Curriculum Vitae

. Prof dr Bambanq Irawan FIHA FAsCC FInaSIM

• Internist [ PB PAPDI ] 1981

• Internist Cardiovascular Consultant [ PB PAPDI ] 1996

• Cardiologist and FIHA [ PP PERKI ] 2004

• Cardiologist Consultant [ PP PERKI ] 2005

• Profesor in Cardiology [ DIRJEN DIKTI ] 2006

• FAsCC [ Asean Society of Cardiology ] 2008

• FinaSIM [ PB PAPDI ] 2009
Simple Guideline for Acute Coronary
Syndrome (ACS)

Bambang Irawan SpPD[K], SpJP[K], FIHA,

FInaSIM, FAsCC
Divisi Cardiology Departement of Cardiology
Faculty of Medicine Gadjah Mada University
Coronary Heart Disease
 Ischemic heart disease :
epidemiology
• Annual incidence of angina: 213/100.000
population > 30 years old
• Ischemic heart disease (IHD) is the main cause
of death in Europe and USA
• Cardiovascular mortality in patients with chronic
stable angina: 1.3-10 %/year
• Chronic stable angina is the initial symptom of
IHD

Murray CJL.,ed,Lopez AD. The Global Burden of Disease: a Comprehensive Assessment of Mortality and Disability from
disease, Injurues and Risk Farctors in 1990 and projected to 2020.Cambridge, Mass:Harvard University Press;1996
Supply-Demand Mismatch

O xygen Supply O xygen Dem and

- Blood Flow - Heart rate
-O2 Carrying -Contractility
Capacity -W all stress
 Hb Level O2 Saturation
Exercise O2 Content
Heart rate
Afterload Collaterals
wall Coronary blood flow
stress O2 VS O2
Demand Supply Vasoconstriction
Heart size
Spasm
Contractility

Ischemic Oxygen Balance

 CLINICAL CLASSIFICATION OF
CHEST PAIN
Typical angina (definite)
• Substernal chest discomfort with a characteristic quality
and duration that is
• provoked by exertion or emotional stress and
• relieved by rest or nitroglycerin

Atypical angina (probable)

meets 2 of the above characteristics

Noncardiac chest pain

meets <=1 of the typical angina characteristics

Diamond GA. J Am Coll Cardiol 1983;1:574

 CCS Classification

• I : Angina occurring with strenous but not

ordinary physical activity
• II : Slight limitation of ordinary physical activity
• III : Marked limitation of ordinary physical
activity
• IV : Inability to carry on any physical activity
without discomfort, symptoms may be
present at rest.
 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

kerja

Elevasi ST ST/T- Normal atau

ECG menetap abnormalities Tdk dpt ditentukan ECG
3
Bio-
chemistry Troponin (+) Troponin
2 kali negatif
Stratifikasi
Risiko tinggi Risiko rendah
risiko

Diagnosis STEMI NSTEMI Angina tidak stabil

Pengobatan Reperfusi Invasive Non-Invasive

 Karakteristik Angina pd ACS
• Terlokalisir terutama (tapi tidak selalu) di
daerah prekordium
• Menyebar ke lengan, leher, punggung, atau
epigastrium
• Tidak berubah dengan posisi atau pergerakan
• Sering terasa seperti menekan, “constricting”
atau “crushing”
• Episode > 20 menit
• Diikuti sesak, pusing, mual, atau berkeringat
 Possible presentation of ACS

• Angina at rest, with pain episodes lasting >

20 min
• New onset ( within < 2 months ) exertional
angina of at least CCSC III
• Recent increase ( < 2 months ) in anginal
severity to at least CCSC III
• Angina post MCI
 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

kerja

Elevasi ST ST/T- Normal atau

ECG menetap abnormalities Tdk dpt ditentukan ECG
3
Bio-
chemistry Troponin (+) Troponin
2 kali negatif
Stratifikasi
Risiko tinggi Risiko rendah
risiko

Diagnosis STEMI NSTEMI Angina tidak stabil

Pengobatan Reperfusi Invasive Non-Invasive

 CHARACTER
OF
ANGINAL PAIN

• Localized usually at precordium

• Radiate to arm, neck, shoulder, back or
epicardium
• Feels like being pressed by heavy object, or
constricting or crushing.
• Episode > 20 min
• Concomitant systemic symptoms: dyspnea,
dizziness, nausea, diaphoresis
The Grip of Angina
 Atherosclerosis Timeline
Foam Fatty Intermediate Fibrous Complicated
Cells Streak Lesion Atheroma Plaque Lesion/Rupture

Endothelial Dysfunction
From first decade From third decade From fourth decade
Smooth muscle Thrombosis,
Growth mainly by lipid accumulation and collagen hematoma

