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Detailed understanding of gross pathology is mandatory for successful patholo-
gists, but this knowledge also provides a sound foundation for those intending to
become surgeons, internists, and obstetrician/gynecologists. Some knowledge of
gross pathology is important for members of the allied health professions and
dental students. For pathologists, pathology residents, and pathology assistants,
knowledge of gross pathology is essential for guidance in selecting the correct
areas of pathologic lesions to sample for microscopy and frozen section examina-
tion. This atlas aims to provide a comprehensive illustration and description of a
wide range and number of pathologic processes and diseases affecting all the
major organs of the body. Emphasis is placed on how the anatomic structure of
different organs may determine the pattern of involvement by disease processes
and how such patterns may aid in the correct diagnosis of the gross pathology. In
some cases, multiple illustrations of disease processes are given to show evolu-
tion of the disease. Histologic illustrations of selected gross lesions are also
included where relevant. The atlas is illustrated with more than 1,200 color pho-

Dr. Alan G. Rose, MD, FRCPath, FACC, is Professor of Pathology at the University
of Minnesota Medical School. He is also the Director of Autopsy Service at the
University of Minnesota Medical Center, Fairview; the Residency and Fellowship
Training Program; and the Medical School Pathology Teaching Program at the
University of Minnesota.
with Histologic Correlation
University of Minnesota
Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo

Cambridge University Press
The Edinburgh Building, Cambridge CB2 8RU, UK
Published in the United States of America by Cambridge University Press, New York

Information on this title: www.cambridge.org/9780521868792
© Alan G. Rose 2008

This publication is in copyright. Subject to statutory exception and to the
provision of relevant collective licensing agreements, no reproduction of any part
may take place without the written permission of Cambridge University Press.
First published in print format 2008

ISBN-13 978-0-511-43679-6 eBook (EBL)

ISBN-13 978-0-521-86879-2 hardback

Cambridge University Press has no responsibility for the persistence or accuracy
of urls for external or third-party internet websites referred to in this publication,
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.
Every effort has been made in preparing this publication to provide accurate and
up to date information that is in accord with accepted standards and practice at the
time of publication. Nevertheless, the authors, editors, and publisher can make no
warranties that the information contained herein is totally free from error, not least
because clinical standards are constantly changing through research and
regulation. The authors, editors, and publisher therefore disclaim all liability for
direct or consequential damages resulting from the use of material contained in
this publication. Readers are strongly advised to pay careful attention to
information provided by the manufacturer of any drugs or equipment that they
plan to use.

Cardiac Diseases
1 1

Pulmonary Pathology
2 90

Kidneys, Ureters, and Urinary Bladder
3 157

Liver, Biliary System, and Pancreas
4 207

Salivary Glands and GIT
5 272

Female Genital Tract and Breast
6 358

Diseases of the Male Genital System
7 428

Bones and Joints
8 460

Diseases of the Spleen, Lymph
9 515
Nodes, and the Thymus Gland

Pituitary, Carotid Body, Thyroid
10 541
Gland, and Adrenals

Skin and Soft Tissues
11 566

Central Nervous System
12 607

Index 655
1 Cardiac Diseases


1-1. Unicuspid unicommissural aortic valve has become stenotic in
middle age due to calci¬cation of the abnormally stressed single cusp.

1-2. Congenital aortic stenosis due to a bicuspid aortic valve with
thick, dysplastic cusps. Each cusp is approximately the same length
as the other (i.e., stenosis occurs because no abnormally long con-
joined cusp is present).

Cardiac Diseases 1


1-3. A. Aortic stenosis due to calci¬ed congenital
bicuspid aortic valve in a 50-year-old man. The
longer conjoined cusp on the left is characterized
by the presence of a raphe (arrow) that does not
reach up to the free margin of the cusp. B. Micro-
scopic section through the raphe shows ¬brous tis-
sue and no evidence of two preexisting separate
aortic cusps (that may have fused).

2 Cardiac Diseases
1-4. Infective endocarditis affecting a bicuspid aortic valve in a
patient who also has a small perimembranous ventricular septal
defect situated immediately below the valve.

