Prof. Dr. dr.

Idris Idham, SpJP (K),

FIHA, FACC, FESC, FASCC, FSCAI
SR Negeri Tabing, Padang, Tahun 1957
SMPN Kuranji, Padang, Tahun 1960
SMAN I Padang, Tahun 1963
Dokter Umum Fakultas Kedokteran Universitas Gadjah Mada; (S1)
Tahun 1972
Dokter Spesialis Jantung dan Pembuluh Darah FK UI; (S2) Tahun1983
Post Graduate Course on Invasive Cardiology, Nuclear Cardiology
Austin Hospital Melbourne, Australia, 1992
Post Graduate Course on Non-Invasive Cardiology Pacemaker
Implantation, Royal Melbourne Hospital, Australia, 1993
Pendidikan Dokter Universitas Airlangga; (S3) Tahun 2000
Guru Besar tetap Universitas Indonesia; Tahun 2004
Education
Prof. Dr. dr. Idris Idham, SpJP (K),
FIHA, FACC, FESC, FASCC, FSCAI
Staf senior, Dept. Kardiologi & Kedokteran Vaskular FKUI &
Pusat Jantung Nasional Harapan Kita
Chief cardiologist, RS Medika BSD
Sekretaris Kolegium Pengurus Pusat Perhimpunan Dokter
Spesialis Kardiovaskular (PP PERKI) 2008-sekarang
Fellow of Indonesian Heart Association (FIHA)
Fellow of American College of Cardiology (FACC)
Fellow of European Society of Cardiology (FESC)
Fellow of ASEAN Federation of Cardiology (FAsCC)
Fellow of Society of Cardiovascular Angiography and
Intervention (FSCAI)
Head of Cardiovascular Devision Medika BSD Hospital
Cardiovascular Emergency :
Focus On Acute Coronary Syndromes
Roles of Primary Physicians


Idris Idham
RS MEDIKA BSD

Spectrum of CV Emergency
Congenital Heart Diseases
Acute Coronary Syndrome : UAP,
NSTEMI, STEMI
Acute Lung Edema
Acute Aortic Dissection
Acute Limb Ischemia
Deep Veins Thrombosis


Hypertensive Crisis : emergency,
urgency
Arrhythmia : AFRVR, SVT, VT, VF,
TAVB
Cardiomyopathy : PPCM, HCM, DCM.
CARDIOVASCULAR SPECIALIST
COMPETENCY

FRONTLINE DOCTORS


FROM PALPITATION TO CVD

Front-line medical practitioners

Play very important role in fighting
cardiovascular diseases (CVD), the no.1 killer
in Indonesia
1

Front liners are doctors who first encounter
the patient, including family physicians
Patients will benefit from early diagnosis and
prompt treatment
Competent of recognizing important signs &
symptoms of CVD, e.g. chest pain

1
Dept. of Health, RI. 2002.
Chest Pain
One of the most challenging symptoms
1

Diagnosis ranges from benign esophageal
reflux to fatal MCI
Failure to manage fatal conditions lead to
complications including death
Over management of low risk conditions causes
unnecessary burden
Acute or escalating chronic chest discomfort is
most challenging.

1
Harrisons principles of internal medicine: McGraw-Hill, 2005.
Evaluation Aim
To assess the general clinical condition of
patient
To determine the working diagnosis
To initiate immediate management plan
Should be performed rapidly yet
accurately
General Clinical Assessment
Stratify patient : stable vs unstable
condition; based on level of
consciousness & vital signs.
Stabilize the patient first! Secure ABC
(airway, breathing, circulation)

Determining Working Diagnosis
Largely a clinical work, accurate anamnesis
is the key.
Characteristics of chest pain should be
thoroughly explored:
Quality, duration, location, precipitating &
relieving factors, other associated features.
Based on characteristics, determine the
organ(s) or system(s) causing the pain.

