coronary arterial disease

7/23/2019 Coronary Arterial Disease

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Intactendothelium

Anti-aggregatory

via prostacycline

Vasodilatory

via nitric oxide

Fibrinolytic

via tPA

Antithromboticvia

thrombomodulin



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



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



CAD is characterized by

obstruction of the coronary artery

most commonly by atheromatous

pla!ue irrespective of the

occurrence of symptoms and

signs"



#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



(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



CA#





M%ocardial I'chemia

pla.(e

STALE AN/INA



CA#





M%ocardial I'chemia

pla.(e

STALE AN/INA

UNSTALE

PLA0UE



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.(



intima

endothelium

platelet

v 5 F

3 p I b

C o l



v 5 F

C o l



Platelet adhesion



/ 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%



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



Platelet aggregation



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

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6IIIa 6III

3,afer A. 199

/issuefactor



5hite thrombus




CA#




M%ocardial I'chemia

Coro!ar%hrom*o'i'




CA#




M%ocardial I'chemia

Coro!ar%hrom*o'i'

Ac(e coro!ar%'%!drome'



pla!ue

0table anginaPla!ue ruptureCoronary thrombosis1on-0/-.levation AC0<A710/.(I

0/.(I



(2#CA+DIA= I0C4.(IA



(yocardial ischemia is characterized by an

imbalance bet>een myocardial oxygen supply

and demand"

Causes?

5 contractiledysfunction

5 arrhythmias

5 infarction

5 death



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/



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



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



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



<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"



.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



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



A00.00(.1/ #F

3=#8A= +I0 F#+

C#+#1A+2 A+/.+2

DI0.A0.



=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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Age

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Cholesterol $mg7dl%

&, '', ) ),

Cholesterol

&, ' ', ) ),

+is:levelVery high

#ver *

4igh

'-*

(oderate

&-'

(ild

,-&

=o>

<nder ,

1onsmo:er 0mo:er



(.1

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Age

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Cholesterol $mg7dl%

&, '', ) ),

Cholesterol

&, ' ', ) ),

+is:levelVery high

#ver *

4igh

'-*

(oderate

&-'

(ild

,-&

=o>

<nder ,



&-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



P+.V.1/I#1 #F

C#+#1A+2 A+/.+2

DI0.A0.



.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



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



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



(A1A3.(.1/

(anaging stable angina patients based



(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



/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

coronary arterial disease

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