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Ischemic Heart Disease

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Presentation on theme: "Ischemic Heart Disease"— Presentation transcript:

1 Ischemic Heart Disease
Dr S.Sadeghian

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
Reduced Oxygen Supply Increased Oxygen Demand 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

4 Endothelial Dysfunction
Pathophysiology of CAD: Atherosclerosis Complicated Lesion/ Rupture Foam Cells Fatty Streak Intermediate Lesion Atheroma Fibrous Plaque Atherosclerosis is a progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as UA, myocardial infarction, and stroke. Pepine CJ. The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: potential role in myocardial ischemia. Am J Cardiol. 1998; 82(suppl 10A): Endothelial Dysfunction From First Decade From Third Decade From Fourth Decade 9

5 Hemostatic Thrombotic
Cardiovascular Risks Cardiovascular Risks Slide 2. Beyond cholesterol: predicting cardiovascular risk in the 21st century As we understand more about the biology of atherothrombosis, we need to move beyond standard cholesterol screening if we are to appreciate the promise of preventive early intervention therapies. While hyperlipidemia, hypertension, and diabetes, as well as the behavioral risk factors of smoking and diet, remain major critical modifiable risk factors for vascular disease, we have learned over the years that many hemostatic and thrombotic markers such as lipoprotein(a), D-dimer, and homocysteine, inflammatory markers such as C-reactive protein (CRP), fibrinogen, and interleukin-6, and genetic markers are all part of the evolving understanding of cardiovascular risk. Keywords: markers, risk factors Slide type: figure (chart) Lipids HTN Diabetes Behavioral Hemostatic Thrombotic Inflammatory Genetic

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

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

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


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
Comment Definition Canadian 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 Pharmacologic Treadmill
Bicycle, upright or supine Pharmacologic Vasodilators Dipyridamol Adenosine Positive inotropes/chronotropes Dobutamine

13 Types of Documents Imaging Exercise 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
Angina Control Improved Prognosis/ Prevention Of MI Nitrates Yes No BB CCBs Dihydropyridines: Short acting Long acting Nondihydropyridines: Diltiazem, Verapamil Poor No (prognosis ↓) ? ?No Aspirin Statins ?yes ACEIs PTCA CABG


17 Acute Coronary Syndrome

The ACSs consist of acute myocardial infarction, which is subdivided into Q wave and non-Q infarctions, and a related condition referred to as UA. As their name implies, Q wave MI (QMI) and non-Q wave MI (NQMI) are differentiated by the presence or absence of a pathological Q wave on the 12-lead ECG. Both produce tissue necrosis, QWMI tends to produce more necrosis and, therefore, may be a larger infarct. UA (USA) does not produce infarction, that is does not show evidence of tissue necrosis, but is included in ACS because of its common pathophysiology. UA NSTEMI STEMI

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 Usually no Q waves at presentation CPK, LDH + Troponin release STEMI ST elevation + Q waves at discharge

23 The Three I 1. Ischemia Epicardial Coronary Artery Lateral Wall of LV Septum Left Ventricular Cavity The vessel lumen is now narrowed by a clot. If the clot is incomplete or collateral circulation is good, only the hardworking, poorly perfused sub-endocardial tissue will become ischemic. This is represented on the ECG by ST depression or T wave inversion. Positive Electrode Interior Wall of LV

24 The Three I 2. Injury Thrombus If the clot is complete or the collateral circulation is poor, the ischemia will be transmural (through to wall). This is seen on the ECG as ST segment elevation. Most often this occurs due to a complete and persistent clot. Spontaneous lysis at this point is rare and the tissue is expected to infarct unless acute reperfusion therapy can be rapidly initiated. ST segment elevation is presumptive evidence of ACUTE MI. Ischemia

25 The Three I 3. Infarction Thrombus Infarcted Area Electrically Silent During the evolution of an infarct, Q waves, ST elevation, and T inversion may occur together. ST elevation is the most important finding to the emergency care provider. It is presumptive evidence of acute myocardial infarction. Ischemia Depolarization

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

Definite ACS Noncardiac Diagnosis Chronic Stable Angina Possible ACS No ST-Elevation ST-Elevation Treatment as indicated by alternative diagnosis ACC/AHA Chronic Stable Angina Guidelines ST and/or T wave changes Ongoing pain Positive cardiac biomarkers Hemodynamic abnormalities Nondiagnostic ECG Normal initial serum cardiac biomarkers Observe ≥ 12 h from symptom onset Evaluate for reperfusion therapy 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) ACC/AHA STEMI Guidelines Negative Potential diagnoses: nonischemic discomfort; low-risk ACS 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. Arrangements for outpatient follow-up

29 Risk Scores TIMI GRACE History Age Hypertension DM Smoking
↑ Cholesterol Family history History of CAD Presentation Severe angina Aspirin within 7 days Elevated markers ST-segment deviation  HR  SBP Elevated creatinine Heart failure Cardiac arrest 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.


31 Likelihood That S&S Represent an ACS Secondary to CAD
LOW LIKELIHOOD INTERMEDIATE LIKELIHOOD HIGH LIKELIHOOD FEATURE 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 pain Character of pain Age >70 Pulmonary edema, most likely caused by ischemia New or worsening MR murmur S3 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 normal Slightly elevated elevated Cardiac markers

33 Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy
Recurrent 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%) Conservative Low 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
New 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.


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 Anterior AMI

47 Inferior Wall MI Inferior AMi

48 Inferior + RV MI Inferolateral AMI

49 Posterior Wall MI

50 Lateral Wall MI High lateral AMI


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. 3rd 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 D5W to KVO Vital signs: Q 1/2 hr until stable, then q 4 hr and PRN. Notify if HR <60 or >110; BP <90 or >150; RR <8 or >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 Complications of AMI Extension / Ischemia Arrhythmia Pericarditis
Expansion / Aneurysm AMI RV Infarct Heart Failure 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* Nl LV SF  LV SF Nl LV SF  LV SF Stress Imaging or Catheterization Stress Imaging Direct Cath Normal Angiography Revascularization * (Re) MI or CP, VT, CHF, Prior MI, Prior Revascularization


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