Ischemic Heart Disease

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

14. Cut section of a coronary artery with complete occlusion

15. Histologic section with recent thrombosis

16. Rupture of Plaque

17. Progression of Myocardial necrosis after occlusion

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

19. 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

20. 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

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

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

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

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

26. 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

27. 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

28. Key Events in Ischemic Damage

29. 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

30. Acute myocardial infarct

31. Acute myocardial infarct

32. Acute MI - 4 days

33. Acute MI

34. Myocardial changes

35. 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

36. Normal myocardium – note central nuclei and intercalated disks

37. Early ischemia- contraction bands

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

39. Early coagulation necrosis- loss of myocyte nuclei

40. MI 4days

41. Later coagulation necrosis – infiltration of neutrophils

42. Remote infarct – fibrous scar

43. 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

44. Complications of MI – Hemopericardium due to rupture

45. Area of infarct Rupture of myocardial infarct hemopericardium

46. MI with rupture

47. Rupture of myocardial infarct

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

49. Rupture of papillary muscle

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