Introduction to Cardiovascular Pathology - Fred Clayton

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Introduction to Cardiovascular Pathology- Fred
Clayton

• Systemic Pathology of Congestive Heart Failure
• Pathology of Myocarditis
• Pathology of Cardiomyopathy
• Dilated Cardiomyopathy
• Hypertrophic Cardiomyopathy
• Restrictive Cardiomyopathy

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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

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CHF Bodys 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

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Left-sided Heart Failure

• Ischemic heart disease
• Hypertension
• Aortic and mitral valve disease
• Myocardial disease

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Lungs Pulmonary edema

• Dyspnea breathlessness
• Orthopnea dyspnea lying down
• Paroxysmal nocturnal dyspnea extreme dyspnea

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Lung Pulmonary Edema pale pink edema fluid
filling alveoli
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Lung alveolar hemorrhage, heme-filled macrophage
s heart failure cells, with iron stain to right
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Kidneys reduced perfusion

• Ischemic tubular necrosis / ATN
• Prerenal azotemia

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Kidney -ATN
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Brain in CHF cerebral hypoxia

• Irritability
• Loss of attention span
• Restlessness
• Stupor
• Coma

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Right-sided heart failure

• Pure cor pulmonale
• Consequence of left-sided failure
• Myocardial myocarditis, cardiomyopathy,
  constrictive pericarditis

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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

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Liver chronic passive congestion blood pools
near the central veins
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Liver chronic passive congestion
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Liver chronic passive congestion blood pools
near the central veins
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Liver chronic passive congestion red cell
pooling near central veins and pericentral
necrosis of the hepatocytes
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CHF final pathway to death

• Ischemic heart disease
• Hypertensive heart disease
• Valvular heart disease
• Cardiomyopathy
• Myocarditis
• Specific heart muscle diseases

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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

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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

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Dilated, globoid heart in myocarditis
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Myocarditis meets Dallas criteria of a T
lymphocyte infiltrate and myocyte necrosis or
dropout. This is usually either viral or of
unknown cause.
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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.
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Bacterial colony in myocarditis
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Toxoplasmosis
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Chagas disease
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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

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Giant Cell Myocarditis
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Giant Cell Myocarditis
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Cardiomyopathies
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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

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Dilated cardiomyopathy
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Cardiomyopathy loss of myofibrils
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Cardiomyopathy trichrome stain showing
extensive fibrosis (blue) between the myocytes.
The myocytes also vary in size, and some have
partial loss of myofibrils.
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Normal Heart - EM
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Loss of fibrils in cardiomyopathy. The myocyte at
lower left is about normal the others have an
extensive loss of myofibrils.
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Cardiomyopathy loss of fibrils and a small
contraction band in the top center.
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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)

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Hypertrophic cardiomyopathy
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Hypertrophic cardiomyopathy
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Hypertrophic cardiomyopathy
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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.
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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).

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Restrictive Cardiomyopathy

• Amyloidosis
• Endomyocardial fibrosis subendocardial fibrosis
• Loefflers endocarditis eosinophilic
  infiltrate
• Endocardial fibroelastosis

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Amyloidosis notice the pink material between
the myocytes.
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Amyloidosis Congo Red is very, very positive.
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Amyloidosis this heart is thickened, pale, and
has a rubbery consistency that interferes with
cardiac expansion during diastole.
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Endomyocardial fibrosis fibrosis under the
endocardium and in the the inner third of the
myocardium.
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Endomyocardial fibrosis of a ventricular wall.
When extensive, this would cause restrictive
heart failure too.
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Endocardial fibroelastosis elastic stain
(black) is very positive. This disease, which
occurred in young children and was once 15,000
births, now is almost never seen. Etiology is not
known (? viral such as mumps).
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Endocardial fibroelastosis
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Specific Heart Muscle Diseases

• Toxic alcohol, catecholamines, cocaine,
  Adriamycin
• Metabolic hemochromatosis, hyperthyroidism
• Neuromuscular muscular dystrophy
• Storage disease glycogen, Fabrys disease
• Infiltrative - sarcoidosis

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Heart - Beckers muscular dystrophy looks like
idiopathic dilated cardiomyopathy.
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Note the fibrosis and loss of myofibrils in some
cells.
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By electron microscopy, this was Adriamycin
toxicity. See the clear vacuoles (they are
dilated sarcoplastic reticulum) and severe loss
of myofibrils.
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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.
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Cardiac Sarcoidosis well defined granuloma with
giant cells. Dosent infiltrate destroy
myocardium like giant cell myocarditis.
Eosinophils are less common in sarcoidosis than
in giant cell myocarditis.
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Hemochromatosis - note the brown perinuclear
deposits of hemosiderin. It is, however, the
soluble iron, not the hemosiderin, that is
considered toxic.
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Hemochromatosis iron stain (iron is blue).
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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.