This PowerPoint presentation provides images and descriptions of normal heart anatomy and various cardiovascular pathologies. It begins with images of the normal heart structures, including the coronary arteries, myocardium, and valves. It then covers atherosclerotic cardiovascular disease, showing examples of atherosclerotic plaques, aneurysms, thrombi, and infarcts. Other sections address arterial dissection, infective endocarditis, pericarditis, and myocarditis. The presentation is intended to enable offline study of cardiovascular pathology images for medical licensing exam preparation.

1. A Basic PowerPoint conversion :
For study, sharing and download as a tool in preparation to
sit for the USMLE Step 1
Source of Images
Webpath- University of Utah
Hypermedia Image Source Tables included
Conversion prepared and presented by
Marc Imhotep Cray, M.D.
Basic Medical Sciences Teacher

2. Webpath Hypermedia Source Tables
http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html
Purpose
The purpose of this PowerPoint conversion is
1. To enable the learner to bring Webpath Cardiovascular
Pathology image plates to their desktop for offline study
2. To contribute to mobile device viewing diversity
3. It serves as a part of the IVMS ANS and Cardiovascular
Pharmacology Sequenced Course Demonstration
 Open Demo
2

3. Normal Heart
3

4. Normal Heart
•Normal heart, gross
•Normal aortic valve, gross
•Normal tricuspid valve, gross
•Normal coronary artery, microscopic
•Normal myocardium, medium power microscopic
4

5. Normal heart, gross
• This is the external
appearance of a normal
heart.The epicardial surface
is smooth and glistening.
• The amount of epicardial fat
is usual.The left anterior
descending coronary artery
extends down from the aortic
root to the apex
5

6. Normal tricuspid valve, gross
• This is the tricuspid
valve. The leaflets and
thin and delicate.
• Just like the mitral valve,
the leaflets have thin
chordae tendineae that
attach the leaflet margins
to the papillary muscles
of the ventricular wall
below
6

7. Normal coronary artery,
microscopic
• This is a normal
coronary artery.
• The lumen is large,
without any narrowing
by atheromatous
plaque. The muscular
arterial wall is of
normal proportion
7

8. Normal myocardium, medium
power microscopic
• This is the normal
appearance of
myocardial fibers in
longitudinal section.
• Note the central
nuclei and the
syncytial arrangement
of the fibers, some of
which have pale pink
intercalated disks
8

9. Atherosclerotic
Cardiovascular
Disease
9

10. Atherosclerotic
Cardiovascular Disease (1)
•Coronary artery with atherosclerotic narrowing, microscopic
•Coronary artery with recanalized thrombosis, microscopic
•Coronary artery with calcific atherosclerosis, microscopic
•Coronary artery atherosclerosis, occlusive, microscopic
•Coronary artery thrombosis, recent, microscopic
•Atheromatous plaque, high power, microscopic
•Aorta with rare lipid streaks, gross
•Aorta with lipid streaks, gross
•Aortas demonstrating various degrees of atherosclerosis, gross
10

11. Coronary artery with
atherosclerotic narrowing,
microscopic
• The coronary artery
shown here has
narrowing of the lumen
due to build up of
atherosclerotic plaque.
• Severe narrowing can
lead to angina,
ischemia, and infarction
11

12. Coronary artery with recanalized
thrombosis, microscopic
• This section of
coronary artery
demonstrates remote
thrombosis with
recanalization to leave
only two small, narrow
channels
12

13. Coronary artery with calcific
atherosclerosis, microscopic
• There is a severe degree of
narrowing in this coronary
artery.
• It is "complex" in that there is
a large area of calcification
on the lower right, which
appears bluish on this H&E
stain.
• Complex atheroma have
calcification, thrombosis, or
hemorrhage. Such
calcification would make
coronary angioplasty difficult
13

14. Aortas demonstrating various
degrees of atherosclerosis, gross
• These three aortas
demonstrate mild, moderate,
and severe atherosclerosis
from bottom to top.
• At the bottom, the mild
atherosclerosis shows only
scattered lipid plaques.
• The aorta in the middle
shows many more larger
plaques. The severe
atherosclerosis in the aorta at
the top shows extensive
ulceration in the plaques
14

15. Aorta, atherosclerotic
aneurysm, gross
• Here is an example of an
atherosclerotic aneurysm of the
aorta in which a large "bulge"
appears just above the aortic
bifurcation.
• Such aneurysms are prone to
rupture when they reach about
6 to 7 cm in size.
• They may be felt on physical
examination as a pulsatile mass
in the abdomen.Most such
aneurysms are conveniently
located below the renal arteries
so that surgical resection can
be performed with placement of
a dacron graft
15