Determining Working Diagnosis
Consider anatomical structure of thorax
& adjacent abdominal organs ; each
organ has typical characteristics
Important : features may not always
present ; several features may occur
simultaneously
Anatomy of Thoracic Cavity
I.I. - 09 / PDKI Pekanbaru
Features of Major Causes of
Chest Pain
Angina: sensation of pressure, tightness,
squeezing, heaviness, burning ; located
retrosternal, often radiate (detailed later)
Aortic dissection : abrupt onset of tearing or
ripping sensation, knife-like pain in anterior
chest, often radiate to back
Pleuritis : pleuritic pain, influenced by
breathing ; accompanied by cough, fever.
1
Harrisons principles of internal medicine: McGraw-Hill, 2005.
Features of Major Causes of
Chest Pain
Esophageal reflux : burning, substernal or
epigastric pain, relieved by antacids
Musculoskeletal : aching, worsened by
movement, may be reproduced by localized
pressure
Herpes zoster : sharp, burning, dermatomal
distribution, with vesicular rash

Differential Diagnosis of
Chest Pain
Cardiac
ACS: infarct,angina
MVP
Aortic Stenosis
Hypertrophic cardio-
myopathy
Pericarditis

Lungs
Lung Emboli
Pneumonia
Pneumothorax
Pleuritis
Gastrointestinal
Esophageal reflux
Esophageal rupture
Gall bladder disease
Peptic Ulcer
Pancreatitis

Vascular
Aortic dissection/aneurysm

Others
Musculoskeletal
Herpes zoster
General Approach for First liners
Targetted anamnesis and thorough physical
exams
Consider most likely diagnoses
If more than one, consider the worst one
Closely monitor vital signs
Administer essential first-line drugs
Refer to higher facility if required, after
patient is reasonably stabilized
Focus on:
Acute Coronary Syndromes
I.I. - 09 / PDKI Pekanbaru
A spectrum of clinical syndromes due to
sudden, significantly compromised coronary
circulation ranging from unstable angina to
NSTEMI and STEMI.
Further stages of stable angina pectoris

Topol EJ, ed. Textbook of cardiovascular medicine 2007.
DEFINITION
PATHOPHYSIOLOGY
Foam
Cells
Fatty
Streak
Intermediate
Lesion
Atheroma
Fibrous
Plaque
Complicated
Lesion/Rupture
Endothelial Dysfunction
Smooth muscle
and collagen
From first decade From third decade From fourth decade
Growth mainly by lipid accumulation
Thrombosis,
hematoma
Stary HC et al. Circulation 1995;92:1355-1374.
Atherosclerosis Timeline
DIAGNOSIS
Presentation
(Clinical, Initial ECG)
ST-Seg Elevation
Myocardial Infarction
Non-STSeg Elevation
Acute Coronary Syndr
ST-Seg Elevation
MCI
Non-ST-seg-
Elevation MCI
Unstable
Angina
Working
diagnosis
Time

Evolution of
ECG &
Biomarkers
Final
diagnosis
National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
Biomarker (-) Biomarker (+)
I.I. - 09 / PDKI Pekanbaru
CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
revascularization
Medical therapy,
coronary angiography

P
e
r
f
o
r
m
e
d

i
n

1
0

m
i
n

{on serial
ECG}
Troponin,
CKMB (+)
Clinical Classification of Angina
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
UA/NSTEMI
THREE PRINCIPAL PRESENTATIONS
Rest Angina* Angina occurring at rest and
prolonged, usually > 20 minutes

New-onset Angina New-onset angina of at least CCS
Class III severity

Increasing Angina Previously diagnosed angina that
has become distinctly more
frequent, Longer in duration, or
lower in threshold (i.e., increased
by > 1 CCS) class to at least CCS
Class III severity
CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
revascularization
Medical therapy,
coronary angiography

P
e
r
f
o
r
m
e
d

i
n

1
0

m
i
n

{on serial
ECG}
Troponin,
CKMB (+)
EVOLVING ECG
A. Normal ECG
B. Tall or peaked T waves
C. ST
D. & E. ST with inverted T
waves
F. Abnormal Q
ECG pattern
Ischemia : ST , tall T,
inverted T
Injury : ST
Infarction : pathologic Q
CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
revascularization
Medical therapy,
coronary angiography

