coronary arterial disease
TRANSCRIPT
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Intactendothelium
Anti-aggregatory
via prostacycline
Vasodilatory
via nitric oxide
Fibrinolytic
via tPA
Antithromboticvia
thrombomodulin
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ARTERIALINTIMA
VESSELLUMEN
MCP-1
Macrophage Foam cell
Oxidaio! o"L#L
L#L
L#L
Modi$edL#L
Mo!oc%e
C%o&i!e'
Adhe'io!molec(le
Barter P. EurHeart J 2004;69(suppl 6):A19-A22
)#L i!hi*i
)#L i!hi*i MCP-1expre''io!
)#L i!hi*i
)#L promoe chole'erol e+(x
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CA#
E!doheliald%'"(!cio!
Ri'& Facor'#%'lipidemia ,↑ P, #M,
I!'(li! Re'i'a!ce, Plaele',Fi*ri!oge!, ec
Adapted from!au et al. Am Heart J. 1991;121:1244-126"
pla.(e
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CAD is characterized by
obstruction of the coronary artery
most commonly by atheromatous
pla!ue irrespective of the
occurrence of symptoms and
signs"
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#ther causes of CAD
$non-atherosclerotic causes%
&"Congenital abnormality of the coronary
arteries
'"(yocardial bridging
)"Coronary arteritis
*"+adiation-induced coronary disease
,"Vasospasm in non-diseased coronary
arteries
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(1) #$%% A&' A%tma% E. E%*l J ed 200";"49:16"6(2) +,e + A %est$*ators. /$r 199";:"
/hrombus in the left anterior
descending artery $'%
0tenosis in the right coronary
artery $&%
C#+#1A+2 A+/.+I#3+AP42
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CA#
E!doheliald%'"(!cio!
Ri'& Facor'#%'lipidemia ,↑ P, #M,
I!'(li! Re'i'a!ce, Plaele',Fi*ri!oge!, ec
Adapted from!au et al. Am Heart J. 1991;121:1244-126"
M%ocardial I'chemia
pla.(e
STALE AN/INA
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CA#
E!doheliald%'"(!cio!
Ri'& Facor'#%'lipidemia ,↑ P, #M,
I!'(li! Re'i'a!ce, Plaele',Fi*ri!oge!, ec
Adapted from!au et al. Am Heart J. 1991;121:1244-126"
M%ocardial I'chemia
pla.(e
STALE AN/INA
UNSTALE
PLA0UE
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Ahero'clero'i' I!ole'
More Tha! 2(' Lipid'
Thi!$*ro(' cap
I!3ammaor%cell'
Fe4SMC'
Eroded
e!doheli(mAciaedmacrophage'
Thic&$*ro(' cap
Foam cell'
I!ac
e!doheli(m
MoreSMC'
Adapted from Libby. Circulation. 1995;91:2844-2850
Lac& o" i!3ammaor%cell'
U!'a*le Pla.(eU!'a*le Pla.(e Sa*le Pla.(Sa*le Pla.(
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intima
endothelium
platelet
v 5 F
3 p I b
C o l
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v 5 F
C o l
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Platelet adhesion
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/ 4 +
. P I
3 p I b
v 5 F
C o l
/6A'
A D P
AA
P33'
P34'
/6A'
ADP
Aspirin
Platelet activation
/hienopyridine$Clopidogrel
ticlopidine%
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v 5 F
C o l
/ 4 +
. P I
3 p I I b 7
I I I a
3 p I b
/ 6 A '
A D
P
F I 8
3pIIb7IIIainhibitor
–
3pIIb7IIIaPlatelet aggregation
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Platelet aggregation
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6II
VII VIIa
VIIa7/F
I6
I6a
6Ia
6I
Ca99
6IIa
6 6a
Ca99
VIIIa VIII
P/ /h
Va V
Fibrinogen Fibrin monomer
Fibrin polymer
Cross-lin:ed ;brin
6IIIa 6III
3,afer A. 199
/issuefactor
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5hite thrombus
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Adapted from!au et al. Am Heart J. 1991;121:1244-126"
CA#
E!doheliald%'"(!cio!
Ri'& Facor'#%'lipidemia ,↑ P, #M,
I!'(li! Re'i'a!ce, Plaele',Fi*ri!oge!, ec
M%ocardial I'chemia
Coro!ar%hrom*o'i'
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Adapted from!au et al. Am Heart J. 1991;121:1244-126"
CA#
E!doheliald%'"(!cio!