16. Atherosclerotic
Cardiovascular Disease (2)
•Aorta, atherosclerotic aneurysm, gross [CT]
•Aorta, atheroma, low power, microscopic
•Aorta, atheroma, high power, microscopic
•Aorta, ulcerative atherosclerosis with mural thrombosis, gross
•Cholesterol emboli in kidney, medium power microscopic
•Coronary artery, mild atherosclerosis, gross
•Coronary artery, severe atherosclerosis, gross
•Coronary artery, hemorrhage into plaque, gross
•Coronary artery, occlusive atherosclerosis, gross
•Heart and LAD coronary artery with recent thrombus, gross
•Coronary artery with recent thrombus, longitudinal section, gross
•Coronary artery with recent thrombus, cross section, gross
16

17. CT scan with contrast
• This abdominal high
speed CT scan with
contrast demonstrates
an abdominal aortic
aneurysm approximately
6 cm in diameter.
• At this size, there is
increased risk for
rupture
17

18. Coronary artery, mild
atherosclerosis, gross
• A coronary artery has been
opened longitudinally.
• The coronary extends from left
to right across the middle of the
picture and is surrounded by
epicardial fat. Increased
epicardial fat correlates with
increasing total body fat.
• There is a lot of fat here,
suggesting one risk factor for
atherosclerosis.
• This coronary shows only mild
atherosclerosis, with only an
occasional yellow-tan lipid
plaque and no narrowing
18

19. Coronary artery, severe
atherosclerosis, gross
• This is the left coronary
artery from the aortic root
on the left.
• Extending across the
middle of the picture to
the right is the anterior
descending branch.
• This coronary shows
severe atherosclerosis
with extensive
calcification. At the far
right, there is an area of
significant narrowing
19

20. Coronary artery, hemorrhage
into plaque, gross
• This is coronary
atherosclerosis with the
complication of
hemorrhage into
atheromatous plaque,
seen here in the center
of the photograph.
• Such hemorrhage
acutely may narrow the
arterial lumen
20

21. Heart and LAD coronary artery
with recent thrombus, gross
• The anterior surface of the
heart demonstrates an opened
left anterior descending
coronary artery.
• Within the lumen of the
coronary can be seen a dark
red recent coronary thrombosis.
• The dull red color to the
myocardium as seen below the
glistening epicardium to the
lower right of the thrombus is
consistent with underlying
myocardial infarction
21

22. Myocardial Infarction
22

23. Myocardial Infarction
•Heart, left ventricle, acute myocardial infarction, gross
•Heart, left ventricle and septum, myocardial infarction, gross
•Myocardium, contraction band necrosis, microscopic
•Myocardium, acute myocardial infarction, 1 to 2 days, microscopic
•Myocardium, acute myocardial infarction, 1 to 2 days, microscopic
•Myocardium, acute myocardial infarction, 3 to 4 days, microscopic
•Myocardium, intermediate myocardial infarction, 1 to 2 weeks, microscopic
•Heart, transmural myocardial infarction with rupture and hemopericardium,
gross
•Heart, transmural myocardial infarction with rupture, gross
•Heart, remote myocardial infarction, medium power microscopic
•Heart, remote myocardial infarction, low power microscopic
•Heart, remote myocardial infarction, gross
•Heart, left ventricular aneurysm, gross
•Heart, left ventricular aneurysm, gross
•Heart, coronary artery bypass graft, gross
23

24. Heart, left ventricle, acute
myocardial infarction, gross
• This is the left ventricular
wall which has been
sectioned lengthwise to
reveal a large recent
myocardial infarction.
• The center of the infarct
contains necrotic muscle
that appears yellow-tan.
• Surrounding this is a zone
of red hyperemia.
Remaining viable
myocardium is reddishbrown
24

25. Heart, left ventricle and septum,
myocardial infarction, gross
• This cross section through the
heart demonstrates the left
ventricle on the left.
• Extending from the anterior
portion and into the septum is
a large recent myocardial
infarction.
• The center is tan with
surrounding hyperemia.
• The infarction is "transmural"
in that it extends through the
full thickness of the wall
25

