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ACUTE CORONARY SYNDROME (ACS)

MAJOR CLINICAL MANIFESTATIONS OF ATHEROTHROMBOSIS


Ischemic stroke Myocardial infarction
Transient ischemic attack

Angina:
Stable Unstable

Peripheral arterial disease:



Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 16.

Intermittent claudication Rest Pain Gangrene Necrosis

Atherothrombosis is commonly found in more than one arterial bed in an individual patient*
Cerebrovascular disease Coronary disease

24.7%

7.4% 3.3%

29.9%

3.8%

11.8% 19.2%
Peripheral arterial disease

* Data from CAPRIE study (n=19,185) Coccheri S. Eur Heart J 1998; 19(suppl): P1268.

IDENTIFYING THOSE AT RISK OF ATHEROTHROMBOSIS


Local factors Elevated prothrombotic factors: fibrinogen, CRP, PAI-1 Blood flow patterns, vessel diameter, arterial wall structure Systemic conditions History of vascular events Hypertension Hyperlipidemia Hypercoagulable states Homocystinemia

Generalized disorders Obesity Diabetes

Atherothrombosis manifestations (myocardial infarction, stroke, vascular death)

Genetic Genetic traits Gender Age

Lifestyle Smoking Diet Lack of exercise

Yusuf S et al. Circulation 2001; 104: 274653. 2. Drouet L. Cerebrovasc Dis 2002;13(suppl 1):16.

KONSEP DAN TEORI ATEROSKLEROSIS

Konsep

Teori

Penyakit

Infiltrasi lipid Kerusakan endotel Radikal bebas Imunologi

Inflamasi

Aterosklerosis/ PJK

Interaksi Beberapa Proses Pada Proses Aterosklerosis

Serum LDL LDL infiltrasi

Radikal Bebas

Oksidasi LDL

Kerusakan Endotel Faktor Pertumbuhan Platelet Agregasi

Sel Busa

Garis Lemak

Proliferasi Sel Kalsifikasi

ATHEROGENESIS
(MCP-1, CSF, EDRF, TF) (GF, Cytokines)

Endothelial Cell D

Smooth Muscle Cell E

Ox - LDL A
Monocyte C

B Macrophage Foam Cell Foam Cell

(IL, Apo E, Pretease)

Endothelial Injury Fibrinoid necrosis

Plasma solutes Callogen Elastin

Hyperplasia

Proliferative arteriolarsclerosis

Fibrosis

Hyaline arteriosclerosis

Normal vessel

Pal-1

EC
SMC

Pal-1

tPA

Atherosclerotic plaque

Pal-1 EC SMC

Pal-1 tPA

Christ et al., Senescent SMCs Increase Vascular Wall PAI-1 Expression

CONSTRICTOR

DILATOR

PRO

ANTI

Endothelium-1 Angiotensin-II Vasconstrictor Prostaglandins

Prostacyclin Nitric oxide Other EDRF-Like Substances

Platelet-activating factor Tissue factor Von willebrand factor Plasminogen activator Inhibitor-1 Other Coagulation factors

Prostacyclin Thrombomodulin Ecto-ADPase Tissue Plasminogen Activator Urokinase Heparin-Like Molecules

Early atherogenesis

1. Vaskuler injury 2. Monocyte recruitment Macrophage formation

Lysis
Progression 3. Lipid deposition 4. Platelet and growth factor 5. SMCs 6. Sysnthesis of extracelluler matrix 7. Plaque disruption

Late atherogenesis Acute coronary syndrome

8. Trombosis Monocyte recruitment

Macrophage formation
Lysis

Unstable Coronary Artery Disease (II)

Thrombus forms and extends into the lumen

Thrombus

Lipid core

Adventitia

Inflammation

Repair

STATINS

Unstable plaque

Stable plague
Weissberg, 1999

Clinical classification of ACS


Acute Coronary Syndrome (ACS)

No ST Elevation
Unstable Angina Pectoris
MI (NSTEMI)

ST Elevation
MI (STEMI)

No Q-wave

Q-wave

National Heart Foundation of Australia, Cardiac Society of Australia and New Zealand. Med J Aust 2000;173 (suppl):S65S88

MANAJEMEN SKA
- Oklusi > 4-6 jam Nekrosis miokard irreversible IMA dengan gel q (IMA-Q)

- Reperfusi

Menurunkan morbiditas - mortalitas

- Fase

Pre hospital stage Hospital stage : - IGD - CVCU

PENGOBATAN SKA

I. Tahap Awal : Oksigenisasi Nitrogliserin Aspirin Antitrombin II. Tahap Lanjut :

morphin

Heparin, LMWH warfarin Inhibitor glycoprotein IIb/IIIa, Trombolitik, PCI / IKP, CABG Obat-obat : CCA, ACEI, Blocker, Nitrat

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Iskemia Miokard