Stary HC, et al. Circulation. 1995;92:1355-74. Artery wall often gets

larger with increasing plaque-Glagov NEJM 1987
 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

kerja

Elevasi ST ST/T- Normal atau

ECG menetap abnormalities Tdk dpt ditentukan ECG
3
Bio-
chemistry Troponin (+) Troponin
2 kali negatif
Stratifikasi
Risiko tinggi Risiko rendah
risiko

Diagnosis STEMI NSTEMI Angina tidak stabil

Pengobatan Reperfusi Invasive Non-Invasive

 3 ELEKTROKARDIOGRAM
EKG 12 Sandapan Pertama

TENTUKAN:
•Irama
•Elevasi SEGMENT ST ?
•Depresi SEGMENT ST ?
•LEFT BUNDLE BRANCH BLOCK (BARU)?
•T inverted ?
•Gelombang Q ?
•NON DIAGNOSTIK atau EKG normal
 .
• .
Inferior Wall MI
Anterior Wall MI
New LBBB
T inverted
 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

kerja

Elevasi ST ST/T- Normal atau

ECG menetap abnormalities Tdk dpt ditentukan ECG
3
Bio-
chemistry Troponin (+) Troponin
2 kali negatif
Stratifikasi
Risiko tinggi Risiko rendah
risiko

Diagnosis STEMI NSTEMI Angina tidak stabil

Pengobatan Reperfusi Invasive Non-Invasive

4
SPEKTRUM KLINIS SKA
 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

kerja

Elevasi ST ST/T- Normal atau

ECG menetap abnormalities Tdk dpt ditentukan ECG
3
Bio-
chemistry Troponin (+) Troponin
2 kali negatif
Stratifikasi
Risiko tinggi Risiko rendah
risiko

Diagnosis STEMI NSTEMI Angina tidak stabil

Pengobatan Reperfusi Invasive Non-Invasive

5
TIMI Risk Score UA / NSTEMI

HISTORICAL POINTS RISK OF CARDIAC EVENTS (%)

Age ≥ 65 1 BY 14 DAYS IN TIMI 11B*

≥ 3 CAD risk factors RISK DEATH DEATH, MI OR

(FHx, HTN, ↑ chol, DM, active smoker) 1 SCORE OR MI URGENT REVASC

Known CAD (stenosis ≥ 50%) 1 0/1 3 5

ASA use in past 7 days 1 2 3 8
PRESENTATION 3 5 13
Recent (≤ 24H) severe angina 1 4 7 20
↑ cardiac markers 1 5 12 26
ST deviation ≥ 0.5 mm 1
6/7 19 41
RISK SCORE = Total Points (0 - 7)
*Entry criteria:UA or NSTEMI defined as ischemic pain
Low = 0-2 points, Medium = 3-4 points
at rest within past 24H, with evidence of CAD (ST segment
High = 5-7 points deviation or +marker)
 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

kerja

Elevasi ST ST/T- Normal atau

ECG menetap abnormalities Tdk dpt ditentukan ECG
3
Bio-
chemistry Troponin (+) Troponin
2 kali negatif
Stratifikasi
Risiko tinggi Risiko rendah
risiko

Diagnosis STEMI NSTEMI Angina tidak stabil

Pengobatan Reperfusi Invasive Non-Invasive

 Elevation of oxygen supply

Reduction of the extravasal Prolongation of the Dissolution or Prevention

coronary resistance diastolic interval Of Intravasal obstruction
Nitro vasodilatators B Blockers Inhibitor of pletelet
ACE-I CCBs Aggregation
In case of HF Thrombvolytic agents

Providing relief for the ischemic heart

Nitro CCBs CCBs

ACE-I B Blockers
compounds

Reduction of Reduction of Reduction of Reduction of

Preload afterload contractility Heart rate

Reduction of the oxygen demand

 Treatment Delayed is Treatment Denied

Symptom Call to PreHospital ER Cath Lab

Recognition Medical System

Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy

Immediate Assessment in ER
• Vital signs, including blood pressure
• Oxygen saturation
• IV access
• 12-leads ECG < 10 minutes
• Brief, targeted history and physical exam (to
identify reperfusion candidates)
• Fibrinolytic check list; check contraindications
• Obtain initial cardiac markers
Immediate Assessment in ER
• Portable Chest X-ray < 30 min
• Assess for the following :
-Heart rate > 100 bpm and SBP < 100 mmHg
-Pulmonary edema/rales or
-Signs of shock
• If any of these conditions is present,
consider triage to a facility capable of
cardiac catheterization and
revascularization
TERAPI PADA SINDROMA KORONER AKUT
PERAWATAN DI RUMAH SAKIT
1. Antiplatelet (Aspirin 160 mg)
2. Pain killer (morfin) M
3. Suplemen O2
4. Terapi anti iskemia O
Nitrat N
5. Antiplatelet dan antikoagulan
Clopidogrel 300 mg, Ticlopidine A
Heparin atau Low Molecular Weight Heparin
Hirudin
Tranquilizer
5. a. STEMI : tentukan segera pilihan revaskularisasi
( Fibrinolitik Vs PCI)
b. Non STEMI : segera lakukan stratifikasi risiko
 PAIN KILLER