26. Heart, transmural myocardial infarction
with rupture and hemopericardium,
gross
• One complication of a transmural
myocardial infarction is rupture of the
myocardium.
• This is most likely to occur in the
first week between 3 to 5 days
following the initial event, when the
myocardium is the softest.
• The white arrow marks the point of
rupture in this anterior-inferior
myocardial infarction of the left
ventricular free wall and septum.
• Note the dark red blood clot forming
the hemopericardium. The
hemopericardium can lead to
tamponade
26

27. Heart, left ventricular aneurysm,
gross
• A cross section through
the heart reveals a
ventricular aneurysm
with a very thin wall at
the arrow.
• Note how the aneurysm
bulges out. The stasis in
this aneurysm allows
mural thrombus, which is
present here, to form
within the aneurysm
27

28. Arterial Dissection
28

29. Arterial Dissection
•Aorta, dissection with tear in arch, gross
•Heart, dissection with tear through media, low power microscopic
•Hemopericardium with cardiac tamponade, gross
•Aorta, dissection, gross
•Aorta, dissection, microscopic
•Carotid artery, dissection with compression, gross
•Aorta, dissection, microscopic
•Aorta, dissection, Marfan's syndrome, gross
•Floppy mitral valve with prolapse, Marfan's syndrome, gross
•Floppy mitral valve with prolapse, Marfan's syndrome, gross
•Aorta, cystic medial necrosis, Marfan's syndrome, Mucin stain, microscopic
•Arachnodactyly, Marfan's syndrome, gross
29

30. Aorta, dissection with tear in
arch, gross
• There is a tear (arrow)
located 7 cm above the
aortic valve and
proximal to the great
vessels in this aorta
with marked
atherosclerosis.
• This is an aortic
dissection
30

31. Hemopericardium with cardiac
tamponade, gross
• An aortic dissection may
lead to hemopericardium
when blood dissects
through the media
proximally.
• Such a massive amount of
hemorrhage can lead to
cardiac tamponade
31

32. Aorta, dissection, gross
• This aorta has been opened
longitudinally to reveal an area of
fairly limited dissection that is
organizing.
• The red-brown thrombus can be
seen in on both sides of the section
as it extends around the aorta. The
intimal tear would have been at the
left.
• This creates a "double lumen" to
the aorta.
• This aorta shows severe
atherosclerosis which, along with
cystic medial necrosis and
hypertension, is a risk factor for
dissection
32

33. Aorta, dissection, microscopic
• Here, the dissection went into
the muscular wall. In any
case, an aortic dissection is
an extreme emergency and
can lead to death in a matter
of minutes.
• The blood can dissect up or
down the aorta.
• Blood dissecting up around
the great vessels can close off
the carotids.
• Blood can dissect down to the
coronaries and shut them off
33

34. Carotid artery, dissection with
compression, gross
• The right carotid artery is
compressed by blood dissecting
upward from a tear with aortic
dissection.
• Blood may also dissect to
coronary arteries.
• Thus patients with aortic
dissection may have symptoms
of severe chest pain (for distal
dissection) or may present with
findings that suggest a stroke
(with carotid dissection) or
myocardial ischemia (with
coronary dissection).
34

35. Infective Endocarditis
35

36. Non-infective Endocarditis
•Non-bacterial thrombotic endocarditis, gross
•Non-bacterial thrombotic endocarditis, gross
•Non-bacterial thrombotic endocarditis, microscopic
•Libman-Sacks endocarditis (and mitral rheumatic
valvulitis), gross
•Mitral valve, acute rheumatic vegetations, gross
•Mitral valve, rheumatic mitral stenosis, gross
36

37. Aortic valve, infective
endocarditis, gross
• This is infective endocarditis.
The aortic valve demonstrates
a large, irregular, reddish tan
vegetation.
• Virulent organisms, such as
Staphylococcus aureus,
produce an "acute" bacterial
endocarditis, while some
organisms such as
Streptococcus viridans produce
a "subacute" bacterial
endocarditis
37

38. Infective endocarditis spreading to
myocardium, gross
• In this case, the infective
endocarditis
demonstrates how the
infection tends to spread
from the valve surface.
• Here, vegetations can be
seen on the endocardial
surfaces, and the
infection is extending into
to underlying myocardium
38

39. Infective endocarditis,
microscopic
• Microscopically, the valve
in infective endocarditis
demonstrates friable
vegetations of fibrin and
platelets (pink) mixed
with inflammatory cells
and bacterial colonies
(blue).
• The friability explains
how portions of the
vegetation can break off
and embolize
39

