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Penanganan Mutakhir Penyakit Jantung Koroner : Sindroma Koroner Akut

Prof. dr. Harmani Kalim, MPH,Sp.JP (K), FIHA, FASCC

Departemen Kardiologi dan Kedokteran Va k!ler FK"I P! at Jant!ng #a ional$%S Jant!ng Harapan Kita

Epidemiologi

Survei Kesehatan Rumah Tangga (SKRT) Departemen Kesehatan menunjukkan, penyakit jantung memberikan kontribusi sebesar 1 ,! " dari seluruh penyebab kematian pada tahun 1 #$ %ngka tersebut meningkat menjadi &',' " pada tahun 1 ! (asil SKRT tahun &))1, *+K telah menempati urutan pertama dalam deretan penyebab utama kematian di ,ndonesia$

Atherosclerosis Timeline
"oam Cells "att# Strea$ %ntermediate At'eroma &esion "i(rous Pla)ue Compli*ated &esion+ ,upture

/ndot'elial -#sfun*tion "rom "irst -e*ade "rom .'ird -e*ade "rom "ourt' -e*ade

Adapted from Pepine CJ. Am J Cardiol. 1998;82(suppl 10A):23S 2!S.

*athogenesis o%theros.leroti. *la/ues


ndothelial damage Protective response results in production of cellular adhesion molecules Monocytes and T lymphocytes attach to sticky surface of endothelial cells Migrate through arterial wall to subendothelial space Macrophages take up o!idised L"L-# Lipid-rich foam cells $atty streak and pla%ue

The 0%.tivated1 Endothelium


endothelium cytokines -eg. *L-/0 T,$-1 chemokines -eg.M#P-/0 *L-21 growth factors -eg. P"3$0 $3$1
attracts monocytes and T lymphocytes which adhere to endothelial cells

activated

# LL&LA' A"( )*+, M+L #&L )

induces cell proliferation and a prothrombic state

4oenig 5. Eur Heart J Suppl /6667/-)uppl T17T/689:.

0am(aran ,o(e$n#a Pla$ (Pla)ue) disertai Proses .rom(osis

Unstable coronary artery disease

Thrombus Forms and Extends into the lumen

Thrombus

Lipid core

Adventitia

%.ute 2oronary Syndrome 3 2lini.al *erspe.tive


144&3 2lini.al des.ription o- progression o- angina symptoms to myo.ardial in-ar.tion and death 1 1)3 *re5in-ar.tion angina 1 413 ,ntrodu.tion o- terminology o- unstable angina 1 !!3 2on.ept o- a.ute .oronary syndrome 1 )51 63 Risk strati-i.ation5Troponins

7ilestones in 7anagement o%.ute 2oronary Syndrome


1 1 1 1 1 1 !#3%spirin therapy !63 Thrombolyti. therapy !!3 %spirin and heparin 43 8o9 mole.ular 9eight heparin !3 :*,,b;,,,a and aspirin and heparin 3 2atheter based; ,nvasive treatment (*2,;2%<:) &))13 2lopidogrel 9ith aspirin &))63 =hat1s ne9>>

Sindroma Koroner %kut

%ngina *ektoris terstabil ,n-ark miokard non elevasi segmen ST (STE7,) ,n-ark 7iokard dengan elevasi segmen ST (?STE7,)

*ato-isiologi sama *ersentasi sama %turan& pengelolaan a9al sama STE7, perlu evaluasi untuk intervensi reper-usi akut

2lini.al 2lassi-i.ation o- 7yo.ardial ,n-ar.tion3 E@pert 2onsensus

Type , Spontaneous 7, related to is.hemia due to a primary .oronary event su.h as a pla/ue erosion and;or rupture, -issuring, or disse.tion Type & 7, se.ondary to is.hemia due to either A& demand or de.reased supply (.oronary artery spasm, .oronary embolism, anemia, (T?, hypotension, arrhythmia)

Thygesen, K. et.al. Circulation 2007; 116: 2634 2653.

2lini.al 2lassi-i.ation o- 7yo.ardial ,n-ar.tion3 E@pert 2onsensus

Type # Sudden une@pe.ted .ardia. death, in.luding .ardia. arrest, o-ten 9ith symptoms suggestive o- myo.ardial is.hemia, a..ompanied by presumably ne9 ST elevation, or ne9 8<<<, or eviden.e o- -resh thrombus in a .oronary artery by angiography and;or at autopsy, but death o..urring be-ore blood tests .ould be obtained, or at a time be-ore the appearan.e o- .ardia. biomarkers in the blood$

Thygesen, K. et.al. Circulation 2007; 116: 2634 2653.

2lini.al 2lassi-i.ation o- 7yo.ardial ,n-ar.tion3 E@pert 2onsensus

Type 'a 7, asso.iated 9ith *2, Type 'b 7, asso.iated 9ith stent thrombosis as do.umented by angiography or at autopsy Type 6 7, asso.iated 9ith 2%<:

Thygesen, K. et.al. Circulation 2007; 116: 2634 2653.

Baktor *enentu 8uas ,n-ark


1$

1$ &$ #$ '$

8ama oklusi (,ngat3 door to balloon C ) menit dan door to needle C #) menit ) Kolateral Tingkat konsumsi oksigen miokard Keadaan metabolik Keseimbangan -ibrinolitik

Diagnosis o- %ngina

Typi.al anginaD%ll three o- the -ollo9ing


Substernal .hest dis.om-ort Anset 9ith e@ertion or emotional stress Relie- 9ith rest or nitrogly.erin

%typi.al angina

& o- the above .riteria

?on.ardia. .hest pain

1 o- the above

Diagnosis o- Enstable %ngina

*atients 9ith typi.al angina 5 %n episode oangina


,n.reased in severity or duration (as onset at rest or at a lo9 level o- e@ertion Enrelieved by the amount o- nitrogly.erin or rest that had previously relieved the pain

*atients not kno9n to have typi.al angina


Birst episode 9ith usual a.tivity or at rest 9ithin the previous t9o 9eeks *rolonged pain at rest

Diagnosis o- %.ute 7, STE7, ; ?STE7,

%t least & o- the -ollo9ing


,s.hemi.