P
e
r
f
o
r
m
e
d

i
n

1
0

m
i
n

{on serial
ECG}
Troponin,
CKMB ()
Biomarkers
Recommendation : CK, CKMB & Troponin upon admission
and serial in 6-12 hours
LDH, SGOT/SGPT and other enzymes not recommended
Increase of plasma CK plasma & CK-MB happens early, but
less specific
Increase of TnI & TnT are more specific in diagnosing marker
MI ; its level corresponds with prognosis (higher value, worse
prognosis)

0 1 2 3 4 5 6 7 8
50
20
10
5
2
1
Early release myoglobin of
CKMB isoform
Cardiac troponin after classical
myocardial infarction
CK-MB after myocardial infarction
Cardiac troponin after microinfarction
M
u
l
t
i
p
l
e

o
f

t
h
e

A
M
I

c
u
t
o
f
f

l
i
m
i
t

Day after onset of AMI
Time-course of the different cardiac biochemical markers. From Wu AH et al. Clin Chem
1999 ; 45 : 1104, with permission
Biomarkers
CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
revascularization
Medical therapy,
coronary angiography

P
e
r
f
o
r
m
e
d

i
n

1
0

m
i
n

{on serial
ECG}
Troponin,
CKMB ()
I.I. - 09 / PDKI Pekanbaru
High Risk
Repetitive or prolonged (> 10 minutes) pain
Elevated level of cardiac biomarker (troponin or
creatine kinase-MB isoenzyme);
Persistent or dynamic ST depression 0.5 mm or new
T-wave inversion
Transient ST-segment elevation (0.5 mm) in more
than two contiguous leads
Haemodynamic compromise

Guideline ACS 2006 National Heart Foundation Australia
High Risk
Sustained ventricular tachycardia
Syncope
LV systolic dysfunction (ejection fraction <40%);
Prior PCI or CABG within 6 months or prior
Diabetes
Chronic kidney disease (estimated GFR< 60 mL/min)

Guideline ACS 2006 National Heart Foundation Australia
CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
reperfusion
Medical therapy,
coronary angiography

P
e
r
f
o
r
m
e
d

i
n

1
0

m
i
n

{on serial
ECG}
Troponin,
CKMB ()
Initial Management
Monitor and support ABCs
Check vital signs, including O2 saturation
Establish IV access
Administer
Oxygen 4L/min
Aspirin 160-325 mg chewed
Clopidogrel loading dose 300 mg
ISDN 5 mg sublingual, nitroglycerine iv if necessary
Morphine if pain not relieved with NTG
Caution: hemodynamic instability due to pump
failure &/ malignant arrhythmia

Anticoagulation & Reperfusion
Heparin administration (LMWH or UFH)
Reperfusion in STEMI
Fibrinolysis or primary percutaneous coronary
intervention (PCI). GPs should be trained to give
fibrinolytic
Assess onset (12 hours) and contraindication
(bleeding, etc)
Door to needle time: 30 min
Door to balloon time: 90 min
Fibrinolytic Absolute Contraindication
Hemorrhagic stroke, or stroke of unknown origin
Ischemic stroke in preceding 6 months
Central nervous system trauma or neoplasm
Recent major trauma/surgery/head injury (within
preceding 3 weeks)
Gastro-intestinal bleeding within the last month
Known bleeding disorder
Aortic dissection
Non-compressible punctures (e.g liver biopsy, lumbar
puncture)
ESC Guidelines of STEMI, 2008
Algorithm in ACLS
I.I. - 09 / PDKI Pekanbaru
CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
revascularization
Medical therapy,
coronary angiography

P
e
r
f
o
r
m
e
d

i
n

1
0

m
i
n

{on serial
ECG}
Troponin,
CKMB ()
A Aspirin and Anticoagulants

B Beta blockers and Blood Pressure

C Cholesterol and Cigarettes

D Diet and Diabetes

E Education and Exercise

F Fun and Faith
Secondary Prevention Strategy
Invasive Strategy
As secondary prevention
Early catheterization (before discharge):
for patients with moderate-high risk not
receiving primary percutaneous coronary
intervention
Later catheterization: for low risk
patients

