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Chapter
8The
disease
of
cardiovascularsystem8.1
atherosclerosis
(
AS
)z
characterized
by
intimal
lesions
calledatheroma
or
fibrofatty
plaques
that
protrudeinto
the
lumen,weaken
the
underlyingmedia,and
undergo
a
serious
of
complicationsz
Primarily
affects
elastic
arteries
(aorta,carotid,
iliac-arteries)
and
large
and
mediusized
muscular
arteries
(coronary
andpopliteal
arteries)8.1.1
epidemiology
and
risk
factorshyperlipemia
/
hypercholesterolemia:①
LDL/LDL-C
,VLDL,
triglycerides,cholesterol→positive②
HDL/HDL-C,
apoA-I
→negativehypertension:→early
and
severesmoking:→endothelial
damage、CO↑→
PDGF↑,SMC
proliferation
emigration→
ox-LDLDiabetes
and
hyperinsulimemia:hyperglycemia→LDL
glycolate→ox-LDL→hypertriglyceridehyperinsulimemia→SMC↑、HDL↓heredity:
200genes;
HDL-receptorgene
mutation→familyhypercholesterolemia6.
Age
and
sex:age:
age↑→ASfactors
changesarterial
wall
proliferativechangesex:
estrogen→cholesterol↑postmenopausal
female=maleOthers:Obesity
,
stressful
life
type
,
hypoxia
,
dielackofVit.
C
,
infection
ofbacteria
,
viruLack of
exercise
:Intake
of
alcohol
:Protective
role
for
moderate
intake
ofalcohol
:
HDLA
large
amount
of
intake
of
alcohol:hypertension,
cerebral
hemorrhage8.1.3
pathologic
changeselastic
arteries:
aorta,
carotid,
iliaclarge
and
medium-sized
muscular
arteriecoronary,popliteal
A1.
favorite
site:lower
abdominal
aorta,
coronary
A,popliteal
A,
the
descending
thoracic
athe
internal
carotid
A,
the
circle
of
wWhat
does
the
atherosclerotic
vessel
look
lThe
lesion
of
atherosclerosis
is
not
one
spentitybut
a
spectrum
of
arterial
changesincluding
:□Atheromatous
fibro-lipid
plaques
=
fibroplaque
=
fibrotheroma□Fatty
streaks
=
intimal
xanthoma□Intimal
cushion
lesions
=
intimal
mass
lebasic
pathologic
changes1.
fatty
streak:
the
early
lesiongross:tiny
round
or
oval
flat
yellow
dotsarranged
in
rows,
coalesce
to
form
astreak,
1-2mm,
slightly
raised,particularto
theaortic
valve
regionLM:
a
collection
of
foam
cellsfatty
streak:
multipleyellowflatspots(fatty
dotFatty
streak
(sudan
red)(3)
formation:lipid↑→engulfed
by
Mφ,
SMC
→foam
cell(two
sources)(4)
result:reversiblecould
be
seen
in
infants
and
children2.
fibrous
plaque:gross:irregular
grey-white
raisedplaqueLM:
fibrouscap,
foam
cell,lipids圖8-5
主動(dòng)脈粥樣硬化主動(dòng)脈后壁見(jiàn)黃白色纖維斑塊lumenFibrous
capLipid
core,clefMassontrichrome(膠原纖維-藍(lán);肌、纖維素-紅)Media
thinCalcification,neovascular3.
Atheromatous
plaqueor
atheroma(hallmarkof
AS)z
gross:white/whitish
yellow/
yellowirregularelevated
plaque(2)
LM:①
surface:
fibrous
cap(hyaline
degenerationofcollagen,
SMC
embed
in
extra
cellularmatrix)②
necrotic
center:
amorphous
necrotic
materia(cell
debris,lipid,cholesterol
crystals,
casurrounding:
granulation
tissue,
lymphocyte+foam
cells③
media:
atrophy→thinComplicated
lesions:on
the
basis
of
fibrous
plaque
and
atheromatouhemorrhage
within
plaque:acute
obstruction
of
A(
coronary
A
→myocardial
infarction)focal
rupture:lower
abdominal
aorta、iliacarteries、tempArupture→ulceration→thrombosis↓atheromatous→embolism→infarct圖8-8腹主動(dòng)脈粥樣硬化斑塊內(nèi)出血粥樣斑塊纖維帽和壞死物質(zhì)之間可見(jiàn)大量紅細(xì)胞,壞死物內(nèi)可見(jiàn)針形“膽固醇結(jié)晶裂隙”圖8-9腹主動(dòng)脈瘤腎動(dòng)脈下腹主動(dòng)脈粥樣硬化伴局限性明顯擴(kuò)張,動(dòng)脈瘤形成。thrombosis:obstruction→infarctioncalcification:harden,
elasticityaneurysm
formation:rupture→hemorrhageAS
focal
disruption,
thrombomosiPslaque
ruptureThe
atheromatous
plaque
and
the
dynamics
of
plaquestability(三)Lesions
in
organs
&
clinical
features1.
aortic
AS:site:abdominal
aorta>thoratic
A>aorta arch>ascending
Alesions:atheromatous
and
secondarychangesulceration、calcification、hemorrhage,abdominal
aortic
aneurysm→Rupture→Death2.
