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Pathology of the Endocardium

Alfonso López

Professor of Anatomic Pathology
Dept. Pathology and Microbiology
Atlantic Veterinary College
University of Prince Edward Island
Canada

Jan 5, 2013
Endocardium
• The endocardium, the most internal layer of the heart
is in intimal contact with the blood.
• It lines the atria ventricles and valves. E
• Purkinje fibers are located mostly in the ventricular n
sub-endocardium. d
o
c
a
r
d
Purkinje cell i
u
m

Myocardium

Subendocardium
Normal Endocardium

Endocardium covering the myocardium, valves and chordae


tendinae (dotted arrows)

Endocardium

Right Ventricle
Left Ventricle

Note how thin is the endocardium, on the right ventricle is almost completely
transparent while in the left ventricle is paper-thin (thick arrow)
Valve leaflets Normal Valves
Aortic Valve
Note how thin and translucent the
valves are.

Chordae Tendinae

Bicuspid Valve
Remember to gently wash the
valves for proper gross
examination.

Papillary Muscle
Endocardial
Mineralization
Endocardial
Valvular
Fibrosis
Cysts

Endocardial
Diseases

Myxomatous
Degeneration Endocarditis
Rupture
Chordae
Tendinae
Endocardial Fibrosis and Fibroelastosis

Generalized (primary) endocardial fibroelastosis occurs as a hereditary disease in humans 
and Burmese and Siamese cats in which there is no underlying cardiac disease.  The 
pathogenesis is uncertain.

Acquired (secondary) focal fibroelastosis can be focal or diffuse and the most common 
causes are:

• Abnormal blood turbulences in the atria or ventricles cause the so‐called "jet 
lesions." These lesions occur when mechanical injury caused by turbulence damage 
the endocardium.  Jet lesions are commonly seen in valvular insufficiencies. 

• Diffuse sub‐endocardial fibrosis secondary to prolonged cardiac dilation.

Gross lesions and Microscopic Lesions:  On gross examination, the endocardium appears 
thickened and often shows a rough or corrugated surface .  Endocardial thickening is the 
result of an abnormal deposition of collage and elastic fibres.

Clinical Relevance:  Generalized fibroelastosis can impair and reduce stroke volume leading 
to congestive heart failure.
Subendocardial Fibroelastosis Secondary to
Congenital Heart Diseases

Increase collagen deposition in the sub-endocardium was secondary to


chronic blood turbulence caused by a congenital heart defect in this dog.

Note diffusely thickened endocaridum

Fig. 10-54 Subendocardial fibroelastosis, heart, left ventricle, dog. (Zachary and McGavin.
Pathologic Basis of Veterinary Disease, 5th Edition. Elsevier Health Sciences, p. 569).
Subendocardial Fibroelastosis

Thickened
Endocardium

Myocardium

C-M03 (VSPO) Endocardial fibroelastosis (EFE), cat.


Note thickened and corrugated
The endocardium is uniformly thickened up to 250 um
appearance
(20x normal) by relatively dense fibrous connective
tissue .
Endocardial Mineralization
Endocardial Mineralization  is an abnormal deposition of calcium or mineral in the 
endocardium.  According to the pathogenesis endocaridal mineralization could be:
• Metastatic: High levels of circulating Ca++  in hypercalcemic states
• Dystrophic:  Secondary calcification in injured endocardium.

Endocardial mineralization occurs in all species 

The most common causes of endocardial mineralization in domestic animals are:

• Hypervitaminosis D :

• When animals are given excess amounts of vitamin D (iatrogenic hypervitaminosis).
• When animals ingest Vitamin D analogs which are present in some rodenticides or toxic 
plants such as Solanum malacoxylon and Cestrum diurnum.  

• Cachexia:  Markedly cachectic animals, particularly bovines with paratuberculosis or 
tuberculosis, often show endocardial and arterial mineralization.  The pathogenesis of 
this particular lesion is poorly understood.

• Uremia: Mineralization is also seen in uremic dogs (uremic endocarditis).
Subendocardial Mineralization

Note corrugation and thickening of the endocardium (star). Mineralization is


also present in the aorta (arrows)
Valvular Cysts
• Particularly common in calves
• Considered just as an Incidental finding
• Cysts generally rupture into circulation and disappear
• There is no clinical significance

According to content, cyst are classified as:


• Lymphocyst when the content is clear fluid
• Hemocyst when the content is blood)
Valvular Lymphocyst

Incidental post-mortem finding in a calf

Note valvular cyst filled with clear fluid (star)

1 cm
Valvular Hemocyst

Incidental post-mortem finding in a calf.


Remember, these cyst rupture into circulation which explains
why are not found in adult cattle.

Note cyst filled with blood in the


atrio-ventricular valve (star)
Myxomatous Valvular Degeneration
(Endocardiosis)

• Most common cardiac lesion found at


necropsy in mature dogs.

• The incidence increases with age:


• 1-yr-old = 5%
• 13-yr-old = 75%

• It typically affects the mitral valve.


• It is morphologically characterized by
nodular thickening of the valve with a
smooth shinny surface.

