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This is a normal coronary artery with no atherosclerosis

and a wide lumen that can carry as much blood as the
myocardium requires.

This is mild coronary atherosclerosis. A few

scattered yellow lipid plaques are seen on the
intimal surface of the opened coronary artery
traversing the epicardial surface of a heart. The
degree of atherosclerosis here is not significant
enough to cause disease, but could be the
harbinger of worse atherosclerosis to come.

The degree of atherosclerosis is much greater in

this coronary artery, and the lumen is narrowed
by half. A small area of calcification is seen in the
plaque at the right.

a coronary artery showing narrowing of

the lumen by atheromatous plaque.

Coronary thrombus

Coronary atherosclerosis, thrombosis

This is a low power picture of the classical changes of

atherosclerosis. You will notice that the lumen of the
vessel is about 75% narrowed with a single large
atherosclerotic plaque. The blue crystals are calcium,
which have precipitated because the pH of the interior
of the plaque is so low. You may see long needle like
slits or openings in the plaque, which represent areas
where cholesterol had crystallized. They are now empty
because the cholesterol was washed out of the tissue
during the fixation and processing of the tissue.

These cross sections of the left anterior descending coronary

artery demonstrate more pronounced atherosclerosis with
narrowing at the left, which is the proximal portion of this
artery. Atherosclerosis is generally worse at the beginning of
an artery where turbulence of vascular flow with ongoing
endothelial stress and injury is greater.

Pictured is a cholesterol-filled atherosclerotic coronary artery from a

human body. Researchers at the University of Pennsylvania School of
Medicine have demonstrated the potential of a new type of therapy for
patients who suffer from high cholesterol levels. A new study shows that
targeted inhibition of the microsomal triglyceride transfer protein (MTP)
is highly effective in reducing cholesterol levels in very high risk patients.

This is an atheromatous plaque in a coronary artery

that shows endothelial denudation with disruption and
overlying thrombus formation at the right. The arterial
media is at the left.

Here is occlusive coronary atherosclerosis. The coronary at the left

is narrowed by 60 to 70%. The coronary at the right is even worse
with evidence for previous thrombosis with organization of the
thrombus and recanalization such that there are three small lumens
remaining, one of which contains additional recent thrombus.

This is the gross appearance of severe coronary

atherosclerosis, which involves virtually 100% of the surface
of this coronary artery. There is extensive calcification,
especially at the right where the lumen is narrowed.

Here is a coronary artery with atherosclerotic plaques.

There is recent hemorrhage into the plaque. This is one of
the complications of atherosclerosis. Such hemorrhage
could acutely narrow the lumen and produce an acute
coronary syndrome with ischemia and/or infarction of the
myocardium.

 Here is the anterior

surface of the heart
with the left anterior
descending coronary
artery opened
longitudinally. This is
coronary thrombosis,
one of the
complications of
atherosclerosis. The
occlusive dark red
thrombus is seen within
the lumen of the
coronary artery. This
produces an acute
coronary syndrome.

Here is the coronary thrombosis at higher

magnification. The thrombus occludes the
lumen and produces ischemia and/or
infarction of the myocardium.

A coronary thrombosis is seen microscopically

occluding the remaining small lumen of this coronary
artery. Such an acute coronary thrombosis is often
the antecedent to acute myocardial infarction.

The interventricular septum of the heart has

been sectioned to reveal an extensive acute
myocardial infarction. The dead muscle is tanyellow with a surrounding hyperemic border.

This cross section through the heart reveals a large

myocardial infarction involving the anterior left
ventricular wall and septum. The infarct is beginning to
heal, but still has a necrotic center. The ejection fraction
from the left ventricle would be significantly reduced.

The tan to white areas of myocardial scarring seen from

the endocardial surface here represent a remote healed
myocardial infarction. This healed infarct is most
prominent over the septum but also involves the left
ventricle.

There has been a

previous extensive
transmural myocardial
infarction involving the
free wall of the left
ventricle. Note that the
thickness of the
myocardial wall is normal
superiorly, but inferiorly
is only a thin fibrous wall.
The thinned area
represents a ventricular
aneurysm that has
developed as a
consequence of the
healed infarct. Such an
aneurysm represents
non-contractile tissue
that reduces stroke
volume and strains the
remaining myocardium.
The stasis of blood in the
aneurysm predisposes to
mural thrombosis.

The pale yellow lipid streaks in the aorta are the

earliest lesion of atherosclerosis.

Put down that extra slice of pizza and look carefully at this
aorta. The white arrow denotes the most prominent fatty
streak in the photo, but there are other fatty streaks scattered
over the aortic surface. Fatty streaks are the earliest lesions
seen with atherosclerosis in arteries. Increased total cholesterol
and decreased HDL cholesterol contribute to this process.

Three aortas are shown to demonstrate

mild, moderate, and severe
atherosclerosis from bottom to top.

