Definisi

Arteriosclerosis adalah istilah umum yang

menggambarkan pengerasan apapun ( dan
hilangnya elastisitas ) dari arteri medium hingga
besar
Arteriolosclerosis adalah setiap pengerasan (dan
hilangnya elastisitas ) dari arteriol ( arteri kecil )
Aterosklerosis adalah pengerasan arteri khusus
karena plak ateromatosa .
Aterosklerosis adalah proses perkembangan plak
ateromatosa

Epidemiologi

Faktor Resiko Atherosclerosis

Tidak bisa
dimodifikasi
Usia
Jenis kelamin
Genetik
Riwayat keluarga

Dapat dimodifikasi
Hyperlipidemia
HDL/LDL ratio.
Hipertensi.
Merokok .
Diabetes.

 Lesser, or Non quantitated risk factors

Obesity
Physical inactivity
Stress
Postmenopausal estrogen deficiency
High carbohydrate intake
Alcohol
Lipoprotein a
Hardened unsaturated fat intake
Chlamydia pneumoniae

PATHOGENESIS

Response to injury hypothesis,

Aterosklerosis dianggap respon
peradangan kronis pada dinding arteri
diprakarsai oleh cedera pada endotel .

Hipotesis injury

Cedera endotel kronis

Akumulasi lipoprotein ke dalam dinding pembuluh terutama LDL dengan konten

kolesterol tinggi ...... .Kemudian oksidasi lipoprotein

Adhesi monosit darah & leukosit lain di endotelium , & migrasi ke intima &
transformasi menjadi makrofag & foam cell

Adhesi trombosit

Pelepasan faktor dari trombosit diaktifkan, makrofag atau sel endotel vaskular
yang menyebabkan migrasi SMCs dari media ke intima .

Proliferasi SMCs di intima , elaborasi matriks ekstraselular , yang mengarah ke

penumpukan kolagen & proteoglikan .

Peningkatan akumulasi lipid dalam makrofag & SMCs & ekstraseluler

1. Cedera endotel kronis

Evolusi perubahan dinding arteri dalam
disfungsi
endotel , menyebabkan
peningkatan permeabilitas , adhesi
leukosit , dan trombosis

2. Akumulasi Liporotein
terutama LDL dan bentuk teroksidasi ) di dinding
pembuluh darah . Low - density molekul lipoprotein ( LDL )
menjadi teroksidasi ( LDL - ox ) oleh radikal bebas ,
terutama oksigen bebas ( ROS ). Ketika LDL teroksidasi
kontak dengan dinding arteri, serangkaian reaksi terjadi
untuk memperbaiki kerusakan pada dinding arteri yang
disebabkan oleh LDL teroksidasi . Kolesterol dapat
bergerak dalam aliran darah yag dibawa liporotein

Respon pembuluh darah pada

hipotesis injury

Pathogenesis in short:
1.
2.
3.
4.
5.
6.

intimal injury
Inflamasi, Nekrosis
Akumulasi Lipid kolesterol (soft.atheroma)
Fibrosis, ploriferasi otot polos (hard.atheroma)
Destruksi pembuluh darah
Komplikasi - Thrombosis, embolism, aneurism,
dissection & rupture.

A r te r io s c le r o s is
A r te r io s c le r o s is
H a r d e n in g

A th e r o s c le r o s is
L a rg e B V
In tim a

M e d ia l C a lc ific
S c le r o s is
M e d ia

A r te r io lo s c le r o s is
S m a ll v e s s e l
F u ll th ic k n e s s

H y a lin e

H y p e r p la s tic

This is Monckeberg's medial calcific sclerosis, which is

the most insignificant form of arteriosclerosis.
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.

Atherosclerosis
DEFINITION
Chronic inflammatory disorder of intima of
large arteries characterised by formation
of fibrofatty plaques called atheroma,
which protrudes into and obstructs the
vascular lumen & weakens the underlying
media & may be associated with serious
complications.

ATHEROMA

Morphology of atheroma
(GP)
Athermo plaque consists of:
a raised focal lesion, soft , yellow core of
lipids( mainly cholestrol & cholestrol esters),
covered by a firm, white fibrous cap.
0.3-1.5 cms. In diameter, sometimes coalesce to
form larger lesions.
Involve partial circumference of arterial wall
( (eccentric), patchy & variable along the length of
vessel.
First the patches are focal & sparse then gradually
increase in size & become diffuse

GP
1.

Fatty dots
not raised , so do not cause obstruction to the flow
Multiple, yellow , flat spots < than 1mm in diameter
composed of lipid laden foam cells

2.

