1. Introduction to Cardiovascular Pathology - Fred Clayton
Systemic Pathology of Congestive Heart Failure
Pathology of Myocarditis
Pathology of Cardiomyopathy
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy

2. Congestive Heart Failure
Cardiac output insufficient for metabolic requirements of the body
Systolic dysfunction – decreased myocardial contractility
Diastolic dysfunction – insufficient expansion for ventricular volume
Problems are accentuated by increased demand – high output heart failure

3. CHF – Body’s Compensation
Tachycardia
Frank-Starling – increased End Diastolic Volume
Myocardial hypertrophy
Renin-angiotensin-aldosterone system
Catecholamines – positive inotropic effect
Adrenergic redistribution of blood flow
Increase oxygen extraction from hemoglobin

4. Left-sided Heart Failure
Ischemic heart disease
Hypertension
Aortic and mitral valve disease
Myocardial disease

6. Lungs – Pulmonary edema
Dyspnea – breathlessness
Orthopnea – dyspnea lying down
Paroxysmal nocturnal dyspnea – extreme dyspnea

7. Lung – Pulmonary Edema – pale pink edema fluid filling alveoli

8. Lung – alveolar hemorrhage, heme-filled
macrophages “heart failure cells”, with
iron stain to right

9. Kidneys – reduced perfusion
Ischemic tubular necrosis / ATN
Prerenal azotemia

10. Kidney -ATN

11. Brain in CHF – cerebral hypoxia
Irritability
Loss of attention span
Restlessness
Stupor
Coma

12. Right-sided heart failure
Pure cor pulmonale
Consequence of left-sided failure
Myocardial – myocarditis, cardiomyopathy, constrictive pericarditis

14. Right failure - systemic effects
Liver – chronic passive congestion
Spleen – congestive splenomegaly
Kidneys – congestion and hypoxia
Sub-Q – peripheral edema and anasarca
Pleural space – effusions
Brain – venous congestion and hypoxia
Portal - ascites

15. Liver – chronic passive congestion – blood pools near the central veins

16. Liver – chronic passive congestion

17. Liver – chronic passive congestion – blood pools near the central veins

18. Liver – chronic passive congestion – red cell pooling near central veins
and pericentral necrosis of the hepatocytes

19. CHF – final pathway to death
Ischemic heart disease
Hypertensive heart disease
Valvular heart disease
Cardiomyopathy
Myocarditis
Specific heart muscle diseases

20. Myocarditis Etiology Viral – Coxsackie A, ECHO, Influenza
Chlamydia and Rickettsia – psittaci & typhi
Bacteria – diphtheria, TB, Strep
Fungal & Protozoa – Trypanosomes, Toxo
Hypersensitivity – SLE, RHD, drugs
Physical Agents – Radiation
Idiopathic – Giant cell myocarditis

21. Myocarditis Morphology
Gross –dilated, flabby heart, pale patches with hemorrhage
Microscopic – interstitial inflammatory infiltrate with myocyte necrosis, fibrosis
Mononuclear cells – idiopathic or viral
Neutrophils – bacterial
Eosinophils –hypersensitivity or protozoa
Granulomatous – TB or sarcoid

22. Dilated, globoid
heart in
myocarditis

23. Myocarditis – meets Dallas criteria of a T lymphocyte infiltrate and myocyte
necrosis or dropout. This is usually either viral or of unknown cause.

24. Diphtheria myocarditis – due to a toxin rather than bacterial invasion
Diphtheria myocarditis – due to a toxin rather than bacterial invasion. There is
some inflammation, myocyte changes (see the big nucleolus). Myocyte necrosis
(not shown) also happens.

25. Bacterial colony in myocarditis

26. Toxoplasmosis

27. Chagas disease

28. Giant Cell Myocarditis
Myocyte necrosis
Multinucleated giant cells
Lymphocytes, plasma cells, macrophages, eosinophils, and neutrophils
Often fulminant, rapid progression to death
Differential diagnosis – cardiac sarcoidosis

29. Giant Cell Myocarditis

30. Giant Cell Myocarditis

31. Cardiomyopathies

32. Dilated Cardiomyopathy
Gross – increased weight, dilatation, endocardial fibrosis, normal valves and coronary arteries
Microscopic – myocyte hypertrophy, myofibrillar loss and interstitial fibrosis
Etiology – viral, genetic, toxins
Clinical significance – heart failure & death

34. Dilated cardiomyopathy

35. Cardiomyopathy – loss of myofibrils

36. Cardiomyopathy – trichrome stain showing extensive fibrosis (blue) between
the myocytes. The myocytes also vary in size, and some have partial loss of
myofibrils.

