CURRICULUM VITAE

Name Dr Muhammad Syukri SpJP, (K) FIHA, FAPSIC, FSCAI

Telephon Mobile : +628126660998, E-mail : Musyukri@ yahoo.com

Education

: Graduation of General Practitioner Faculty of medicine Andalas University, Padang, 1992

: Graduation of Cardiologist Faculty of medicine University of Indonesia, Jakarta , 2003

Current Position

: Head of Division of Cath Laboratorium, Cardiac Center RS DR M Djamil

Padang, West Sumatera, Indonesia
Training

: Introduction of Interventional Cardiology, NUH, Singapore, 2006

: Fellowship Intervention Cardiology, RS harapan Kita, Jakarta, 2007
: Workshop Trans Radial Intervention, Bangkok, 2008
: Workshop Intervention Bifurcation, Malaysia, 2009
: Workshop Advance Interventional cardiology, Crossroad institute, Japan, 2010
: Fall Fellow SCAI, Las Vegas, Nevada USA 2011
: Myocardial Perfusion Scanning / SPECT, GVI Medical Devices, Twinsburg, OH, USA 2014
ORGANIZATION

: Former Chairman of Indonesian Heart Association, Branch of Padang, West Sumatera

: Member of Indonesian Medical Association
: Member of Indonesian Society of Intervention Cardiology
: Member of Fellow Asia Pacific Society Interventional Cardiology ( Asia Pacific )
: Member of Fellow Society for Cardiovascular Angiography and Intervensions ( USA )
PUSAT
JANTUNG

SINDROMA KORONER AKUT

Dr. MUHAMMAD SYUKRI, Sp JP

BAGIAN KARDIOLOGI DAN KEDOKTERAN VASKULAR

FK UNIVERSITAS ANDALAS
JANTUNG SEBAGAI POMPA

Kanan Kiri
 Capaian Pembelajaran
• Menjelaskan
– Epidemiologi
– Etiologi dan Faktor Risiko S
– Patofisiologi K
– Klasifikasi
– Gambaran Klinis
A
– Penatalaksaan
– Komplikasi dan Prognosis
 Penyakit Kardiovaskuler :
Masalah Yang Berakibat Fatal
Kondisi Ibu Hamil dan
Persalinan
Lain-lain &
defisiensi Peny.Infeksi &
nutrisi parasit

Kecelakaan

Kanker
Peny.Respirasi
Non infeksi 30%
Infeksi Respirasi

Penyebab kematian
Kardiovaskular nomor I di dunia dan
Indonesia

Survey Kesehatan Indonesia 2001

WHO World Health Report, 2001
 Faktor Risiko Penyakit Jantung Koroner
Tidak dapat dimodifikasi
1. Usia : Tua > Muda
2. Gender : Laki-laki > Perempuan
3. Riwayat Keluarga ( PJK )
4. Riwayat PJK
Dapat dimodifikasi !!!!!
1. Merokok
2. Hipertensi
3. Diabetes Mellitus
4. Diet : Tinggi Lemak Jenuh dan Kolesterol
5. Peningkatan Kadar Kolesterol Total dan LDL
6. Kadar Kolesterol HDL Rendah
7. Obesitas
8. Kurang Aktivitas Fisik
6
 Proses penyempitan/Penyumbatan pembuluh darah
(Atherothrombosis)
Plak pecah
Penyempitan Dan tersumbat
Garis lemak Tumpukan UAP
Normal lemak

MCI
MATI

STROKE

Gejala tersembunyi Sakit dada Critical Leg

Ischemia

Umur Meningkat sesuai umur

MCI = Serangan Jantung
Sindroma Koroner Akut

• Suatu Spektrum Klinis peny. Jantung Koroner :

– NON STEMI
• unstable angina
• non-Q wave MI
– STEMI
• Ditandai dengan adanya Plaque Ruptur
sebagai dasar Patofisiologi secara umum
• Terbentuk thrombus, Vasokonstriksi Koroner
5/98 MedSlides.com 8
Patofisiologi SKA
 Peran Platelets pada Proses
Atherothrombosis
1 •Adhesion

Platelets

2 •Activation
Plaque
rupture
Activated
platelets
3 •Aggregation
TxA2
ADP Fibrinogen
ASA, Clopidogrel

