1. Pericardial Diseases
 Associated with diseases in heart and surrounding
structures, or secondary to systemic disorders.
 Isolated pericardial disease is unusual.
Pericardial effusion and haemopericardium:
 Normally, there is 30 to 50 mL of thin, clear,
straw-colored fluid in pericardial sac.
 Parietal pericardium undergoes distention by fluid
of variable composition (pericardial effusion).

2.  The consequences depend on: ability of parietal
pericardium to stretch, speed of accumulation,
and amount of fluid.
 Thus, with slowly accumulating effusions, the only
clinical significance is globular enlargement of
heart shadow on chest x-ray.
 In contrast, rapidly developing fluid collections
in haemopericardium caused by ruptured MI ,or
traumatic perforation may produce fatal cardiac
tamponade.

3. pericarditis: Causes:-
Infectious Agents
Viruses
Pyogenic bacteria
Tuberculosis
Fungi
parasites
Immunologically Mediated
Rheumatic fever
Systemic lupus erythematosus
Scleroderma
Postcardiotomy syndrome
Postmyocardial infarction (Dressler) syndrome
Drug hypersensitivity reaction
Miscellaneous
Myocardial infarction
Uremia
Following cardiac surgery
Neoplasia
Trauma
Radiation

4. Acute Pericarditis:
Serous Pericarditis:
 produced by:
o Non infectious inflammations: RF, SLE, scleroderma,
tumors, and uremia.
o Viral infection elsewhere: upper respiratory tract
infection, pneumonia, parotitis.
o Viral pericarditis that accompany viral myocarditis
(myopericarditis).

5. Morphology:
 An inflammatory reaction with scant numbers
of polymorphnuclear leukocytes, lymphocytes,
and macrophages.
 The volume of fluid is not large (50 to 200 mL)
and accumulates slowly.
 The fluid has low specific gravity, and low protein
content.
serous fluid, at the bottom of pericardial cavity (arrow).

6. Fibrinous and Serofibrinous Pericarditis:
 Composed of serous fluid mixed with fibrinous
exudate.
 Common causes: acute MI , postinfarction (Dressler)
syndrome , uremia, chest radiation, RF, SLE, and
trauma.
 A loud pericardial friction rub is characteristic of
fibrinous pericarditis.
 Pain , systemic febrile reactions, and signs of
cardiac failure may be present.

7. Morphology:
 The surface is dry with a fine granular roughening.
 An increased inflammatory process induces more
and thicker fluid which is yellow and cloudy owing
to leukocytes and erythrocytes and often fibrin.
 Fibrin may be digested with resolution of exudate,
or it may become organized.

8. Purulent or Suppurative Pericarditis:
 Invasion of pericardial space by infective organisms
which may reach pericardial cavity by :
(1) direct extension from neighboring inflammation:-
an empyema of pleural cavity, lobar pneumonia,
or mediastinal infections.
(2) seeding from blood.
(3) lymphatic extension.
(4) direct introduction during cardiotomy.

9. Morphology:
 The exudate ranges from a thin to a creamy pus .
 The serosal surfaces are reddened, granular, and
coated with exudate .
 Microscopically:
o There is an acute inflammatory reaction.
o Organization is the usual outcome.
o Resolution is infrequent.

10. Hemorrhagic Pericarditis:
 An exudate composed of blood admixed with
fibrinous or suppurative effusion.
 Commonly caused by malignant neoplastic
involvement of pericardial space.
 May also be found in bacterial infections,
in patients with an underlying bleeding diathesis,
and in tuberculosis.
 Often follows cardiac surgery and sometimes
is responsible for significant blood loss or even
cardiac tamponade.

11. Caseous Pericarditis:
 Caseation within pericardial sac, until proved
otherwise, is tuberculous in origin.
 Infrequently, fungal infections evoke a similar
reaction.
 Pericardial involvement occurs by direct spread from
tuberculous foci within tracheobronchial nodes.
 It is rare but is the most frequent cause of
fibrocalcific chronic constrictive pericarditis.

12. Chronic or Healed Pericarditis:
 In some cases, organization produces plaque-like
fibrous thickening of serosal membranes.
 This fibrosis yields adhesion between parietal and
visceral pericardium called adhesive pericarditis.
 In other cases, organization results in complete
obliteration of pericardial sac.

13. Constrictive Pericarditis:
 The heart encased in a dense fibrous or fibrocalcific
scar that limits diastolic expansion and seriously
restricts cardiac output.
 History of previous pericarditis may or may not be
present.
 The pericardial space is obliterated.
 The major therapy is surgical removal of the shell
of constricting fibrous tissue (pericardiectomy).

