SKA [Autosaved]

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SINDROMA KORONER AKUT

SMF JANTUNG DAN PEMBULUH DARAH

RSI SITI RAHMAH PADANG

Indry Putri Festari


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JANTUNG SEBAGAI POMPA JANTUNG SEBAGAI POMPA

Kanan K


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PenyakitKardiovaskuler :Masalah Yang BerakibatFatal

C VC V

Kanker

Peny.Infeksi &

parasit

Lain-lain

Kecelakaan

Peny.RespirasiNon infeksi

Infeksi Respirasi

Kondisi Ibu Hamil dan

Persalinan&

defisiensi

nutrisi

ur!ey Kese"atan Indonesia #$$%

H' orld Healt" Report( #$$%

Penyebab kematian

nomor I di dunia danIndonesia

30%30%


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NormalNormal

Garis lemak Garis lemak TumpukanTumpukan

lemak lemak

PenyempitanPenyempitanPlak pecahPlak pecah

Dan tersumbatDan tersumbat

MCIMCI

STRK!STRK!

Critical "e#Critical "e#

IschemiaIschemiaGe$ala tersembunyiGe$ala tersembunyi

M%TIM%TI

Menin#kat sesuai umurMenin#kat sesuai umur

Sakit dadaSakit dada

&%P&%P

Proses penyempitan pembuluh darah(Aterosklerosis)


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AWASSERANGAN JANTUNG !!!


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SAKIT DADA


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1. Lifestyle

DietSmoking

Obesity Physical

inactivity

2. ↑ Blood Pressure

3. Plasma lipids

↑LDL-

↑↑ !"

↑↓ #DL-↑$ther Lipid %actors &

'poliproprotein B

Lipoprotein (a)

3. Dia*etes+ ,nsulin esistance

. /merging isk %actors &

- ↑ Plasma #omocysteine (t#cy)

-- !hrom*ogenic %actors

-- ↑ plasma 0*rinogen

-- Plasminogen 'ctivator ,nhi*itor (P',-

-- arkers of ,nammation

. "enetics

%amily history

Faktor Risiko


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Gangguan metabolisme

Faktor risikoFaktor risiko Batas NilaiBatas Nilai

4egemukan4egemukan( Lingkaran Perut )( Lingkaran Perut )

LakiLaki

5anita5anita

6172 cm (67 in)6172 cm (67 in)

688 cm (63 in)688 cm (63 in) !rigliserida !rigliserida ≥≥17 mg+dL17 mg+dL

#DL-#DL-

LakiLaki

5anita5anita

97 mg+dL97 mg+dL

97 mg+dL97 mg+dL !ekanan Darah !ekanan Darah ≥≥137+137+≥≥8 mm #g8 mm #g

"ula Puasa"ula Puasa ≥≥117 mg+dL117 mg+dL JAMA. 2771:28&28;-2


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PREVENTIVE

REVENTIVE

M%T

CRP


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FAKTOR RISIKO

S,>D$' 4$$>/ '4?!


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Acute Coronary Syndrome

• The spectrum of clinical conditions ranging from:

unstable angina pectoris

Non ST elevasi (Non-STEMI)

ST elevasi myocard infarct (STEMI)

• Characterized by the common pathophysiology of adisrupted atheroslerotic plaque


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Acute Coronary Syndrome

,schemic Discomfort?nsta*le Symptoms

>o S!-segmentelevation S!-segmentelevation

Unstable Non-Q Q-Wave

angina AMI AMI

/"

'cute

eperfusion

#istoryPhysical /@am


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Unstable Angina - Definition

• Angina at rest (> 20 minutes)

• new-onset (< 2 months) exertional angina (at least CCSCIII in severity)

•

recent (< 2 months) acceleration of angina (increase inseverity of at least one CCSC class to at least CCSC classIII)

• Angina Post MI


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Unstable Angina Likelihood of CAD

• Previous history of CAD

• Presence of risk factors

• Older age

• ST-T wave ischemic ECG changes


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Unstable Angina precipitating factors

• Inappropriate tachycardia

anemia, fever, hypoxia, tachyarrhythmias,thyrotoxicosis

• High afterload

aortic valve stenosis, LVH

• High preload

high cardiac output, chamber dilatation

• Inotropic state

sympathomimetic drugs, cocaine intoxication


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Unstable Angina prognosticindicators