symptoms Diagnosti. E2: .hanges Serum .ardia. marker elevations

Enstable %ngina
Non occlusive thrombus Non specific ECG Normal cardiac enzymes

,)T M*
Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression + ! T "ave inversion on ECG Elevated cardiac enzymes

STE7,
Complete thrombus occlusion ST elevations on ECG or ne" #$$$ Elevated cardiac enzymes %ore severe symptoms

Sasaran *era9atan Kardiak


1$ &$ #$

'$

6$

7engurangi luasnya in-ark 7empertahankan -ungsi ventrikel kiri 7en.egah kejadian kardiak atau komplikasi major 7engatasi komplikasi yang mengan.am ji9a 7ulai melakukan pen.egahan sekunder

%.ute 7anagement

,nitial evaluation F stabiliGation E--i.ient risk strati-i.ation Bo.used .ardia. .are

Evaluation

E--i.ient F dire.t history ,nitiate stabiliGation interventions

1**urs simultaneousl#

*lan -or moving rapidly to indi.ated .ardia. .are &irected Therapies


are Time Sensitive'

2hest pain suggestive o- is.hemia


(mmediate assessment "ithin )* %inutes
(nitial labs and tests

Emergent care
*; access #ardiac monitoring +!ygen Aspirin ,itrates

+istory & ,hysical


stablish diagnosis 'ead #3 *dentify complications Assess for reperfusion

1& lead E2: Abtain initial .ardia. enGymes ele.trolytes, .b. lipids, bun;.r, glu.ose, .oags 2HR

Bo.used (istory

%id in diagnosis and rule out other .auses

*alliative;*rovo.ative -a.tors Iuality o- dis.om-ort Radiation Symptoms asso.iated 9ith dis.om-ort 2ardia. risk -a.tors *ast medi.al history 5 espe.ially .ardia.

Reper-usion /uestions

Timing opresentation E2: .;9 STE7, 2ontraindi.ation to -ibrinolysis Degree o- STE7, risk

Targeted *hysi.al

E@amination

Jitals 2ardiovas.ular system Respiratory system %bdomen ?eurologi.al status

Re.ogniGe -a.tors that in.rease risk


(ypotension Ta.hy.ardia *ulmonary rales, +JD, pulmonary edema, ?e9 murmurs;heart sounds Diminished peripheral pulses Signs o- stroke

,e$aman /20 'arus se*epatn#a dila$u$an dan diinterpretasi saat pasien ti(a di %0Standar waktu 10 menit

:amm &an*et 3=8:1=33<2001

Presentation Workin !"

%s*'emi* -is*omfort A*ute Coronar# S#ndrome

-a4ies 8J :eart 83:3;1< 2000

#C$

3o S. /le4ation 3S./8%

S. /le4ation

%ioc&em. Marker 'inal !" 5nsta(le An6ina

Myocardial Infarction 378% 79 8%

Normal or non-diagnostic EKG

ST Depression or Dynami. T 9ave ,nversions

ST5Segment Elevation 7,

?e9 8<<<

7,S > 0.12 se* & A?is de4iation Prominent S 9a4e @1 @3 Prominent , 9a4e 1< a@&< @= @;

Ese o- 2ardia. 7arkers in %2S


5,& E 99t' Ftile of ,eferen*e Control 0roup

=0
8ultiples of t'e 5,&

20 10 = 2 1 0 1
5pper referen*e limit

Cardia* troponin after A*lassi*alB A8% C2 8C after A8% Cardia* troponin after Ami*roinfar*tionB

2 3 D = ; -a#s After 1nset of A8%

Modified from( #SC)ACC Comm MI redefined* JACC +,( -.-/0000 Wu A1 et al. Clin C&em 1---23.(1103.

2ardia. markers

Troponin ( T, ,)

2K57< isoenGyme

Jery spe.i-i. and more sensitive than 2K Rises '5! hours a-ter injury 7ay remain elevated -or up to t9o 9eeks 2an provide prognosti. in-ormation Troponin T may be elevated 9ith renal dG, poly;dermatomyositis

Rises '5K hours a-ter injury and peaks at &' hours Remains elevated #K5 '! hours *ositive i- 2K;7< L 6" o- total 2K and & times normal Elevation .an be predi.tive o- mortality Balse positives 9ith e@er.ise, trauma, mus.le dG, D7, *E

*rognosis 9ith Troponin


8 7
8ortalit# at D2 -a#s

7.5 F 6.0 F 3.4 F 1.0 F


831

6 5 4 3 2 1 0

3.7 F

1.7 F
1!D 1D8 13D =0 ;!
9.0

0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 Cardiac troponin I (ng/ml)

S*EKTRE7 K8,?,S SK%

Current definitions and prognosis of ACS


1&hr serum troponin T .on.entration (ug;8) < 0.01 BCS ESC&ACC ()* +0-da# mortalit# 1-mont! mortalit# ACS it! unsta"le angina 'nsta"le angina 'nsta"le angina ,.-. 2.1. 0.1 and < 1.0 ACS it! m#oc#te necrosis $% 'nsta"le angina 10.,. 12.3. ACS $% $% $% 1/.0. 10./. 1.0 it! clinical

A*ute Coronar# S#ndrome 3o S. /le4ation S. /le4ation

5isk Stratification
Pur4oses .ria6e + .ransfer for .ertiar# Care ,esour*e Allo*ation Sele*tion of ,? Strate6# Pro6nosis

Continuous Process Presentation: :istor#< ACS features< Ciomar$ers< P/? %n :ospital: /4ents< ,esponse to ,? -is*'ar6e: &@ "un*tion< Arr'#t'mias< %s*'emia

Risk Strati-i.ation
STE%( ,atient/
$ased on initial Evaluation- ECG- and Cardiac mar.ers

0ES

NO

- Assess for reperfusion


- )elect < implement reperfusion therapy - "irected medical therapy

E% or ?STE7, 5 Evaluate -or ,nvasive vs$ .onservative treatment 5 Dire.ted medi.al therapy