40. Pericarditis
40

41. Pericarditis
•Serous pericarditis, diagram
•Fibrinous pericarditis, diagram
•Fibrinous pericarditis, gross
•Fibrinous pericarditis, gross
•Fibrinous pericarditis, gross
•Fibrinous pericarditis, microscopic
•Hemorrhagic pericarditis, gross
•Hemorrhagic pericarditis, gross
•Purulent pericarditis, gross
41

42. Fibrinous pericarditis, gross
• A window of adherent
pericardium has been
opened to reveal the
surface of the heart.
• There are thin strands of
fibrinous exudate that
extend from the epicardial
surface to the pericarial
sac.
• This is typical for a
fibrinous pericarditis
42

43. Hemorrhagic pericarditis, gross
• The pericarditis here not
only has fibrin, but also
hemorrhage. Thus, this is
called a "hemorrhagic
pericarditis".
• It is really just fibrinous
pericarditis with
hemorrhage. Without
inflammation, blood in the
pericardial sac would be
called "hemopericardium
43

44. Myocarditis
44

45. Myocarditis
•Heart, microabscesses, gross
•Heart, microabscess, gross
•Heart, microabscess, microscopic
•Acute rheumatic carditis, microscopic
•Acute rheumatic carditis, microscopic
•Acute rheumatic carditis, microscopic
•Chronic rheumatic valvulitis, gross
•Interstitial viral myocarditis, microscopic
45

46. Heart, microabscesses, gross
The epicardial surface of the
heart is smooth and
glistening, but there are
small scattered pinpoint
yellowish microabscesses.
(Higher magnification in next
photo).
46

47. Heart, microabscess, gross
This magnification of the preceding
photograph shows the small yellowish
pinpoint microabscesses on the
epicardial surface. Microabscesses
may appear in persons who are septic.
They may also represent emboli from
an infective endocarditis in which small
portions of a vegetation have
embolized out the coronary arteries.
47

48. Heart, microabscess,
microscopic
The microscopic
appearance of a
microabscess is shown
here.
The center consists of
blue bacterial colonies
and is surrounded by
acute inflammatory
cells.
48

49. Acute rheumatic carditis,
microscopic (1)
Microscopically, acute
rheumatic carditis is marked
by a peculiar form of
granulomatous inflammation
with so-called "Aschoff
nodules" seen best in
myocardium.
These are centered in
interstitium around vessels as
shown here. The myocarditis
may be severe enough to
cause congestive heart failure.
49

50. Acute rheumatic carditis,
microscopic (2)
Here is an Aschoff nodule at
high magnification.
The most characteristic
component is the Aschoff giant
cell.
Several appear here as large
cells with two or more nuclei
that have prominent nucleoli.
Scattered inflammatory cells
accompany them and can be
mononuclears or occasionally
neutrophils.
50

51. Acute rheumatic carditis,
microscopic (3)
Another peculiar cell seen
with acute rheumatic
carditis is the Anitschkow
myocyte.
This is a long, thin cell with
an elongated nucleus.
51

52. Chronic rheumatic valvulitis,
gross
In time, chronic rheumatic
valvulitis may develop by
organization of the acute
endocardial inflammation along
with fibrosis, as shown here
affecting the mitral valve.
Note the shortened and
thickened chordae tendineae.
52

53. Interstitial viral myocarditis,
microscopic
The interstitial lymphocytic
infiltrates shown here are
characteristic for a viral
myocarditis, which is probably
the most common type of
myocarditis.
Many of these cases are
probably subclinical.
Some may be a cause for
sudden death in young
persons. There is usually little
necrosis.
The most common viral
agent is Coxsackie B.
53

54. Neoplasia
54

55. Neoplasia
•Heart, rhabdomyoma, gross
•Heart, atrial myxoma, gross
•Heart, atrial myxoma, microscopic
•Heart, epicardium, metastases, gross
•Heart, myocardium, metastatic melanoma, microscopic
55

56. Heart, rhabdomyoma,
gross
• This two year old child
died suddenly. At
autopsy, a large firm,
white tumor mass was
found filling much of the
left ventricle.
• This is a cardiac
rhabdomyoma. Such
primary tumors of the
heart are rare
56