• Presence of ST-T-wave changes with pain

• Hemodynamic deterioration

pulmonary edema, new mitral regurgitation,

3rd heart sound, hypotension

• Other predictors

left ventricular dysfunction, extensive CAD, age,comorbid conditions (diabetes mellitus, obstructive

pulmonary disease, renal failure, malignancy)


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Unstable Angina pathogenesis

•Plaque disruption

• Acute thrombosis

• Vasoconstriction


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NoralNoralFattyFatty

Streak Streak FibrosFibrosPla"ePla"e

O##lsi$eO##lsi$eAt%eros#leroti#At%eros#leroti#

Pla"ePla"e

Pla"ePla"eR&tre'R&tre'Fissre (Fissre (

T%robosisT%robosis

MIMI

StrokeStroke

Criti#al )e*Criti#al )e*

Is#%eiaIs#%eiaCli+i#ally Sile+tCli+i#ally Sile+t

Coro+aryCoro+ary

,eat%,eat%

I+#reasi+* A*eI+#reasi+* A*e

E-ort A+*i+aE-ort A+*i+a

Cla.i#atio+Cla.i#atio+

U+stableU+stable

A+*i+aA+*i+a

Atherosclerosis: A Progressive Process

ourtesy of P "anA.


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Non-Q-Wave MI clues to diagnosis

• Prolonged chest pain

• Associated symptoms from the autonomic nervous system

nausea, vomiting, diaphoresis• Persistent ST-segment depression after resolution of chestpain


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Unstable Angina Risk Stratification

Low Risk

•new-onset exertional angina

•

minor chest pain during exercise•pain relieved promptly by nitroglycerine

Management

•

can be managed safely as an outpatient (assumingclose follow-up and rapid investigation)


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Intermediate Risk

•prolonged chest pain

•diagnosis of rule-out MI

Management

•observe in the ER or Chest Pain Unit

•monitor clinical status and ECG

•

obtain cardiac enzymes (troponin T or I) every 8 to 12hours


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High Risk

• recurrent chest pain

•

ST-segment change• hemodynamic compromise

• elevation in cardiac enzymes

Management

• monitor in the Coronary Care Unit


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Risk Stratification by ECG

The risk of death or MI at 30 days is strongly related to theECG at the time of chest pain.

• ST depression 10%

• T-wave inversion 5%

• No ECG changes1-2%


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Unstable Angina Therapeutic Goals

Therapeutic Goals

• Reduce myocardial ischemia

•

Control of symptoms• Prevention of MI and death

Medical Management

• Anti-ischemic therapy

•

Anti-thrombotic therapy


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Unstable Angina Medical Therapy

• Anti-ischemic therapy nitrates, beta blockers, calcium antagonists

• Anti-thrombotic therapy Anti-platelet therapy

aspirin, ticlopidine, clopidogrel,GP IIb/IIIa inhibitors

Anti-coagulant therapy

heparin, low molecular weight heparin (LMWH),

warfarin, hirudin, hirulog


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Unstable Angina Anti-ischemicTherapy

• restrict activities

• morphine

•

oxygen• nitroglycerine

pain relief, prevent silent ischemia, control hypertension,improve ventricular dysfunction

nitrate free period recommended after the first 24-48 hours


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Unstable Angina Anti-ischemicTherapy

• beta-blockers

lowering angina threshold

prevent ischemia and death after MI

particularly useful during high sympathetic tone

• calcium antagonists

particularly the rate-limiting agents

nifedipine is not recommended without concomitant ß-

blockade


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Unstable Angina Anti-thromboticTherapy

• Thrombolytics are not indicated

• “lytic agents may stimulate the thrombogenic process andresult in paradoxical aggravation of ischemia and myocardialinfarction”

Cir#latio+ /0012 304/5156/557


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Platelets in Acute CoronarySyndromes

•Platelets play a key role in ACS

•Sources of platelet activation (triggers) thromboxane A2 (TXA2)

ADP

epinephrine

collagen

thrombin


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Unstable Angina Anti-plateletTherapy

• aspirin is the “gold standard”

irreversible inhibition of the cyclooxygenase pathway inplatelets, blocking formation of thromboxane A2, andplatelet aggregation

in AMI, ASA reduced the risk of death by 20-25%in UA, ASA reduced the risk of fatal or nonfatal MI by 71%during the acute phase, 60% at 3 months, and 52% at 2years

bolus dose of 160-325 mg, followed by maintenance dose of

80-160 mg/d


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Unstable Angina Anti-plateletTherapy