Bibrinolysis indi.ations

ST segment elevation L1mm in t9o .ontiguous leads ?e9 8<<< Symptoms .onsistent 9ith is.hemia Symptom onset less than 1& hrs prior to presentation

%bsolute .ontraindi.ations -or -ibrinolysis therapy in patients 9ith a.ute STE7,


%ny prior ,2( Kno9n stru.tural .erebral vas.ular lesion (e$g$, %J7) Kno9n malignant intra.ranial neoplasm (primary or metastati.) ,s.hemi. stroke 9ithin # months EH2E*T a.ute is.hemi. stroke 9ithin # hours Suspe.ted aorti. disse.tion %.tive bleeding or bleeding diathesis (e@.luding menses) Signi-i.ant .losed5head or -a.ial trauma 9ithin # months

%dvantages oBibrinolyti. Therapy


7ore universal a..ess Shorter time to treatment :reater .lini.al trial eviden.e o-3

redu.tion in in-ar.t siGe improvement o- 8J -un.tion

Results less dependent on physi.ian e@perien.e 8o9er system .osts


42

Ad4antages of primar# 5C% o4er t!rom"ol#sis


2lini.al indi.es Event rate 6!rom"ol#sis S!ort term mortalit# 7,-1 ee8s9 :ong term mortalit# 71-12mont!s9 Stro8e ;e-infarction ;ecurrent isc!aemia <eat! or non-fatal re-infarction Need for CABG 2. 2. /. 2. 12. 1/. 1+. 5C% -. -. <1. +. 3. 3. 2. %bsolute RR +. +. /. -. 11. -. -. Relative RR +1. +2. 1,. -0. -0. ,,. +2. ??T

++ ++ -0 /0 /0 /0 /0

2omparing out.omes

STE7, .ardia. .are

STE* 13 %ssessment Time sin.e onset o- symptoms

) min -or *2, ; 1& hours -or -ibrinolysis

,s this high risk STE7,>


K,88,* .lassi-i.ation ,- higher risk may manage 9ith more invasive r@

Determine i- -ibrinolysis .andidate

7eets .riteria 9ith no .ontraindi.ations

Determine i- *2, .andidate

<ased on availability and time to balloon r@

7edi.al Therapy 7A?% M <%(

7orphine (.lass ,, level 2) %nalgesia Redu.e pain;an@ietyDde.rease sympatheti. tone, systemi. vas.ular resistan.e and o@ygen demand 2are-ul 9ith hypotension, hypovolemia, respiratory depression A@ygen (&5' liters;minute) (.lass ,, level 2) Ep to 4)" o- %2S patient demonstrate hypo@emia 7ay limit is.hemi. myo.ardial damage by in.reasing o@ygen delivery;redu.e ST elevation

?itrogly.erin (.lass ,, level <) %nalgesiaDtitrate in-usion to keep patient pain -ree Dilates .oronary vesselsDin.rease blood -lo9 Redu.es systemi. vas.ular resistan.e and preload %spirin (1K)5#&6mg .he9ed F s9allo9ed) (.lass ,, level %) ,rreversible inhibition o- platelet aggregation StabiliGe pla/ue and arrest thrombus Redu.e mortality in patients 9ith STE7,

<eta5<lo.kers (.lass ,, level %) 1'" redu.tion in mortality risk at 4 days at &#" long term mortality redu.tion in STE7, %ppro@imate 1#" redu.tion in risk oprogression to 7, in patients 9ith threatening or evolving 7, symptoms Reassess -or therapy as .ontraindi.ations resolve %2E5,nhibitors ; %R< (.lass ,, level %) Start in patients 9ith anterior 7,, pulmonary .ongestion, 8JEB C ')" Start in -irst &' hours %R< as substitute -or patients unable to use %2E5,

(eparin (.lass ,, level 2 to .lass ,,a, level 2) 87=( or EB( (ma@ ')))u bolus, 1)))u;hr) ,ndire.t inhibitor o- thrombin %djun.t to surgi.al revas.ulariGation and thrombolyti. ; *2, reper-usion &'5'! hours o- treatment 2oordinate 9ith *2, team (EB( pre-erred) Esed in .ombo 9ith aspirin and;or other platelet inhibitors 2hanging -rom one to the other not re.ommended

STE7, .are 22E

7onitor -or .ompli.ations3

re.urrent is.hemia, .ardiogeni. sho.k, ,2(, arrhythmias

Revie9 guidelines -or spe.i-i. management o- .ompli.ations F other spe.i-i. .lini.al s.enarios

*2, a-ter -ibrinolysis, emergent 2%<:, et.N

De.ision making -or risk strati-i.ation at hospital dis.harge and;or need -or 2%<:

Enstable angina;?STE7, .ardia. .are

Evaluate -or .onservative vs$ invasive therapy based upon3


Risk

o- a.tual %2S T,7, risk s.ore %2S risk .ategories per %(% guidelines #o" +igh

(ntermediate

Hig !i"# $C% (&$/'%()*I)


)l+,at+d cardiac mar#+r" '+- or pr+".m+d n+- %( d+pr+""ion !+c.rr+nt i"c +mia d+"pit+ t +rap/ !+c.rr+nt i"c +mia -it +art 0ail.r+ Hig ri"# 0inding" on non1in,a"i,+ "tr+"" t+"t 2+pr+""+d "/"tolic l+0t ,+ntric.lar 0.nction H+mod/namic in"ta3ilit/ %."tain+d 4+ntric.lar tac /cardia 5CI -it 6 mont " 5rior 6/pa"" ".rg+r/

#o" ris.

(ntermediate

ris.

+igh ris.

