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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 William J Hunter MD

  2. Types of Heart Disease • Acquired Heart Disease • Congenital Heart Disease

  3. Acquired Heart Disease • Ischemic Heart Disease • Hypertensive Heart Disease • Valvular Heart Disease • Myocardial Heart Disease

  4. Ischemic Heart Disease • Supply of oxygen in the coronary arterial blood is inadequate to provide for the oxygen demands of the heart.

  5. Epidemiology of ischemic heart disease • 500,000 die • Overall rate has fallen since 1980 • Prevention - working on risk factors: smoking, hypertension, cholesterol, better diabetic control, aspirin prophylaxis • Therapeutic advances- new medications, coronary care units, thrombolysis, angioplasty, stents and coronary bypass surgery

  6. Results of Ischemic HD • Angina Pectoris - ASVD • Stable angina • Prinzmetal’s angina - spasm • Preinfarction (unstable) angina - MI • Myocardial Infarct- myocardial necrosis • Sudden cardiac death • Chronic ischemic HD with heart failure- ‘focal fibrosis’ or presbycardia

  7. Acute Coronary Syndromes • The new ‘in’ word- TV ads • A spectrum -from unstable angina to acute myocardial infarct • Atherosclerotic plaque disruption and associated platelet-fibrin thrombus formation • Sudden death

  8. Acute coronary Syndrome

  9. Etiology of Ischemic HD • 95-98% Atherosclerotic Narrowing with plaques • Coronary embolism (rare) • Dissecting aneurysm (rare) • Arteritis (polyarteritis, rheumatoid, Kawasaki Disease) (rare) • Syphilis (rare) • Cocaine abuse

  10. Coronary Atherosclerosis • 90% have at least one 75% occlusion- the key is acute change of the plaque • Hemorrhage into the atheroma • Rupture of the plaque with thrombosis • Erosion or ulceration of the plaque with thrombosis • Most have two arteries involved • Most blocks are in the epicardial arteries

  11. Atherosclerotic plaque

  12. Hemorrhage into plaque compromises lumen

  13. Cut section of a coronary artery with complete occlusion

  14. Histologic section with recent thrombosis

  15. Rupture of Plaque

  16. Progression of Myocardial necrosis after occlusion

  17. Myocardial Infarct • Most have • >75% occlusion of coronary by plaque • multi-vessel disease • 80% have recent thrombus • LAD most commonly involved

  18. Typical MI • Most have multivessel disease • Ulcerative stenotic plaque or hemorrhage into the plaque • Platelets aggregate • Tissue thromboplastin released • Vasoactive amines released • Thrombosis and spasm occur • Ischemic necrosis

  19. Arteries involved • LAD (40 - 50%) Anterior wall, apex, Anterior 2/3 septum • RCA (30- 40%) Post wall, post 1/3 septum • LCA (15- 20%) Lateral wall

  20. Role of Hemodynamic Changes • Sudden drop in BP • Must be difference in pressure between coronary ostia and coronary sinus

  21. Role of Vasospasm • Vasospasm documented in angina • Spasm can cause rupture of plaques • Rare cases of MI after spasm

  22. Role of Platelet • Rupture of Plaques > adherence • The aggregation contributes to blockage • Thromboxane, histamine, serotonin => vasospasm • ASA helps

  23. Supply of O2 in the Blood • Anemia • CO and cyanide • O2 demand • Hypertension • Valvular disease • Hyperthyroidism • Fever • Catecholamines • (? personality types)

  24. Role of acute Plaque Change in MI • Hemorrhage into the atheroma - expanding its volume • Rupture or fissuring, exposing the highly thrombogenic plaque constituent • Erosion or ulceration • Note that the original plaque may not have been a significant lesion (no critical stenosis

  25. Time of Day • Peak incidence of MI: 6am to noon • Adrenergic stimulation of awakening can put more stress on the plaque • Surge of blood pressure at same time frame

  26. Key Events in Ischemic Damage

  27. Gross Changes of MI • Up to 5 hours- no changes • 6-24 hour- pallor • 24-48 hours- central pallor - hyperemia at margins • 2-5 days - hyperemic border, yellow band, soft dull center • 5-10 days- broader yellow border and thin new pink border • 10 days-3 wks - islands of red brown tissue surrounded by red-purple granulation tissue • 3-6 weeks - fibrosis

  28. Acute myocardial infarct

  29. Acute myocardial infarct

  30. Acute MI - 4 days

  31. Acute MI

  32. Myocardial changes

  33. Histology of MI • 0-6 hours - none (? waviness) • 6-24 hours- eosinophilia, loss of cross striation • 24-48 hours- coagulative necrosis, PMN • 2-5 days- phagocytosis, granulation tissue • 10 days - 3weeks increasing fibrosis, PMN’s disappear • 3-6 weeks - maturing fibrosis

  34. Normal myocardium – note central nuclei and intercalated disks

  35. Early ischemia- contraction bands

  36. Early MI – coagulation necrosis. Pyknosis and karyolysis of nuclei

  37. Early coagulation necrosis- loss of myocyte nuclei

  38. MI 4days

  39. Later coagulation necrosis – infiltration of neutrophils

  40. Remote infarct – fibrous scar

  41. Complications of MI • Arrhythmias (90%) • CHF 60% • Cardiogenic shock 10% • Rupture (wall, septum, PAP M.) 5-10% • Mural thrombus and embolism • Pericarditis • Ventricular Aneurysms • Papillary muscle dysfunction

  42. Complications of MI – Hemopericardium due to rupture

  43. Area of infarct Rupture of myocardial infarct hemopericardium

  44. MI with rupture

  45. Rupture of myocardial infarct

  46. Rupture of ventricular septum– giving rise to Acute right heart failure

  47. Rupture of papillary muscle

  48. Infarct of papillary muscle – leading to mitral valve dysfunction