ACUTE CORONARY

SYNDROME

Nizam Akbar
Dept of Cardiology & Vascular medicine
Universitas Sumatera Utara
Adam Malik Hospital - Medan
 Major clinical manifestations
of atherothrombosis
Ischemic Transient
stroke ischemic attack

Myocardial Angina:
infarction • Stable
• Unstable

Peripheral arterial
disease:
• Intermittent claudication
• Rest Pain
• Gangrene
• Necrosis

Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6.

 FAKTOR RESIKO
P J K

TIDAK DAPAT DAPAT

DIRUBAH DIRUBAH
Usia > 40 thn (lk) MEROKOK
Pr : Menopause HIPERTENSI
DIABETES
Jenis kelamin
HIPERKOLESTEROL
Riwayat Keluarga
FAKTOR RESIKO PJK DI INDONESIA
INA – MONICA 1993

Merokok Hipertensi Hiperkolesterol D M

What Is Atherothrombosis?

Atherosclerosis

Thrombosis
PENYAKIT JANTUNG KORONER :
PENYEMPITAN PEMBULUH ARTERI
KORONER JANTUNG OLEH PLAK
(TUMPUKAN ) ATEROSKLEROSIS

PLAK ATEROSKLEROSIS :
KOLESTEROL (UTAMA),KALSIUM, JARINGAN IKAT,
OTOT POLOS, KOMPONEN DARAH, FIBRIN, KARBOHIDRAT
Kapan Atherosklerosis Terjadi?

Atherosklerosis
Berawal dari usia balita sampai dengan
lansia

Tedjasukmana P
 The normal artery wall

Endothelial cells
Early atherosclerosis (I) –
Endothelial dysfunction
Lipid accumulates in
the intimal space and is
associated with
abnormal endothelial
cell function

Lipid
 Early atherosclerosis (II) –
The consequences of endothelial dysfunction
Activated endothelial
cells express adhesion
molecules and recruit
inflammatory cells,
predominantly monocytes

Lipi
d
 Early atherosclerosis (III) –
Formation of the fatty streak
Monocytes migrate
into the intima,
differentiate into
macrophages
and ingest lipid to
form foam cells

Lipid T-lymphocytes
accompany the
monocytes on
migration into
the intima
Proses Terjadinya Atherosklerosis
Manifestasi Klinis
Penyakit Jantung Koroner

Nyeri dada
( Angina, Chest Pain )

Serangan Jantung
( Heart Attack, Myocard Infark )

Kematian mendadak
( Sudden Death, Cardiac Arrest )
Chronic PJK
Dimana Rasa Nyeri Dirasakan??
The Role of Platelets in Atherothrombosis

1 3 Aggregation
Adhesion

2
Activation
Lefkovits et al.NEJM 332:1553,1995.
 Platelets: Role in Thrombosis
High Flow Slow Flow

Fibrin RBCs Platelets Fibrin RBCs Platelets

White Thrombus Coagulation Thrombus

RBCs, red blood cells.

 CLOPIDOGREL C

ADP

ADP

Collagen thrombin
GPllb/llla
(Fibrinogen receptor) Activation TXA
2

ASA COX

COX (cyclo-oxygenase)
ADP (adenosine diphosphate) TXA 2
TXA2 (thromboxane A2)

1. Jarvis B, Simpson K. Drugs 2000; 60: 347–77.

Activated Clopidogrel
Platelet Ticlopidine

To neighboring
platelet

Gp IIb/IIIa
Aspirin
fibrinogen
receptor
IV Gp IIb/IIIa
Thrombin
Inhibitors Serotonin
COX Epinephrine
Collagen
Activation

Adhesive proteins
thrombospondin
α δ
fibrinogen Degranulation
p-selectin
vWF Platelet agonists
ADP
Inflammatory factors ATP
Coagulation factors serotonin
platelet factor 4 calcium
factor V CD 154 (CD 40 ligand) magnesium
factor XI
PDGF
PAI-1

TXA, thromboxane; PDGF, platelet-derived growth factor.

 Atherothrombosis:
The Pathologic Process

Atherosclerotic Plaque Thrombus Thrombus Embolism

Plaque Fissure/ Formation Incorporated
Cracking into Atheroma
/
Rupture

Stabilized Occlusion
Plaque
Chronic Ischemia Medical Training Asia Middle East Acute Event
3L
 Atherothrombosis:
A Generalized Condition

Medical Training Asia Middle East

3R
Ruptured Carotid Artery Plaque with Thrombus
 Surface of a Thrombus

Nilsson, 1984 M3
 Acute Coronary Syndrome

EKG: ST Elevation (-) ST Elevation (+)

Biomarkers

UAP NSTEMI/ STEMI/

Non-Q MI Q MI

UAP: Unstable angina pectoris, Non-Q MI: Non-Q wave myocardial infarction
NSTEMI: Non ST-elevation myocardial infarction
STEMI: ST-elevation myocardial infarction, Q MI: Q wave myocardial infarction
ANGINA PECTORIS
Proses Tersumbatnya Pemb. Darah
 Kriteria Diagnosis
1. Nyeri dada khas infark atau ekuivalen lebih dari 20 menit,
tidak hilang dengan pemberian nitrat

2. Gambaran EKG dan evolusinya yang khas IMA

a) Pada STEMI ditandai oleh elevasi 2mm di precordial lead
atau 1 mm di extremity lead atau new BBB, semua perubahan
terjadi minimal pada dua lead yang berhubungan
b) Pada non STEMI EKG bisa normal atau berubah tapi
tidak memenuhi kriteria STEMI

3. Gambaran laboratorium : peningkatan enzim ( CK MB,

Troponin T, dll )
 Pertolongan Pertama :
MONA

Morphine (M)

Oksigen (O)

Nitrat (N)

Aspirin (A)
 CURRENTLY AVAILABLE
ANTITHROMBOTIC DRUGS

ANTIPLATELET AGENTS ANTICOAGULANTS THROMBOLYTIC

AGENTS

ORAL PARENTERAL ORAL PARENTERAL -PARENTERAL

GPIIb/IIIa -STREPTOKINASE
Aspirin Coumarin
antagonists Heparin -UROKINASE
Dipyridamol LMWH -tPA
Ticlopidin melagatran
Hirudin
Clopidogrel Argatroban
Cilostazol Fondaparinux
 Therapy

STEMI : Revascularisasi secepatnya

< 3 jam : PCI (Percutaneus Coronary Intervention>
<12 Jam : Thrombolytyc Therapy

UAP / Non-STEMI :
Anticoagulant dgn Heparinisasi

Lain-lain :
Antiplatelet Agents : Aspirin and Clopidogrel
Nitrat, Betabloker, Calcium Antagonist, ACE Inhibitor
Kateterisasi jantung / Angiografi koroner
Angiografi Koroner
Coronary Artery Bypass Graft
( CABG )
Coronary Artery Bypass Graft