Summary
Acute Coronary Syndrome as one of
potentially fatal cardiovascular emergency
should be recognized immediately

Early diagnosis and prompt treatment should
be managed to overcome good results and
avoid myocardial damage (Time is muscle)
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, belum terdapat landasan
ilmiah yang kuat.
ACC/AHA Guideline of STEMI 2004
I.I. - 09 / PDKI Pekanbaru

ANTIPLATELET

ASPIRIN
CLOPIDOGREL
TICLOPIDINE
Gp IIb / IIIa inhibitor
I.I. - 09 / PDKI Pekanbaru
Aspirin
MANFAAT : menurunkan angka reinfark
50% dalam 30hari ; 20% penurunan
mortaliti dlm 2 tahun
Dosis 81-325 mg P.O.
Trials: ISIS (88), Antiplatelet Trialist Group
(94), HART (90)


Aspirin kunyah segera diberikan meskipun
belum ada hasil EKG
(non coated/slow released)
I.I. - 09 / PDKI Pekanbaru
Adenosine Diphosphate
Inhibitors
ADP disekresi oleh platelet (aktivasi dan
agregasi platelet)
P2T cell surface receptors
Ticlodipine
Clopidogrel
Efek samping : Neutropenia, trombositopenia
I.I. - 09 / PDKI Pekanbaru
COX (cyclo-oxygenase)
ADP (adenosine diphosphate)
TXA
2
(thromboxane A
2
)
CLOPIDOGREL
ASA
COX
ADP
ADP
C
GPllb/llla
(Fibrinogen receptor)
Collagen thrombin
TXA
2
Activation
TXA
2

ASA
Synergistic Mode of Action with
Clopidogrel and ASA
1
1. Schafer AI. Am J Med 1996; 101: 199209.
I.I. - 09 / PDKI Pekanbaru
Clopidogrel
Gol Thienopyridine yg memblok P2Y reseptor ADP
Menghambat aktivasi platelet
Digunakan pada pasien UA/NSTEMI :
Diberikan pada semua pasien
Bukan kandidat CABG
Pasien yg direncanakan kateterisasi dlm
24-36 jam stlh masuk

I.I. - 09 / PDKI Pekanbaru
Glycoprotein IIb/IIIa Inhibitors
50,000 receptors per platelet
Aggregation final common pathway
Passivation; stops deposition
Abciximab (Reopro); tirofiban (Aggrastat);
eptifibatide (Integrilin) and lamifiban (Canada)
Pre-PCI/ Procedural Coronary Intervention
I.I. - 09 / PDKI Pekanbaru

Anti Ischemia

NITRAT
B BLOKER
ANTAGONIS KALSIUM
I.I. - 09 / PDKI Pekanbaru
Nitrat
Indikasi : pada Anterior MI, iskemja persisten, CHF, hipertensi
Manfaat: dapat memperbaiki perfusi koroner
Hati-hati pd: inferior MI dengan perluasan atau keterlibatan
RV
Trials: GISSI-3 (94), ACC/AHA (96)
Pemberian Sublingual
Pemberian per IV
Dosis awal 5Ug/mnt ditingkatkan tiap 5 menit
disesuaikan dengan gejala klinis dan EKG

I.I. - 09 / PDKI Pekanbaru
Beta-bloker
Effektif untuk pengobatan simtomatik dan
pencegahan infark miokard.
Vasokonstriktor moderat
Dipilih obat yang kardio-selektif
Berhubungan dengan nitrat.
Kontraindikasi:vasospastik angina, blok SV derajat II
atau III, asma, gagal jantung dlm
dekompensasi,penyakit arteri perifer yg berat
I.I. - 09 / PDKI Pekanbaru
Beta-bloker

Metoprolol IV
Metoprolol oral
Atenolol oral
Propranolol oral
Bisoprolol oral
Carvedilol oral

5 15 mg
2 x 25 100 mg
1 x 25 100 mg
3 x 20 80 mg
1 x 5 10 mg
1 x 25 mg
I.I. - 09 / PDKI Pekanbaru
Antagonis kalsium
Pd UAP atau NSTEMI bila ada indikasi kontra B-
bloker

Tidak ada bukti manfaatnya pada pencegahan
infark miokard.