GP IIb/IIIa Inhibitors

Cannon, Braunwald, Heart Disease. 2001;1232-1263

Peran Platelets pada Proses
Atherothrombosis
 Chest pain

ST elevation ST depression ST segment N

ECG

Bio-chemistry Troponin rise / Troponin normal

fall

Diagnosis

STEMI NSTEMI UA
Adapted from Hamm CW et al. Eur Heart J 2011;32:2999 – 3054, Davies MJ. Heart 2000;83:361–366 12
Sindroma Koroner Akut
Ischemic Discomfort History
Unstable Symptoms Physical Exam

No ST-segment ST-segment
ECG
elevation (NTEMI) elevation ( STEMI )

Unstable Non-Q Q-Wave Acute

angina AMI AMI Reperfusion

5/98 MedSlides.com 13
 AWAS !!!!
SERANGAN JANTUNG !!!
SAKIT DADA
Unstable Angina - Definition

• angina at rest (> 20 minutes)

• new-onset (< 2 months) exertional angina (at least CCSC III
in severity)
• recent (< 2 months) acceleration of angina (increase in
severity of at least one CCSC class to at least CCSC class III)
Unstable Angina Likelihood of CAD

• Previous history of CAD

• presence of risk factors
• older age
• ST-T wave ischemic ECG changes
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
Unstable Angina prognostic indicators

• 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)
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 (assuming
close follow-up and rapid investigation)
Unstable Angina Risk Stratification

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
12 hours
Unstable Angina Risk Stratification

High Risk
• recurrent chest pain
• ST-segment change
• hemodynamic compromise
• elevation in cardiac enzymes
Management
• monitor in the Coronary Care Unit
Risk Stratification by ECG

The risk of death or MI at 30 days is strongly related to the

ECG at the time of chest pain.
• ST depression 10%
• T-wave inversion 5%
• No ECG changes 1-2%
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
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
Unstable Angina Anti-ischemic Therapy

• 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
Unstable Angina Anti-ischemic Therapy

• 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
Unstable Angina Anti-thrombotic Therapy

• Thrombolytics are not indicated

• “lytic agents may stimulate the thrombogenic process and
result in paradoxical aggravation of ischemia and myocardial
infarction”

Circulation 1994; 89:1545-1556

Platelets in Acute Coronary Syndromes

• Platelets play a key role in ACS

• Sources of platelet activation (triggers)
– thromboxane A2 (TXA2)
– ADP
– epinephrine
– collagen
– thrombin
Unstable Angina Anti-platelet Therapy

• aspirin is the “gold standard”

– irreversible inhibition of the cyclooxygenase pathway in
platelets, blocking formation of thromboxane A2, and
platelet 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 2
years
– bolus dose of 160-325 mg, followed by maintenance dose
of 80-160 mg/d
Unstable Angina Anti-platelet Therapy

• Thienopyridines
– ticlopidine (Ticlid; Hoffmann-La Roche)
– clopidogrel (Plavix; Bristol-Myers Squibb)

block platelet aggregation induced by ADP and

the transformation of GP IIb/IIIa into its high
affinity state
GP IIb/IIIa Receptor
Final Pathway to Platelet Aggregation

• Platelet activation and aggregation are early events in

the development of coronary thrombosis
• GP IIb/IIIa receptors on activated platelets undergo
a conformational change allowing recognition and
binding of fibrinogen
• Fibrinogen “acts like glue”, bridging GP IIb/IIIa
receptors on adjacent platelets, leading to platelet
aggregation
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 a

monoclonal antibody or by synthetic compounds
mimicking the RGD sequence for fibrinogen binding
prevents platelet aggregation
Unstable Angina
Anti-coagulant Therapy
• Heparin
– recommendation is based on documented efficacy in
many trials of moderate size
– meta-analyses (1,2) of six trials showed a 33% risk
reduction in MI and death, but with a two fold
increase in major bleeding
– titrate PTT to 2x the upper limits of normal

1. Circulation 1994;89:81-88
2. JAMA 1996;276:811-815
Unstable Angina
Anti-coagulant Therapy

• Low-molecular-weight heparin
advantages over heparin:
– better bio-availability
– higher ratio (3:1) of anti-Xa to anti-IIa activity
– longer anti-Xa activity, avoid rebound
– induces less platelet activation
– ease of use (subcutaneous - qd or bid)
– no need for monitoring
 N ST E M I
(Non ST Segment Elevation Mycardial Infarction)

