Prof. Dr. dr.

Idris Idham, SpJP (K),

FIHA, FACC, FESC, FASCC, FSCAI
Education
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
 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 Indonesia1
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

1Dept. of Health, RI. 2002.

 Chest Pain
One of the most challenging symptoms1
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.

1Harrisons 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.

1Harrisons 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 Gastrointestinal
ACS: infarct,angina Esophageal reflux
MVP Esophageal rupture
Aortic Stenosis Gall bladder disease
Peptic Ulcer
Hypertrophic cardio-
Pancreatitis
myopathy
Pericarditis
Vascular
Aortic dissection/aneurysm
Lungs
Lung Emboli Others
Pneumonia Musculoskeletal
Pneumothorax Herpes zoster
Pleuritis
 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

 DEFINITION

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.

PATHOPHYSIOLOGY
 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;92:1355-1374.

DIAGNOSIS
 Presentation
(Clinical, Initial ECG)

Working ST-Seg Elevation Non-STSeg Elevation

diagnosis Myocardial Infarction Acute Coronary Syndr

Time

Evolution of
ECG & Biomarker (+) Biomarker (-)
Biomarkers

Final ST-Seg Elevation Non-ST-seg- Unstable

diagnosis MCI Elevation MCI Angina
National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
I.I. - 09 / PDKI Pekanbaru
 Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial

ECG
ST elevation ST elevation ECG}

Bio- - ACS unlikely

Troponin, Troponin, - NSTEMI
chemistry
CKMB (+) CKMB (+) - STEMI

Risk Risk: high / low

Stratification

Initial management,
Management revascularization

Secondary Medical therapy,

prevention
coronary angiography Modified from ESC 2007
 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
 Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial

ECG ECG}
ST elevation ST elevation

Bio- Troponin, Troponin, - ACS unlikely

chemistry CKMB (+) - NSTEMI
CKMB (+)
- STEMI

Risk Risk: high / low

Stratification

Initial management,
Management revascularization

Secondary Medical therapy,

prevention
coronary angiography Modified from ESC 2007
ECG pattern
Ischemia : ST , tall T,
inverted T
Injury : ST
Infarction : pathologic Q

EVOLVING ECG
A. Normal ECG
B. Tall or peaked T waves
C. ST
D. & E. ST with inverted T
waves
F. Abnormal Q
 Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial

ECG
ST elevation ST elevation ECG}

Bio- Troponin, - ACS unlikely

Troponin, - NSTEMI
chemistry CKMB ()
CKMB (+) - STEMI

Risk
Risk: high / low
Stratification

Initial management,
Management revascularization

Secondary Medical therapy,

prevention
coronary angiography Modified from ESC 2007
 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)
 Biomarkers Early release myoglobin of
CKMB isoform

50 Cardiac troponin after classical

Multiple of the AMI cutoff limit

myocardial infarction

20 CK-MB after myocardial infarction

10 Cardiac troponin after microinfarction

5
2
1

0 1 2 3 4 5 6 7 8
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
 Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial

ECG
ST elevation ST elevation ECG}

Bio- Troponin, Troponin, - ACS unlikely

chemistry CKMB (+) - NSTEMI
CKMB ()
- STEMI

Risk
Stratification
Risk: high / low

Initial management,
Management revascularization

Secondary Medical therapy,

prevention
coronary angiography Modified from ESC 2007
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

 Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial

ECG
ST elevation ST elevation ECG}

Bio- Troponin, Troponin, - ACS unlikely

chemistry CKMB (+) - NSTEMI
CKMB ()
- STEMI

Risk Risk: high / low

Stratification
Initial management,
Management reperfusion

Secondary Medical therapy,

prevention
coronary angiography Modified from ESC 2007
 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

