Coronary Arthery Disease

dr. Abraham Ahmad A.F., SpJP

INTERNAL DEPT – MEDICAL FACULTY - UNUSA

ATHEROSCLEROSIS
PATHOGENESIS

▶ Atherogenesis occurs over a period of many years –

decades
▶ Acute clinical event may first herald the presence of
atherosclerosis
Endothelial Cell Injury
Vascular endothelium
normally resist attachment
of the white blood cells
and other blood
components.
Smoking, elevated low-
density lipoprotein (LDL)
levels, immune
mechanisms, and
mechanical stress
associated with
hypertension share the
potential for causing
endothelial injury with
adhesion of monocytes
and platelets

4
Migration of Inflammatory Cells
Endothelial cells begin to express selective
adhesion molecules that capture
monocytes and other inflammatory cells
initiate development of atherosclerotic
lesions.
After monocytes adhere to endothelium,
they migrate between the endothelial cells
to localize in the intima, transform into
macrophages, and engulf lipoproteins,
largely LDL particales

Lipid Accumulation and Smooth

Muscle Cell Proliferation
Activated macrophages release toxic
oxygen species that oxidize LDL. The
oxidized LDL aggressively ingested by the
macrophages resulting in the formation of
foam cells (primary component
atherosclerotic lesions). Activated
macrophages also produce growth factors
that contribute to migration
and proliferation of smooth muscle cells
(SMCs) and the elaboration of extracellular
5
matrix (ECM)
Plaque Structure
Atherosclerotic plaques : aggregation of SMCs, macrophages, and other
leukocytes; ECM, including collagen and elastic fibers; and intracellular and
extracellular lipids.
Superficial fibrous cap : SMCs and dense ECM.
Beneath and to the side of the fibrous cap is cellular area (the shoulder) consisting
macrophages, SMCs, and lymphocytes
Below fibrous cap is a central core of lipid-laden foam cells and fatty debris.
Rupture, ulceration, or erosion of an unstable or vulnerable brous cap may lead to
hemorrhage into the plaque or thrombotic occlusion of the vessel lumen 6
MANIFESTASI KLINIS PJK

1. Asimptomatik (silent myocardial ischemia)

2. Angina pektoris
A. Angina pectoris stabil
B. Angina pectoris tidak stabil
C. Variant angina (prinzmental angina)
3. Infark miokard akut
4. Dekompensasi kordis
5. Aritmia jantung
6. Mati mendadak (sudden death)
7. Syncope
1. ASIMPTOMATIK (SILENT
MYOCARDIAL ISCHEMIA)

▶ Diketahui secara kebetulan (check up)

▶ Tidak terdapat keluhan
▶ EKG menunjukkan depresi segment ST
▶ Pemeriksaan lain dalam batas normal
▶ Mekanisma diduga karena
A. nilai ambang nyeri meningkat,
B. neuropati otonomik (px DM),
C. meningkatnya produksi endomorfin,
D. derajat stenosis yang ringan.
2.a. ANGINA PEKTORIS STABIL
(STABLE ANGINA)

▶ Gejala Klinis
A. Nyeri dada saat aktifitas
B. Bersifat kronis(>2 bulan)
C. Nyeri precordial daerah retrosternal
D. Seperti tertekan benda berat atau terasa
panas
E. Seperti diremas atau tercekik
▶ Menjalar ke
A. lengan kiri atas/ bawah medial
B. Ke leher, daerah maksila
C. Hingga dagu atau punggung
D. Jarang ke lengan kanan
2.a. ANGINA PEKTORIS STABIL
(STABLE ANGINA)

▶ Mekanisme terjadinya iskemia

a. Karena gangguan keseimbangan antara
suplai dan kebutuhan oksigen miokard
b. Karena adanya aterosklerosis aliran koroner
berkurang
c. Terutama saat kebutuhan meningkat
(aktifitas)
d. Terjadilah iskemia
e. Ischemia on effort
2.a ANGINA PEKTORIS STABIL (STABLE
ANGINA)

▶ Pengobatan
▶ Prinsip
▶ Menjaga agar suplai oksigen selalu seimbang
dengan kebutuhan oksigen miokard