57. Heart, atrial myxoma, gross
• The left atrium has been
opened to reveal the most
common primary cardiac
neoplasm--an atrial myxoma.
• These benign masses are
most often attached to the
atrial wall, but can arise on a
valve or in a ventricle.
• They can produce a "ball
valve" effect by intermittently
occluding the atrioventricular
valve orifice. Embolization of
fragments of tumor may also
occur. Myxomas are easily
diagnosed by
echocardiography
57

58. Heart, epicardium, metastases,
gross
• Primary tumors of the heart
are uncommon.
• Metastases to the heart are
more common, but rare overall
(only about 5 to 10% of all
malignancies have cardiac
metastases).
• Seen over the surface of the
epicardium are pale white-tan
nodules of metastatic tumor.
Metastases may lead to a
hemorrhagic pericarditis.
58

59. Congenital Heart
Disease
59

60. Congenital Heart Disease
•Congenital heart disease, table
•Heart, probe patent foramen ovale, and paradoxical embolus, gross
•Heart, atrial septal defect, gross
•Heart, atrial septal defect, Eisenmenger's complex, gross
•Heart, ventricular septal defect, gross
•Heart, atrial septal defect and ventricular septal defect, gross
•Aorta, coarctation, gross
•Aorta, coarctation, gross
•Pulmonic valve, quadricuspid, gross
•Aortic valve, bicuspid, gross
•Aortic valve, senile calcific aortic stenosis, gross
•Heart, tetralogy of Fallot, diagram
•Heart, persistent truncus arteriosus, diagram
•Heart, transposition of great vessels, diagram
60

61. Congenital Heart Disease
Type of Defect Mechanism
61

62. Type of Defect Mechanism
• Ventricular Septal Defect (VSD) There is a hole within the
membranous or muscular portions of the intraventricular septum that
produces a left-to-right shunt, more severe with larger defects
•
Atrial Septal Defect (ASD) A hole from a septum secundum or
septum primum defect in the interatrial septum produces a modest
left-to-right shunt
•
• Patent Ductus Arteriosus (PDA) The ductus arteriosus, which
normally closes soon after birth, remains open, and a left-to-right
shunt develops
62

63. Type of Defect
Mechanism
• Tetralogy of Fallot Pulmonic stenosis results in right ventricular
hypertrophy and a right-to-left shunt across a VSD, which also has
an overriding aorta
• Transposition of Great Vessels The aorta arises from the right
ventricle and the pulmonic trunk from the left ventricle. A VSD, or
ASD with PDA, is needed for extrauterine survival. There is right-toleft shunting
• .
• Truncus ArteriosusThere is incomplete separation of the aortic and
pulmonary outflows, along with VSD, which allows mixing of
oxygenated and deoxygenated blood and right-to-left shunting
63

64. Type of Defect
Mechanism
• Hypoplastic Left Heart Syndrome There are varying
degrees of hypoplasia or atresia of the aortic and mitral
valves, along with a small to absent left ventricular
chamber
• Coarctation of Aorta Either just proximal (infantile
form) or just distal (adult form) to the ductus is a
narrowing of the aortic lumen, leading to outflow
obstruction
• Total Anomalous Pulmonary Venous Return
(TAPVR) The pulmonary veins do not directly connect to
the left atrium, but drain into left innominate vein,
coronary sinus, or some other site, leading to possible
mixing of blood and right-sided overload
64

65. Heart, atrial septal defect,
gross
• In the region of the foramen
ovale on the interatrial
septum is a small atrial
septal defect, as seen in this
heart opened on the right
side.
• Here the defect is not
closed by the septum
secundum, so a shunt exists
across from left to right
65

66. Heart, ventricular septal defect,
gross
• This is the heart of a
premature stillborn with
Trisomy 13 in which a
ventricular septal defect is
visible in the membranous
septum.
• About 90% of VSD's are in
the membranous septum and
10% in the muscular septum.
66

67. Aorta, coarctation, gross
• This portion of aorta was
resected from a patient
with a coarctation.
• The aorta narrows
postductally here to about
a 3 mm opening
67

68. Aorta, coarctation, gross
• The aorta is opened
longitudinally here to
reveal a coarctation.
• In the region of the
narrowing, there was
increased turbulence
that led to increased
atherosclerosis.
68

69. Heart, tetralogy of Fallot,
diagram
This diagram depicts the
features of Tetralogy of
Fallot:
1. Ventricular septal defect;
2. Overriding aorta;
3. Pulmonic stenosis;
4. Right ventricular
hypertrophy. The obstruction
to right ventricular outflow
creates a right-to-left shunt
that leads to cyanosis.
69