 Algorithm in Acute Coronary Syndrome

Admission CHEST PAIN

Performed in 10 min
Working Suspected ACS
diagnosis

Persistent No persistent {on serial

ECG
ST elevation ST elevation ECG}

Bio- Troponin, - ACS unlikely

Troponin, - NSTEMI
chemistry CKMB ()
CKMB (+) - STEMI

Risk Risk: high / low

Stratification

Initial management,
Management revascularization

Secondary Medical therapy,

prevention
coronary angiography Modified from ESC 2007
Secondary Prevention Strategy
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

 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)
Thank You
 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

 Synergistic Mode of Action with
Clopidogrel and ASA1

CLOPIDOGREL C

ADP

ADP

GPllb/llla Collagen thrombin

Activation
(Fibrinogen receptor) TXA 2

ASA
ASA COX

TXA 2

COX (cyclo-oxygenase)
ADP (adenosine diphosphate)
TXA2 (thromboxane A2)

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 5 15 mg
Metoprolol oral 2 x 25 100 mg
Atenolol oral 1 x 25 100 mg
Propranolol oral 3 x 20 80 mg
Bisoprolol oral 1 x 5 10 mg
Carvedilol oral 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 Lepas cepat :30 -120 mg 3x/hr

Lepas lambat: 100-360 mg 1x/hr

Verapamil Lepas cepat : 40 160 mg/hr

Lepas lambat: 120-480 mg 1x/hr

I.I. - 09 / PDKI Pekanbaru

 PAIN KILLER

Morfin:
2.5mg-5 mg IV pelan.
Hati hati pada : inferior MCI,
asthma , bradikardia

Pethidin : 12.5-25 mg IV pelan

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 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

LMWH
1mg/kg, SC , bid
Enoxaparine
0,1 ml/10 kg , SC , bid
Nadroparine
2.5 mg
Fondaparinux
I.I. - 09 / PDKI Pekanbaru
 ACC/AHA 2007 Guidelines Update
for UA and NSTEMI1
Class I Recommendations for Antithrombotic Therapy*
Definite ACS with continuing
ischemia or other high-risk
Possible ACS Likely/Definite ACS features or planned PCI

Aspirin Aspirin
Aspirin
+ +
SC LMWH IV heparin/SC LMWH
or +
IV heparin IV GP IIb/IIIa antagonist

+ 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

1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA)
6/12/2011
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
 Fibrinolitik :indikasi kontra relatif
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
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

 Skema sistem fibrinolitik
Plasminogen Activators
(t-PA, u-PA)

Plasminogen Activator
Inhibitors (PA1, PA2, TAFI)

Plasminogen Plasmin

2-Antiplasmin
Fibrin
Fibrin degradation
Product
I.I. - 09 / PDKI Pekanbaru Braunwald, A Textbook of Cardiovascular Medicine. 6th ed
 SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK

Streptokinase Rendah
Actylase (tPA) Tinggi
Reteplase(r-PA) Sedang
Tenecteplase Sangat tinggi
(TNK-tPA)

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

 Complications of Acute MI

Extension / Ischemia Arrhythmia

Pericarditis

Expansion / Aneurysm Acute MI RV Infarct

Mechanical Heart Failure 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

 Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA

Diagnosis Curiga Sindrom Koroner Akut

Kerja

Elevasi ST Tanpa Elevasi Normal atau

ECG
menetap ST menetap Tdk dpt ditentukan

Bio- Troponin Troponin ECG

chemistry (CKMB) Troponin
2 X negative
Stratifikasi
Risiko tinggi Risiko rendah Mungkin bukan SKA
risiko

Pengobatan

Pencegahan
sekunder
Esc/EHJ 2002
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
 Treatment Delayed is Treatment Denied

Symptom Call to PreHospital ED Cath Lab

Recognition Medical System

Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy

I.I. - 09 / PDKI Pekanbaru

 Options for Transport of Patients With STEMI and Initial
Reperfusion Treatment
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.

Noninvasive Risk
Fibrinolysis
Stratification
Not Late
Rescue Ischemia Hospital Care
PCI Capable driven and Secondary
PCI Capable Prevention

PCI or CABG

Primary PCI

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