1-5. Congenital pulmonary stenosis: a small central hole is present
at the top of a tent-like dome of ¬brous tissue. The presence of four
commissures gives an appearance suggesting four cusps are fused in
forming this obstructing ¬brous dome.

Cardiac Diseases 3

1-7. Appearance of a surgically excised mitral valve
1-6. Congenital mitral atresia: no mitral valve is
with double mitral ori¬ce. The ori¬ce of the valve
present, and there is only a central shallow dimple
is subdivided by a mass of abnormal valvular tissue
in the ¬brous tissue occupying the space where the
(*) linking the two cusps.
mitral valve should have been formed.

1-8. Parachute mitral valve, which may be func-
tionally stenotic, is characterized by all of the chor-
dae tendineae of the mitral valve being attached to
a single papillary muscle. The diagnosis may easily
be missed if the other missing papillary muscle is
not noted.

4 Cardiac Diseases
1-9. Recurrent subaortic membranous stenosis
(arrow) after prior resection of an obstructing ¬brous
membrane running across the muscular ventricular
septum and the anterior mitral lea¬‚et. The membrane
may re-form repeatedly after resection in some indi-
viduals. The aortic valve is thickened and deformed
secondary to the effects of the subaortic obstruction-
induced jet lesion.

1-10. Ebstein™s anomaly of the tricuspid valve showing atrialization
of the proximal portion of the right ventricle due to downward dis-
placement of the tricuspid valve ring. The very large, dysplastic tri-
cuspid valve is also plastered down against the underlying right ven-
tricular endocardium in multiple areas, rendering the valve

Cardiac Diseases 5
1-11. Endocardial ¬broelastosis: the left ventricle is lined by a
porcelain-like layer of ¬brous tissue. Some patients give a history of
maternal mumps infection during pregnancy.

1-12. Probe indicates a patent foramen ovale, and a small red throm-
bus is adherent to the nearby margin of the fossa ovalis (right). Trans-
venous atrial closure devices have been developed to seal such defects
and thus prevent passage of thrombus via the patency to reach the
left atrium.

6 Cardiac Diseases
1-13. A paradoxical embolus occurs when a throm-
bus passes from the right atrium into the left atrium
and then into the systemic circulation producing
arterial occlusion. A. View from right atrium of a
paradoxical embolus (arrow) passing across a patent
foramen ovale. B. Left atrial view of the other end
of the thromboembolus (arrow) that is passing across
the patent foramen ovale.


Cardiac Diseases 7
1-14. Secundum atrial septal defect at site usually
occupied by the fossa ovalis in the interatrial septum.

8 Cardiac Diseases
1-15. Ostium secundum (upper hole) and ostium
primum (lower hole) defects seen on left side of the
heart. The anterior cusp of the mitral valve has a
cleft (arrow) in it as part of the ostium primum
defect. This 48-year-old woman presented with pul-
monary hypertension due to the long-standing left-
to-right shunt at atrial level. She died while await-
ing a heart-lung transplant.

1-16. Appearance of anterior lea¬‚et of the mitral valve in ostium pri-
mum defect with two separate atrioventricular valves: multiple short
tethering chordae limited the movement of the anterior mitral cusp
during left ventricular systole. In addition to closing the defect with
a patch, the surgeon needs to cut these abnormal chordae to allow
normal mitral valve function.

Cardiac Diseases 9
1-17. Aneurysm of the fossa ovalis (¬‚ap valve) may be a primary
abnormality per se or may be associated with valvular disease (e.g.,
mitral valve atresia). The aneurysm always points into the lower
pressure zone. Such aneurysms may also be acquired in later life.

1-18. Perimembranous ventricular septal defect: the hole
includes the area of the membranous septum plus some sur-
rounding muscular tissue.

10 Cardiac Diseases
1-19. Right ventricular end of a small muscular ventricular septal
defect shows surrounding endocardial ¬brous thickening due to tur-
bulent blood ¬‚ow (jet lesion).