14. This photograph showed pericardial fibrosis and calcification (Hematoxylin and
eosin stainx40).

15. Tumors of the Heart
 Primary tumors of heart are rare.
 In contrast, metastatic tumors to heart occur in
about 5% of patients dying of cancer.
 The most common primary tumors , in descending
order of frequency are: myxomas, fibromas,
lipomas, papillary fibroelastomas, rhabdomyomas,
angiosarcomas, and other sarcomas.
 The first five tumors are all benign and account
for 80% to 90% of primary tumors of the heart.

16. PRIMARY CARDIAC TUMORS :
Myxoma:
 Most common primary tumor of heart in adults.
 90% are located in atria, with left-to-right ratio
of 4:1.
 The major clinical manifestations are due to
valvular "ball-valve" obstruction and emboli.
 Echocardiography to identify these masses
noninvasively.
 Surgical removal is usually curative.
 Rarely , the neoplasm recurs months or years later.

17.  10% of patients have familial cardiac myxoma
syndrome (known as Carney syndrome).
Morphology:
 Almost always single.
 Fossa ovalis in atrial septum is favored site .
 Range from small ( 1 cm) to large (up to 10 cm).
 Sessile or pedunculated masses.
 Vary from globular hard masses mottled with
hemorrhage, to soft papillary or villous lesions
having a gelatinous appearance.

18. The left atrium has been opened to reveal the most common
primary cardiac neoplasm - atrial myxoma.

19.  Histologically :
 Composed of stellate or globular myxoma ("lepidic")
cells , smooth muscle cells, and undifferentiated cells.
 Embedded within abundant acid mucopolysaccharide
ground substance.
 Covered on the surface by endothelium.
 Hemorrhage and mononuclear inflammation are
usually present.

20. Lipoma:
 May occur in subendocardium , in subepicardium,
or within myocardium.
 Localized poorly encapsulated masses.
 May be asymptomatic, can create ball-valve
obstruction as myxomas, or may produce
arrhythmias.
 Most often located in left ventricle, right atrium,
or atrial septum.

21. Papillary Fibroelastoma:
 Most often identified at autopsy.
 They may embolize and become clinically important.
Morphology:
 Generally located on valves.
 They constitute a distinctive cluster of hair-like
projections up to 1 cm in diameter ( sea anemone
appearance).

22. On light microscopy: fronds of connective tissue are eosinophilic (pink) and show minimal
cellularity. The most conspicuous cells are endothelial cells on the surface of "papillary"
fronds. (right) shows yellow collagen with concentric discontinous layers of elastic lamellae
in the core. Thus the name fibroelastoma

23. Rhabdomyoma:
 Most frequent primary tumor of heart in infants and
children.
 Frequently discovered in first year of life because
of obstruction of valvular orifice or cardiac chamber.
 High frequency of tuberous sclerosis in patients
with cardiac rhabdomyomas.
 A recent study suggested that cardiac rhabdomyomas
may be due to a defect in apoptosis during
developmental cardiac remodeling.

24. Morphology:
 Small gray-white myocardial masses up to several
centimeters in diameter located on either left or
right side of heart and protruding into ventricular
chambers.
 Histologically:
Composed of large rounded or polygonal cells
containing numerous glycogen-laden vacuoles which
separated by strands of cytoplasm running from
plasma membrane to more or less centrally located
nucleus, the so-called spider cells.

25. Gross appearance of cardiac rhabdomyoma.
Multiple rhabdomyomas (arrows) in a child
with Tuberous Sclerosis (at autopsy).

26. Metastatic tumors to the heart:
 The most frequent primaries are:
carcinomas of lung and breast, melanomas,
leukemias, and lymphomas.
 Metastases can reach heart and pericardium by:
o Lymphatic extension (most carcinomas).
o Hematogenous seeding (many tumors).
o Direct contiguous extension (primary carcinoma of
lung, breast, or esophagus).

27.  Clinical symptoms: either by
o Pericardial spread with pericardial effusion that
causes tamponade.
o Tumor bulk that is sufficient to directly restrict
cardiac filling.
 Bronchogenic carcinoma or malignant lymphoma
may infiltrate mediastinum causing compression,
or invasion of superior vena cava with resultant
obstruction to blood coming from head and
upper extremities (superior vena cava syndrome).

28.  Renal cell carcinoma can grow in lumen of renal vein,
and into inferior vena cava and blocking venous
return to heart.
 Noncardiac tumors cause indirect cardiac effects
via circulating tumor-derived substances ( NBTE ,
and carcinoid heart disease).
 Complications of tumor radiotherapy:
o Radiation can cause pericarditis, pericardial effusion,
and myocardial fibrosis.