Trombus menutup koroner secara komplit kurang dari 1

jam kemudian terjadi aliran darah
Predictor in hospital death
Thrombosis in an enemy but bleeding is not a friend
 ACUTE STEMI
ST Segment Elevation Mycardial Infarction

 Diagnosis
 Risk Stratification
 Acute Therapy
 Reperfusion
 Adjunctive
 Complications
 Pre-Discharge Management
 Diagnosis of Acute STEMI
History

• Classic symptoms: intense, oppressive chest

pressure radiating to left arm
• Other symptoms:
 chest heaviness, burning
 radiation to jaw, neck, shoulder, back, arms
 nausea, vomiting
 diaphoresis
 dyspnea
 lightheadedness
• Symptoms may be mild or subtle
 Diagnosis of Acute MI
Physical Examination

• Tachycardia or bradycardia
• Extrasystoles
• S3 or S4, mitral regurgitation murmur
• Lung rales
• Hypertension or hypotension
• Pallor, distress
 Diagnosis of Acute MI
Electrocardiogram

Defines location, extent, and prognosis of infarction

• ST elevation diagnostic of coronary occlusion
• Q-waves do NOT signify completed infarction
• ST depression or T inversion: unlikely total coronary
occlusion
• ST elevation in RV4 for RV infarction
• Observe up to 24 hrs for non-diagnostic ECG
• Differentiate from early repolarization in V1-2
 Diagnosis of Acute MI
Echocardiography

• Not diagnostic, but supportive

• Identify regional wall motion abnormalities
• Absence of contralateral wall hyperkinesia suggests
multivessel disease or IRA recanalization
• Assess LV function, prior infarcts
• More sensitive than ECG for RV infarction
 Diagnosis of Acute MI
Differential Diagnosis

Ischemic Heart Disease

• angina, aortic stenosis, hypertrophic CMP
Nonischemic Cardiovascular Disease
• pericarditis, aortic dissection
Gastrointestinal
• esophageal spasm, gastritis, PUD, pancreatitis,
cholecystitis
Pulmonary
• pulmonary embolism, pneumothorax, pleurisy
Management of Acute MI

 Diagnosis
 Risk Stratification
 Acute Therapy
 Reperfusion
 Adjunctive
 Complications
 Pre-Discharge Management
 Acute MI - Risk Stratification
ECG Classification - GUSTO I Outcome
Category Occlusion Site ECG 1-Year
Mortality
1. Prox LAD before septal  ST V1-6, I, aVL 25.6%
fasicular or BBB
2. Mid LAD before diagonal  ST V1-6, I, aVL 12.4%
3. Distal LAD beyond diagonal  ST V1-4 or 10.2%
Diagonal in diagonal  ST I, aVL, V5-6
4. Moderate-to- proximal RCA  ST II, III, aVF and 8.4%
large inferior or LCX V1, V3R, V4R or
(post, lat, RV) V5-6 or
R > S V1-2
5. Small inferior distal RCA or  ST II, III, aVF only 6.7%
LCX branch
 Acute MI - Risk Stratification
Ejection Fraction

50% Mortality (2-Year)

40%

30%

20%

10%

0
20 30 40 50 60 70
Ejection Fraction (%)

Gottlieb et al. Am J Cardiol 1992;69:977-984

 Acute MI - Risk Stratification
Hemodynamic Subgroups - Killip Class

GISSI-1 (%)
Killip Definition Incidence Control Lytic
Class Mortality Mortality
I No CHF 71 7.3 5.9
II S3 gallop or 23 19.9 16.1
basilar rales
III Pulmonary edema 4 39.0 33.0
(rales >1/2 up)
IV Cardiogenic shock 2 70.1 69.9
Management of Acute MI

 Diagnosis
 Risk Stratification
 Acute Therapy
 Reperfusion
 Adjunctive
 Complications
 Pre-Discharge Management
 PENANGANAN STEMI
PENANGANAN DI RUMAH
ACS DI RUMAH SAKIT
SAKIT

TUJUAN UTAMA

STRATEGI PENGOBATAN

45 % – 75 %
Pasien dilakukan penanganan secara NON STENT / Non PCI
 Myocardial Reperfusion
The Original Paradigm

Re-establish Infarct
Limit Infarct Size  Mortality
Vessel Patency
 STEMI Management
STEMI Diagnosis

Primary-PCI capable EMS or non primary-PCI

center capable center

Preferably PCI possible < 120 min?

