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ACUTE CORONARY SYNDROME

Dr. Zainal Safri, SpPD, SpJP

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PATHOFISIOLOGY OFACUTE CORONARY SYNDROME

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Endothelial

DysfunctionFoamCells

FattyStreak

IntermediateLesion Atheroma

FibrousPlaque

ComplicatedLesion/Rupture

Endothelial injurynitric oxideendothelin-1vasodilation

Lipidaccumulationadhesion molecules(ICAM, VCAM)

monocyte adhesion

macrophage LDLuptake

Inflammationcontinued macrophage/lipidaccumulation

leukocyte accumulationcytokines (IL-6, TNFa, IFNg

MMP's

CRP(hepatic)

oxidized LDL

homocysteinesmokingaginghyperglycemiahypertension

Pathophysiology of Atherosclerosis

35-45 yrs 45-55 yrs 55-65 yrs >65 yrs

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The Process

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nical Manifestations of Arterial Thrombo

UA/NSTEMI:Partially-occlusive thrombus

(primarily platelets)

Intra-plaque

thrombus (plateletdominated)

Plaque core

STEMI:occlusive thrombus (platelets,

red blood cells, and fibrin)

Intra-plaquethrombus (platelet

dominated)

Plaque core

SUDDEN DEATH

Adapted from Davies MJ Circulation1990

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Non ST Elevation MI

90% of acute MIs are caused by thrombus formation from rupture of unstable plaques

Ruptured Plaque

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Occlusive Thrombus

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ANGINA PEKTORIS

INFARK MIOKARD

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Stable Plaque Unstable Plaque Disrupted Plaque

Braunwald E et al. J Am Coll Cardiol2000;36:9701062.

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Stable versus Unstable

Plaque

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Mortalitas dan morbiditas tinggi , 40 %kematian terjadi sebelum sampai di rumah sakit( HARUS SEGERA DIRUJUK!!)

Setidaknya 250.000 kematian sehubunganinfark miokard terjadi dalam 1 jam setelahonset gejala dan sebelum terapi dimulai (USA)

DalamSATUtahun hampirsetengah kematianterjadi pada4 minggu pertamasetelahdiagnosa.

Mengapa SKA harus segeraditangani?

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Risk Factors Aterosklerosis

faktor genetik/riwayat keluargakandung

merokok dislipidemia hipertensi diabetes

obesitas usia Dll.*Pernah infark miokard dan/atau stroke

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DIAGNOSISACUTE CORONARY SYNDROME

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Angina:

Gejala angina dapat dibedakan darinyeri non jantung atau nyerikardiogenik lain, berdasarkananamnesis,

dan k/p ditunjang pemeriksaan fisik

EKG,dan laboratorium.

Berkaitan dengan kejadian iskemiapada otot jantung

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KELUHAN UTAMA SINDROM KORONER AKUT

Sakit dada atau nyeri hulu hati yang berat, asalnya non-

traumatik, dengan ciri-ciri tipikal iskemia miokard atauinfark:

Dada bgn tengah/substernal rasa tertekan atau sakitseperti diremas

Rasa sesak, berat/tertimpa beban , mencengkeram,terbakar,sakitsakit perut yg tdk dpt dijelaskan, sendawa, nyeri huluhatiPenjalaran ke leher, rahang, bahu, punggung atau 1

atau ke 2 lenganDisertai sesakDisertai mual dan/atau muntahDisertaiberkeringat

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Keluhan :SAKIT DADA/ANGINA

PECTORIS

Sifat & kualitas

LokasiPenjalaranLamaKeluhan dan Gejala penyerta

Anamesis harus terarah

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Angina Pectoris Stabil

ANGINA STABIL, ditandai nyeri dada atau rasa tidakenak sewaktu adanya beban (aktivitas, beban

mental) dimana kebutuhan miokardium tidak dapatdipenuhi dengan suplai yang cukup.

Angina Stabil dapat diprediksi dan dapat hilang atauberkurang dengan istirahat dan nitrogliserin.

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Dimana Rasa Nyeri Dirasakan??

