Atherosclerosis is a condition where plaque builds up inside arteries. It is caused by inflammation in response to cholesterol and fat accumulation. Plaque can be stable or unstable. Unstable plaque is prone to rupturing, causing blood clots that can restrict blood flow and lead to heart attacks and strokes. Risk factors include high cholesterol, smoking, diabetes, and hypertension. Treatment focuses on lifestyle changes and medications to reduce cholesterol and other risk factors. Statins are commonly used but can have side effects, so low doses are preferred.

1. ATHEROSCLEROSIS

2. ASVD
• Definition
• Atherosclerosis also called
arteriosclerotic vascular disease or ASVD)
1-is a condition in which an artery wall thickens as a result of the
accumulation of fatty materials cholesterol and triglyceride.
2-Also is a syndrome affecting arterial blood vessels,
• a chronic complex inflammatory response in the walls of arteries,
• caused largely by the accumulation of macrophages
(a type white blood cell that ingests blood cell foreign material,
it is key player in the immune response to foreign invaders of the
body) white blood cells promoted by low-density lipoproteins
(LDL, in the Intima plaque of mid and large arteries.

3. Regarding the plaque ASVD divides in 2 groups
. A-Stable atherosclerosis
• B-unstable (also called vulnerable).
• stable atherosclerotic plaques, which tend to be
asymptomatic, are rich in extracellular matrix and
smooth muscle cells,
• while, unstable plaques are rich in macrophages and
foam cells and the extracellular matrix separating the
lesion from the arterial lumen (also known as the
fibrous cap) is usually weak and prone to rupture

4. . Ruptures of the fibrous cap expose thrombogenic
material, such as collagen to the circulation and
eventually induce thrombus formation in the
lumen.
• Upon formation, intraluminal thrombi can
occlude arteries outright (e.g. coronary occlusion),
• but more often they detach, move into the
circulation
• eventually occluding smaller downstream
branches causing thrombo embolism.

5. • The Atheroma ("lump of gruel",(cereal) which
is the nodular accumulation of a soft, flaky,
yellowish material at the center of large
plaques, Underlying areas of cholesterol
crystals Calcification at the outer base of older
• composed of macrophages nearest the lumen
of the artery Atherosclerotic lesions,

6. • the risk may be higher while in the blood
stream.
• However, LDL particles have a half-life of only
a couple of days and their content (LDL
particles carry cholesterol,
cholesteryl esters(disease) (is a rare genetic
disorder characterized by sub total defect of
an enzyme known as lisosomal acid lipase
(LIPA or LAL)

7. • Once inside the vessel wall, LDL particles get
stuck and their content becomes more prone
to oxidation.
• Than The damage caused by the oxidized LDL
molecules triggers a cascade of immune
responses which over time can produce an
atheroma.

8. • The body's immune system responds to the damage to
the artery wall caused by oxidized LDL by sending
specialized white blood cells (macrophages and T-
lymphocytes) to absorb the oxidized-LDL forming
specialized foam cells.
• These white blood cells are not able to process the
oxidized-LDL, and ultimately grow then rupture,
depositing a greater amount of oxidized cholesterol
into the artery wall.
• This triggers more white blood cells, continuing the
cycle.

9. • Ther 2 type of plaque
• The fibro-lipid (fibro-fatty) plaque is
characterized by an accumulation of lipid-
laden cells underneath the intima of the
arteries,
• The fibrous plaque
• is also localized under the intima, within the
wall of the artery resulting in thickening and
expansion of the wall and, sometimes, spotty
localized narrowing of the lumen with some
atrophy of the muscular layer.