Memberikan hasil yang baik dalam jangka pendek
pada episode iskemik.


I.I. - 09 / PDKI Pekanbaru
Antagonis kalsium

Diltiazem


Verapamil

Lepas cepat :30 -120 mg 3x/hr
Lepas lambat: 100-360 mg 1x/hr

Lepas cepat : 40 160 mg/hr
Lepas lambat: 120-480 mg 1x/hr
I.I. - 09 / PDKI Pekanbaru
Morfin:
2.5mg-5 mg IV pelan.
Hati hati pada : inferior MCI,
asthma , bradikardia

Pethidin : 12.5-25 mg IV pelan
PAIN KILLER
I.I. - 09 / PDKI Pekanbaru
ANTITROMBOTIK DAN
ANTIKOAGULAN
Heparin ( Unfractionated Heparin)
Low Molecular Weight Heparin
I.I. - 09 / PDKI Pekanbaru
Heparin (UFH)
Terikat pada AT III (anti-thrombin III)
,menginaktivasi trombin
Tidak ada efek pada Factor Xa
Hospitalization/ PTT/ bleeding
Benefit in UA/ rebound effect
Anti-Xa: Anti-thrombin 1:1
Memperpanjang APTT
I.I. - 09 / PDKI Pekanbaru
Low Molecular Weight Heparin
Depolimerasi dari UFH standar dengan
berat molekul lebih kecil dari pada UFH
SQ injections/ 90% bio-
available/predictable
Anti-Xa: Anti-thrombin 2-4:1
FDA menyetujui pemakaian enoxaparin/
dalteparin untuk SKA
I.I. - 09 / PDKI Pekanbaru
UFH
LMWH
I.I. - 09 / PDKI Pekanbaru
KELEMAHAN UFH
Bioavailability kurang baik
Tidak dapat menghambat trombin yang terikat pada
bekuan (clot-bound thrombin)
Tergantung pada kofaktor AT III
Efek variabel
Monitor APTT berkala untuk mendapatkan kadar
terapeutik
Rebound iskemia setelah penghentian
Risiko heparin-induced thrombocytopenia (HIT)
Panduan Terapi SKA tanpa ST Elevasi PERKI 2004
I.I. - 09 / PDKI Pekanbaru
KEUNGGULAN DARI LMWH
Mengurangi ikatan pada protein pengikat heparin
Efek yang dapat diprediksi lebih baik
Tidak memerlukan pengukuran APTT
Pemakaian subkutan,menghindari kesulitan dalam
pemakaian secara IV
Berkaitan dengan kejadian perdarahan yang kecil, namun
bukan perdarahan besar
Stimulasi trombosit kurang dari UFH dan jarang
menimbulkan HIT
Penghematan biaya perawatan (dari studi ESSENCE)
Panduan Terapi SKA tanpa ST Elevasi PERKI 2004
I.I. - 09 / PDKI Pekanbaru
TEHNIK INJEKSI LMWH SUBKUTAN
I.I. - 09 / PDKI Pekanbaru
DOSIS YANG DIREKOMENDASIKAN
UFH




LMWH
Enoxaparine
Nadroparine
Fondaparinux
Initial I.V BOLUS 60 UI/Kg max 4000 UI
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




1mg/kg, SC , bid
0,1 ml/10 kg , SC , bid
2.5 mg
I.I. - 09 / PDKI Pekanbaru
6/12/2011
Definite ACS with continuing
ischemia 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 LMWH
or
IV heparin
ACC/AHA 2007 Guidelines Update
for UA and NSTEMI
1
+ Clopidogrel + Clopidogrel
*
During hospital care

Clopidogrel should be administered to hospitalized patients who are unable to take ASA
because of hypersensitivity or major GI intolerance