•Thienopyridines ticlopidine(Ticlid; Hoffmann-La Roche)

clopidogrel(Plavix; Bristol-Myers Squibb)

block platelet aggregation induced by ADP andthe transformation of GP IIb/IIIa into its highaffinity state

GPIIb/IIIR


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GP IIb/IIIa ReceptorFinal Pathway to Platelet Aggregation•Platelet activation and aggregation are early eventsin the development of coronary thrombosis

•GP IIb/IIIa receptors on activated platelets undergo

a conformational change allowing recognition andbinding of fibrinogen

•Fibrinogen “acts like glue”, bridging GP IIb/IIIareceptors on adjacent platelets, leading to platelet

aggregation


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Unstable Angina Anti-platelet Therapy

• GP IIb/IIIa inhibitors

abciximab (monoclonal antibody)

eptifibatide (peptidic inhibitor)

lamifiban and tirofiban (non-peptides)

direct occupancy of the GP IIb/IIIa receptor by amonoclonal antibody or by synthetic compoundsmimicking the RGD sequence for fibrinogen binding prevents platelet aggregation


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Unstable Angina Anti-coagulant Therapy

• Heparinrecommendation is based on documented efficacy inmany trials of moderate size

meta-analyses(1,2)of six trials showed a 33% riskreduction in MI and death, but with a two foldincrease in major bleeding

titrate PTT to 2x the upper limits of normal

/8 Cir#latio+ /00123043/633

98 JAMA /00729:743//63/5


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Unstable Angina Anti-coagulant Therapy

• Low-molecular-weight heparinadvantages over heparin:

better bio-availability

higher ratio (3:1) of anti-Xa to anti-IIa activitylonger anti-Xa activity, avoid rebound

induces less platelet activation

ease of use (subcutaneous - qd or bid)

no need for monitoring


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NEW ACLS - ACS ALGORITHM ACC / AHAUpdate 2007

M o + a; C o

ACC'A


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Diagnosa penatalaksanaan dan persiapan+pre hospital oleh /S &

- onitor support 'B. Persiapan untuk P dan de0*rilasi

- Berikan oksigen aspirin nitroglycerin dan morphine *ila di*utuhkan

- Cika tersedia periksa /" 12 lead ika terdapat S!-/levasi &

E #u*ungi rumah sakit yang dituu dengan DF pasien

E ulai mem*uat 0*rinolytic checklist

- S yang dituu harus menyaiapkan Go*iliAe #ospital esourcesH untuk

merespon pasien S!/,

Diagnosa cepat oleh /mergency Departemen Penatalaksanaan umum cepat oleh/.D(917min)

- heck vital signs evaluasi saturasi $2 - Morphin ,I ika nyeri tidak *erkurang dengan- Pasang ,I line nitroglycerin

- /" 12 lead - O2 L+mnt pertahankan saturasi $2 6


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S! /levasi atau LBBB *aru ataudiasumsikan *aru: dicurigai kuat

S!-/levasi , (S!/,)

S! depresi atau ! inverted:dicurigai kuat suatu ischemia

esiko tinggi unsta*le angina + >onS! /levation , ('?+>S!/,)

>ormal atau tidak ada peru*ahansegmen S! atau gelom*ang !

esiko rendah atau sedang untukunsta*le angina

ulai terapi tam*ahan sesuaiindikasi. Cangan menundareperfusi

-Clopidogrel-β-adrenergic reseptor *lockers-#eparin (?%# or L5#)

ulai terapi tam*ahan sesuai

indikasi

-Clopidogrel->itroglycerin-β-adrenergic reseptor *lockers-#eparin (?%# or L5#)-"lycoprotein ,,*+,,,a inhi*itor

Berlanut memenuhi kriteria

sedang atau tinggi (ta*el3)atau troponin positive

$nset geala 9 12 am$pname di ruangan dgn

Gmonitoring *edH !entukan status resiko

Pertim*angkan opname di /Dchest paint unit atau Gmonitored*edH di /DLanutkan dengan &Serial cardiac marker (termasuktroponin)?lang /" monitor segmen S!Pertim*angan stress test

Strategi reperfusi& !erapi ditetapkan *erdasarkankeadaan pasien dan centercriteriaenyadari tuuan terapi reperfusi&Door-to-*alloon ination (P,) M


