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Ischemic Heart Disease

Ischemic Heart Disease

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Ischemic Heart Disease

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  1. Ischemic Heart Disease DrS.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 From First Decade From Third Decade From Fourth Decade

  5. LipidsHTNDiabetes Behavioral HemostaticThrombotic Inflammatory Genetic Cardiovascular Risks Cardiovascular Risks

  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 TransientLV Dysfunction ProgressiveLV Dysfunction Angina & ACS Breathlessness Arrhythmia Most myocardial ischemia is painless (“silent”) … Sudden Death

  8. AnginaClassification • Exertional • Variant • Anginal equivalent syndrome • Prinzmetal’s angina • Syndrome-X • Silent ischemia

  9. 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.

  10. Grading of Angina of Effort by the Canadian Cardiovascular Society

  11. Types of Stressors • Exercise • Treadmill • Bicycle, upright or supine • Pharmacologic • Vasodilators • Dipyridamol • Adenosine • Positive inotropes/chronotropes • Dobutamine

  12. Types of Documents • Imaging • Scintigraphy • Echo • CT angio • Angiography • Exercise

  13. 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

  14. Effects of Treatment of Chronic Stable Angina

  15. Acute Coronary Syndrome

  16. ACSs ACS UA NSTEMI STEMI

  17. 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

  18. Pathophysiology of Acute Coronary Syndromes

  19. Unstable Plaque

  20. 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

  21. The Three I1. Ischemia Epicardial Coronary Artery Lateral Wall of LV Septum Left Ventricular Cavity Positive Electrode Interior Wall of LV

  22. The Three I2. Injury Thrombus Ischemia

  23. The Three I3. Infarction Thrombus Infarcted Area Electrically Silent Ischemia Depolarization

  24. 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

  25. 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

  26. SYMPTOMS SUGGESTIVE OF ACS 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

  27. Risk Scores 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.

  28. Likelihood That S&S Represent an ACS Secondary to CAD

  29. ACC/AHA System for Risk Stratification of Patients with UA

  30. Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy

  31. Angina: Prognosis • LV function • Number of coronary arteries with significant stenosis • Extent of jeoporized myocardium

  32. 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

  33. Preparation for Discharge After UA/NSTEMI • Antiplatelet Rx • ASA 75 - 162 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)

  34. Acetaminophen, ASA, tramadol, narcotic analgesics (short term) Nonacetylated salicylates Non 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 NSAIDs with some COX-2 selectivity COX-2 selective NSAIDs New Pharmacological Therapy for Musculoskeletal Symptoms With Known CVD or Risk Factors for IHD *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.

  35. Myocardial Infarction

  36. 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.

  37. Etiology • Formation of a blood clot on a cholesterol plaque • Occasionally: rupture of the surface of the cholesterol plaque

  38. 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

  39. 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

  40. 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

  41. AMI - Wavefront Phenomenon

  42. Anterolateral Wall MI

  43. Inferior Wall MI

  44. Inferior + RV MI

  45. Posterior Wall MI

  46. Lateral Wall MI