Class 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; 2007.
I.I. - 09 / PDKI Pekanbaru
OBAT-OBATAN LAINNYA
Tranquilizer e,g diazepam 5mg bid
Stool softener
I.I. - 09 / PDKI Pekanbaru
TERAPI FIBRINOLITIK
I.I. - 09 / PDKI Pekanbaru
Fibrinolitik : 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 block yg baru
Syok kardiogenik pd IMA ( bila kateterisasi dan
revaskularisasi tdk dapat dilakukan )


Fibrinolitik door to needle time < 30 menit !!
PCI pada IMA lebih unggul bila dpt dilakukan
dlm 90 30 menit
I.I. - 09 / PDKI Pekanbaru
Fibrinolitik : indikasi kontra
Absolut
Riwayat stroke hemoragik,kapanpun terjadinya
Riwayat stroke iskemik dalam 3 bulan kecuali stroke iskemik
dengan onset < 3 jam
Neoplasma intrakranial
Perdarahan internal aktif(tidak termasuk menstruasi)
Kecurigaan suatu diseksi aorta
Luka kepala tertutup yg signifikan atau trauma facial dalam 3
bulan
Kelainan struktural atau pembuluh darah cerebral
ACC/AHA guideline of STEMI 2004
I.I. - 09 / PDKI Pekanbaru
Hipertensi berat saat datang ke unit emergency yaitu BP> 180 / 110 mmHg
Pungsi vaskuler yg tak dapat dikompresi
Perdarahan internal 2 4 mgg sebelumnya
Konsumsi antikoagulan oral
prolonged CPR ( > 10 minutes) or operasi mayor dlm jangka waktu 2-4
minggu
Untuk Streptokinase : pemberian sebelumnya ( 5 hari-2 tahun) atau riwayat
reaksi alergi
Kehamilan
Active peptic ulcer
Riwayat hipertensi kronis yg tak terkontrol
Riwayat stroke iskemik lebih dari 3 bulan,demensia atau patologi serebral
lainnya yg blm tercantum dalam indikasi kontra
Fibrinolitik :indikasi kontra relatif
ACC/AHA guideline of STEMI 2004
I.I. - 09 / PDKI Pekanbaru
Perbandingan terapi trombolitik
dengan terapi standar pada IMA
Mulai trombolisis Tambahan Jiwa yg
diselamatkan per 1000
pasien yg diobati
-------------------------------------------------------------------

Pd jam pertama 65
Pd jam kedua 37
Pd jam ketiga 29
Antara jam ke 3-6 26
Antara jam 6-12 18
Antara jam 12-24 9
I.I. - 09 / PDKI Pekanbaru
AGEN FIBRINOLITIK
Streptokinase (SK)
Actylase (tPA)
Reteplase (r-PA)
Tenecteplase (TNK-tPA)
I.I. - 09 / PDKI Pekanbaru
Plasminogen Activators
(t-PA, u-PA)
Skema sistem fibrinolitik
Plasminogen Plasmin

2
-Antiplasmin
Fibrin
Fibrin
degradation
Product
Plasminogen Activator
Inhibitors (PA1, PA2, TAFI)
Braunwald, A Textbook of Cardiovascular Medicine. 6th ed I.I. - 09 / PDKI Pekanbaru
SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK
Streptokinase
Actylase (tPA)
Reteplase(r-PA)
Tenecteplase
(TNK-tPA)
Rendah
Tinggi
Sedang
Sangat tinggi
I.I. - 09 / PDKI Pekanbaru
CARA PEMBERIAN FIBRINOLITK
Streptokinase ( Streptase )
1.5 million Unit in 100 ml D5W or 0.9% saline selama
30-60 mnt
without heparin : Inferior MCI
with heparin : anterior MCI
tPA
15 mg IV bolus kemudian 0.75 mg/Kg selama 30
mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt berikutnya
I.I. - 09 / PDKI Pekanbaru
Streptokinase (SK, Streptase)
Keuntungan : lebih baik pada anterior
MCI, age <75; lebih murah
Komplikasi: antigenic, perdarahan
intraserebral pada studi GUSTO 0.6%
Trials: GISSI-1, ISIS-2 (88)
I.I. - 09 / PDKI Pekanbaru
TPA Alteplase, rTPA
Keuntungan : clot specific, baik pada
anterior MCI
Komplikasi : 1% perdarahan intrakranal
Biaya: lebih mahal dari SK
Trials: ASSENT, GUSTO (93) TIMI-IIIB (94)
I.I. - 09 / PDKI Pekanbaru
Extension / Ischemia
Complications of Acute MI
Acute MI
Arrhythmia
Heart Failure
Expansion / Aneurysm
RV Infarct
Pericarditis
Mechanical Mural Thrombus
I.I. - 09 / PDKI Pekanbaru