Coronary
AS:coronary
heart
disease3.Carotid
A、Cerebral
A
ASsite:basilar
A,middle
cerebral
A,Williscirclelesion①ischemicatrophy②infarction:thrombosis→occuludetemporal
lobe,
caudate
nuclears,lenticularnucleus,thalamus③
hemorrhage:AS→aneurysm
rupture圖8-10
大腦基底動(dòng)脈粥樣硬化
圖8-11腦軟化↑示動(dòng)脈粥樣硬化斑塊
↑示篩狀軟化灶Renal
A
AS:sites:ostia
ofrenal
A
majorbranch,proximal
segmentlesion
:
infarctor
hypertension
AS
of
extremities:narrowing→claudication→thrombosis→gangreneSmall
intestine
AS:
infarction8.2
pathogenesis1.
Response
to
injury
theory
andinflammation
theory:---
Current
view
of
the
pathogenesis
of
ASAS
plaque
as
the
response
of
endothelial
celto
damaging
factorsdamage
factors:mechanical
denudation、
LDL、hypercholesterolemia、immunecomplex、ox-LDL、smokingz
Central
to
this
thesis
are
the
followingeventsRoles
ofLipidsEndothelial
injurySmooth
muscle
proliferationMacrophage(Mφ)zz
①
Role
of
lipidsIncrease
endothelial
permeabilityImpairendothelial
functionOX-LDLingested
by
Mφ→foaming
from
cellschemotactic
for
circulating
monocytesincrease
monocyte
adhesionstimulate
release
of
growth
factorschemotactic
to
endothelial
cells
(EC)smooth
muscle
cells
(SMC)②
Role
of
EC
injury:
initial
lesionMechanical
injurySmokingRisk
Factors
HypoxiaHyperlipidemiaHypertensionEC
injuryNon-denuding
EC
dysfunctionEC
denudingIncreased
EC
permeabilityEnhanced
monocyte,
platelet
adhesionRelease
GF→SMC
proliferationz
③
role
of
macrophage:
key
stepy
Platelet
,
EC,
Monocyte,
SMCGrowth
Factors
(PDGF,FGF,etc)emigrationproliferationadhere→emigrant
subendothelially→
foam
cellsMatrixGF→SMC↑z
④
role
of
SMC
proliferation:GF
→
SMC
proliferation
in
media→
emigration→intimaaccounting
for
the
progressive
growth
of
ASphenotype
change(constrictive→synthesis)surface
LDL
receptor→foam
cell
(SMC
derived)collagen
,
elasticfiber
protein,
proteoglycansinteraction→formation
of
AS
plaque2.
Lipid
infiltration
theory:hyperlipemia↓EC
damage→permeability↑→lipoprotein
deposit→Mφcleanup↓SMC↑↓atheroma3.
Smooth
muscle
mutagenic
theory①SMC
in
AS
plaque→monoclone②
etiology:chemical
mutagenic
agentsvirus4.
Macrophage
receptor
defect
theory(1)normal①cell
membrane:
LDL
receptor→combine
withLDL→engulf→intracellular②
intake→LDL
receptor→change
with
the
needof
cholesterol(2)
AS:
LDL
receptors↓↓→LDL
cleaning↓→LDL
in
blood↑(2)
ox-LDL①
not
be
recognized
by
nativeLDL
receptor②
engulf
mediate
by
scavenger
recept(Mφsurface)→foam
cell③
chemotactic
to
monocytes↑④chemotactic
to
EC、SMC↑GF↑8.2
coronary
AS
and
coronaryheart
diseasecoronary
atherosclerosisdistribution:①left>right,large
branch>small
branch,proximal
segment>distant
segment②
left
anterior
descending
coronary
A>rightCA>left
CA>left
circumflex
CAThe
progression
of
myocardial
necrosis
after
coronary
a.RCALCXLADfeatures:cutfacecrescent
plaquemyocardial
side,eccentric
stenosin4
grades:Ⅰ
<
25%
;
Ⅱ
26-50%;
Ⅲ
51-75%;
Ⅳ
>76%ischemic
heart
disease
(IHD)8.2.2
coronary
heart
disease
(CHD)1.