10. Lipid fraction and the risk of CAD
• Cholesterol is caried primarily 3 defferent
lipoprotien
• The VLDL,LDL,and HDL molecules
• 1- Total cholesterole= HDL+VLDL+LDL
• 2-VLDL cholesterole= Triglyceride/5
• 3-LDL = Total chol-HDL chol-Trigly /5 = mg/dl
SI unit
• 4-LDL= Total chol-HDL chol-Trigly/2 = mmol/l
• mmol/L -mmol/L- Trigly/2.2= mmol/l

11. • Interestingly, chronically expanding
lesions are often asymptomatic until
lumen stenos is is so severe (usually over
80%) that blood supply to downstream
tissue(s) is insufficient, resulting in
ischemia.

12. • These complications of advanced
atherosclerosis are chronic, slowly progressive
and cumulative.
• Most commonly, soft plaque suddenly
ruptures , causing the formation of a
thrombus that will rapidly slow or stop blood
flow,
• leading to death of the tissues fed by the
artery in approximately 5 minutes.
• This catastrophic event is called an infarction.

13. • One of the most common recognized
scenarios is called coronary thrombosis of a
coronary artery emboli ,
• causing myocardial infarction (a heart attack).
• The same process in an artery to the brain is
commonly called stroke.
• Another common scenario in very advanced
disease is claudicating from insufficient blood
supply to the legs, typically caused by a
combination of both stenosis and aneurysm
segments narrowed with clots called
thrombophilibitis .

14. Atherosclerosis affects
• the entire artery tree, but mostly larger, high-
pressure vessels such as the
• coronary,
• renal,
• femoral,
• cerebral,
• and carotid arteries.
• These are termed "clinically silent" because the
person having the infarction does not notice the
problem and does not seek medical help,
• or when they do, physicians do not recognize
what has happened.

15. Signs and symptom
• Clinically, atherosclerosis is typically associated with
men over the age of 45y.
• Sub-clinically, the disease begins to appear at early
childhood, and perhaps even at birth.
• Noticeable signs can begin developing at puberty.
• Though symptoms are rarely exhibited in children,
• Early screening of children for cardiovascular
diseases could be beneficial to both the child and
his/her relatives.
• ATheroma in arm, or more often in leg arteries,
which produces decreased blood flow is called
peripheral artery occlusive disease (PAOD).

16. • While coronary artery disease is more
prevalent in men than women, atherosclerosis
of the cerebral arteries and strokes equally
affect both sexes.
• According to United States data for the year
20013,
• for about 66% of men and 47% of women, the
first symptom of atherosclerotic
cardiovascular disease is heart attack or
sudden cardiac death (death within one hour
of onset of the symptom).

17. • Most artery flow disrupting events occur at
locations with less than 50% lumen narrowing
• Diagnosis
• Cardiac stress testing,
• traditionally the most commonly performed non-
invasive testing method for blood flow limitations,
in general, detects only lumen narrowing of ~75%
or greater,
• Nuclear STRESS TEST
• Although some physicians claim that nuclear stress
methods can detect as little as 50%.

18. • A famous case study involved autopsies of
American soldiers killed in World War II and
the Korean War.
• Although these were mostly young, healthy
men in their 20s, many already had
evidence of developing atherosclerosis.
• Other studies done on soldiers in the
Second Indochina War showed similar
results, although often worse than the ones
from the earlier wars.
• Theories include high rates of tobacco use
and (in the case of the Vietnam soldiers),
the advent of processed foods after WWII.

19. Herpes virus infection of arterial smooth muscle
cells has been shown to cause cholesteryl
ester (CE) accumulation.
Cholesteryl ester accumulation is associated
with atherosclerosis.
Also, cytomegalovirus (CMV) infection is
associated with cardiovascular diseases.