• Morfin:
2.5mg-5 mg IV perlahan
Hati –hati pada : inferior MCI,
asthma, bradikardia

• Pethidin : 12.5-25 mg IV pelan

 OKSIGEN
• Pemberian suplemen O2 diberikan pada pasien
dengan desaturasi O2 (SaO2 <90%)
• Suplemen O2 mungkin membatasi injury
miokard atau bahkan mengurangi elevasi ST
• Pemberian suplemen O2 rutin > 6 jam pertama
pd kasus tanpa komplikasi

ACC/AHA Guideline of STEMI 2004

 ANTI ISKEMIK
•NITRAT
•B BLOKER (jika tidak ada kontraindikasi)
•ANTAGONIS KALSIUM (UAP/NSTEMI)

VASODILATOR
•INHIBITOR ACE (EF < 40%, anterior MCI, HF)
•NITRAT IV (jika AHF)
ANTITROMBOTIK DAN
ANTIKOAGULAN

•Heparin ( Unfractionated Heparin)

•Low Molecular Weight Heparin
•Anti Xa
 DOSIS YANG DIREKOMENDASIKAN

• Initial I.V BOLUS 60 UI/Kg max 4000 UI

UFH
• Infus :12-15 UI/kg BB/jam max 1000
UI/jam
• Monitor APTT : 3, 6, 12, 24 jam setelah
mulai terapi
• Target APTT 50-70 msec (1,5 -2 x
kontrol)

LMWH
Enoxaparine • 1mg/kg, SC , bid (5 hari)
Fondaparinux • 2,5 cc , satu kali sehari (5 hari)
 REVASKULARISASI
PADA STEMI < 12 jam

Apa pilihan kita?

FIBRINOLITIK
VS
PCI
Fibrinolitik lebih dianjurkan jika:
( 3 Point)
1. Presentasi STEMI akut ≤ 3 jam
2. Jika presentasi STEMI > 3 jam namun
tindakan PCI tidak bisa dikerjakan atau
akan terlambat dikerjakan;
Waktu antara pasien tiba sampai dengan
inflasi balon >90 menit
3. Tidak ada kontraindikasi fibrinolitik

Catatan:
Fibrinolitik harus dikerjakan dalam waktu < 30 mnt
(Door to Needle time < 30 menit)
PCI primer lebih dianjurkan jika:
( 5 Point )
1. Presentasi ≥3 jam
2. Presentasi < 3 jam namun terdapat
kontraindikasi fibrinolitik
3. Tersedia fasilitas PCI dan waktu kontak
antara pasien tiba sampai dengan inflasi
balon <90 menit
4. STEMI akut dengan risiko tinggi ( gagal
jantung Killip ≥3 dan syok kardiogenikl)
5. Diagnosis STEMI masih diragukan
 STRATIFIKASI RISIKO
pada Non-STEMI / UAP
 MENENTUKAN STRATEGI
TATALAKSANA NON STEMI/UAP

Strategi Invasif
(angiografi akan dilakukan
dalam 48 jam)

VS

Strategi Konservatif
(angiografi tidak akan
dilakukan/direncanakan elektif)
 Complications of Acute MI

Extension / Ischemia Arrhythmia

Pericarditis

Expansion / Aneurysm Acute MI RV Infarct

Mechanical Heart Failure Mural Thrombus

 Komplikasi awal :
9Aritmia
9Disfungsi LV dan gagal jantung
9Ruptur ventrikel
9Regurgitasi mitral akut
9Gagal fungsi RV
9Syok kardiogenik
 Komplikasi lambat :
9Trombosis mural dan
9Emboli sistemik
9Aneurisma LV
9DVT
9Emboli paru
9Sindrome Dressler
How to reduce plaque formation
Intervention on risk fact
How to reduce the risk of plaque
rupture
 KESIMPULAN
1. Tatalaksana STEMI dimana tersedia fasilitas PCI
adalah PCI primer. Jika sarana PCI tidak tersedia
diberikan trombolitik sesuai indikasi dan kontraindikasi.
2. Tatalaksana NSTEMI meliputi strategi invasif dini dan
strategi konservatif sesuai stratifikasi risiko.
3. Klopidogrel direkomendasikan sebagai antiplatelet
(klas 1) untuk penanganan ACS baik STEMI maupun
UA/NSTEMII dan diberikan bersama ASA. Clopidogrel
diberikan tunggal jika terdapat kontraindikasi ASA
(ACC-AHA / ESC Guideline).
4. GPIIb-IIIa inhibitor diberikan pada pasien yang
menjalani PCI primer.
5. Fondaparinux dan Enoksaparin efektif pada SKA.