< 60 min
Immediate transfer to
PCI center
Primary-PCI Yes No
Preferably ≤ 90 min
(≤ 60 min in early
Preferably
Rescue-PCI presenters)
≤ 30 min
Immediately Immediate transfer to
No PCI center
Succesful Immediate
fibrinolysis ? fibrinolysis ?
Yes
Preferably 3-24 h

Coronary angiography Steg G et al. Eur Heart J. 2012;33:2569-619

 Primary PCI
Treatment of
choice for Acute MI

Acute Myocardial Infark = Serangan Jantung

BALON ANGIOPLASTI ( PTCA )
STENTING ( CINCIN )
OPERASI BYPASS KORONER
Dasar THERAPY pada THROMBOSIS
Berdasarkan pada PATOFISIOLOGIS
PATHOGENESIS THERAPY

RISK FACTORS PREVENTION

- PLATELET ADHESION

ANTIPLATELET
-PLATELET AGGREGATION

-BLOOD COAGULATION ANTICOAGULANT

-THROMBOSIS THROMBOLYTIC
 Acute MI Management
Pharmacologic Therapy on Hospital Discharge

 Aspirin indefinitely (ticlopidine or clopidogrel for aspirin

allergy or intolerance)
 Beta blockers for at least 2-3 years
 ACE inhibitors for CHF, LVEF<40%, or large infarction
(even with preserved LVEF)
 Lipid lowering agents
 Coumadin for mural thrombus, extensive anterior
infarct, DVT, atrial fibrillation
 Thrombolysis in Acute MI
Relative Contraindications

 Uncontrolled HTN (BP > 180/110) on presentation

 History prior CVA beyond 1 yr
 Anticoagulant Rx with INR > 2-3; bleeding diathesis
 Recent trauma (within 2-4 wks)
 Noncompressible vascular punctures
 Recent internal bleeding (within 2-4 wks)
 Pregnancy
 Active peptic ulcer
 Prior exposure (5 day - 2 yr) for SK or APSAC
 Thrombolysis in Acute MI
Absolute Contraindications

 Previous hemorrhagic stroke

 CVA within previous yr

 Intracranial neoplasia or AVM

 Active internal bleeding (not menses)

 Suspected aortic dissection

 Thrombolytic: Placebo-Control
Meta-Analysis
Odds
Agent Trial Name Deaths/Patients Odds Ratio Reduction
Active Control (& 95% Cl) (± s.d.)

Streptokinase GISSI 495/4865 623/4878 23% ± 6

ISAM 50/842 61/868 16% ± 18
ISIS-2 471/5350 648/5360 30% ± 5

APSAC AIMS 32/502 61/502 50% ± 16

t-PA ASSET 182/2516 245/2495 28% ± 9

Overall: any thrombolytic 1230/14075 1623/14103 27% ± 3

Patients < 6 hours 8.7% 11.6%

0.0 0.5 1.0 1.5 2.0

Lytic better Lytic worse
 Thrombolysis for Acute MI
Time to Therapy and Mortality Reduction
Pooled Analysis of Randomized Trials
Absolute Mortality Reduction per 1000 Patients
40


30


20 


10


0
0 6 12 18 24
Time from Symptom Onset to Randomization (h)
Fibrinolytic Therapy Trialists. Lancet 1994;343:311.
 Aspirin in Acute MI
ISIS-2
35 Day Mortality (%)
20

15
13.2
10 10.7 10.4
8
5
4300 4295 4300 4292
0
Placebo ASA SK SK + ASA

ISIS-2 Collaborative Group, Lancet 1988;2:349.