CHD:
ischemic
heart
disease(IHD)–
agroup
of
closely
related
syndromeresulting
from
myocardial
ischemia2.etiology
and
pathogenesis:①insufficient
blood
supply:
AS、sp②
increase
in
cardiac
energy
demand:BP↑↑,overworked,excite→work
load
of
heart↑An
imbalancebetween
the
perfusion
anddemand
of
the
heart
for
oxygenated
blooangina
pectorisz
1.
angina
pectorisA
symptom
complex
of
IHD
characterized
byparoxymal
and
usually
attacks
of
substernal
oprecordial
chest
discomfort
(constricting,squeezing,
chocking
or
kinfelike)cardiac
oxygendemand↑↑acute、temporarily,comparatively
coronary
Ablood
supply2.
clinical
typesstable
or
typical
angina:reliveby
rest
or
nitroglycerin,
chronicstenosing
coronary
AS(>75%)prinzmetal
or
variant
angina:episodic
angina,
occure
at
rest,
duecoronary
spasm,
ECG:S-T
elevated,unrelated
to
BP,
rate,
activity,vasodilators
respond
promptly(3)unstable
or
crescendo
angina:occure
with
progressively
increasingfrequencytend
to
be
of
more
prolonged
durationInduced
by
disruption
of
an
AS
plaque
witsuperimposed
partial
thrombosis
andembolization
or
vasospasm
(preinfarctiangina)myocardial
infarction,(MI)concept:acute
ischemic
necrosisdue
to
severe
sustainedischemia,heart
attacktypes:95%
LV,
transmural
orsubendocardial
infarction(1)subendocardial
myocardial
infarctio①
concept:an
area
of
ischemic
necrosis
l
to
the
inner
1/3,
at
most
?
of
the
ventric
wall
(papillary
muscle,
trabeculae
carn②
lesion:multiple
different
in
size
focnecrosis③
circumferential
infarction:entire
LV
endocardium(2)transmural
myocardial
infarctiontypical
infarction:①
the
ischemic
necrosis
involves
the
fulnearly
full
thickness
of
the
ventriculawall
in
the
distribution
of
a
singlecoronary
artery
>2/3→thick
layer
infarz②
favorite
sites:LAD
40-50%Anterior
wall
of
LV
nearapex,anterior
portion
ofventricular
septrm,
apexcircumferentiallyRCA
30-40%Inferior-posterior
wall
of
LV,posteriole
portion
ofventricular
septum,
inferior-posterior
RV
free
wallLCX
15-20%Lateral
wall
of
LV
exceptat
apex3.lesion:anemic
infarct,yellow
or
gray-red,dryirregular12hr
naked
eye?-1hr
EMz4.Lab:z1/2hr:
glycogen↓z6-12hr:myoglobin
↑z24hr:
GOT,LDH,GPT,CPK↑gross?-4hr4-12hrOccasionally
dark
motting12-24hrDark
motting1-3dMotting
with
yellow-tan
infarct
center3-5dHyperemic
border,
center
yellow-tan
softing7-10dMaximally
yellow-tan
and
soft
with
depressed
red-tan
margins10-14dRed-gray
depressed
infarct
borders3wGray-white
scar,
progressive
from
border
to
coreof
infarct>2mScarring
completeLM?-4hrVariable
waviness
of
fibers
at
border4-12hrBeginning
coagulationnecrosis,edema,hemorrhage12-24hrOngoing
coagulation
necrosis,
myocytehypereosinophilia,
marginal
contraction
bandnecrosis1-3dCoagulation
necrosis,with
loss
of
nuclei
andstriation,
interstitial
infiltrate
of
neutrophils3-7dBeginning
disintegratin
of
dead
myofibers,
earlyphagocytosis7-10dWell-developed
phagocytosis
of
dead
cells,earlyformation
of
fibrovascular
granulation
at
margin10-14dWell-estabished
granulation
and
collagendeposition2-8wIncreased
collagen
deposition>2mDense
collagenous
scar圖7-14心肌梗死心肌梗死48h后,心肌細(xì)胞核消失,肌漿變成均質(zhì)細(xì)顆粒狀,橫紋幾乎消失。擴(kuò)大的心肌間隙中可見(jiàn)多量嗜中性粒細(xì)胞浸潤(rùn)。圖7-15心肌凝固性壞死(肌漿凝集)梗死的心肌纖維肌漿內(nèi)可見(jiàn)明顯增厚的波浪狀橫帶(收縮帶)圖7-16
心肌梗死心肌梗死7天后,心肌細(xì)胞核幾乎消失,肌漿變成紅染無(wú)結(jié)構(gòu)。可見(jiàn)增生的肉芽組織。圖7-17急性心肌梗死左心室前壁線形破裂5.complication①
myocardial
rupture:acute,severe,1-3days
or
1week(within
2weefavorite
siteresultVentricular
free
wallHemopericardium
andcardiac
tamponadeventricular
septumLeft-to-right
shuntpapillary
muscleSevere
mitral
regurgitation②
ventricularaneurysm:a
late
complication,from
a
largetransmuralanteroseptal
infarct,paradoxicallybulgesduringsystole③mural
thrombos
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