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Workshop nr.

14

PATHOLOGY OF THE ARTERIAL SYSTEM


1. Atherosclerosis - ATS
a. Aortic atherosclerosis (MA' MI)
. Fibro-lipidic plaque
b. Coronarian atherosclerosis (MA, MI)
o Fibro-lipidic plaque or fibrotic plaque with
atheromatous core
. Calcified fibrotic plaque
o Thrombotic fibrotic plaque
c. Cerebral atherosclerosis (MA)
2. Systemic hypertension
MI - Benign nephroangiosclerosis
MA
o Concentric hypertrophy of the left ventricle
. Benignnephroangiosclerosis
o Cerebral hematoma with ventricular flood
1. Atherosclerosis
Atherosclerosis is an arterial disease:
o involving large and medium-sized arteries
o elastic arteries (e.g., aorta, carotid and iliac arteries)
o large and medium sized muscular arteries (e.g., coronary and popliteal
arteries, cerebral arteries & lower extremity arteries)
o Is characteized by the formation of intimal atherosclerotic plaques (fibrofatty
plaques) with secondary involvement of the medial muscular layer.
The fundamental lesion in atherosclerosis is fibrolipidic plaque. The lesions have
the same morphological appearance regardless of location.
a. Aorticatherosclerosis
MA
. The lesions are localized in the aortic abdominal segment, at branching or
bifurcation of iliac arteries and around the orifices of the emerging collaterals.
. In severe forms are involved other segments, as well: the thoracic aorta and more
rarely ascending aorta.
According with American Heart Association (AHA), there are six atherosclerotic
lesions: (l) fatty dots, (2) fatty streaks, (3) lipid plaques, (4) atheromatoqs plaques,
(5) fibroatheromatous plaques, (6) complicated atherosclprotic plaques (calcification,
ulceration, thrombosis and embolism, aneurysm formation).

"*l
iTr'[*' H:ili:'lT,'ffiil]iJ]"J;:Hrany dots (FD) which are
less than 1 mm in diameter. Subsequently they form elongated
lesions (l mm width and 1 cm long or longer) proiemining on the
intimal aortic surface.

'''.""ff ::#j;Hl[ffi:il",]:ii',1:",j'J;Xxliffi theintima


lntralumenal prnieminent lesion, whitish-yellow in colour (core of
lipids and a covering fibrous cap), of round to oval shape and I-2
cm in diameter.

""',-f:Tl.lilir#ir11tr,:-ffir?Jff
i*o,o,,,u,"deposi,sor
calcium salts leading to a lesional image of egg-shell appearance

'.:-?l$1j-iiii;:i:i**";::*lf;T'nT';."guru,marginsand
yellow, granular deposits on the surface
By elimination of the atheromatous core are resulting cholesterol
emboli

*T-fri,':dftiff,T*:*;ffidffi;;]l";,"".,
of ulcerated lesions, which are a sourse of emboli
MI- Fibro-tipidic plaque
Cross section through the aortic wall (Simionescu staining):
- At the plaque lsvel the aortic rvall is thickened
- The fUro-tip;O plaque is located at the level of the intima with secondarv
involvement of the media
. The intimalPiaque
subendoteliallayer - compact acellular layer composed of coliagen fibers
{blue in Simionescu staining)
-
i';:*$i*l f,{fi
"'ffim;:F*:u-
' fibrin (red)
fibrotic base, containing capillary vessels of neoformation
" Medial atrophy and fibrosis, which affects the elasticity and strenglh of the wall
b. Coronarian atherosclerosis
MA
Coronarian atherosclerosis (fibrotic and fibro atheromatous plaques) has a
stenotic feature leading to myocardiai chronic ischemia'
branches. on the first 6 cm of
" The lesions arslocated on extramyocardial coronaryattery}
their origin {anterior descending artety, circumflex
. The consequence of coronary ats is coronary stenosis and myocardial chronic
ischemia
, The chronic myocardial ischemia is manifested as myocafiial atrophy and fibrosis
in adjacent mYocardium
M{ - Coronarian atheroscierosis
, Cross section through an extramyocardial coronary artery, r,r'hich presents on 2
. opposite walls 2 ATS plaques: fibro-lipidic plaque and calcified fibrous plaque
. At the plaque levelthe wall is thickened
. The plaques are located in the intima, causing secondary medial layer damage by
compression
. The media becomes thinned and fibrotic (atrophy by compression) and affects the
elasticity and strength of the wall
' The lumen is stenotic
I ) Fibro-lipidic plaque
. Cross section through an extramyocardial coronary artery (HE)
. The intimal plaque
subendothelial level - fibrous cap compact, acellular layer of collagen
fibers