Komplikasi awal :
-aritmia
-disfungsi LV dan gagal jantung
-ruptur ventrikel
-regurgitasi mitral akut
-gagal fungsi RV
-syok kardiogenik

I.I. - 09 / PDKI Pekanbaru
Komplikasi akhir :
-trombosis mural dan emboli sistemik
-aneurisma LV
-DVT
-emboli paru
-sindrome Dressler

I.I. - 09 / PDKI Pekanbaru
SAKIT DADA
Masuk RS
Diagnosis
Kerja
ECG
Bio-
chemistry
Stratifikasi
risiko
Pengobatan
Pencegahan
sekunder
Curiga Sindrom Koroner Akut
Elevasi ST
menetap
Tanpa Elevasi
ST menetap
Normal atau
Tdk dpt ditentukan
Troponin
(CKMB)
Troponin
ECG
Troponin
2 X negative
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
Esc/EHJ 2002
Mungkin bukan SKA
I.I. - 09 / PDKI Pekanbaru
TERAPI INTERVENSI
PADA SINDROMA
KORONER AKUT
I.I. - 09 / PDKI Pekanbaru
Angioplasty
Keberhasilan Primer : 85 - 95 %

Kematian : 0.3 - 1.3 %

Infark Miokard : 1.6 - 6.3 %

Operasi By-pass darura : 1 - 7 %

Stenosis lebih lanjut
sblm era stent : 30 - 40 %
era stent : 15-20%
Drug eluting stent : almost 0%
I.I. - 09 / PDKI Pekanbaru
Primary PTCA/PCI
Keunggulan: ICH 0%,
Syarat : jumlah tindakan primary PCI>100
kasus/th/operator ;>600/yr/rumah sakit
Mortaliti: reinfark 5 vs 12% untuk TPA; 30 hari
sama dengan TPA; namun pada AMI Anterior
; age>70 pulse >100 angka 2% vs 10% for TPA
Trials: RITA, PAMI (93); MITI (96)
I.I. - 09 / PDKI Pekanbaru
I.I. - 09 / PDKI Pekanbaru
Symptom
Recognition
Call to
Medical System
ED
Cath Lab
PreHospital
Delay in Initiation of Reperfusion Therapy
Increasing Loss of Myocytes
Treatment Delayed is Treatment Denied
I.I. - 09 / PDKI Pekanbaru
Patients receiving fibrinolysis should be risk-stratified to identify need for
further revascularization with percutaneous coronary intervention (PCI) or
coronary artery bypass graft surgery (CABG).
All patients should receive late hospital care and secondary prevention of
STEMI.
Fibrinolysis
Primary PCI
Noninvasive Risk
Stratification
Late
Hospital Care
and Secondary
Prevention
PCI or CABG
Not
PCI Capable
PCI Capable
Rescue
Ischemia
driven
Options for Transport of Patients With STEMI and Initial
Reperfusion Treatment
I.I. - 09 / PDKI Pekanbaru
I.I. - 09 / PDKI Pekanbaru
Chest pain: focus on
acute coronary syndromes
What doctors should know
IDRIS IDHAM
Department of Cardiology and Vascular Medicine
Fakultas of Medicine University of Indonesia
National Cardiovascular Center Harapan Kita
I.I. - 09 / PDKI Pekanbaru
Thank you
I.I. - 09 / PDKI Pekanbaru