Chest ,ain center

Conservative therapy

(nvasive therapy

,nvasive therapy option E%;?STE7,

2oronary angiography and revas.ulariGation 9ithin 1& to '! hours a-ter presentation to ED Bor high risk %2S (.lass ,, level %) 7A?% M <%( (EB() 2lopidogrel

&)" redu.tion death;7,;Stroke O 2ERE trial 1 month minimum duration and possibly up to

months

:ly.oprotein ,,b;,,,a inhibitors

2onservative Therapy -or E%;?STE7,


Early revas.ulariGation or *2, not planned 7A?% M <%( (87= or EB() 2lopidogrel :ly.oprotein ,,b;,,,a inhibitors

Anly in .ertain .ir.umstan.es (planning *2,, elevated Tn,;T) Serial E2:s Serial 7arkers

Surveillen.e in hospital

7edi.ation Ese at Dis.harge and 15year 7ortality

%-ter adjusting -or age, previous 7,, 2(B, Killip .lass, abnormal biomarker, ST deviation;<<< on presentation, the dis.harge use o- the -ollo9ing medi.ations 9as asso.iated 9ith lo9er 15year mortality P3 %S% QARR)$'! ()$#K to )$K#), *C)$))1S <eta5blo.ker QARR)$4& ()$6K to )$ &), *C)$)1S %2E inhibitor QARR)$4K ()$K) to )$ K), *R)$)&S 8ipid lo9ering agent QARR)$4& ()$64 to )$ &), *C)$)1S
= +'> odds ratio -6?@ confidence interval1

Comprehensive Medical Therapy For 2nd Prevention for Patients ith C!" or #ther $ascular "isease
'isk 'eduction

A A A A A

A)A= Deta Dlockers= A# inhibitors= )tatins= )moking #essation

9B-CB@ 9B-C?@ 99-9?@ 9?-E9@ ?B@

%The four medications every atherosclerosis patient should be treated ith& unless contraindications exist and are documented

*en.egahan Sekunder
% 3 %S%, antikoagulan, %2E5,;%R< (8JD, (B, (T?, D7) < 3 <eta5blo.ker, <= redu.tion, <* 2ontrol (<*C 1#);!) mm(g) 2 3 2igarette smoking .essation 2holesterol .ontrol (K58D8C4) mg;dl) D 3 Diet ( %(% step & diet ) Diabetes management ( %.C4") E 3 E@er.ise regularly Edu.ation B 3 Bamily Support : 3 :o to (ospital

)econdary Prevention of #oronary "isease


Secondary Prevention
#A"
,on-#oronary Atherosclerosis

Primary Prevention

)ubclinical Atherosclerosis Multiple 'isk $actors nvironmental0 3enetic $actors that Produce 'isk

Population Wellness

*revention ne9sN
$rom /66E to 9BBE the death rate from coronary heart disease declinedFCC@... Dut the actual number of deaths declined onlyF/2@F

3etting better with treatmentG Dut more patients developing disease 8 need for primary prevention focus

Kesimpulan

SK% men.akup %*TS, ?STE7,, dan STE7, Bokus penatalaksanaan 5 penilaian dan intervensi segera ( 7A?% M <%( ) 5 strati-ikasi resiko ( %*TS;?STE7, JS STE7, ) 5 reper-usi .epat pada STE7, (Bibrinolitik vs *2, ) 5 strategi konservati- vs invasi- dini pada %*TS; ?STE7, *en.egahan sekunder agresi- pada pasien SK% 5 <<, %2E51;%R<, %S%, statin

=>ara!$utiaraSari)armani

*"?ecti4es

<efine @ delineate acute coronar# s#ndrome ;e4ie


$anagement Guidelines

'nsta"le Angina & NS6E$% S6E$%

;e4ie

secondar# pre4ention initiati4es

Acute Coronar# S#ndromes

'nsta"le Angina Non-S6-Segment Ele4ation $% 7NS6E$%9 S6-Segment Ele4ation $% 7S6E$%9

Similar pat!op!#siolog#

Similar presentation and earl# management rules

S6E$% reAuires e4aluation for acute reperfusion inter4ention

<iagnosis of Acute $% S6E$% & NS6E$%

At least / of t!e follo ing


%sc!emic

s#mptoms <iagnostic ECG c!anges Serum cardiac mar8er ele4ations

<iagnosis of Angina

6#pical anginaBAll t!ree of t!e follo ing


Su"sternal c!est discomfort *nset it! eCertion or emotional stress ;elief it! rest or nitrogl#cerin

At#pical angina

/ of t!e a"o4e criteria

Noncardiac c!est pain

<iagnosis of 'nsta"le Angina

5atients angina

it! t#pical angina - An episode of

%ncreased in se4erit# or duration )as onset at rest or at a lo le4el of eCertion 'nrelie4ed "# t!e amount of nitrogl#cerin or rest t!at !ad pre4iousl# relie4ed t!e pain

5atients not 8no n to !a4e t#pical angina


>irst episode it! usual acti4it# or at rest t!e pre4ious t o ee8s 5rolonged pain at rest

it!in

'nsta"le Angina
Non occlusive thrombus Non specific ECG Normal cardiac enzymes

,)T M*
Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression + ! T "ave inversion on ECG Elevated cardiac enzymes

S6E$%
Complete thrombus occlusion ST elevations on ECG or ne" #$$$ Elevated cardiac enzymes %ore severe symptoms

Acute $anagement

%nitial e4aluation @ sta"iliDation Efficient ris8 stratification >ocused cardiac care

Efficient @ direct !istor# 1**urs %nitiate sta"iliDation inter4entions simultaneousl


#

E4aluation

5lan for mo4ing rapidl# to indicated cardiac care


&irected Therapies are Time Sensitive'

C!est pain suggesti4e of isc!emia


(mmediate assessment "ithin )* %inutes
(nitial labs and tests

1/ lead ECG *"tain initial cardiac enD#mes electrol#tesE c"c lipidsE "un&crE glucoseE coags CF;

Emergent care A *; access A #ardiac monitoring A +!ygen A Aspirin A ,itrates

+istory & ,hysical


A stablish diagnosis A 'ead #3 A *dentify complicatio ns A Assess for reperfusion

>ocused )istor#

Aid in diagnosis and rule out ot!er causes

5alliati4e&5ro4ocati4e factors Gualit# of discomfort ;adiation S#mptoms associated it! discomfort Cardiac ris8 factors 5ast medical !istor# -especiall# cardiac

;eperfusion Auestions

6iming of presentation ECG c& S6E$% Contraindication to fi"rinol#sis <egree of S6E$% ris8

6argeted 5!#sical

ECamination

Iitals Cardio4ascular s#stem ;espirator# s#stem A"domen Neurological status

;ecogniDe factors t!at increase ris8


)#potension 6ac!#cardia 5ulmonar# ralesE HI<E pulmonar# edemaE Ne murmurs&!eart sounds <iminis!ed perip!eral pulses Signs of stro8e

8odified from &i((# P Cir* 10D:3;=<2001

A*ute Coronar# S#ndrome

Superfi*ial /rosion

,uptured "i(rous Cap

:amm &an*et 3=8:1=33<2001

Presentation Workin !"