1-20. Top Dacron patch seals atrial septal defect and lower Dacron
patch sealing ventricular septal defect (VSD) is the site of infection
(infective endocarditis of VSD patch). The patch has been sampled
for microbiology and histology.

Cardiac Diseases 11
1-21. Postoperative tetralogy of Fallot showing
dehiscence of Dacron patch sealing right side of an
infracristal ventricular septal defect. A probe passes
1-22. Total anomalous pulmonary venous drainage:
upward from the right ventricle behind the free
the con¬‚uence of the four pulmonary veins has no
margin of the patch to enter the left ventricle (not
connection to the left atrium, but in this patient
seen in this view).
drained inferiorly below the diaphragm. Note that
the apex of the heart has been displaced vertically
to expose the major pulmonary veins.

12 Cardiac Diseases
1-23. Cor triatriatum results from failure of incor-
poration of the common pulmonary vein into the
left atrium during the ¬fth week of embryological
development. A ¬bromuscular diaphragm subdi-
vides the left atrium into two chambers linked by a
small hole. A. Upper chamber with small hole in
its ¬‚oor (probe). B. Lower chamber that leads
directly into mitral valve ori¬ce.


Cardiac Diseases 13

1-24. Patent ductus arteriosus (*) passes upward from
pulmonary artery to join the aorta.

1-25. Surgically resected coarctation of the aorta
has been bisected longitudinally to reveal a curtain-
like fold of aortic tissue that affects the superior,
anterior, and posterior portions of the aorta, but
spares its inferior portion. One theory of causation
attributes ectopic ductal tissue as the cause of the

14 Cardiac Diseases
1-26. Transposition of the great arteries. The aorta
(note the origins of the arch branches) is seen to be
arising from the right ventricle at the expected ori-
gin of the pulmonary artery, and the latter (not vis-
ible in this view) arises from the left ventricle. The
descending thoracic aorta had a left-sided descent.

Cardiac Diseases 15


1-27. A. Glycogen storage disease has produced massive concentric
hypertrophy of the cardiac chambers. B. Histology shows swollen, vac-
uolated myocytes due to massive accumulation of glycogen.

16 Cardiac Diseases
1-28. A. Bosselated appearance of left ventricular
endocardium in histiocytoid cardiomyopathy. B.
Histologic appearance of innermost portion of left
ventricle showing vacuolated Purkinje ¬bers and
myocytes expanding the subendocardium.


Cardiac Diseases 17
1-29. A. Biventricular coronary-cameral ¬stulae
have led to marked ectasia and elongation of the
major coronary arteries so that they resemble a “bag
of worms” in appearance. The coronary arteries
have had to carry much more blood than normal to
compensate for blood lost into the cardiac chambers.
B. Histologic appearance of left ventricle showing
large arterial branches reaching to the endocardial


18 Cardiac Diseases
1-30. Congenital diverticulum arising from the apex of the left ven-
tricle passed through the diaphragm anterior to the liver to terminate
in the abdomen. Patient had pulsating umbilical swelling during life.
Death was due to a hypoplastic left ventricle.

Cardiac Diseases 19

1-31. A. Senile calci¬c aortic stenosis due to cal-
cium deposits in a tricuspid aortic valve that ren-
der the cusps relatively immobile. The deposits are
mainly situated on the out¬‚ow aspect of all three
cusps. B. Lipid deposits (central pale area) within
the cusp that develop with age form the nidus for
development of the calci¬cation. C. Massive calci-
¬cation expands the thickness of the cusp.



20 Cardiac Diseases
1-32. Acquired bicuspid aortic valve due to fusion (arrow) of one
commissure. The fusion reaches right up to the free margin of the
two united cusps and is unlike a raphe of a congenital bicuspid valve
that would not reach up this high.


1-33. A. Acquired aortic stenosis due to rheumatic
fever shows the typical triangular ori¬ce due to par-
tial fusion of all three commissures. Note also the
thickness of the cusps. B. Surgically excised speci-
men of acquired aortic stenosis due to tricommis-
sural fusion shows similar features.