70. Heart, transposition of great
vessels, diagram
• In the diagram, transposition of the
great vessels is shown
• occurs when the trunco-conal septum
does not spiral down. Instead, it
descends straight down. As a result,
outflow of right ventricle is into aorta
and outflow from left ventricle is into
the pulmonic trunk.
• In order for this system to work, there
must be a connection between the
system and pulmonic circulations.
• Sometimes this is through a
ventricular septal defect or an atrial
septal defect.
• In the diagram at the left, this is
through a patent ductus arteriosus
70

71. Cardiomyopathies
71

72. Cardiomyopathies
•Cardiomyopathies, table
•Heart, dilated cardiomyopathy, gross [XRAY]
•Heart, dilated cardiomyopathy, gross
•Heart, cardiomyopathy, microscopic
•Heart, hypertrophic cardiomyopathy, explanted heart, gross
•Heart, restrictive cardiomyopathy from hemochromatosis, microscopic
•Heart, restrictive cardiomyopathy from amyloidosis, microscopic
•Myocardium, amyloidosis, apple-green birefringence with polarized
light, Congo red stain, microscopic
•Heart, hypertension with left ventricular hypertrophy, gross
•Heart, hypertrophy with hypertension, gross
72

73. Type of CMP Findings
• Dilated (Congestive) All four chambers are dilated, and there is
also hypertrophy. The most common cause is chronic alcoholism,
though some may be the end-stage of remote viral myocarditis.
•
Hypertrophic The most common form, idiopathic hypertrophic
subaortic stenosis (IHSS) results from asymmetric interventricular
septal hypertrophy, resulting in left ventricular outflow obstruction.
•
Restrictive The myocardium is infiltrated with a material that results
in impaired ventricular filling. The most common causes are
amyloidosis and hemochromatosis.
73

74. Heart, dilated cardiomyopathy,
gross
• This very large heart has a
globoid shape because all of
the chambers are dilated.
• It felt very flabby, and the
myocardium was poorly
contractile.
• This is an example of a
cardiomyopathy.
• This term is used to denote
conditions in which the
myocardium functions poorly
and the heart is large and
dilated, but there is no specific
histologic finding
74

75. Heart, dilated cardiomyopathy,
[XRAY]
• This chest radiograph
demontrates marked
cardiomegaly, with
the left heart edge
appearing far to the
left
75

76. Heart, cardiomyopathy,
microscopic
• Microscopically, the
heart in cardiomyopathy
• demonstrates
hypertrophy of
myocardial fibers
(which also have
prominent dark nuclei)
along with interstitial
fibrosis
76

77. Heart, hypertrophic cardiomyopathy,
explanted heart, gross
• There is marked left ventricular
hypertrophy, with asymmetric bulging of
a very large interventricular septum into
the left ventricular chamber.
• This is hypertrophic cardiomyopathy.
About half of these cases are familial,
though a variety of different genes may
be responsible for this disease.
• Both children and adults can be affected,
and sudden death can occur. Seen here
is the explanted heart. Pacemaker wires
enter the right ventricle.
• The atria with venous connections, along
with great vessels, remained behind to
connect to the transplanted heart
(provided by someone who cared
enough to make transplantation
possible).
77

78. Heart, hypertension with left
ventricular hypertrophy, gross
• This left ventricle is very
thickened (slightly over 2 cm
in thickness), but the rest of
the heart is not greatly
enlarged.
• This is typical for
hypertensive heart disease.
• The hypertension creates a
greater pressure load on the
heart to induce the
hypertrophy
78

79. Heart, hypertrophy with
hypertension, gross
• The left ventricle is
markedly thickened in
this patient with severe
hypertension that was
untreated for many
years.
• The myocardial fibers
have undergone
hypertrophy
79

80. Arterial and Venous
Diseases
80

81. Renal arteriole, fibrinoid necrosis with
malignant hypertension, microscopic
• One complication of
hyperplastic
arteriolosclerosis with
malignant hypertension is
fibrinoid necrosis, as seen
here in a renal arteriole
81

82. Varicose veins, gross
• The prominent veins shown
here on the lower leg are
varicosities. Varicose veins are
a common problem with aging.
The venous valves become
incompetent.
• There may be muscular
atrophy with less tone to
provide a massage effect on
the large superficial veins, and
skin becomes less elastic with
time.
• Hydrostatic pressure from
standing for long periods
exacerbates the problem
82