%s*'emi* -is*omfort A*ute Coronar# S#ndrome

-a4ies 8J :eart 83:3;1< 2000

#C$

3o S. /le4ation 3S./8%

S. /le4ation

%ioc&em. Marker 'inal !" 5nsta(le An6ina

Myocardial Infarction 378% 79 8%

5,& E 99t' Ftile of ,eferen*e Control 0roup

Ese o- 2ardia. 7arkers in %2S


=0 20 10 = 2 1 0 1
5pper referen*e limit

8ultiples of t'e 5,&

Cardia* troponin after A*lassi*alB A8% C2 8C after A8% Cardia* troponin after Ami*roinfar*tionB

2 3 D = ; -a#s After 1nset of A8%

Modified from( #SC)ACC Comm MI redefined* JACC +,( -.-/0000 Wu A1 et al. Clin C&em 1---23.(1103.

A*ute Coronar# S#ndrome 3o S. /le4ation S. /le4ation

5isk Stratification
Pur4oses .ria6e + .ransfer for .ertiar# Care ,esour*e Allo*ation Sele*tion of ,? Strate6#

Pro6nosis

Continuous Process Presentation: :istor#< ACS features< Ciomar$ers< P/? %n :ospital: /4ents< ,esponse to ,? -is*'ar6e: &@ "un*tion< Arr'#t'mias< %s*'emia

Symptoms suggestive o- %2S


5a4id 7ria e 89tain %iomarkers

Assess 12 lead /C0

$oal 6 10 min

3on Cardia* -ia6nosis

C'roni* Sta(le An6ina

Possi(le ACS ASA

-efinite ACS

As Per 1t'er -?

8edi*al ,?

Antit'rom(in Ceta Clo*$er ACS Proto*ol

S#mptoms Su66esti4e of ACS Possi(le ACS 3o S. ele4. G 12' &#ti* eli6i(le :ytic
(- 3 G 30 m)

-efinite ACS S. ele4. > 12' 3ot a reperfusion *andidate


Consider 5e4erfusion for Sym4toms

&#ti* ineli6i(le PCI;


(- C G 90)
Consider: 0P %%(+%%%a H stent

Medical 5"
(AC/%)

;Skilled 84er.)7eam 5a4idly A<aila9le

S#mptoms Su66esti4e of ACS


Possi(le ACS 3o S. ele4. -efinite ACS S. ele4. /4aluate for reperfusion

3on d? /C0 3e6. *ard. mar$ers 1(ser4e f+u studies 3e6 3e6 1utpt f+u Stress Pos Pos

S. .9 *'an6es 1n6oin6 pain Positi4e *ard mar$ers :emod#nami* a(nl.

-? of ACS *onfirmed Admit to 'ospital A*ute is*'emia pat'9a#

-e4elopment of at'eros*lerosis and 4ulnera(le pla)ue

2hronology o%theros.leroti. Jas.ular Disease *ro.ess


A*ute Coronar# S#ndrome Se*ondar# Pre4ention

%s*'emi* :eart -isease Cere(ro4as*ular -isease Perip'eral @as*ular -isease

8odified from &i((# P Cir* 10D:3;=<2001

6roponins for E4aluation and $anagement of ACS


Ad4anta6es

-isad4anta6es

'isk )tratificaton )ensH)pec I #4MD "etect 'ecent M* )election of '! "etect 'eperfusion

Low sens. early -J :h1 'epeat at 2-/9 h if neg. Limited ability to detect late minor reinfarction

,e*ommendation Useful as single test to efficiently Dx NSTE ! "linicians s#ould familiari$e t#emselves %it# Dx &cutoffs' in local la(

ECG assessment
ST Elevation or ne" #$$$ STE%(
ST &epression or dynamic T "ave inversions

NSTE%(
Non!specific ECG

1nstable 2ngina

Normal or non-diagnostic EKG

S6 <epression or <#namic 6 %n4ersions

a4e

S6-Segment Ele4ation $%

Ne

:BBB

7,S > 0.12 se* & A?is de4iation Prominent , 9a4e @1 @3 Prominent S 9a4e 1< a@&< @= @; 9it' t 9a4e in4ersion

Cardiac mar8ers

6roponin 7 6E %9

CK-$B isoenD#me

Ier# specific and more sensiti4e t!an CK ;ises ,-2 !ours after in?ur# $a# remain ele4ated for up to t o ee8s Can pro4ide prognostic information 6roponin 6 ma# "e ele4ated it! renal dDE pol#&dermatom#ositis

;ises ,-1 !ours after in?ur# and pea8s at /, !ours ;emains ele4ated +1-,2 !ours 5ositi4e if CK&$B J -. of total CK and / times normal Ele4ation can "e predicti4e of mortalit# >alse positi4es it! eCerciseE traumaE muscle dDE <$E 5E

5rognosis
8 7 8ortalit# at D2 -a#s 6 5 4 3 2 1 0

it! 6roponin
7.5 F 6.0 F

3.4 F 1.0 F
831

3.7 F

1.7 F
1!D 1D8 13D =0 ;!
9.0

0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 Cardiac troponin I (ng/ml)

;is8 Stratification
STE%( ,atient/
$ased on initial Evaluation- ECG- and Cardiac mar.ers

0ES

NO

- Assess for reperfusion


- )elect < implement reperfusion therapy - "irected medical therapy

'A or NS6E$% - E4aluate for %n4asi4e 4s. conser4ati4e treatment - <irected medical t!erap#