Cardiac Diseases 21
1-34. Acquired aortic stenosis in patients with left ventricular assist
devices. For the assist pump to work well, the aortic valve stays per-
manently closed, favoring thrombosis and organization leading to
commissural fusion. Left lower picture shows organizing thrombus
on the in¬‚ow aspect of the aortic valve. Right lower picture shows
commissural fusion leading to aortic stenosis.

1-35. Marantic endocarditis: note the large vegetations (thrombotic
deposits) on the aortic valve in a patient with prior coronary arterial
bypass grafts. Note hemoglobin staining of the aortic intima by
intravascular hemolysis due to septicemia. Vegetations showed no
sign of infection microscopically.

22 Cardiac Diseases
1-36. A. Small, ¬rmly adherent, verrucous vegeta-
tions of acute rheumatic fever lie on contact area of
the mitral valve cusps. Left atrium posterior wall has
a MacCallum™s patch (i.e., area of endocardial thick-
ening due to the trauma of a regurgitant jet of blood
from mitral incompetence). In acute rheumatic fever,
increased numbers of Aschoff bodies may be found
at this site of mechanical injury. B. Histology of rheu-
matic vegetation showing an Aschoff body with over-
lying ¬brin deposition. C. Two Aschoff bodies in the
proliferative phase lie on either side of a small
intramyocardial coronary artery.



1-37. Tight mitral stenosis with a ¬sh mouth ori¬ce due to
repeated attacks of acute rheumatic fever.

Cardiac Diseases 23
1-38. Severe postrheumatic mitral stenosis showing thickened, short-
ened cusps; fused commissures; and fused chordae tendineae.

1-39. Surgically excised mitral stenosis due to calci¬cation at one
commissure. The presence of the calci¬cation (yellow-brown, ulcer-
ated-looking area on the right) prevents the use of valvotomy to treat
the stenosis. The calci¬cation should not be mistaken for infective
endocarditis. Infection rarely affects mitral stenosis and is more com-
mon in mitral regurgitation.

24 Cardiac Diseases
1-40. Several mitral valve chordae are thickened in this patient with
micronodular cirrhosis. This association has been noted more often
in patients with alcoholic cirrhosis, and the pathogenesis is believed
to be related to failure to detoxify an unknown substance that elicits
an endocardial overlay lesion in some chordae.

Cardiac Diseases 25


1-41. A. Mitral stenosis in Whipple disease: healing vegetations lie
along the contact area of the cusps, which show ¬brosis and chordal
fusion. B. Histology shows histiocytes containing abundant periodic
acid-Schiff“positive intracellular material with ghost outlines of bac-
teria in between.

26 Cardiac Diseases


1-42. A. Radiograph of heart with an aortic prosthesis showing mas-
sive calci¬cation of the mitral annulus, which is C shaped due to the
anterior mitral lea¬‚et making up part of the annulus. B. Mitral annu-
lar calci¬cation (arrow) lies behind the mitral cusp in this sectioned
heart. In patients who receive hemodialysis, the calci¬ed material
may become liqui¬ed and may mimic an abscess in appearance.

Cardiac Diseases 27
1-43. Floppy mitral valve. A. Left atrial view of
intact mitral valve showing hemorrhoidal appear-
ance due to multiple hooding of the valve. B.
Opened mitral valve showing multiple redundant
folds (hoods) on posterior lea¬‚et prolapsing back
into the left atrium. Intervening portions of the cusp
appear normal. C. Hoods develop at sites of absent
¬brosal collagen and expanded spongiosa (loose
connective tissue rich in acid mucopolysaccharide).
(continued on next page)



28 Cardiac Diseases
1-43. (Continued) D. Endocardial friction lesion of
endocardium behind chordae. E. Histologic appear-
ance of the friction lesion showing red staining col-
lagen layer expanding the endocardium. Chordal
rupture may result in some cases.


Cardiac Diseases 29
1-44. Floppy mitral valve of long duration shows diffuse cuspal
¬brosis and chordal thickening that may mimic healed rheumatic

1-45. Infective endocarditis complicating a ¬‚oppy mitral valve.

