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1
Atherosclerosis
Logman Mohammed
LOGMAN
Vessel wall structure
LOGMAN 2
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
4
Atherosclerosis
 COMMON RISK FACTORS ARE
1 INCREASING AGE
2 MALE GENDER
3 FAMILY HISTORY
4 GENETIC ABNORMALITIES
LOGMAN
5
Atherosclerosis
 POTENTIAL CONTROLLABLE RISK
FACTORS ARE
1 HYPERLIPIDEMIA
2 HYPERTENTION
3 DIABETES MELLITUS
4 CIGARETTE SMOKING
LOGMAN
6
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
LOGMAN
7
Pathogenesis of Atherosclerosis
According to injury hypothesis
considers
atherosclerosis to be a chronic
inflammatory Response of the
arterial wall initiated by injury:
LOGMAN
8
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
LOGMAN
9
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
LOGMAN
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
11
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.
LOGMAN
12
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
LOGMAN
13
 There are two types of atherosclerotic
plaque
 vulnerable
 stable
atherosclerotic plaque
LOGMAN
Clinical Classification of Atherosclerosis
 Pre-clinical (asymptomatic) period
 Clinical period
– Ischemic stage
– Necrotic stage
– Sclerotic stage
LOGMAN 14
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.
LOGMAN 15
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)
LOGMAN 16
17
CEREBRAL FORM OF
ATHEROSCLEROSIS
LOGMAN
18
RENAL FORM OF
ATHEROSCLEROSIS
 Acute form may be as
infarction
 Chronic form is called
Atherosclerotic
Nephrosclerosis or
Primary contracted
kidney
LOGMAN
19
Intestinal form of atherosclerosis
 Acute form may be as
gangrenous necrosis
of the intestine
 Chronic form may be
as ischemic
enterocolitis
LOGMAN
20
Extremity form of atherosclerosis
 Acute form may be as gangrenous
necrosis.
LOGMAN
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
LOGMAN 21
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
LOGMAN 22
thanks
23LOGMAN

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Atherosclerosis (1)

  • 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
  • 4. 4 Atherosclerosis  COMMON RISK FACTORS ARE 1 INCREASING AGE 2 MALE GENDER 3 FAMILY HISTORY 4 GENETIC ABNORMALITIES LOGMAN
  • 5. 5 Atherosclerosis  POTENTIAL CONTROLLABLE RISK FACTORS ARE 1 HYPERLIPIDEMIA 2 HYPERTENTION 3 DIABETES MELLITUS 4 CIGARETTE SMOKING LOGMAN
  • 6. 6 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 LOGMAN
  • 7. 7 Pathogenesis of Atherosclerosis According to injury hypothesis considers atherosclerosis to be a chronic inflammatory Response of the arterial wall initiated by injury: LOGMAN
  • 8. 8 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 LOGMAN
  • 9. 9 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 LOGMAN
  • 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
  • 11. 11 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. LOGMAN
  • 12. 12 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 LOGMAN
  • 13. 13  There are two types of atherosclerotic plaque  vulnerable  stable atherosclerotic plaque LOGMAN
  • 14. Clinical Classification of Atherosclerosis  Pre-clinical (asymptomatic) period  Clinical period – Ischemic stage – Necrotic stage – Sclerotic stage LOGMAN 14
  • 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. LOGMAN 15
  • 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) LOGMAN 16
  • 18. 18 RENAL FORM OF ATHEROSCLEROSIS  Acute form may be as infarction  Chronic form is called Atherosclerotic Nephrosclerosis or Primary contracted kidney LOGMAN
  • 19. 19 Intestinal form of atherosclerosis  Acute form may be as gangrenous necrosis of the intestine  Chronic form may be as ischemic enterocolitis LOGMAN
  • 20. 20 Extremity form of atherosclerosis  Acute form may be as gangrenous necrosis. LOGMAN
  • 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 LOGMAN 21
  • 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 LOGMAN 22

Editor's Notes

  1. Small arterioles within the adventitia (termed vasa vasorum, literally "vessels of the vessels") supply the outer 50% to 65% of the media.
  2. Arteriosclerosis literally means "hardening of the arteries with loss of elasticity”.