Cardiac Care Goals


<ecrease

necrosis 5reser4e :I function 5re4ent ma?or ad4erse cardiac e4ents 6reat life t!reatening complications

amount of m#ocardial

S6E$% cardiac care

STE* 1K Assessment 6ime since onset of s#mptoms

00 min for 5C% & 1/ !ours for fi"rinol#sis

%s t!is !ig! ris8 S6E$%L


K%::%5 classification %f !ig!er ris8 ma# manage rC

it! more in4asi4e

<etermine if fi"rinol#sis candidate

$eets criteria

it! no contraindications

<etermine if 5C% candidate

Based on a4aila"ilit# and time to "alloon rC

>i"rinol#sis indications

S6 segment ele4ation J1mm in t o contiguous leads Ne :BBB S#mptoms consistent it! isc!emia S#mptom onset less t!an 1/ !rs prior to presentation

A"solute contraindications for fi"rinol#sis t!erap# in patients it! acute S6E$%


An# prior %C) Kno n structural cere"ral 4ascular lesion 7e.g.E AI$9 Kno n malignant intracranial neoplasm 7primar# or metastatic9 %sc!emic stro8e it!in + mont!s EFCE56 acute isc!emic stro8e it!in + !ours Suspected aortic dissection Acti4e "leeding or "leeding diat!esis 7eCcluding menses9 Significant closed-!ead or facial trauma it!in + mont!s

Relative .ontraindi.ations -or -ibrinolysis therapy in patients 9ith a.ute STE7,


)istor# of c!ronicE se4ereE poorl# controlled !#pertension Se4ere uncontrolled !#pertension on presentation 7SB5 greater t!an 120 mm )g or <B5 greater t!an 110 mm)g9 )istor# of prior isc!emic stro8e greater t!an + mont!sE dementiaE or 8no n intracranial pat!olog# not co4ered in contraindications 6raumatic or prolonged 7greater t!an 10 minutes9 C5; or ma?or surger# 7less t!an + ee8s9

Relative .ontraindi.ations -or -ibrinolysisN$$

;ecent 7 it!in /-, ee8s9 internal "leeding Noncompressi"le 4ascular punctures >or strepto8inase&anistreplaseK prior eCposure 7more t!an - da#s ago9 or prior allergic reaction to t!ese agents 5regnanc# Acti4e peptic ulcer Current use of anticoagulantsK t!e !ig!er t!e %N;E t!e !ig!er t!e ris8 of "leeding

S6E$% cardiac care

STE* &K <etermine preferred reperfusion strateg#


P#* preferred ifK A P#* available A "oor to balloon J 6Bmin A "oor to balloon minus door to needle J /hr A $ibrinolysis contraindications A Late Presentation I C hr A (igh risk )T M* 4illup C or higher A )T M* d! in doubt

$ibrinolysis preferred ifK A JC hours from onset A P#* not availableHdelayed door to balloon I 6Bmin door to balloon minus door to needle I /hr A "oor to needle goal JCBmin A ,o contraindications

Comparing outcomes

$edical 6!erap# $*NA M BA)

7orphine 7class %E le4el C9 Analgesia ;educe pain&anCiet#Bdecrease s#mpat!etic toneE s#stemic 4ascular resistance and oC#gen demand Careful it! !#potensionE !#po4olemiaE respirator# depression A@ygen 7/-, liters&minute9 7class %E le4el C9 'p to 30. of ACS patient demonstrate !#poCemia $a# limit isc!emic m#ocardial damage "# increasing oC#gen deli4er#&reduce S6 ele4ation

?itrogly.erin 7class %E le4el B9 AnalgesiaBtitrate infusion to 8eep patient pain free <ilates coronar# 4esselsBincrease "lood flo ;educes s#stemic 4ascular resistance and preload %spirin 7110-+/-mg c!e ed @ s allo ed9 7class %E le4el A9 %rre4ersi"le in!i"ition of platelet aggregation Sta"iliDe plaAue and arrest t!rom"us ;educe mortalit# in patients it! S6E$%

<eta5<lo.kers 7class %E le4el A9 1,. reduction in mortalit# ris8 at 3 da#s at /+. long term mortalit# reduction in S6E$% ApproCimate 1+. reduction in ris8 of progression to $% in patients it! t!reatening or e4ol4ing $% s#mptoms ;eassess for t!erap# as contraindications resol4e %2E5,nhibitors ; %R< 7class %E le4el A9 Start in patients it! anterior $%E pulmonar# congestionE :IE> < ,0. Start in first /, !ours A;B as su"stitute for patients una"le to use ACE-%

(eparin 7class %E le4el C to class %%aE le4el C9 :$() or '>) 7maC ,000u "olusE 1000u&!r9 %ndirect in!i"itor of t!rom"in Ad?unct to surgical re4asculariDation and t!rom"ol#tic & 5C% reperfusion /,-,2 !ours of treatment Coordinate it! 5C% team 7'>) preferred9 'sed in com"o it! aspirin and&or ot!er platelet in!i"itors C!anging from one to t!e ot!er not recommended

Additional medication t!erap#

%ldosterone blo.kers 7class %E le4el A9

5ost-S6E$% patients
no significant renal failure 7cr < /.- men or /.0 for omen9 No !#per8alemis J -.0 :IE> < ,0. S#mptomatic C)> or <$

S6E$% care CC'

$onitor for complicationsK

recurrent isc!emiaE cardiogenic s!oc8E %C)E arr!#t!mias

;e4ie guidelines for specific management of complications @ ot!er specific clinical scenarios

5C% after fi"rinol#sisE emergent CABGE etcN

<ecision ma8ing for ris8 stratification at !ospital disc!arge and&or need for CABG

'nsta"le angina&NS6E$% care

cardiac

E4aluate for conser4ati4e 4s. in4asi4e t!erap# "ased uponK


;is8

of actual ACS 6%$% ris8 score ACS ris8 categories per A)A guidelines #o" (ntermediate +igh

*redi.ts risk o- death, ne9;re.urrent 7,, need -or urgent revas.ulariGation 9ithin 1' days

T,7, Risk S.ore

ACS ris8 criteria 7'A&NS6E$%9


&o9 ,is$ ACS
3o intermediate or 'i6' ris$ fa*tors G10 minutes rest pain 3on dia6nositi* /C0 3on ele4ated *ardia* mar$ers A6e G !0 #ears

%ntermediate ,is$ ACS


8oderate to 'i6' li$eli'ood of CA>10 minutes rest pain< no9 resol4ed . 9a4e in4ersion > 2mm Sli6'tl# ele4ated *ardia* mar$ers

Hig !i"# $C% (&$/'%()*I)


/le4ated *ardia* mar$ers 3e9 or presumed ne9 S. depression ,e*urrent is*'emia despite t'erap# ,e*urrent is*'emia 9it' 'eart failure :i6' ris$ findin6s on non in4asi4e stress test -epressed s#stoli* left 4entri*ular fun*tion :emod#nami* insta(ilit# Sustained @entri*ular ta*'#*ardia PC% 9it' ; mont's Prior C#pass sur6er#

#o" ris.

