PUSAT

JANTUNG
Regional

ACUTE STEMI

Dr. MUHAMMAD SYUKRI, Sp JP (K), FAPSIC. FSCAI

PUSAT JANTUNG REGIONAL

REGIONAL CARDIVASCULAR CENTER
RS. DR. M DJAMIL, PADANG
JANTUNG SEBAGAI POMPA

Kanan Kiri
 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
nomor I di dunia dan
CV Indonesia

Survey Kesehatan Indonesia 2001

WHO World Health Report, 2001
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

5/98 MedSlides.com 4
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 5
 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
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

The role of platelets in atherothrombosis is depicted here, with three steps of platelet
function leading up to platelet thrombus formation. The first step is platelet adhesion by
the glycoprotein 1B receptor that forms a platelet monolayer on top of the ruptured
plaque.

The second step is platelet activation, where the platelets will change in shape and
release thromboxane, ADP, and other mediators including serotonin. Also, the platelets
will express and activate the IIb/IIIa receptor.

The third step is platelet aggregation via fibrinogen, shown in orange. This will cross-link
the platelets to each other and form the platelet plug thats the nidus of the growing
platelet-rich thrombus.

The three classes of drugs available are shown here. Both aspirin and clopidogrel will
decrease platelet activation by different pathways but both will decrease the number of
angry platelets circulating in the blood stream. In contrast, the IIb/IIIa receptor
inhibitors will prevent progression of the acute thrombus by blocking the IIb/IIIa receptor.
Again, this is relevant to short-term therapy but not to long-term therapy.
Peran Platelets pada Proses
Atherothrombosis
 AWAS !!!!
SERANGAN JANTUNG !!!
SAKIT DADA
 Faktor Risiko

1. Lifestyle 3. Diabetes/ Insulin Resistance

Diet 4. Emerging Risk Factors :

Smoking - Plasma Homocysteine (tHcy)
Obesity
-- Thrombogenic Factors
Physical inactivity
-- plasma fibrinogen
2. Blood Pressure
-- Plasminogen Activator Inhibitor (PAI-1)
3. Plasma lipids
LDL-C -- Markers of Inflammation

TG 5. Genetics
HDL-C Family history

Other Lipid Factors :

Apoliproprotein B
Lipoprotein (a)
 Gangguan metabolisme

Faktor risiko Batas Nilai

Kegemukan
( Lingkaran Perut )
Laki >102 cm (>40 in)
Wanita >88 cm (>35 in)
Trigliserida 150 mg/dL
HDL-C
Laki <40 mg/dL
Wanita <50 mg/dL
Tekanan Darah 130/85 mm Hg
Gula Puasa 110 mg/dL
JAMA. 2001;285:2486-2497.
 FAKTOR RISIKO

SINDROMA KORONER AKUT

 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
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

 Myocardial Reperfusion
The Original Paradigm

Re-establish
Limit Infarct
Infarct Vessel Mortality
Size
Patency
 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

4/23/2016
 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 )
 GUIDELINE 2007
AUSSIE ( Australia & New Zealand )
Non STEMI
In Hospital ( Early Initiation )
Pengobtan awal segera harus dimulai dengan ASA dan Clopidogrel ( 300 mg LD
and 75 mg/hari) dengan mempertrimbangkan:
Clopidogrel harus dihindari pada pasien yang akan menjalani emergency coronary
bypass surgery
Jika memungkinkan, clopidogrel, harus dihentikan 5 hari sebelum coronary bypass
surgery.

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, khususnya
setelah 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 Kardiovaskular berulang
 GUIDELINE 2007
AUSSIE ( Australia & New Zealand )
STEMI
Semua pasien yang mendapatkan reperfusion therapy pada
STEMI ( PCI atau Fibrinolysis ) harus diberikan ASA dan
CLOPIDOGREL kecuali ada kontra indikasi.

- Fibrinolytic Therapy
Pada pasien dengan fibrinolytic therapy, Clopidogrel (300 mg
LD ) harus ditambahkan pada ASA, kecuali kontraindikasi,
Clopidogrel (75 mg/hari ) harus dilanjutkan paling tidak 1
bulan setelah fibronolytic therapy
CRUSADE

Kepatuhan pada Guidelines

Menurunkan angka Mortality di Rumah Sakit

Increased Adherence to Guidelines Decreases Mortality

In-hospital Mortality (%)

CRUSADE is a national quality improvement initiative of the Duke Clinical Research Institute. Partial funding for CRUSADE is
provided by the Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership.
CRUSADE Data Q3 2006. Cumulative CRUSADE data through September 2003.
Duke Clinical Research Institute. Available at: http://www.crusadeqi.com. Accessed February 13, 2007.
 LEARNING FROM GUIDELINES
1. Clopidogrel di indikasikan pada pasien dengan UA, NSTEMI, dan STEMI dan

diberikan bersama ASA. Clopidogrel diberikan tunggal jika ASA

kontraindikasi.

2. Efek yang cepat dan memberikan perlindungan yang lebih besar jika

pemberian clopidogrel therapy dimulai dengan loading dose 300-mg. dosis

3. Clopidogrel direkomendasikan sebagai antiplatelet Class 1 untuk

penanganan ACS baik STEMI maupun NON STEMI. ( ACC-AHA / ESC /

AUSSIE )
BALON ANGIOPLASTI
STENTING ( CINCIN )
OPERASI BYPASS KORONER

OSAMA BIN LADEN