 Aspirin in Acute MI
Recommendations

• Indicated in ALL patients with acute MI, except for

true aspirin allergy (not intolerance)

• Initiate orally with chewable compound, at least

160 mg stat
some data suggest first dose should be
650 mg to achieve full antiplatelet effect

• Continue 325 mg per day indefinitely

 Acute MI
Heparin

• Intravenous heparin recommended with t-PA

(intial bolus 5000 U, infusion 1000 U/hr, adjust for
weight < 50 kg)
• No clear data for benefit with streptokinase and
increased bleeding
• Discontinue after 24 hrs, except for:
 atrial fibrillation
 recurrent ischemia
 anteroapical MI for CVA prophylaxis
 ACE Inhibitors in Acute MI
Pooled Analysis of Randomized Trials

Study Agent N Mortality Odds Ratio & 95% CI

ISIS-4 Captopril 58,050 

During GISSI-3 Lisinopril 19,394 

MI
CONSEN II Enalaprilat 6,090 

SAVE Captopril 2,231 

Post
AIRE Ramipril 2,006 
MI
TRACE Trandolapril 1,749 

0 1 2
Rx Better Control Better
Hennekens et al. NEJM 1996;335:1660.
 Adjunctive Therapy for Acute MI
Calcium Channel Antagonists
Agent N Odds Ratio & 95% CI Ca+2Ant Control

Nifedipine 1358  15.0% 13.0%

Verapamil 1775  10.8% 13.3%

Diltiazem 2466  13.5% 13.5%

Verapamil/ 4241  12.4% 13.4%

Diltiazem

Pooled 5599  13.0% 13.3%

0 1 2
Less Mortality More Mortality
Held et al, in Topol: Text Int Cardiol 2nd Ed 1993, p.52.
Management of Acute MI

 Diagnosis
 Risk Stratification
 Acute Therapy
 Reperfusion
 Adjunctive
 Complications
 Pre-Discharge Management
 Complications of Acute MI

Extension / Ischemia Arrhythmia

Pericarditis

Expansion / Aneurysm Acute MI RV Infarct

Mechanical Heart Failure Mural Thrombus

 Management of Acute MI

 Diagnosis
 Risk Stratification
 Acute Therapy
 Reperfusion
 Adjunctive
 Complications
 Pre-Discharge Management
 Acute MI
Pre-Discharge Management

• Risk stratification

• Catheterization and revascularization strategy

• Electrophysiologic evaluation for VT or VF

• Lifestyle modification: diet, exercise, tobacco

• Pharmacologic therapy
 GUIDELINE PENANGANAN PASIEN
ACS NON STENT

BAGAIMANA GUIDELINES MENURUT ESC & ACC-AHA

NEW ACLS - ACS ALGORITHM
ACC / AHA
Update 2007
 ACC/AHA ACLS ACS Algorithm
2006
1
Nyeri dada (kecurigaan ischemia)

2
Diagnosa, penatalaksanaan dan persiapan/pre hospital oleh EMS :
- Monitor, support ABC. Persiapan untuk CPR dan defibrilasi
- Berikan oksigen, aspirin, nitroglycerin dan morphine bila dibutuhkan
- Jika tersedia, periksa ECG 12 lead, jika terdapat ST-Elevasi :
• Hubungi rumah sakit yang dituju dengan DX pasien
• Mulai membuat fibrinolytic checklist
- RS yang dituju harus menyaiapkan “Mobilize Hospital Resources” untuk
merespon pasien STEMI

Diagnosa cepat oleh Emergency Departemen Penatalaksanaan umum cepat oleh E.D
(<10min)

- Check vital signs, evaluasi saturasi O2
- Pasang IV line
- ECG 12 lead
- Anamnese singkat, terarah, pemeriksaan fisik
- Periksa awal level cardiac marker, elektrolit
Dan faal hemostatis
- Periksa Rontgen dada (<30 m)
- Morphin IV jika nyeri tidak berkurang dengan
nitroglycerin
- O2 4 L/mnt, pertahankan saturasi O2 > 90%
- Nitroglycerin SL atau spray atau IV
- Aspirin 160 samapai 325 mg (jika tidak
diberikan oleh EMS)
 4