(ntermediate

ris.

+igh ris.

Chest ,ain center

Conservative therapy

(nvasive therapy

Se.ondary prevention behavioral intervention

Smo8ing cessation

Cessation-classE medsE counseling Goal +0 - 10 minutes dail# ;is8 assessment prior to initiation <AS) dietE fi"erE omega-+ fatt# acids <3. total calories from saturated fats

5!#sical Acti4it#

<iet

*r ma#"e ?ust mo4eN.

Secondar# pre4ention cogniti4e

5atient education

%n-!ospital O disc!arge Ooutpatient clinic&re!a" <epression&anCiet# assessment @ treatment Social support s#stem

$onitor ps#c!osocial impact


Antiplatelet agent

$edication C!ec8list after ACS

AspirinP and&or Clopidorgrel StatinP >i"rate & Niacin & *mega-+ Beta "loc8erP ACE-%P&A;B Aldactone 7as appropriate9

:ipid lo ering agent


Anti!#pertensi4e agent

Summar#

ACS includes 'AE NS6E$%E and S6E$% $anagement guideline focus %mmediate assessment&inter4ention 7$*NAMBA)9 ;is8 stratification 7'A&NS6E$% 4s. S6E$%9 ;A5%< reperfusion for S6E$% 75C% 4s. 6!rom"ol#tics9 Conser4ati4e 4s %n4asi4e t!erap# for 'A&NS6E$% Aggressi4e attention to secondar# pre4ention initiati4es for ACS patients Beta "loc8erE ASAE ACE-%E Statin

Cardio4ascular disease and dia"etes


I;=F of deat's are to C@ disease due

Coronar# 'eart disease deat's 2 to D fold

Cardio4as*ular *ompli*ations of .2-8

Stro$e ris$ 2 to D fold

:eart failure 2 to = fold


.2-8 E t#pe 2 dia(etes mellitus
Cell -S:. !ia9etes Care. 2003;2;:2D33 D1. Centers for -isease Control (C-C). 999.*d*.6o4.

%bnormal glu.ose metabolism in 2%D


n E 210! inpatients 9it' a*ute CA-; n E 28=D outpatients 9it' sta(le CA2no9n dia(etes 10..J =8 =1

60

60

.otal patients (F)

40

32

30

PatientsJ (F)

40

20

20

0 Inpati+nt" 7.tpati+nt"

0 Inpati+nt"
%0. %"0

7.tpati+nt"
3e9 -8

Jn E 1920 9it'out $no9n dia(etes 10.. E oral 6lu*ose toleran*e test; %0. E impaired 6lu*ose toleran*e; %"0 E impaired fastin6 6lu*ose

Cartni$ 8 et al. #ur 1eart J. 200D;2=:1880 90.

?e95onset hypergly.emia linked to highest rate o- in5hospital mortality


3 E 2030 'ospital patients
40 30 *ortalit/ 20 (9) 10 0 'ormogl/c+mia 8no-n dia3+t+" '+- /p+rgl/c+mia

%C5 patients
JP G 0.01 4s normo6l#*emia and $no9n dia(etes

3on %C5 patients

5mpierreK 0/ et al. J Clin #ndocrinol Meta9. 2002;8!:9!8 82.

Stress hypergly.emia in %7,3 %sso.iation 9ith mortality risk in patients 9ithout kno9n diabetes
,eferen*e 1MSulli4an 1991 &e9ando9i*K 19!9 Soler 1981 1s9ald 198; Cellodi 1989 ,a4id 19!= Se9darsen 1989 Pooled 0 1 2 3 D = ; ! 8 9 10 11 12 13
:#per6l#*emia definition (m6+d&)

>1DD N121 N110 N1DD >121 >121 N1DD

5nadLusted ,, of in 'ospital mortalit# after 8%J


J4s patients 9it' normo6l#*emia
Capes S/ et al. :ancet. 2000;3==:!!3 8.

<aseline -asting plasma glu.ose levels predi.t (B hospitaliGation in high5risk patients


13.A,0/.+.,A3SC/3-; 3 E 31<=D; 9it' C@- or -8 H end or6an dama6e
0.0; 0.0= 0.0D Proportion 9it' in*ident :" 'ospitaliKation 0.03 0.02 0.01 0.0 0 200 D00 ;00 800 1000 1200 "ollo9 up (da#s)
&o6 ran$ P G 0.001
:eld C et al. Circulation. 200!;11=;13!1 =.

3ormal lo9 3ormal 'i6' %"0 3e9 -8 -8

23F in :" 'ospitaliKation per 18 m6+d& 6lu*ose in patients 9it' no $no9n dia(etes

%dmission glu.ose and glu.ose .hange 9ithin &' hours predi.t mortality risk
3 E 1D;9 9it' A8% (n E 1219 9it'out -8)
12 10 30 da# mortalit# (F) 8 6 4 2 0 0 G12= 12=OG1D0 1D0OG1!0 Caseline 6lu*ose (m6+d&) N1!0 9F in 30 da# mortalit# per 11 m6+d& 6lu*ose in first 2D 'r (P E 0.002)J

0lu*ose (2D 'r 4s (aseline) N30 m6+d& de*rease 3o *'an6e to G30 m6+d& de*rease
J8ulti4ariate anal#sis

%n*rease

0o#al A et al. #ur 1eart J. 200;;2!:1289 9!.