30 Cardiac Diseases


1-46. A. Infective endocarditis of a normal aortic valve with perfo-
ration of two valve cusps. B. Histologic appearance of aortic valve
infective endocarditis with focal basophilia due to presence of pus
cells within vegetation on the cusp.

Cardiac Diseases 31
1-47. Massive ring abscess of aortic valve in a patient with Q fever
endocarditis due to Coxiella burnetii infection. Surgical correction,
including aortic root replacement, would be the only way to cure this
patient. Alternatively, a valved tube graft from the cardiac apex to
the aorta, combined with occlusion of the aortic root, may have been

1-48. Severe destruction of chordae and anterior cusp of mitral valve
due to infective endocarditis caused by a virulent Staphylococcus
aureus organism.

32 Cardiac Diseases
1-49. Surgically excised tricuspid valve for infective endocarditis.

1-50. Because of the low right-sided blood pressure and gentler cir-
culation, vegetations on the right-sided heart valves may attain a
much larger size than on the left side of the heart. These two vege-
tations ¬lled much of the right ventricle and the right atrium.

Cardiac Diseases 33
1-51. Endocardial vegetation (arrow) close to pulmonary valve due
to infection by Candida albicans.

1-52. Ruptured mycotic aneurysm of anterior lea¬‚et of mitral valve
due to infective endocarditis. Note that the aneurysm faces into the
lower-pressured left atrium.

34 Cardiac Diseases
1-53. Prosthetic valve endocarditis occurs in the
host tissue adjacent to the prosthesis and leads to
prosthetic ring sutures pulling out of the infected
host tissue, causing incompetence of the valve.
Plastic probe indicates this area in the photograph.

Cardiac Diseases 35


1-54. A. Calci¬cation of a Hancock porcine aortic
valve prosthesis has produced severe mitral stenosis
in this young girl. Thrombus overlying the atriotomy
wound site attests to the short duration that the pros-
thesis had been in situ. B. Histology of a cusp shows
central calci¬cation of the cuspal collagen in an area
that would have become ¬xed last during glu-
taraldehyde ¬xation. Unlike formaldehyde, glu-
taraldehyde is a poorly penetrating ¬xative.

36 Cardiac Diseases
1-55. Massive thrombus ¬lls the valve pockets on the out¬‚ow aspect
of this porcine aortic valve prosthesis, leading to prosthetic valvular

1-56. Surgical suture looped around one strut of this bovine peri-
cardial heart valve prosthesis has tilted up the prosthesis so that it
greatly obstructs the subaortic out¬‚ow tract of the left ventricle and
led to death of the patient soon after surgery. The prosthesis was
inserted from the left atrial aspect, and the strut and suture were
invisible to the surgeon performing the operation.

Cardiac Diseases 37
1-57. Pannus tissue overgrowth has produced stenosis of this
Ionescu-Shiley bovine pericardial mitral valve prosthesis and
obscured the original cusps. Some bland ¬brin-platelet thrombus is
present on the free margins of the cusps.

1-58. Severe prosthetic stenosis of this St. Jude Medical mechanical
prosthesis has resulted from bilateral thrombus at the hinge mecha-
nism area that has led both cusps to be ¬xed in the slightly open

38 Cardiac Diseases
1-60. Totally occlusive thrombus ¬lls the lumen of
1-59. Cloth wear in this Starr-Edwards ball valve
this atherosclerotic coronary artery.
mitral prosthesis has led to partial detachment of
the cloth from the cage struts. Abundant thrombus
had become attached to the free cloth, and the cloth
wear became apparent only after the thrombus had
been cleared from the cloth surface.

1-61. Top panel shows a recent regional, anteroseptal, transmural
myocardial infarct (left) as a pale area in the left ventricle. Propagated
red thrombus is seen within sections of the left anterior coronary artery
(right). Bottom panel (left) shows a ventricular slice with a healed pos-
terior myocardial infarct, plus a more recent, reperfused infarct that
appears hemorrhagic in appearance. The thrombosed causative coro-
nary occlusion is seen in sections of the coronary artery (right).

