ACUTE CORONARY

SYNDROME

Nizam Akbar

Dept of Cardiology & Vascular medicine

Universitas Sumatera Utara

Adam Malik Hospital - Medan

Major clinical manifestations

of atherothrombosis

Transient ischemic attack

Angina:• Stable• Unstable

Ischemicstroke

Myocardial infarction

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

Peripheral arterialdisease:• Intermittent claudication• Rest Pain• Gangrene• Necrosis

FAKTOR RESIKO FAKTOR RESIKO FAKTOR RESIKO FAKTOR RESIKO

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TIDAK DAPAT

DIRUBAH

DAPAT

DIRUBAH

Usia > 40 thn (lk) MEROKOKUsia > 40 thn (lk)

Pr : Menopause

Jenis kelamin

Riwayat Keluarga

MEROKOK

HIPERTENSI

DIABETES

HIPERKOLESTEROL

FAKTOR RESIKO PJK DI INDONESIA

INA – MONICA 1993

Merokok Hipertensi HiperkolesterolD M

What Is Atherothrombosis?

� Atherosclerosis

Thrombosis� Thrombosis

PENYAKIT JANTUNG KORONER :PENYAKIT JANTUNG KORONER :

PENYEMPITAN PEMBULUH ARTERI

KORONER JANTUNG OLEH PLAK

(TUMPUKAN ) ATEROSKLEROSIS

PLAK ATEROSKLEROSISPLAK ATEROSKLEROSIS ::

KOLESTEROL (UTAMA),KALSIUM, JARINGAN IKAT,

OTOT POLOS, KOMPONEN DARAH, FIBRIN, KARBOHIDRAT

Kapan Atherosklerosis Terjadi?

AtherosklerosisBerawal dari usia balita sampai dengan lansia

Tedjasukmana P

The normal artery wall

Endothelial cells

Early atherosclerosis (I) Early atherosclerosis (I) ––

Endothelial dysfunctionEndothelial dysfunction

Lipid accumulates in

the intimal space and is

associated with

abnormal endothelial

cell function

Lipid

cell function

Early atherosclerosis (II) Early atherosclerosis (II) ––

The consequences of endothelial dysfunctionThe consequences of endothelial dysfunction

Activated endothelial

cells express adhesion

molecules and recruit

inflammatory cells,

Lipi

d

inflammatory cells,

predominantly monocytes

Monocytes migrate

into the intima,

differentiate into

macrophages

and ingest lipid to

Early atherosclerosis (III) Early atherosclerosis (III) ––

Formation of the fatty streakFormation of the fatty streak

Lipid

and ingest lipid to

form foam cells

T-lymphocytes

accompany the

monocytes on

migration into

the intima

Proses Terjadinya Atherosklerosis

�Nyeri dada

( Angina, Chest Pain )

�Serangan Jantung

Manifestasi KlinisPenyakit Jantung Koroner

�Serangan Jantung

( Heart Attack, Myocard Infark )

�Kematian mendadak

( Sudden Death, Cardiac Arrest )

Chronic PJK

Dimana Rasa Nyeri Dirasakan??

Adhesion

The Role of Platelets in Atherothrombosis

Aggregation1 3

Activation2

Lefkovits et al.NEJM 332:1553,1995.

High Flow Slow Flow

Platelets: Role in Thrombosis

Fibrin PlateletsRBCs

White Thrombus

Fibrin PlateletsRBCs

Coagulation Thrombus

RBCs, red blood cells.

CLOPIDOGREL

ADP

ADP

C

ASA COX

GPllb/llla(Fibrinogen receptor)

Collagen thrombin

TXA2

Activation

TXA2

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

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

Thrombin

Activated

Platelet

AspirinGp Gp IIb/IIIa

fibrinogenfibrinogen

receptorreceptor

To neighboringTo neighboring

plateletplatelet

Clopidogrel

Ticlopidine

IV Gp IIb/IIIaInhibitors Thrombin

SerotoninEpinephrineCollagen

Activation

COXCOX

Degranulationαααααααα δδδδδδδδ

Platelet agonists

ADPATPserotonincalciummagnesium

Adhesive proteinsthrombospondinfibrinogenp-selectinvWF

Coagulation factors

factor Vfactor XIPAI-1

Inflammatory factors

platelet factor 4

CD 154 (CD 40 ligand)

PDGF

Inhibitors

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

Atherothrombosis:

The Pathologic Process

Medical Training Asia Middle East

3L

Occlusion

Acute Event

Embolism

Chronic Ischemia

AtheroscleroticPlaque

PlaqueFissure/Cracking

/ Rupture

Thrombus Incorporated

into Atheroma

Thrombus Formation

Stabilized Plaque

Atherothrombosis:

A Generalized Condition

Medical Training Asia Middle East

3R Ruptured Carotid Artery Plaque with Thrombus

Surface of a Thrombus

M 3Nilsson, 1984

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

Acute Coronary Syndrome

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

BiomarkersBiomarkers

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)�Oksigen (O)

�Nitrat (N)

�Aspirin (A)

CURRENTLY AVAILABLEANTITHROMBOTIC DRUGS

ANTIPLATELET AGENTS ANTICOAGULANTS THROMBOLYTIC

AGENTS

ORAL PARENTERAL ORAL PARENTERAL

Aspirin

Dipyridamol

Ticlopidin

Clopidogrel

Cilostazol

GPIIb/IIIa

antagonistsCoumarin

Heparin

LMWH

Hirudin

Argatroban

Fondaparinux

melagatran

-PARENTERAL

-STREPTOKINASE

-UROKINASE

-tPA

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