8odified from &i((# P Cir* 10D:3;=<2001

A*ute Coronar# S#ndrome

Superfi*ial /rosion

,uptured "i(rous Cap

:amm &an*et 3=8:1=33<2001

Presentation Workin !"

%s*'emi* -is*omfort A*ute Coronar# S#ndrome

-a4ies 8J :eart 83:3;1< 2000

#C$

3o S. /le4ation 3S./8%

S. /le4ation

%ioc&em. Marker 'inal !" 5nsta(le An6ina

Myocardial Infarction 378% 79 8%

6roponins for E4aluation and $anagement of ACS


Ad4anta6es

-isad4anta6es

'isk )tratificaton )ensH)pec I #4MD "etect 'ecent M* )election of '! "etect 'eperfusion

Low sens. early -J :h1 'epeat at 2-/9 h if neg. Limited ability to detect late minor reinfarction

,e*ommendation Useful as single test to efficiently Dx NSTE ! "linicians s#ould familiari$e t#emselves %it# Dx &cutoffs' in local la(

A*ute Coronar# S#ndrome 3o S. /le4ation S. /le4ation

5isk Stratification
Pur4oses .ria6e + .ransfer for .ertiar# Care ,esour*e Allo*ation Sele*tion of ,? Strate6#

Pro6nosis

Continuous Process Presentation: :istor#< ACS features< Ciomar$ers< P/? %n :ospital: /4ents< ,esponse to ,? -is*'ar6e: &@ "un*tion< Arr'#t'mias< %s*'emia

Symptoms suggestive o- %2S


5a4id 7ria e 89tain %iomarkers

Assess 12 lead /C0

$oal 6 10 min

3on Cardia* -ia6nosis

C'roni* Sta(le An6ina

Possi(le ACS ASA

-efinite ACS

As Per 1t'er -?

8edi*al ,?

Antit'rom(in Ceta Clo*$er ACS Proto*ol

S#mptoms Su66esti4e of ACS Possi(le ACS 3o S. ele4. G 12' &#ti* eli6i(le :ytic
(- 3 G 30 m)

-efinite ACS S. ele4. > 12' 3ot a reperfusion *andidate


Consider 5e4erfusion for Sym4toms

&#ti* ineli6i(le PCI;


(- C G 90)
Consider: 0P %%(+%%%a H stent

Medical 5"
(AC/%)

;Skilled 84er.)7eam 5a4idly A<aila9le

S#mptoms Su66esti4e of ACS


Possi(le ACS 3o S. ele4. -efinite ACS S. ele4. /4aluate for reperfusion

3on d? /C0 3e6. *ard. mar$ers 1(ser4e f+u studies 3e6 3e6 1utpt f+u Stress Pos Pos

S. .9 *'an6es 1n6oin6 pain Positi4e *ard mar$ers :emod#nami* a(nl.

-? of ACS *onfirmed Admit to 'ospital A*ute is*'emia pat'9a#

-e4elopment of at'eros*lerosis and 4ulnera(le pla)ue

2hronology o%theros.leroti. Jas.ular Disease *ro.ess


A*ute Coronar# S#ndrome Se*ondar# Pre4ention

%s*'emi* :eart -isease Cere(ro4as*ular -isease Perip'eral @as*ular -isease

8odified from &i((# P Cir* 10D:3;=<2001

/le*tro*ardio6rap'i* C'an6es

129

Causes of S6 segment Ele4ation


Acute m#ocardial infarction Benign earl# repolariDation :eft "undle "ranc! "loc8 :eft 4entricular !#pertrop!# Ientricular aneurs#m Coronar# 4asospasm 5ericarditis Brugada S#ndrome Su"arac!noid !emorr!age
130

%nitial 8ana6ement in /1. /. +. ,. -. 1. 3.

%nitial e4aluation

it! ECG in C 1) min

*/ "# nasal prongsE %I accessE continual ECG Su"lingal N6G unless SB5<00 or ); <-0 or J100 Analgesia 7morp!ine or meperidine9 Aspirin 7+/- mg po c!e ed9 :ipid panelE electrol#tesE magnesiumE C%5s 6!rom"ol#sis or 5C% if S6 J1mI or :BBB 7door-needle < +0 min or door-"alloon < 00 min9

Thrombolyti.s
7e.hanism o- %.tion
(trepto)inase Proactivator Activator Plasmino'en tPA *eteplase Tenecteplase Plasmin

Activates plasmino'en that is bound to fibrin

Fibrin

Fibrin de'radation products

Thrombolyti.s
7e.hanism o- %.tion
(trepto)inase Proactivator Activator Plasmino'en tPA *eteplase Tenecteplase Plasmin

Activates plasmino'en that is bound to fibrin

Fibrin

Fibrin de'radation products

Thrombolyti.s

%bsolute 2ontraindi.ations

*re.autions

5re4ious !emorr!agic stro8e at an# timeP or ot!er stro8es it!in one #ear Kno n intracranial neoplasm Acti4e internal "leeding Suspected aortic dissection

Se4ere uncontrolled )6N 7B5J120&100mm)g9 Current use of anticoagulants in t!erapeutic dose 7%N; /-+9 ;ecent trauma 7 it!in /-, ee8s9E including !ead trauma or traumatic or prolonged C5; or ma?or surger#7<+ ee8s9 Noncompressi"le 4ascular punctures ;ecent internal "leeding 7 it!in /-, ee8s9 Acti4e 5'< )&* c!ronic se4ere )6N

Thrombolyti.s

7onitoring *arameters

EKG B5 Sites of "leeding CBC 7)&)E platelets9

5i4otal 6!rom"ol#tic Clinical 6rials

+,((,-.
/.0123

+,((,-2
/.0063

A((E7T-2
/.0003

A((E7T-4
/266.3

,(,(-2
/.0113

+U(T#-,
/.0043

+U(T#-,,,
/.0053

+U(T#-$
/266.3

136

Ad4antages of >i"rinol#tic 6!erap#


$ore uni4ersal access S!orter time to treatment Greater clinical trial e4idence ofK

reduction in infarct siDe impro4ement of :I function

;esults less dependent on p!#sician eCperience :o er s#stem costs


137

Comparing outcomes

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