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Introduction to Cardiovascular Pathology - Fred Clayton

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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.

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