20. • Risk factors
• Various anatomic and physiological risk factors
for atherosclerosis are known.
• These can be divided into various categories:
• A-Congenital
• B- Acquired,
• C-Modifiable ,
•

21. • Risks multiply, with two factors increasing the
risk of atherosclerosis fourfold.
• Hyperlipidemia, hypertension and cigarette
smoking together increases the risk seven
times.
• Modifiable Diabetesor Impaired glucose
tolerance (IGT)

22. • Lesser or uncertainThe following factors are of
relatively lesser importance, are uncertain or
unquantified:
• Obesity - (in particular central obesity, also
referred to as abdominal or male-type obesity) +
• Postmenopausal syndrom estrogen deficiency
• High intake of saturated fat (may raise total and
LDL cholesterol
• Intake of trans fat (may raise total and LDL
cholesterol while lowering HDL cholesterol)(is the
worst type of fat also called unsaturated which
has double carbon means (E-esomer) and fatty
acid (s)

23. • High carbohydrate intake[
• Elevated serum levels of triglycerides+
• Elevated serum levels of homocysteine(is a
naturally occuring amino acid found in plasma .
• Elevated serum levels of uric acid (also
responsible for gout)
• Elevated serum fibrinogen concentrations(is a
protien produce by the liver –help stop bleeding
–helping blood to create clot
• Elevated serum lipoprotein(a) concentrations[
(contain both protien and lipids allows fat to move
through the water inside and outside the cell

24. • Chronic systemic inflammation as reflected by
upper normal WBC concentrations, elevated
hs-CRP and many other blood chemistry
markers, most only research level at present,
not clinically done.
• Hyperthyroidism (an over-active thyroid)
• Elevated serum insulin levels +
• Short sleep duration
• Chlamydia pneumoniae infection

25. • Stenoses can be slowly progressive, whereas
plaque ulceration is a sudden event that
occurs specifically in atheromas with
thinner/weaker fibrous caps that have
become "unstable".

26. • Examples of anatomical detection methods
include
• (1) coronary calcium scoring by CT,
• (2) carotid IMT (intimal media thickness)
measurement by ultrasound, and
• (3) intravascular ultrasound (IVUS). Examples of
physiologic measurement methods include (1)
lipoprotein subclass analysis,
• (2) HbA1c,
• (3) hs-CRP, and
• (4) homocysteine.

27. • Screeing of patients –called framingham 10
years CAD risk projection are the standard
• Depend of age of patients gaving special
score.
• Treatment plan
• 1- reduction of LDL and other risk factors
Smoking .hypertension ,dibetis ,alcohole use
,sedentary life style ,non of exercise ,deitary
life style

28. Pharmacologic therapy
• KEEP LDL less than 100mg/L (2.6 mmol/L) with
asprin 81mg reduce the risk to 10-20%
• 1-Niacin (nicotinic acid ) 3-4,5mg/daily reduce
chance of CHD 15-20% -but cause flushing (hot
flushes ) which reduced the use
• 2-Cholestyramin (Bile Acid-Binding resins )
reduce the risk 20%- unfortunately increased
triglyceride to be careful

29. 3-Statin- Hydroxymethylglutaryl
A (HMG-COA)reductase inhibitors
Include atorvastatin –fluvastatin-lovastain-pitavastatin-
pravstatin –rosuvastatin- and simivastatin they reduce
the enzymes which creating cholesterole.
Reduce MI-STROKE,
Atrovastatin 10-40mg/d
Rosuvastatin5-40mg/d
Fluvastatin 20-40mg/d
Pravastatin 10-40mg/d
Simvastatin 5-40mg/d
Side effect muscle aches-GI effect-livetr effect myositis
and rhabdomyolysis

30. D-Fibric Acid derivative
• Reduce LDL –and plasma triglycerid 10 to 15%
• Include gemfebrozil-600mg once or twice daily
• Ciprofibrate and bezafibrate
• Side effect are include
chlelithithisis,hepatitis,myosistis reduce the
use now
E- Ezitimibe
Reduce the absorbtion of dietary cholesterole in
intestine -10-15mg/d have les side effect

31. • Best with low risk medication are
• 1-HMG-COA statines better to use with low
dose
• 2-Niacine can be used with combination must
be carefull
• 3-Resins (cholestyramin ) is safe during
pregnancy
• 4-combination of those medication would
creating side effects on liver –GI and musles