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+tk UA ' NSTEMIRekoe+.asi +tk A+ti&latelet .a+ A+ti#oa*la+t /

)o> Risk ACS


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ESC Guidelines 2007

•ASA ( Klas 1 A )Direkomendasikan pada semua pasien NSTE-ACS bila tidak ada

kontra indikasi, dengan initial LD 160-325 (non enteric) dan dosipemeliharaan 75 – 100 mg untuk jangka panjang

•CLOPIDOGREL ( Klas 1A )

Untuk semua pasien ACS, SEGERA berikan Clopidogrel 300mg Ldilanjutkan dengan 75mg/ hari, Clopidogrel harus dilanjutkanhingga 12 bulan, kecuali ada resiko tinggi perdarahan.

Untuk pasien yang kontra indikasi terhadap ASA, Clopidogrel

harus digunakan sebagai penggantinya ( 1B )

GUIDELINE2007


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GUIDELINE 2007• AUSSIE ( Australia & New Zealand )Non STEMI

In Hospital ( Early Initiation ) Pengobtan awal segera harus dimulai dengan ASA dan Clopidogrel ( 300 mg LDand 75 mg/hari) dengan mempertrimbangkan:

Clopidogrel harus dihindari pada pasien yang akan menjalani emergency coronarybypass surgery

Jika memungkinkan, clopidogrel, harus dihentikan 5 hari sebelum coronary bypasssurgery.

Long-term management (Discharge Medication)

Semua pasien harus diberikan ASA 75 – 150 mg/hari kecuali kontra indikasi

Clopidogrel harus diberikan selama 12 months setelah diagnosa ACS, khususnyasetelah pemasangan stent, dengan lamanya therapy tergantung tipe stent dan

keadaan lokasi pemasangan Clopidogrel juga dapat diberikan sebagai alternative kontraindikasi thd ASA,atau sebagai tambahan ASA, pada pasien UA atau kejadian Kardiovaskularberulang

GUIDELINE2007


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GUIDELINE 2007• AUSSIE ( Australia & New Zealand )

STEMI

Semua pasien yang mendapatkan reperfusion therapy pada STEMI ( PCI atau Fibrinolysis ) har

diberikan ASA dan CLOPIDOGREL kecuali ada kontra indikasi.

-Fibrinolytic Therapy

Pada pasien dengan fibrinolytic therapy, Clopidogrel (300 mg LD ) harus ditambahkan pada ASA, kecukontraindikasi, Clopidogrel (75 mg/hari ) harus dilanjutkan paling tidak 1 bulan setelah fibronolyttherapy

KepatuhanpadaGuidelines

CRUSA,E


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Kepatuhan pada GuidelinesMenurunkan angka Mortality di Rumah Sakit

?S'D/ is a national uality improvement initiative of the Duke linical esearch ,nstitute. Partial fundingfor ?S'D/ is provided *y the Bristol-yers Sui**+Sano0 Pharmaceuticals Partnership.?S'D/ Data Q3 277;. umulative ?S'D/ data through Septem*er 2773.Duke linical esearch ,nstitute. 'vaila*le at& http&++KKK.crusadei.com. 'ccessed %e*ruary 13 277=.

I + 6 % o s & i t a

l M o r t a l i t y @ D A

I + 6 % o s & i t a l M o r t a l i t y @ D A

I+#rease. A.%ere+#e to Gi.eli+es ,e#reases

Mortality

I+#rease. A.%ere+#e to Gi.eli+es ,e#reases

Mortality

LEARNING FROM GUIDELINES


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/8 Clo&i.o*rel .i i+.ikasika+ &a.a &asie+ .e+*a+ UA NSTEMI .a+

STEMI .a+ .iberika+ bersaa ASA8 Clo&i.o*rel .iberika+ t+**a

ika ASA ko+trai+.ikasi8

98 Eek ya+* #e&at .a+ eberika+ &erli+.+*a+ ya+* lebi% besar

ika &eberia+ #lo&i.o*rel t%era&y .ilai .e+*a+ loa.i+* .ose

H==6*8 .osis

H8 Clo&i.o*rel .irekoe+.asika+ seba*ai a+ti&latelet Class / +tk

&e+a+*a+a+ ACS baik STEMI a&+ NON STEMI8 @ ACC6A


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STENTING ( CINCIN )

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