Atherosclerosis is a disease where plaque builds up inside arteries. It is a chronic inflammatory response in the artery walls caused by injury and risk factors like age, gender, family history, hyperlipidemia, hypertension, and smoking. The plaque is made up of fat, cholesterol, and other substances in the blood. Over time, the plaque can grow and harden, narrowing the arteries. This restricts blood flow and can lead to problems like heart attacks or strokes if a plaque ruptures. The buildup of plaque tends to occur most commonly in arteries supplying the heart, brain, kidneys and lower body. Prevention focuses on lifestyle changes like a healthy diet, exercise, not smoking, and treating conditions like high

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Atherosclerosis
Logman Mohammed
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2. Vessel wall structure
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3. Atherosclerosis
• Atherosclerosis is a specific type of
arteriosclerosis (thickening & hardening of arterial
walls) affecting primarily the intima of large and
medium-sized muscular arteries.
 Chronic inflammatory response in the walls of
arteries.
 Slowly progressive.
 A build-up of fat (cholesterol) within the artery
wall.
 Characterized by intimal lesions called:
atheromas, atheromatous or plaquesLOGMAN 3

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Atherosclerosis
 COMMON RISK FACTORS ARE
1 INCREASING AGE
2 MALE GENDER
3 FAMILY HISTORY
4 GENETIC ABNORMALITIES
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Atherosclerosis
 POTENTIAL CONTROLLABLE RISK
FACTORS ARE
1 HYPERLIPIDEMIA
2 HYPERTENTION
3 DIABETES MELLITUS
4 CIGARETTE SMOKING
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Atherosclerosis
 OTHER RISK FACTORS ARE
1 OBESITY
2 PHYSICAL INACTIVITY
3 STRESS
4 POSTMENOPOUSAL ESTROGEN DEFICIENCY
5 High Cholesterol
6 HIGH CARBOHYDRATE INTAKE
7 CHLAMYDIA PNEUMONIA
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Pathogenesis of Atherosclerosis
According to injury hypothesis
considers
atherosclerosis to be a chronic
inflammatory Response of the
arterial wall initiated by injury:
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Pathogenesis of Atherosclerosis
 1 chronic endothelial injury
2 insudation of lipoproteins [LDL]
3 modification of lipoproteins by
oxidation
4 adhesion of blood monocytes
5 adhesion of platelets
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Pathogenesis of Atherosclerosis
6 migration of smooth muscle cells
from the media into the intima
7 proliferation of smooth muscle cells
in the intima
8 enhanced accumulation of intra and
extra cellular lipids
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10. Endothelial cell Monocyte Macrophage Foam cell Smooth muscle
cell
Internal elastic
lamina
Vessel lumen
1. Endothelial
permeability
4. SMC
migration2. Monocyte
adhesion and
transmigration
Increased stiffness
3. Macrophage
transformation
into foam cells
The major cellular events in the
progression of atherosclerosis

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ATHEROSCLEROTIC PLAQUE
 The change of the large arterial
intima is called atherosclerotic plaque
or atheroma
 atherosclerotic plaque is the intimal
thickening with lipid accumulation
 It consists of fibrous cap, necrotic core
and fibrous basis.
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atherosclerotic plaque
 It has three principle components:
 1 cells –smooth muscle cells, macrophages
other leukocytes
2 Extra cellular matrix- collagen, elastic fibers,
proteoglycans
3 Intra cellular and extra cellular lipids
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 There are two types of atherosclerotic
plaque
 vulnerable
 stable
atherosclerotic plaque
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14. Clinical Classification of Atherosclerosis
 Pre-clinical (asymptomatic) period
 Clinical period
– Ischemic stage
– Necrotic stage
– Sclerotic stage
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15. Clinical Manifestations
 The clinical manifestations of atherosclerosis depend on the
vessels involved and the extent of vessel obstruction.
 Atherosclerotic lesions produce their effects through:
– narrowing of the vessel and production of ischemia;
– sudden vessel obstruction caused by plaque hemorrhage or
rupture;
– thrombosis and formation of emboli resulting from damage
to the vessel endothelium;
 In larger vessels such as the aorta, the important complications
are those of thrombus formation and weakening of the vessel
wall.
 In medium-size arteries such as the coronary and cerebral
arteries, ischemia and infarction caused by vessel occlusion are
more common.
 Although atherosclerosis can affect any organ or tissue, the
arteries supplying the heart, brain, kidneys, lower extremities,
and small intestine are most frequently involved.
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16. Clinical manifestations of Atherosclerotic Vascular Disease
Vascular basin Acute manifestation Chronic
manifestation
Coronary arteries Acute coronary syndromes:
- unstable angina
- AMI
- sudden cardiac death
Stable angina
Vasospastic angina
Carotid and cerebral
arteries
Transient ischemic attack
Stroke
Chronic cerebral
ischemia
(“discirculatory
encephalopathy”)
Aorta Aortic dissection Aortosclerosis
Aortic aneurysm
Mesenteric arteries Mesenteric thrombosis Chronic intestinal
ischemia (“abdominal
angina”)
Renal arteries Cholesterol emlolism of renal
artery
Renovascular
hypertension
Renal failure
Pelvical and lower
extremities arteries
Acute limb ischemia Erectile dysfunction
Chronic limb ischemia
(intermittent
claudication)
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CEREBRAL FORM OF
ATHEROSCLEROSIS
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RENAL FORM OF
ATHEROSCLEROSIS
 Acute form may be as
infarction
 Chronic form is called
Atherosclerotic
Nephrosclerosis or
Primary contracted
kidney
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Intestinal form of atherosclerosis
 Acute form may be as
gangrenous necrosis
of the intestine
 Chronic form may be
as ischemic
enterocolitis
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Extremity form of atherosclerosis
 Acute form may be as gangrenous
necrosis.
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21. Diagnostic Approaches in
Atherosclerosis
 Gold standard of diagnosis –
angiography (X-ray, CT or MRI
techniques)
 Electron-beam CT – “coronary calcium
score” – assessment for total plaque
burden
 Doppler ulstrasound – used to detect
renal or carotid lesions, assessment of
intima-media thickness .
 IVUS – unique information on plaque
structure, volume and area
 Angioscopy – mostly used in scientific
studies
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22. Prevention of Atherosclerosis and its
Complications
 Dietary modification: restriction of cholesterol (<200
mg/day), sat fats; DASH-type eating plan; dietary sodium
restriction.
 TG elevation: restriction of plain carbohydrates, total fat
and total calories; refrain from alcohol
 Body mass decrease and increase aerobic physical activity
 Smoking cessation.
 Hypertension treatment.
 Control of diabetes.
 Low-dose aspirin (75-100 mg/day) is indicated in patients
at high risk. It acts as antiaggregant and prevents clot
formation on the plaque
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23. thanks
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