Fatty streaks =coalesce of multiple fatty dots

Elongated, 1 cms longer or more
contain T- lymphocytes & extracellular lipid < than plaques
Appear in aorta in some children younger than 1 year & all
children older than 10years ,

3. Fatty streaks may be precursor of plaque but not all fatty

streaks are converted into fibrous plaque or more
advanced lesions

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.

Common sites:
1. Abdominal aorta compared to thorasic aorta &
lesions are more common around the ostia of
major branches
2. Other common arteries in descending order after
aorta is coronaries, popliteal, internal carotid
& cicle of Willis
3. Vessels of the upper extremities are usually
spared
4. Mesenteric & renal arteries are also spared but
ostias can be involve

COMPONENTS OF ATHEROMATOUS PLAQUE (MP)

1.

*Superficial fibrous cap is composed of SMCs & relatively

dense collagen
2.
*cellular zone containing, SMCs , macrophages,
Lymphocytes (T cells)
*Foam cells : are monocytes derived from blood & SMCs can
also become foam cells

*Deep to the fibrous cap is central necrotic core ,

containing a disorganized mass of lipids( cholestrol&
cholestrol esters) cholestrol clefts, debris from dead cells ,
foam cells, fibrin

*Below & to the sides of cap ( shoulder) is a cellular area

cosisting of macrophages, SMCs, T lymphocytes

At the periphery area of neovascularization is present

Generally plaque undergo remodelling ( degeneration ,
synthesis of ECM & organization of thrombus.

Atheroma Aorta:

Atheroma Aorta:

Atheroma Coronary Artery:

Calcification

COMPLICATIONS & clinical significance

A) Advanced lesions of atheromas are
vulnerable to following pathological changes:

Thrombosis & calcification

Emboli formation , cholestrol emboli or
atheroemboli which are discharged into blood
stream.
Rupture, ulceration, erosions.
Hemorrhage: due to rupture of fibrin cap or thin
walled capillaries that vascularize the plaque &
contained hematoma expand & rupture the plaque
Aneurysmal dilatation: Fusiform, dissecting, or
berry etc., due to pressure or ischemic atrophy
of media with loss of elastic tissue causing
weakness & rupture.

This is severe atherosclerosis of the aorta in which the

atheromatous plaques have undergone ulceration along with
formation of overlying mural thrombus.

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 aorta shows a large atheroma. Cholesterol clefts are

numerous in this atheroma. The surface shows ulceration
and hemorrhage.

COMPLICATIONS & clinical

significance
B) ATH mostly involves arteries supplying the
heart , brain. Kidneys & lower extremities
1. Myocardial infarction ( heart attack)
2. Cerebral infarction ( stroke)
3. Chronic IHD
4. ischemic encephalopathy
5. Aortic aneurysms
6. Peripheral vascular disease ( gangrene of the
legs)
7. mesenteric occlusion
8. Sudden cardiac death

Coronary
Thrombosis
With Infarction

Thrombo-embolism

Aorta Dissecting Aneurisms:

Subarachnoid
Haemorrhage:

American heart association classified

ATH into six types or stages

Type I Fatty dots - Foam cells

Type II Fatty streak
Type III Intermediate stage (Extracellular lipid pool)
Type IV Atheroma Core of lipid
Type V Fibroatheroma Fibrotic layer
Type VI Complicated lesion ( Ulcer, Ca+
Hemorrhage, thrombus, embolism, aneurysm).

Prevention
Three factors need improvement
1. life style, cigarette smoking
2.Reduced consumption of cholestrol &
saturated animal fat & control of
hypertension
3. Prevention of recurrences in those who
have previously suffered from serious
ATH related clinical events

Aterosclerosis Brain

SVD
pertama kali terlihat di arteri dari ganglia
basal , terutama di putamen dan globus
pallidus , yang menunjukkan kapal kecil
AS dan lipohialinosis .
Kedua , arteri kecil megandung materi
putih menjadi terpengaruh oleh
arteriolosclerosis atau lipohialinosis .

 arteri Leptomeningeal dari belahan dan

otak kecil mengembangkan kapal kecil AS
di paralel. arteri batang otak , termasuk
yang berada antara inti pontine , biasanya
berkembang
lipohialinosis
atau
arteriolosclerosis hanya dalam tahap akhir
SVD

Summary:
Disease of elastic & medium sized muscular
arteries.
Fatty dots, streaks, plaques & complications.
Risk factors Males, age, Hypertension,
smoking, DM, life style.
High LDL & low HDL.
Major cause of ischemic organ damage &
death. Stroke, MI, Aneurysms, Gangrene

Tatalaksana