Ulang pemeriksaan ECG 12 lead

13
5
9
ST Elevasi atau LBBB baru atau ST depresi atau T inverted; dicurigai kuat Normal atau tidak ada perubahan segmen
diasumsikan baru; dicurigai kuat ST- suatu ischemia ST atau gelombang T
Elevasi MI (STEMI) Resiko tinggi unstable angina / Non ST Resiko rendah atau sedang untuk unstable
Elevation MI (AU/NSTEMI) angina
6
10 14
Mulai terapi tambahan sesuai indikasi.
Jangan menunda reperfusi Mulai terapi tambahan sesuai indikasi Berlanjut memenuhi kriteria sedang atau
tinggi (tabel 3,4)atau troponin positive?
-Clopidogrel -Clopidogrel
--adrenergic reseptor blockers -Nitroglycerin
-Heparin (UFH or LMWH) --adrenergic reseptor blockers
-Heparin (UFH or LMWH) 15
-Glycoprotein IIb/IIIa inhibitor
Pertimbangkan opname di ED chest
paint unit atau “monitored bed” di ED
Lanjutkan dengan :
11 Serial cardiac marker (termasuk
7 troponin)
Opname di ruangan dgn “monitoring bed” Ulang ECG, monitor segmen ST
Onset gejala < 12 jam Tentukan status resiko Pertimbangan stress test

8
12
Strategi reperfusi:
16
Terapi ditetapkan berdasarkan Pasien High-risk:
keadaan pasien dan center criteria Refractory ischemic chest pain Berlanjut memenuhi kriteria resiko
Menyadari tujuan terapi reperfusi: Recurrent/persistent ST deviation tinggi atau sedang (tabel 3,4)
Door-to-balloon inflation (PCI) = 90 Ventricular tachycardia atau
mnt Hemodynamic tachycardia troponin-positive
Door-to-needle (fibrinolysis) = 30 Signs of pump failure
mnt Strategi invasive awal termasuk
Lanjutkan dengan terapi: kateterisasi & revaskularisasi penderita
ACE inhibitor/angiotensi receptor IMA dgn syok dlm 48 jam 17
blocker (ARB) 24 jam dari onset Lanjutkan pemberian ASA, heparin &
HMG CoA reductase inhibitor (statin terapi lain sesuai indikasi: Jika tidak ada ischemia atau infare,
therapy) ACE inhibitor / ARB maka dapat pulang dengan
HMG CoA reductase inhibitor (statin rencana kontrol
therapy)
Tidak pada resiko tinggi: penentuan
penggolongan resiko dari cardiology
 ACC/AHA 2007 Guidelines Update
untuk UA / NSTEMI
Rekomendasi untuk Antiplatelet dan Anticoagulant 1

Low Risk ACS Intermediate Risk ACS High Risk ACS

Early Conservative Management Early Invasive Management

Aspirin* (Class IA) Aspirin* (Class IA)
Clopidogrel# (Class IA) Clopidogrel (Class IA)
LMWH (enoxaparin)/UFH (Class IA) LMWH (enoxaparin)/UFH (Class IA)

* Or Clopidogrel if contraindicated (IA)

# For at least 1 month (IA) and for up to 9 months (IB)

Gibler, WG, et al. Circul. 2005; 111: 2699-2710

3/6/2019
 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 dosis
pemeliharaan 75 – 100 mg untuk jangka panjang

• CLOPIDOGREL ( Klas 1A )
– Untuk semua pasien ACS, SEGERA berikan Clopidogrel 300mg LD,
dilanjutkan dengan 75mg/ hari, Clopidogrel harus dilanjutkan hingga
12 bulan, kecuali ada resiko tinggi perdarahan.

– Untuk pasien yang kontra indikasi terhadap ASA, Clopidogrel harus

digunakan sebagai penggantinya ( 1B )
 What’s ESC Guidelines NSTEACS 2015 say on
P2Y12 inhibitor ?
A P2Y12 inhibitor is recommended, in addition to aspirin, for 12 months unless there
are contraindications such as excessive risk of bleeds. 1A

Ticagrelor (180 mg loading dose,90 mg twice daily) is recommended,

in the absence of contraindications, for all patients at moderate-to-high
risk of ischaemic events (e.g. elevated cardiac troponins), regardless of 1B
initial treatment strategy and including those pretreated with clopidogrel
(which should be discontinued when ticagrelor is started).

Prasugrel (60 mg loading dose,10 mg daily dose) is recommended in

patients who are proceeding to PCI if no contraindication). 1B
Clopidogrel (300–600 mg loading dose, 75 mg daily dose) is recommended
for patients who cannot receive ticagrelor or prasugrel or who 1B
require oral anticoagulation.

Roffi M et al. European Heart Journal 2015. doi:10.1093/eurheartj/ehv320

83