CARDIOVASCULAR SYSTEMS – 2

(BLOOD AND LYMPHATIC VESSEL)

 CONSEQUENCES OF
ATHEROSCLEROTIC DISEASE

Major targets of atherosclerosis

• Large elastic arteries (e.g., the aorta,
carotid, and iliac arteries)
• Large and medium-sized muscular
arteries (e.g., coronary and popliteal
arteries)
Major consequences of
atherosclerosis
• Myocardial infarction (heart attack)
• Cerebral infarction (stroke)
• Aortic aneurysms
• Peripheral vascular disease (gangrene of the
legs)
The natural history, morphologic features, main
pathogenic events, and clinical complications of
atherosclerosis.
ATHEROSCLEROTIC
PLAQUES
– Susceptible to clinically important changes:
– Rupture, ulceration, or erosion of the intimal surface of atheromatous
– Hemorrhage into a plaque
– Atheroembolism
– Aneurysm formation
ATHEROMA

Coronary heart disease

Cerebrovascular accident

Extremities gangrene
Risk factor
MAJOR MINOR

• Hypertension • Insufficient reguler

• Cigarette smoking physical activity
• Diabetes • Stress
• Obesity
• Oral contraceptive
• Hyperuricemia
• ↑ Carbohydrate intake
• Hyper-homocysteinemia
This is a normal coronary artery. The lumen is large, without any narrowing by
atheromatous plaque. The muscular arterial wall is of normal proportion.
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.
The coronary artery shown here has narrowing of its lumen due to build up of atherosclerotic plaque.
Severe coronary arterial narrowing can lead to angina, ischemia, and infarction, depending on the severity
and chronicity of the occlusion. The plaque shown here is complicated by calcification.
Smooth muscle cell apoptosis or macrophage apoptosis may lead to development of small calcifications
(microcalcifications) which can coalesce into larger calcium deposits within atheromatous plaques.
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.
 Atherosclerotic plaque
rupture
A. Plaque rupture without
superimposed
thrombus

B. Acute coronary thrombosis

superimposed on an
atherosclerotic plaque
with focal disruption of
the fibrous cap, triggering
fatal MCI
There is a pink to red recent thrombosis in this narrowed coronary artery.
The open, needle-like spaces in the atheromatous plaque are cholesterol
clefts.
This high magnification of the atheroma shows numerous foam cells and an occasional cholesterol
cleft. A few dark blue inflammatory cells (lymphocytes) are scattered within the atheroma.
Increasing accumulation of foam cells in an atheroma can predispose to development of a necrotic
core, enhanced by plaque hemorrhage. Larger necrotic cores often have a thin overlying fibrous cap
prone to rupture. Plaque rupture can lead to thrombosis, as can endothelial erosion.
 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.
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.
This microscopic cross section of the aorta shows a large overlying atheroma on
the left. Cholesterol clefts are numerous in this atheroma. The surface on the far
left shows ulceration and hemorrhage. Despite this ulceration, atheromatous
emboli are rare (or at least, complications of them are rare).
This high magnification microscopic view of an aortic atheroma shows
prominent foam cells as well as cholesterol clefts.
This is severe atherosclerosis of the aorta in which the atheromatous plaques have
undergone ulceration along with formation of overlying mural thrombus.
Despite the frequency of aortic atherosclerosis, cholesterol emboli are rare, or at
least insignficant most of the time. Seen here in a renal artery branch
are cholesterol clefts of such an embolus. This patient had severe ulcerative,
friable atheromatous plaques and had undergone angiography, which increases the
risk for such emboli.
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.
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.
Coronary atherosclerosis is shown here complicated by haemorrhage into the
atheromatous plaque. Such hemorrhage acutely may narrow the arterial lumen.
Cross sections of this anterior descending coronary artery demonstrate marked
atherosclerosis with narrowing. This is most pronounced at the left in the more proximal
portion of this artery. In general, the worst atherosclerosis is proximal, where arterial
blood flow is more turbulent. More focal lesions mean that angioplasty or bypass can be
more useful procedures.
 The anterior surface of
the heart demonstrates
an opened anterior
interventricular (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.
At high magnification, the dark red thrombus is apparent in the lumen of the
coronary. The yellow tan plaques of atheroma narrow this coronary significantly,
and the thrombus occludes it completely.
A thrombosis of a coronary artery is shown here in cross section. This acute
thrombosis diminishes blood flow and leads to ischemia and/or infarction with
damage to the myocardial fibers. This can be evidenced clinically by the onset of
chest pain--angina.
This cross section through the heart shows the larger left ventricular chamber and
the small right ventricle. Extending from the anterior portion and into the septum
is a large recent pale myocardial infarction. The center is tan with surrounding
hyperemia. This infarction is "transmural" because it extends through the full
thickness of the ventricular wall.
The earliest change histologically seen with acute myocardial infarction in
the first day is contraction band necrosis. The myocardial fibers are
beginning to lose cross striations and the nuclei are not clearly visible in
most of the cells seen here. Note the many irregular darker pink wavy
contraction bands extending across the fibers.
This high power microscopic view of the myocardium demonstrates an infarction of about 1
to 2 days in duration. The myocardial fibers have dark red contraction bands extending across
them. The myocardial cell nuclei have almost all disappeared. There is beginning acute
inflammation. Clinically, such an acute myocardial infarction is marked by changes in the
electrocardiogram and by a rise in the MB fraction of creatine kinase.
In this microscopic view of a recent myocardial infarction, there is extensive
hemorrhage along with myocardial fiber necrosis with contraction bands and loss
of nuclei.
This myocardial infarction is about 3 to 4 days old. There is an extensive acute
inflammatory cell infiltrate, and many neutrophils are undergoing karyorrhexis. The
myocardial fibers are undergoing necrosis so that the outlines of them are not well
defined. Few cross striations remain, and cell nuclei are no longer visible. The serum
troponin would be elevated.
This is an intermediate myocardial infarction of 1 to 2 weeks in age. Note that
there are remaining normal myocardial fibers at the top. Below these fibers are
many macrophages along with numerous capillaries and little collagenization.
 At 3 to 4 weeks of age the
intermediate myocardial
infarction shown involving a
papillary muscle at low power
above and medium power
below have decreasing
cellularity along with more
prominence of collagen. Note
that there are remaining
normal red myocardial fibers.
Cardiac biomarkers are not
positive at this stage and
myocardial rupture is unlikely.
The degree of cardiac failure
depends upon the extent of
myocardial loss
The myocardium shown demonstrates pale fibrosis with collagenization following healing of a
myocardial infarction. There is minimal cellularity; a few remaining viable red myocardial fibers
are present. This stage is reached about 2 months following the initial ischemic event. This
collagenous scar is nonfunctional for contraction and will diminish the ejection fraction. Such a
scar will not rupture.