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3 Kemungkinan penampilan: Nyeri/angina wkt istirahat ( biasanya terus

> 20 minutes)

Angina baru-New Onset (

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*PENILAIAN AWAL1.ANAMNESIS ( yang terarah) Nyeri dada ariwayat nyeri dada

angina pectoris Faktor risiko Penyakti penyerta lain Obat-obat

2.TANDA VITAL & Pemeriksaan FisikTerfokus

3. ELEKTROCARDIOGRAM : 12 sandapan

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ELECTROCARDIOGRAM

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Acute anteroseptal myocardial infarction.Hyperacute T-wave changes are noted

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Acute Anterior MI

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ST Depresi

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T Inverted

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RECCOMANDATION

Pada pasien yg dicurigai penyakit jantung iskemik akut

1. Harus diperiksa Troponin T atau I waktu masuk dan ,bila normal,diulangi 6-12 jam lagi

2. Mioglobin dan/atau CKMB mass boleh diperiksa pada pasienkeluhan yang baru ( < 6 jam ) sebagai petanda dini infarkmiokard akut dan pada pasien dengan iskemia berulangsetelah 2 minggu infark untuk mendeteksi infark yg lebih

lanjut

Level of evidence : A

ESC/ EHJ 2002

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Creatinine Phosphokinase

Positif 4-12 jam

Iso forms CK-MB1 danCK-MB 2

CK-MB1/CK-MB 2

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Troponin T and I

Tropomyosin complex

MicroinfarctionPertama terdeteksi dlm 2-

4 jam

Nilai Prognostik

Cut-off pointTnT 0.01

ng/ml

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*INITIAL ASSESMENT1.ANAMNESIS/Targeted history

Chest pain / history of chest pain/angina pectoris

Risk factors Other disease ( concomitant disease )

Medications

2.VITAL SIGNS & Focused PHYSICALEXAMINATION

3. ELECTROCARDIOGRAM : 12 Leads

*BIOCHEMICAL MARKERS

*Chest X-Ray

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Penatalaksanaan ACS

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Presentation(Clinical, Initial ECG)

ST-Seg ElevationMyocardial Infarction Non-STSeg ElevationAcute Coronary Syndr

ST-Seg ElevationMCI

Non-ST-seg-Elevation MCI

UnstableAngina

Workingdiagnosis

Time

Evolution ofECG &

Biomarkers

Finaldiagnosis

National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006

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Recommendation for anti ischemic therapy

Class I1. Bed rest, continuous ECG monitoring ( C )2. NTG s.l. or spray followed by IV adm. ( C )3. Oxygen ( C)4. Morphine sulphate IV if symptoms not relieved by NTG (C)5. Beta blocker,if there is ongoing chest pain (( B)6. Calcium Channel blocker if BB if contraindicated (B)

7. ACE inhibitor when hypertension persists despite treatment with NTGand a BB in pts with LV systolic dysfunction or CHF and inPts with diabetes (B)

Class IIa1. Oral long acting CCB for recurrent ischemia in the absence of contra

indication and when BB and nitrates are fully used (C)2. An ACI for all post ACS patients ( level evidence B )3. IABP for severe ischemia that is continuing or recurs frequently

despite intensive medical Tx or for hemodynamically instabibilityin pts before or after coronary angiography

ACC Task Force 2002

P th t Th b i

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Pathway to Thrombosis

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Platelet Activation Pathways

Platelet Aggregation

Fibrinogen

Fibrinogen Binding Site

Thrombin

Platelet

Herbert. Exp Opin Invest Drugs 1994;3:449-455.

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Aspirin

Benefits: decrease 50% reinfarction @30dys; two-year mortality 20%reduction

Doses 81-325 mg P.O. Trials: ISIS (88), Antiplatelet Trialist

Group (94), HART (90)

Aspirin kunyah 160-325 mg segera diberikanmeskipun belum ada hasil EKG

(non coated/slow released)

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Clopidogrel

Diberikan pada ACS loading 300mg ( 4 tablet) class 1A, Trials:

CURE

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Nitrat

Vasodilator

Mengurangi konsumsi Oksigen danmenurunkan jumlah episode iskemik.