Ri'& Facor'#%'lipidemia ,↑ P, #M,
I!'(li! Re'i'a!ce, Plaele',Fi*ri!oge!, ec
M%ocardial I'chemia
Coro!ar%hrom*o'i'
Ac(e coro!ar%'%!drome'
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pla!ue
0table anginaPla!ue ruptureCoronary thrombosis1on-0/-.levation AC0<A710/.(I
0/.(I
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(2#CA+DIA= I0C4.(IA
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(yocardial ischemia is characterized by an
imbalance bet>een myocardial oxygen supply
and demand"
Causes?
5 contractiledysfunction
5 arrhythmias
5 infarction
5 death
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I0C4.(IC CA0CAD.
0upply-demand imbalance
Diastolic dysfunction
0ystolic dysfunction
.C3 changes
Angina
+est 0tress
0 e ! u e n c
e o f i s c h e m
i c e v e n t s
esto ' 5oal,u7 8J. Am J /ard$ol 19;:2"/-"0/
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I0C4.(IC PAI1 $A13I1A%
/2PICA= A13I1A .@<IVA=.1/ A13I1A
&" C4.0/DI0C#(F#+/
'" =#CA/I#1
)" +ADIA/I#1
*" <1=I.=I1.00
&" 1# C4.0/ DI0C#(F#+/
'" =#CA/I#1
)" I1DI3.0/I#1*" <1.6P=AI1.D
5.A1.00
," DIAP#+.0I0
" 04#+/1.00 #F 8+.A/4
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0/A8=. A13I1A D.FI1I/I#1
Angina pectoris $typical or e!uivalent% that
occurs during exertion or emotional stress
and relieved >ithin , to &, minutes by rest
or by the use of sublingual nitroglycerin"
First-onset angina and crescendo angina
that occur during exertion should not be
consider as clinical manifestation of stable
angina
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0table angina? grading of angina pectoris
Clas
s
Canadian Cardiovascular 0ociety functional
classi;cation
I #rdinary physical activity such as >al:ing and climbingstairs does not cause angina" Angina >ith strenuous or
rapid or prolonged exertion at >or: or recreation
II 0light limitation of ordinary activity" 5al:ing or climbing
stairs rapidly >al:ing uphill >al:ing or stair climbing
after meals in cold in >ind or >hen under emotional
stress or only during the fe> hours after a>a:ening"
5al:ing more than t>o bloc:s on the level and climbing
more than one Bight of ordinary stairs at a normal pace
and in normal conditions
III (ar:ed limitation of ordinary physical activity" 5al:ing
one to t>o bloc:s on the level and climbing more than
one Bight in normal conditions
IV Inability to carry on any physical activity >ithout
discomfort anginal syndrome may be present at rest8oldma% et al. /$rulat$o% 191;64:122
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E!doheliald%'"(!cio!
Ri'& Facor'#%'lipidemia ,↑ P, #M,
I!'(li! Re'i'a!ce, Plaele',Fi*ri!oge!, ec
Adapted from!au et al. Am Heart J. 1991;121:1244-126"
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<nstable angina pectoris $<A%?de;nition
Angina pectoris >ith at least one of threefeatures?
&" occurring at rest $or >ith minimal exertion%
and usually lasting more than ' minutes $if not
interrupted by nitroglycerin%
'" being severe and described as fran: pain and
ne> onset $>ithin & month%
)" occurring >ith a crescendo pattern $more
severe prolonged or fre!uent than
previouslyBrau%ald E et al. /$rulat$o% 2002;106:19"
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.Eects of ischemia on themyocardium
(yocardial
hibernation?
myocardial dysfunction due to
chronically reduced coronary
blood Bo> that can be restored
by revascularization
(yocardial stunning
?
prolonged myocardial
dysfunction >ith a gradual
return of contractility after a
brief episode of severe ischemia
(yocardial necrosis
?
cell death due to unrelieved
ischemia
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1#(.1C=A/<+. #F AC</. C#+#1A+2021D+#(.
AC</. C#+#1A+2 021D+#(.
1o 0/ .levation 0/ .levation
<nstable
Angina
1on-0/.(I
1on-@ >ave (I @ >ave (I
Brau%ald et al. JA// 2000;"6:90-1062
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A00.00(.1/ #F
3=#8A= +I0 F#+
C#+#1A+2 A+/.+2
DI0.A0.
