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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. Congestive Heart Failure.

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introduction to cardiovascular pathology fred clayton
Introduction to Cardiovascular Pathology- Fred Clayton
  • Systemic Pathology of Congestive Heart Failure
  • Pathology of Myocarditis
  • Pathology of Cardiomyopathy
    • Dilated Cardiomyopathy
    • Hypertrophic Cardiomyopathy
    • Restrictive Cardiomyopathy
congestive heart failure
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
chf body s compensation
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
left sided heart failure
Left-sided Heart Failure
  • Ischemic heart disease
  • Hypertension
  • Aortic and mitral valve disease
  • Myocardial disease
lungs pulmonary edema
Lungs – Pulmonary edema
  • Dyspnea – breathlessness
  • Orthopnea – dyspnea lying down
  • Paroxysmal nocturnal dyspnea – extreme dyspnea

Lung – alveolar hemorrhage, heme-filled

macrophages “heart failure cells”, with

iron stain to right

kidneys reduced perfusion
Kidneys – reduced perfusion
  • Ischemic tubular necrosis / ATN
  • Prerenal azotemia
brain in chf cerebral hypoxia
Brain in CHF – cerebral hypoxia
  • Irritability
  • Loss of attention span
  • Restlessness
  • Stupor
  • Coma
right sided heart failure
Right-sided heart failure
  • Pure cor pulmonale
  • Consequence of left-sided failure
  • Myocardial – myocarditis, cardiomyopathy, constrictive pericarditis
right failure systemic effects
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

Liver – chronic passive congestion – red cell pooling near central veins

and pericentral necrosis of the hepatocytes

chf final pathway to death
CHF – final pathway to death
  • Ischemic heart disease
  • Hypertensive heart disease
  • Valvular heart disease
  • Cardiomyopathy
  • Myocarditis
  • Specific heart muscle diseases
myocarditis etiology
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
myocarditis morphology
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

Dilated, globoid

heart in



Myocarditis – meets Dallas criteria of a T lymphocyte infiltrate and myocyte

necrosis or dropout. This is usually either viral or of unknown cause.


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.

giant cell myocarditis
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
dilated cardiomyopathy
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

Cardiomyopathy – trichrome stain showing extensive fibrosis (blue) between

the myocytes. The myocytes also vary in size, and some have partial loss of



Loss of fibrils in cardiomyopathy. The myocyte at lower left is about normal; the

others have an extensive loss of myofibrils.

hypertrophic cardiomyopathy
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%)

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.

hypertrophic cardiomyopathy47
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).
restrictive cardiomyopathy
Restrictive Cardiomyopathy
  • Amyloidosis
  • Endomyocardial fibrosis – subendocardial fibrosis
  • Loeffler’s endocarditis – eosinophilic infiltrate
  • Endocardial fibroelastosis

Amyloidosis – this heart is thickened, pale, and has a rubbery consistency that

interferes with cardiac expansion during diastole.


Endomyocardial fibrosis – fibrosis under the endocardium and in the the inner

third of the myocardium.


Endomyocardial fibrosis of a ventricular wall. When extensive, this would cause

restrictive heart failure too.

specific heart muscle diseases
Specific Heart Muscle Diseases
  • Toxic – alcohol, catecholamines, cocaine, Adriamycin
  • Metabolic – hemochromatosis, hyperthyroidism
  • Neuromuscular – muscular dystrophy
  • Storage disease – glycogen, Fabry’s disease
  • Infiltrative - sarcoidosis

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


By electron microscopy, this was Adriamycin toxicity. See the clear vacuoles (they

are dilated sarcoplastic reticulum) and severe loss of myofibrils.


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



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.


Hemochromatosis - note the brown perinuclear deposits of hemosiderin. It is,

however, the soluble iron, not the hemosiderin, that is considered toxic.


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.