Digunakan secara luas

Pemberian per IV

1mg /jam

Disesuaikan dengan gejala klinis dan EKGNitrate sublingual

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Morfin /Beta-blocker/CCB/ Acei

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Coagulation Cascade

XIIa

XIa

IXa

Intrinsic Pathway

(surface contact)

Xa

Extrinsic Pathway

(tissue factor)

VIIa

Thrombin(IIa)

Thrombin-FibrinClot

aPTT

PT

Heparin / LMWH(AT-III dependent)

Hirudin/Hirulog(direct antithrombin)

Courtesy of VTI

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HEPARIN:Mechanism of

Action Both UH and LMWH exert their

anticoagulation activity by catalyzing

antithrombin (AT or AT III) catalyzed AT is accelerated in its

inactivation of the coagulationenzymes thrombin (factor IIa) andfactor Xa.

prolongs aPTT

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DOSAGE UNFRACTIONATED

HEPARIN I.V BOLUS 60 UI/Kg max 4000 UI

Drip/infusion : 12 UI/hour first 24-48hrs

max 1000 UI/hour

= 12.000 UI/12 hours

Monitor APTT : 3, 6, 12, 24 hours after

start of treatment Target APTT 50-70 msec (1 1/2-2X

kontrol )

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Low Molecular Weight Heparin

Dissociate bleeding/ anti-thrombotic

Smaller/ fractionated

SC injections/ 90% bio-available/predictable

Anti-Xa: Anti-thrombin 2-4:1

FDA approved enoxaparin/ dalteparinfor ACS

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Advantages of LMWH over UH

Less inhibition of platelet function

potentially less bleeding risk, but not

shown in clinical use Lower incidence of thrombocytopenia

and thrombosis (HIT syndrome)

less interaction with platelet factor 4

fewer heparin-dependent IgGantibodies

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TEHNIK INJEKSI LOVENOX SUBKUTAN

ACC/AHA 2002 G id li U d t

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4/9/2012

Definite ACS with continuingischemia or other high-risk

features or planned PCI

Aspirin

+IV heparin/SC LMWH

+IV GP IIb/IIIa antagonist

Possible ACS

Aspirin

Likely/Definite ACS

Aspirin

+SC LMWHor

IV heparin

ACC/AHA 2002 Guidelines Updatefor UA and NSTEMI1

+Clopidogrel + Clopidogrel

*During hospital careClopidogrel should be administered to hospitalized patients who are unable to take ASAbecause of hypersensitivity or major GI intoleranceClass IIa: enoxaparin preferred over unfractionated heparin, unless CABG is planned within 24 hours

Class I Recommendations for Antithrombotic Therapy*

1. Braunwald E et al.American College of Cardiology (ACC) and the American Heart Association(AHA) Guidelines, USA: ACC/AHA; 2002.

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T t t D l d i T t t D i d

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Nurses Mini Course

SymptomRecognition Call toMedical System ED

Cath LabPreHospital

Delay in Initiation of Reperfusion TherapyIncreasing Loss of Myocytes

Treatment Delayed is Treatment Denied

/ d k

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FIBRINOLITIK / TROMBOLISIK : Indikasi

Sakit dada khas IMA 12 jam

EKG : 1 mm elevasi seg ST pada 2 sandapan yg

bersebelahan

2mm elevasi seg ST pada 2 sandapan

prekordial

Bundle branch blockyg baru

Syok kardiogenik pd IMA ( bila kateterisasi dan

revaskularisasi tdk dapat dilakukan )

Trombolisis door to needle time < 30 menit !!PCI pada IMA lebih unggul bila dpt dilakukan

dlm 90 30 menit

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FIBRINOLITIK/TROMBOLISIS: ContraIndication

Previous hemorrhagic stroke at any time

Other strokes or cerebrovascular eventsin the preceeding 1 yr

Known intracranial neoplasm

Active internal bleeding is present ( doesnot include menses )

Aortic dissection is suspected

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FIBRINOLITIK

Streptokinase (SK)

Actylase (tPA)Reteplase (r-PA)

Tenecteplase (TNK-tPA)

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CARA PEMBERIANFIBRINOLITIK

Streptokinase ( Streptase )

1.5 million Unit in 100 ml D5W or 0.9%

saline over 30-60 minutewithout heparin : Inferior MCI

with heparin : anterior MCI

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Streptokinase (SK, Streptase)

Manfaat: untuk semua lokasi STEMI,usia

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Contoh instruksi dokter waktu perawatan ACS

Rawat tirah baring NPO/Puasa 8 jam D5W as net Obat-obat:

1.Aspirin dst

2.Nitrat dst3.Beta blocker/CCB4.Heparin dst5.Diazepam dst

6.Laksans dst ECG diulang 12 jam Ro Foto torak Lab : CKMB, Troponin

Rutin : panel lipid, GD, panel renal ,electrolyte

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Operasi pintas koroner ( CABG )

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