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=evels of +is: Associated >ith
0mo:ing 4ypertension and
4ypercholesterolemia
$Adapted from Poulter et al., &)%
x&
4ypertension
Dyslipidemia0mo:ing
x
x*", x
x&" x*
x)
1onsmo:er 0mo:er
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1onsmo:er 0mo:er
Age G
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+is:levelVery high
#ver *
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&-'
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1onsmo:er 0mo:er
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+is:levelVery high
#ver *
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&-'
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<nder ,
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&-2ear Coronary 4eart Disease+is:
J 'CAD or CAD ris:
e!uivalent
=ess than & or &-
'
K '
< &-&
&-year C4D ris: +is: factor
/EP-A+P eport. JAA 2001;2:246-249
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P+.V.1/I#1 #F
C#+#1A+2 A+/.+2
DI0.A0.
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.1D#/4.=IA= D20F<1C/I#1.1D#/4.=IA= D20F<1C/I#1
#CC<+0 I1 +.0P#10. /#
CA+DI#VA0C<=A+CA+DI#VA0C<=A+ +I0 FAC/#+0+I0 FAC/#+0
A1D P+.C.D.0 /4.
D.V.=#P(.(.1/ #F
A/4.+#0C=.+#0I0A/4.+#0C=.+#0I0 A1D C4A13.
P=A@<. 0/A8I=I/2 P=A@<. 0/A8I=I/2 $=.AD /# /4.
D.V.=#P(.1/ #F C#+#1A+2
.V.1/0%
oss . EJ 1999;"40:11-126
$< P. /$rulat$o% 2001;104:"6-"2
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Category +is: factors
Predisposing factors Age sex family history genes
+is:-modifying
behaviors
0mo:ing atherogenic diet
alcohol inta:e physical activity
(etabolic ris: factors Dyslipidemia hypertension
diabetes obesity metabolic
syndrome
Disease mar:ers Calcium score catheterization
result stress test result =V4 on
echocardio-graphy personalhistory of vascular disease $prior
(I or stro:e angina peripheral
vascular disease% inBammatory
state
Four 8asic Categories of +is: Factors
Classi;cation of +is: Factors 8ased #n the
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Classi;cation of +is: Factors 8ased #n the
+esponsiveness to Intervention
Category I
?
Interventions have been proved to lo>er ris: ?
smo:ing =D=-C high-cholesterol diet
hypertension left ventricular hypertrophy
Category
II ?
Interventions are li:ely to lo>er ris: ? diabetes
4D=-C physical inactivity triglycerides small-
dense =D= obesity postmenopausal status
Category
III?
+is: modi;cation might lo>er ris: ? psychosocial
factors =p$a% homocystein oxidative stress no
alcohol consumption
Category IV
?
+is: factors that cannot be modi;ed? age male
gender lo> socioeconomic status family history of
early onset of CVD
Pearso% +A et al. J Am /oll /ard$ol 1996;2:10"9-4
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(A1A3.(.1/
(anaging stable angina patients based
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(anaging stable-angina patients based
on ris: strati;cation
4I34-+I0 PA/I.1/0
$regardless of the
severity of symptoms%
C#+#1A+2
+.VA0C<=A+ILA/I#1
=#5-+I0 PA/I.1/0
>ithout serious
symptoms
P4A+(AC#=#3ICA=
(A1A3.(.1/
Chest discomfort suggestive of ischemia
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/ime from onsetof symptoms
- +eperfusion strategy?PCI $ min% or;brinolysis $) min%
- AC.-I7A+8 >ithin '* h ofsymptom onset%
- 0tatin
&'hours
&' hrs
0tart adMunctivetreatment
1ormal or non-diagnostic
changes in 0/-segment or /-
>aves
0/-depression ordynamic /->ave
inversion stronglysuspicious for inMury
0/ elevation or ne>or presumably ne>
=888 stronglysuspicious for inMury
Chest discomfort suggestive of ischemia
+evie> initial &' lead .C3
Immediate .D assessment and immediate .D generaltreatment
0tart adMunctivetreatment
Admit to monitoredbed
Assess ris: status
- 4igh ris:? earlyinvasivestrategy- Continue A0Aheparin AC.-Istatin
Develops high orintermediate ris:
criteria or troponin-positive
(onitored bed in .D
Develops high orintermediate ris:
criteria or troponin-positive
1o evidence of ischemia and (I? discharge >ith