Cardiac Diseases 39
1-62. Global, subendocardial infarction (arrows) of
the left ventricle has resulted from more than 80%
stenosis of all three major epicardial coronary arter-
ies. The subendocardial myocytes are replaced by
¬brous tissue, and ongoing acute ischemic necrosis
of small groups of myocytes was noted histologically.

1-63. Thrombus (arrow) lies within longitudinally
opened atheromatous coronary artery (top), and seg-
ments (middle) of transversely sectioned coronary
artery contain occlusive thrombus. Bottom picture
shows close-up view of ruptured ¬brous cap of an
atheromatous plaque with thrombus (right) in direct
contact with cholesterol crystals (left).

40 Cardiac Diseases

1-64. A. Thromboembolus (derived from left atrial aspect of mitral
valve prosthesis) totally occludes ostium of left coronary artery in
aortic root. B. Histologic appearance of the occluding thrombus.

1-65. Acute dissecting aneurysm (arrow) of proxi- 1-66. Stent lies within a resected segment of coronary
mal left anterior descending coronary artery. artery.

Cardiac Diseases 41
1-67. A very recent (about 4 hours by history) myocardial infarct of
left ventricle (left) shows only edematous myocardium on its cut sur-
face. Right shows two biventricular slices from the same heart with
a 6-hour duration myocardial infarct; the infarct is well delineated
as the nonstaining area in the blue-stained left slice that had been
incubated with nitroblue tetrazolium.


1-68. Histology of acute myocardial infarction.
A. Edge of an infarct of about 6 hours duration
showing coagulative necrosis (left) and damaged,
viable myocytes (right). B. Edge of expanding
infarct of about 12 hours duration showing con-
traction band necrosis of myocytes, interstitial
edema, plus a prominent polymorphonuclear leuko-
cytic in¬ltration. C. Central portion of a myocardial
infarct of about 4 days duration showing neu-
trophils in¬ltrating between myocytes showing
advanced coagulative necrosis.


42 Cardiac Diseases
1-69. Ruptured papillary muscle head complicating acute myocardial
infarction of left ventricle.

1-70. Acquired ventricular septal defect due to ruptured interven-
tricular septum complicating acute myocardial infarction.

Cardiac Diseases 43
1-71. A. Cardiac aneurysm of left ventricular apex
complicating myocardial infarction. B. Remnants of
the original myocardial wall in the wall of the
aneurysm signify the presence of a true cardiac


44 Cardiac Diseases

1-72. A. Transverse section of ventricles showing
focal hemorrhage within the left ventricle due to a
reperfused myocardial infarct. A large intraepicar-
dial hematoma is present over the right ventricle,
and death occurred due to massive hemoperi-
cardium (cardiac tamponade) that clinically mim-
icked cardiac rupture. B. Section of right coronary
artery shows that a stent has been placed within the
lumen of a dissection of the artery, and the original
lumen is totally compressed. Hemopericardium
resulted from intraepicardial bleeding from the dis-
section, and in turn, this ruptured into the pericar-
dial sac. Bleeding was also favored by the potent
antiplatelet agents given for the stent.

Cardiac Diseases 45
1-73. Transverse biventricular slice of heart show-
ing concentric hypertrophy of left ventricle, incipi-
ent chamber dilatation, and the end-stage kidneys
from this same patient who had renovascular hyper-

1-74. Acute viral myocarditis. A. Dilated, nonhyper-
trophied heart with slightly mottled myocardium. B.
Severe interstitial lymphocytic in¬ltration of the ven-
tricular myocardium with focal loss of myocytes.



46 Cardiac Diseases
1-75. Idiopathic dilated cardiomyopathy. A. Enlarged,
football-shaped, globular heart due to generalized
chamber hypertrophy and dilatation. B. Transverse
slice of heart showing diffuse hypertrophy and dilata-
tion of both ventricles. C. Longitudinal section of
heart showing abundant stasis thrombi at the apices
of both ventricles. (continued on next page)



Cardiac Diseases 47


1-75. (Continued) D. Endocardial scarring near left ventricular apex
due to organization of endocardial thrombi. E. Histologic evidence of
myocyte hypertrophy, namely squared off (box car) nuclei.