• May or may not cause valvular dysfunction


and clinical signs.
Myxomatous Valvular Degeneration (Endocardiosis)

Note thickened and nodular valve with smooth shinny


surface (arrows)
Myxomatous Valvular Degeneration (Endocardiosis)

• Nodular
• Smooth surface
Myxomatous Valvular Degeneration
(Histopathology)

Note thickened and nodular valve composed of loose


connective (myxomatous) tissue (star)
Endocardiosis and Rupture Chordae Tendinae

Sudden collapse and death following exercise

• Post-mortem Diagnosis:
• Endocardiosis, severe, mitral valve
• Rupture chordae tendinae

When you suspect rupture chordae tendinae at the time of necropsy, it is


recommended to open the left atrium, remove the blood, fill the ventricle and atria
with water, and rhythmically compress the heart. If there is rupture, one or more
chordae will whipped out during the “manual systole.”
See endocardiosis and ruptured chordae in gross specimen (arrows)
Endocarditis
(Inflammation of the endocardium)

Endocarditis occurs in all domestic species 

It is most frequently caused by bacteria, and to a much lesser extent, by fungi or parasites.

According to location, endocarditis can be classified as:
• Valvular endocarditis (valves)
• Mural endocarditis (myocardial wall) 

According to gross appearance:
• Vegetative: cauliflower‐like mass of exudate and fibrin attached to a heart valve or endocardium
• Ulcerative when the endocardium is ulcerated.

Common sequels to endocarditis:
• Thromboembolisms:  Mitral or aortic endocarditis often causes renal infarcts;  tricuspid and 
pulmonic endocarditis cause pulmonary infarcts or embolic pneumonia.  
• Ulcerative endocarditis is common in dogs with uremia.
Vegetative Valvular Endocarditis

Vegetative endocarditis is most


commonly seen in cattle and pigs.

Note cauliflower-like exudate in the mitral valve (star)


and pulmonic valve (arrow)
Vegetative Valvular Endocarditis

View from the top of the atrio-ventricular


Vegetative valvular endocarditis is particularly 
valve after opening the atrium.
common in farm animals suffering from 
bacteremia.  It is occasionally seen in dogs and 
cats.

Most common bacteria isolated from 
endocarditis in domestic animals are:

• Streptococcus equi in horses

• Truperella (Arcanobacterium) pyogenes
in cattle

• Erysipelothrix rhusiopathiae and  


Streptococcus suis type II in pigs

• Staphylococcus aureus in dogs
Atrium
• Bartonella and Streptpococcus sp. in 
cats.

Note mass of exudate (star) protruding from


the atrio-ventricular valve.
Vegetative Valvular Endocarditis / Right Sided Heart Failure / Cow
Note hydrothorax (abundant transudate in thorax) due to right sided heart failure

“nutmeg liver”

Note large vegetative mass of exudate (star) on the tricuspid valve (right AV valve) which was causing right
heart failure, ventral edema, ascites and “nutmeg liver”
Vegetative Valvular Endocarditis / Right Sided Heart Failure / Cow

Truprella (Arcanobacterium) pyogenes was isolated from affected valve.

Tricuspid vale

Note severe thickening of the tricuspid valve due to extensive accumulation of exudate.
Sepsis / Pig / Vegetative Valvular Endocarditis
Pig presented for post-mortem examination. The animal showed red discoloration of the skin affecting the
ventral abdomen and legs, and the tips of the ears. Examination of the heart revealed severe vegetative
endocarditis affecting the aortic valve. Streptococcus suis type II was isolated from the lungs and affected
valve.

Aortic valve

Note severe thickening of the aortic valve due to extensive accumulation of exudate.
Vegetative Valvular Endocarditis / Histopathology

Fibrin

Bacterial colonies

Neutrophils and cell debris

Connective tissue, neutrophils and macrophages
VALVE
Vegetative Valvular Endocarditis / Dog

Aortic valve (arrow)

Note severe thickening of the aortic valve due to accumulation of exudate.


Vegetative Valvular Endocarditis / Embolic Pneumonia / Pig

Note accumulation of exudate in tricuspid valve (star) and multiple embolic foci in the lungs (arrows).

Right ventricle
Ulcerative Endocarditis / Uremia / Dog

Fig. 10‐61 Ulcerative endocarditis (uremia), heart, endocardium of left atrium, dog. Note the white‐red, 
thick, wrinkled area (arrows) of endocarditis, mineralization, and fibrous tissue (scar) formation caused 
by uremia in this dog with chronic renal failure. Pathologic Basis of veterinary Diseases page 572
 Thanks to all AVC pathologist for contributing case materials

 Some images were acquired from veterinary colleges of


Canada, United States and Mexico and the names of some
contributing pathologists are unknown. Their valuable
contribution is sincerely acknowledged.

 I would like to thank Dr. Shannon Martinson, Atlantic


Veterinary College, for critically reviewing these modules.
Module : Endocardium

THE END

If you have any comments or criticisms about tutorials or


quizzes please let me know. Also, if you find any errors or
typos please let me know.

lopez@upei.ca
ILD

Thank you very much…

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