF Nl LV SF Stress Imaging or Catheterization Stress Imaging or Catheterization Nl LV SF  LV SF Angiography ± Revascularization Angiography ± Revascularization Stress Imaging Normal Direct Cath Direct Cath * (Re) MI or CP, VT, CHF, Prior MI, Prior Revascularization

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