48 Cardiac Diseases
1-76. Hypertrophic cardiomyopathy. A. Noteworthy
features include massive concentric hypertrophy of
left ventricle, inward bulging interventricular sep-
tum with mirror image plaque of anterior mitral
lea¬‚et, and reactive thickening of anterior lea¬‚et of
mitral valve. Note that the mirror image plaque lies
more inferiorly than the mitral valve because, dur-
ing life, tension in its papillary muscles holds the
valve at a lower level than after death. B. Transverse
biventricular slice showing asymmetric septal
hypertrophy (interventricular septum is thicker
than free wall of left ventricle). C. Myocyte disarray
in a section taken from midportion of the interven-
tricular septum.



Cardiac Diseases 49

1-77. Sigmoid septum (*) associated with aging. The
aorta comes off from the right side of the top of the
interventricular septum rather than straight up from
its summit. Clinically, a cardiologist may have dif-
¬culty distinguishing this entity from true hyper-
trophic cardiomyopathy.

50 Cardiac Diseases

1-78. Restrictive cardiomyopathy. A. Amyloidosis
of the heart with the amyloid deposits being most
visible as granular elevations on the right atrial
endocardial surface. B. Amyloid nodular deposit in
endocardium (Congo Red stain). C. Amyloid
deposits in a small artery and its surrounding con-
nective tissue (sulphated Alcian blue stain).



Cardiac Diseases 51


1-79. A. Cardiac amyloidosis with prominent
involvement of the left-sided heart valves. B. His-
tology of aortic valve cusp showing massive amy-
loid deposits (methyl violet stain).

52 Cardiac Diseases

1-80. Other causes of a restrictive cardiomyopathy.
A. Diffuse interstitial ¬brosis of unknown cause led
to a restrictive cardiomyopathy in this patient. B.
Hemochromatosis: the iron-laden heart is a weak
heart! Note the greater than normal brown color of
the myocardium. C. Histology shows massive blue-
staining iron deposits within cardiac myocytes
(Perl™s Prussian blue stain).



Cardiac Diseases 53


1-81. A. Arrhythmogenic right ventricular dyspla-
sia/cardiomyopathy in a young boy who suffered
sudden, unexpected death. Note the greatly thinned
apical free wall of the right ventricle (RV). Low-
power histology of the RV is shown in the right
panel. B. Isolated myocytes lie within ¬broadipose
tissue and ¬brous tissue. Some cases may show
lymphocytic in¬ltrates.

54 Cardiac Diseases
1-82. A. Noncompaction of the left ventricle
(NCLV) showing absence of the normal smoothness
to the septal wall of the left ventricle; this heart was
explanted at the time of cardiac transplantation
from a 4-year-old girl with severe heart failure.
NCLV will probably be included as a new form of
idiopathic cardiomyopathy in future classi¬cations
of cardiomyopathy. B. Microscopic appearance of
noncompacted left ventricle.


Cardiac Diseases 55
1-83. Idiopathic submitral aneurysm is believed to
result from a developmental weakness of the attach-
ment between the mitral annulus and the left ven-
tricle. The condition is more common in certain
tribes in southern Africa than in Caucasian popula-

1-84. Orthotopic cardiac transplantation. Note the marked difference
in appearance between the normal donor left atrial component and
the postrheumatic calci¬ed organized thrombi in the recipient™s left
atrial component. This donor heart failed due to graft arteriopathy
(chronic rejection). Graft arteriopathy is characterized by histologic
evidence of myocardial ¬brosis and luminal narrowing of both epi-
cardial and intramyocardial coronary arteries (see Fig. 1-86C and D).

56 Cardiac Diseases
1-85. Heterotopic cardiac transplantation (“piggy-
back heart”): the donor heart lies on the left side of
the picture, and a Dacron tube graft links the two
pulmonary arteries.