""f'ftfi*+i*ff**:y'.
' foamy cells
. fibrin
the fibrous basis - collagen
At the plaque angle, there are present capillaries of neoformation
. atrophy and fibrosis of the media
2) Calcified fibrous plaque
' Cross section through an extramyocardial coronary artery (HE)
. subendothelial level -accumulation of collagen fibers
. in the center of the plaque, there are hematoxilinofil deposits of calcium salts
' atrophy and fibrosis of the media
MI- Fibrous plaque complicated by thrombosis
. Cross section through an extramyocardial coronary artery (HE)
. The afiery wall is thickened by a fibrous plaque
. The coronary artery lumen is occluded by a recent thrombus, that consists of a
fibrin network, white cells and red blood cells
. The occlusive thrombus causes acute ischemia (myocardial infarction)

c. Cerebral atherosclerosis
Cerebral atherosclerosis appears at approximatively 15 years after the onset of the
disease. The most frequent involved cerebral arteries are the polygon Willis vessels.
MA
The cerebral arteries of the polygon Willis, located at the brain base, present a
thickened wall by the presence of yellowish fibro-lipidic plaques. On the cross section,
the cerebral atherosclerotic arteries present a perrnanent opaned lumen, resembling with
macaroni (normally, on the cross section, the arteries are collapsed).
Cerebral atherosclerosis (fibrotic and fibro atheromatous plaques) has a stenotic
feature leading to cerebral chronic ischemia (senile dementia)-
Cerebral atherosclerotic complications:
c Plaque thrombosis i Acute cerebral ischemia (cerebral infarct or cerebral
softening )
The rupture wall at the level of the atherosclerotic plaque leading to cerebral
hemorrhage
Aneurismal dilatation involving vertebro-basilar artery (aneurysm - by thinning
of underlying media)

II.
Systemic hypertension
Benign HTA: an increase in the arterial blood pressure
. It represents the persistent increasing of the systolic and diastolic pressure over
normal values
. The main target organs:
Heart (hypertensive cardiopathy) - concentric hypertrophy of the left
ventricle
Kidney- benign nephroangiosclerosis
Brain- Cerebral hematoma with ventricular flood
Arterial system changes
. HTA involves arterioles and small arteries.
. HTA causes the thickening of the wall and narrow of the lumen
(vasoconstriction; damage of the vessel)
MA
Heart - concentric hypertrophy of the left ventricle
Hypertrophy (HT) is a reaction of cell adaptation characterized by increasing of a
tissue or organ volume by increasing in size of cell components. E.g. Concentric
hypertrophy of the left ventricle due to HTA (obstacle in front of LV);
On the extemal surface the heart is increased in size and volume, and on the cross
section, there is a concentric thickening of the left ventricle (over 2 cm in diameter) and a
LV stenotic cavity.
Brain-Cerebral hematoma with ventricular flood
It represents the accumulation of blood in the brain parenchyma. It appears in case
of systemic hypertension due to rupture of an aneurysm of middle cerebral artery.
Macroscopy: a coagulated blood collection, located in the cerebral parenchyma,
adjacent to the lateral cerebral ventricle resulting in ventricular flood and sudden death.
Kidney- benign nephroangiosclerosis
Benign nephroangiosclerosis is an exemple of ischemic atrophy, consisting ln
reducing of arterial circulation in a kidney (chronic ischemia), with consequent loss of
cells.
The consequence is atrophy of the renal parenchyma in HTA: the two kidneys are
atrophic, smaller and paler, with a fine granularity on the external surface. On the cross
section, the renal parenchyma is reduced in volume (the cortex and medulla are not
distinctive) and is associated with hilar adipose tissue hyperplasia.

MI - Kidney- benign nephroangiosclerosis


. Section through the kidney (HE)
. Afferent arteriole with thick wall, homogenized, eosinophilic (hyalinized) and a
stenotic lumen
. Glomeruli in different stages of frbrosis and hyalinization until complete
transformation in spherical structures, homogeneous, eozinofilic without structure
and unfunctional
. Renal tubules:
corresponding to affected glomeruli are atrophied or disappeared being
replaced by connective scar
corresponding to hipertrophied glomeruli are dilated with lumenal hyalin
cylinders