37. Normal Heart - EM

38. Loss of fibrils in cardiomyopathy
Loss of fibrils in cardiomyopathy. The myocyte at lower left is about normal; the
others have an extensive loss of myofibrils.

39. Cardiomyopathy – loss of fibrils and a small contraction band in the top center.

41. Hypertrophic Cardiomyopathy
Hypertrophy of ventricular septum (95%)
Disarray of myofibers (100%)
Volume reduction of ventricles (90%)
Endocardial thickening of LV (75%)
Mitral valve leaflet thickening (75%)
Dilated atria (100%)
Abnormal intramural coronaries (50%)

43. Hypertrophic cardiomyopathy

44. Hypertrophic cardiomyopathy

45. Hypertrophic cardiomyopathy

46. Hypertrophic cardiomyopathy – myofiber dysarray – not all fibers are pulling
the same direction. Thus the contraction is ineffective. However, the cardiac
conduction system can have these same problems, which might cause the
arrhythmias and sudden death these patients tend to die of.

47. Hypertrophic Cardiomyopathy
Etiology – hereditary, mostly autosomal dominant, can appear sporadically
Clinical significance – syncope, arrhythmias and sudden death with a risk of 2-6% per year
Cannot equate with hypertrophy alone! There is variation in heart size without disease. Large hearts correlate with endurance (Secretariat, Lance Armstrong).

49. Restrictive Cardiomyopathy
Amyloidosis
Endomyocardial fibrosis – subendocardial fibrosis
Loeffler’s endocarditis – eosinophilic infiltrate
Endocardial fibroelastosis

50. Amyloidosis – notice the pink material between the myocytes.

51. Amyloidosis – Congo Red is very, very positive.

52. Amyloidosis – this heart is thickened, pale, and has a rubbery consistency that
interferes with cardiac expansion during diastole.

53. Endomyocardial fibrosis – fibrosis under the endocardium and in the the inner
third of the myocardium.

54. Endomyocardial fibrosis of a ventricular wall
Endomyocardial fibrosis of a ventricular wall. When extensive, this would cause
restrictive heart failure too.

55. Endocardial fibroelastosis – elastic stain (black) is very positive
Endocardial fibroelastosis – elastic stain (black) is very positive. This disease,
which occurred in young children and was once 1:5,000 births, now is almost never seen. Etiology is not known (? viral such as mumps).

56. Endocardial fibroelastosis

57. Specific Heart Muscle Diseases
Toxic – alcohol, catecholamines, cocaine, Adriamycin
Metabolic – hemochromatosis, hyperthyroidism
Neuromuscular – muscular dystrophy
Storage disease – glycogen, Fabry’s disease
Infiltrative - sarcoidosis

58. Heart - Becker’s muscular dystrophy – looks like idiopathic dilated cardiomyopathy.

59. Note the fibrosis and loss of myofibrils in some cells.

60. By electron microscopy, this was Adriamycin toxicity
By electron microscopy, this was Adriamycin toxicity. See the clear vacuoles (they
are dilated sarcoplastic reticulum) and severe loss of myofibrils.

61. Cocaine heart – necrosis with contraction bands
Cocaine heart – necrosis with contraction bands. This could happen with any
severe chronic stimulation such as too much pressors in a failing heart or a
pheochromocytoma.

62. Cardiac Sarcoidosis – well defined granuloma with giant cells
Cardiac Sarcoidosis – well defined granuloma with giant cells. Dosen’t infiltrate &
destroy myocardium like giant cell myocarditis. Eosinophils are less common in sarcoidosis than in giant cell myocarditis.

63. Hemochromatosis - note the brown perinuclear deposits of hemosiderin
Hemochromatosis - note the brown perinuclear deposits of hemosiderin. It is,
however, the soluble iron, not the hemosiderin, that is considered toxic.

64. Hemochromatosis – iron stain (iron is blue).

65. Rheumatic fever – Aschoff body – A collection of cells, often near a vessel, with a
few multinucleate cells and some vesicular nuclei with big nucleoli (Aschoff cells). Anichkov myocytes (not shown) are myocytes with very elongated big nucleoli. This is a marker for rheumatic fever, but the serious damage is to the valves.