1-86. A. Severe acute rejection with arteritis lead-
ing to focal areas of ischemic infarction of the left
ventricle in an explanted donor heart. Immunosup-
pression had been discontinued shortly before the
heart was removed and replaced by another donor
heart. B. Histology of severe acute rejection show-
ing marked interstitial lymphocytic in¬ltration.
(continued on next page)


Cardiac Diseases 57

1-86. (Continued) C. Macroscopic appearance of
greatly thickened donor heart coronary artery
(arrow) with pinhole lumen due to graft arteriopa-
thy (chronic rejection). D. Histology of the same
artery showing marked intimal ¬brous thickening,
residual arteritis, and medial hyalinization.


58 Cardiac Diseases


1-87. A. Right ventricular view of incompletely excised rhabdomy-
oma affecting interventricular septum in a young child. B. Histology
shows the typical glycogen vacuolated “spider-like” rhabdomy-

Cardiac Diseases 59

1-88. A. Myxoma of left atrium is attached by a
short stalk to the area of the fossa ovalis. B. Typi-
cal histology of a myxoma showing spindle- and
stellate-shaped cells lying in a loose, myxoid stroma
rich in acid mucopolysaccharides. The tumor cells
may be arranged in cords that later give rise to cap-
illaries. C. Adenomatoid tumor (pointer) of atri-
oventricular node is elevating right atrial endo-
cardium near coronary sinus ostium. D. Histology
of adenomatoid tumor shows large, epithelioid cells
lining a tubular space.



60 Cardiac Diseases

1-89. A. Metastatic lung cancer to the epicardium;
secondary tumors are 20 times more common than
primary cardiac tumors. B. Histology shows moder-
ately differentiated adenocarcinoma occupying the
epicardial layer. C. Polypoid endocardial metastatic
deposit of a plasmacytoma.


Cardiac Diseases 61
1-90. A. Metastatic lymphoma to the heart from
mediastinal lymph nodes usually in¬ltrates via the
interatrial ¬broadipose tissue layer and, in this
patient, extended into the upper portion of the inter-
ventricular septum (seen here from the right side) to
produce complete heart block. Hematogenous spread
may affect any portion of the myocardium. B. His-
tology shows diffuse in¬ltration by atypical lym-
phocytes separating the atrial myocytes.


62 Cardiac Diseases
1-91. Hydatid disease (echinococcosis) of the heart.
A. Hydatid cysts are present within the free wall of
the left ventricle (right) and in the interatrial sep-
tum. B. Histology of the cyst wall (periodic acid-
Schiff stain) shows scolices lying attached to the
germinal epithelium (left).


Cardiac Diseases 63
1-92. Cysticercosis of the heart due to Taenia sagi-
nata (pork tapeworm). A. Innumerable small cysts
(each containing a single scolex) are scattered
throughout all layers of the left ventricle. B. Histol-
ogy of the cyst wall and portion of a scolex.


64 Cardiac Diseases
1-93. A. Macroscopic appearance of a milk spot
(previously called “soldier™s heart”) (arrow). B. His-
tology shows the contrast between the normal, thin
epicardium (top left) and the thickened, organized
epicarditis that has produced the milk spot.


Cardiac Diseases 65

1-94. A. Fibrinous pericarditis (the beloved “bread-
and-butter pericarditis” of pathologists, alluding to
the strands of ¬brin drawn up by the opposing vis-
ceral and parietal layers of the pericardium analo-
gous to pulling apart two slices of buttered bread).
B. Organizing ¬brinous pericarditis showing histio-
cytes engul¬ng ¬brin. C. Cardiac tamponade due to
hemopericardium: removal of the parietal peri-
cardium shows clotted blood ¬lling the pericardial
cavity in a patient with a ruptured myocardial


66 Cardiac Diseases


1-95. A. Fibrinopurulent pericarditis showing pus ¬lling the pericar-
dial cavity. B. Histology of the exudate shows numerous polymor-

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