Microscopically, the aortic atheromatous plaque is thicker

than the remaining media at the right. The plaque contains
amorphous pink material with slit-like "cholesterol clefts" of
lipid material. There is overlying recent hemorrhage at the
left. Thrombus may form on top of such a plaque.

At higher magnification, many foam cells

(macrophages full of lipid material) and a
cholesterol cleft are seen in this atheromatous
plaque.

The cholesterol clefts of lipid, along with a few scattered

foam cells and a couple of lymphocytes, are seen at high
magnification in this atheromatous plaque.

Atherosclerosis
may weaken the
wall of the aorta
such that it
bulges out to
form an
aneurysm. An
atherosclerotic
aortic aneurysm
typically occurs
in the abdominal
portion below
the renal
arteries, as
shown here.
Aortic
aneurysms that
get bigger than
6 or 7 cm are
likely to rupture.

This large abdominal atherosclerotic aortic aneurysm below

the renal arteries at the right and above the bifurcation at
the left has been opened to reveal abundant layered mural
thrombus within the aneurysm [Image contributed by Dr.
John Nicholls, Hong Kong University].

This is a different kind of arteriosclerosis. This is hyperplastic

arteriolosclerosis, which most often appears in the kidney in patients with
malignant hypertension. The arteriolar wall is markedly thickened and the
lumen is narrowed.
Arteriosclerosis, or "hardening of the arteries" is a generic term that
includes atherosclerosis, arteriolosclerosis, and medial calcific sclerosis.

Sometimes the small arteries and arterioles

can be damaged so severely in malignant
hypertension that they demonstrate necrosis
with a pink fibrin-like quality that gives this
process its name--fibrinoid necrosis.

This is hyaline arteriolosclerosis, which can be seen in

patients with diabetes mellitus and with hypertension. This
glomerulus stained with PAS shows nodular deposits of
amorphous material (nodular glomerulosclerosis) along
with a thickened arteriole at the lower right.

This is Monckeberg's medial calcific sclerosis, which is the most

insignificant form of arteriosclerosis (both atherosclerosis and
arteriolosclerosis are definitely significant). Note the purplish blue
calcifications in the media; note that the lumen is unaffected by this
process. Thus, there are usually no real clinical consequences. Remember
this process when calcified muscular arteries show up on a radiograph of
the pelvic region in an older person.

The main pulmonary trunk and pulmonary arteries to

right and left lungs are seen here opened to reveal a
large "saddle" pulmonary thromboembolus. Patients
with such an embolus will have a high mortality rate.

Here is another
large pulmonary
thromboembolu
s seen in cross
section of this
lung. The
typical source
for such
thromboemboli
is from large
veins in the legs
and pelvis.

This pulmonary thromboembolus is occluding the main

pulmonary artery. Persons who are immobilized for weeks are
at greatest risk. The patient can experience sudden onset of
shortness of breath. Death may occur within minutes.

This is the microscopic appearance of a

pulmonary embolus (PE) in a major
pulmonary artery branch.

This pulmonary embolus is adherent to the pulmonary

arterial wall. If the patient survives, the thromboembolus
will organize and, for the most part, be removed.

These are "lines of Zahn" which are the

alternating pale pink bands of platelets with fibrin
and red bands of RBC's forming a true thrombus.

Occlusion of main
pulmonary arteries can
kill the patient suddenly.
Occlusion of small
pulmonary arteries has
no major immediate
effect. Occlusion of a
medium-sized branch of
pulmonary artery can
lead to a pulmonary
infarction in a person with
compromised cardiac or
respiratory status. A
pulmonary infarct is
hemorrhagic because of
the dual blood supply
from the non-occluded
bronchial arteries which
continue to supply blood,
but do not prevent the
infarction.

Here is another
hemorrhagic
pulmonary
infarction in a
patient with a
pulmonary
thromboembolus to
a medium sized
pulmonary artery.
Such infarctions
tend to be based on
the pleural surface
and be roughly
wedge-shaped in
cross section.

Here are petechial

hemorrhages seen
on the epicardium of
the heart. Petechiae
(pinpoint
hemorrhages)
represent bleeding
from small vessels
and are classically
found when a
coagulopathy is due
to a low platelet
count. They can also
appear following
sudden hypoxia.

The blotchy areas of hemorrhage in the skin are called

ecchymoses (singular ecchymosis), or also as areas of
purpura. Ecchymoses are larger than petechiae. They
can appear with coagulation disorders.

Small fibrin thrombi from widespread activation of the coagulation

system with disseminated intravascular coagulopathy (DIC) can
be seen in capillary loops in this glomerulus, highlighted by a
fibrin stain. Laboratory findings with DIC include decreased
platelets, diminished fibrinogen, prolonged prothrombin time,
elevated partial thromboplastin time, and elevated D-dimer.
Consumption of coagulation factors with generation of fibrin split
products, along with platelet consumption, leads to these findings.