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Cardiovascular Pathology (modification of Dr. Veinot’s presentation)

Cardiovascular Pathology (modification of Dr. Veinot’s presentation)

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Cardiovascular Pathology (modification of Dr. Veinot’s presentation)

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  1. Cardiovascular Pathology(modification of Dr. Veinot’s presentation) Michel Dionne MD FRCPC for John P. Veinot MD FRCPC Professor of Pathology University of Ottawa Pathology and Laboratory Medicine Ottawa Hospital

  2. You may only access and use this PowerPoint presentation for educational purposes. You may not post this presentation online or distribute it without the permission of the author.

  3. Overview Atherosclerosis Aneurysms Ischemic heart disease Cardiomyopathies Valvular heart disease Hypertension

  4. CVS Anatomy 101

  5. Endothelium

  6. muscular artery intima media adventitia

  7. Aorta

  8. Media of aorta – an elastic artery

  9. Atherosclerosis Disease of large and medium sized arteries (elastic and muscular), particularly: aorta, iliac, coronary, popliteal, carotid, circle of Willis Develop intimal lesions called atheromas or atheromatous plaques which: protrude into the lumen resulting in stenosis (narrowing of lumen) and possibly occlusion (lumen blocked) can weaken the underlying media, possibly leading to aneurysm formation

  10. Atherosclerosis - risk factors Hyperlipidemia high LDL low HDL Hypertension Smoking Diabetes Age Male gender Family history/ genetics Other: physical inactivity, diet, obesity etc.

  11. Atherosclerosis - pathogenesis • Chronic endothelial injury* resulting in endothelial dysfunction • increased permeability • increased adhesion of leukocytes (monocytes and lymphocytes) and platelets • accumulation of lipids in intima • Migration of monocytes into intima leading to formation of foam cells (lipid-laden macrophages) • Release of cytokines and growth factors result in smooth muscle cell migration into intima, proliferation of smooth muscle cells, deposition of extracellular matrix (e.g. collagen) * From hemodynamic forces, hyperlipidemia, HTN, smoking etc.

  12. From: Robbins and Cotran Pathologic Basis of Disease, 8th Edition

  13. Aorta – fatty streaks

  14. Aorta – fibrofatty/atheromatous plaques

  15. Aorta – complicated plaques

  16. Aortic arch vessels – advanced plaques causing severe stenosis

  17. Coronary artery

  18. Atheromatous material – foam cells (lipid laden macrophages) and cholesterol clefts

  19. From: Robbins and Cotran Pathologic Basis of Disease, 8th Edition

  20. Atherosclerosis - complications Calcification Plaque hemorrhage and rupture Plaque erosion/ulceration Thrombosis Embolization of atheromatous material (atheroemboli) Aneurysm formation and rupture

  21. Renal infarct from embolization

  22. Atherosclerosis - major consequences Symptomatic disease most often affects the heart, brain, kidneys and lower extremities Heart: angina and myocardial infarction Brain: cerebral infarction (stroke) Aorta (particularly abdominal): Aneurysms Stenosis of ostia of major branches leading to visceral ischemia Lower extremities: peripheral vascular (arterial) disease – claudication, gangrene

  23. Aneurysm - definition a localized abnormal dilatation of a vessel

  24. Aneurysm types Atherosclerotic aneurysms are the most common, but there are other types!

  25. Aneurysms - complications Stasis of blood Thrombosis obstruction embolism Mass effect Rupture

  26. Abdominal Aortic Aneurysm (AAA) thrombus

  27. Aneurysm rupture blood lumen tear thrombus vessel wall

  28. AAA rupture Hemorrhage into surrounding tissue

  29. Dissecting “aneurysm”

  30. Coronary artery aneurysms secondary to vasculitis (inflammation of blood vessels)

  31. Left lung SVC Aorta Left atrium Pericardium Right lung Right atrium Left ventricle Right ventricle

  32. Left atrium Right atrium Left ventricle Right ventricle Interventricular septum

  33. Coronary artery anatomy

  34. Coronary artery atherosclerosis affects the epicardial arteries; tends to be more pronounced in the proximal portion of these vessels can involve 1, 2 or all 3 of the main vessels +/- their large branches if degree of obstruction is significant, can result in angina (pain from myocardial ischemia) an atherosclerotic plaque can become unstable (acute plaque lesion): intraplaque hemorrhage plaque rupture or erosion resulting in thrombosis acute plaque lesions can result in an “acute coronary syndrome” (unstable angina, myocardial infarct)

  35. Myocardial infarct terminology

  36. Recent MI - about 24 hours old

  37. Contraction band necrosis

  38. Recent MI - about 3 days old

  39. Recent MI - interstitial infiltrate of neutrophils

  40. Recent MI - 5-7 days old

  41. Recent MI - 7-10 days old “Sick” myocytes bordering the infarct Phagocytosis of dead cells at margin of infarct Residual necrotic myocytes

  42. Remote myocardial infarcts