▶ Medikamentosa
▶ Gol. Nitrat
▶ Calsium antagonis
▶ Beta blocker
▶ Anti-thrombogenik
▶ Statin
2.a. ANGINA PEKTORIS STABIL (STABLE
ANGINA)

a. Penanganan faktor-faktor resiko juga

penting
b. Perlu dipertimbangkan
▶ Percutaneus transluminal coronary angioplasty (PTCA)
▶ Coronary bypass surgery (CABG)
2.b. ANGINA PEKTORIS TIDAK
STABIL

a. Mirip seperti angina stabil, tetapi

b. Nyeri lebih progresif
c. Frekuensi dan lama bertambah
d. Sering saat istirahat
e. Nitrat tidak mengurangi nyeri

Sering disebut “pre-infarction”

2.b. ANGINA PEKTORIS TIDAK
STABIL

▶ Patofisiologi
a. Plaque aterosklerosis mengalami trombosis, akibat
adanya rupture plaque
b. Terjadi juga spasme
c. Oklusi belum total/ intermitten

▶ EKG
▶ Depresi segmen-ST

▶ Enzim jantung belum meningkat

2.b. ANGINA PEKTORIS TIDAK
STABIL

▶ PENGOBATAN
a. Perlu monitor EKG 24 jam
b. Di ruang ICCU

▶ Medikamentosa
a. Obat anti nyeri
b. Oksigen
c. Antitrombotik
d. antikoagulan
e. Nitrat
f. Calsium antagonist
g. Beta blocker
h. Statin
2.b. ANGINA PEKTORIS TIDAK
STABIL

▶ Bila obat-obatan tidak berhasil

1. Dilakukan angiografi koroner

2. PTCA/ CABG
2.c. Variant Angina (prinzmetal`s
angina)

1. Ditemukan th 1959
2. Nyeri selalu saat istirahat
3. Terjadi karena spasme koroner
4. Spasme bersifat lokal
5. Bukan karena peningkatan kebutuhan oksigen
oleh miokard
6. EKG
▶ Bisa terdapat elevasi segmen ST
2.c. Variant Angina (prinzmetal`s
angina)

▶ Maifestasi klinis
1. Sering pada usia muda
2. Tanpa faktor resiko
3. Nyeri sering pada tengah malam – 8 pagi
4. Nyeri sangat hebat

▶ EKG
1. Depresi segmen ST/ elevasi segmen ST
2. Bisa disertai aritmia jantung
 2.c. Variant Angina (prinzmetal`s
angina)

Pengobatan

nitrat
Respon baik dengan Calsium
antagonist
Alfa blocker

Beta blocker Tidak bermanfaat

Antitrombotik
 3. INFARK MIOKARD AKUT

Manifestasi klinis
▶ Gejala prodromal
1. Dada terasa tidak enak (chest discomfort)
2. Sering saat istirahat
3. 30% penderita mengeluh 1-4 mg SMRS
4. 70% < 1 mg SMRS
5. Rasa lemah dan kelelahan
 3. INFARK MIOKARD AKUT

Nyeri dada
Intensitas nyeri sangat berat, Heavy pain
Lama 30 menit – beberapa jam
Compressing
Constricting
Crushing
Kualitas Squeezing
nyeri Choocking
Knife like
burning
 3. INFARK MIOKARD AKUT

Pemeriksaan laboratorium
▶ Serum marker
1. creatin kinase (CK)
▶ Meningkat dalam 4-8 jam, normal dalam
2-3 hari, kadar puncak pada 24 jam
2. CK isoenzim (CK-MB)
▶ Meningkat dalam 3-12 jam, normal
dalam 3-4 hari, puncak pada 18-36 jam
3. Serum glutamic oxaloacetic transaminase
(SGOT)
4. Lactic dehidrogenase (LDH)
▶ Meningkat dalam 10 jam, normal dalam
10-14 hari, puncak pada 24-48 jam
5. Cardiac troponin (cTnI, cTnT)
3. INFARK MIOKARD AKUT

Kriteria diagnostik
▶ Menurut WHO, bila terdapat 2 dari

1.Nyeri dada yang spesifik

2.Perubahan EKG
Gelombang Q patologis, dg
Elevasi segmen ST
3.Peningkatan kadar enzim jantung
3. INFARK MIOKARD AKUT

Obat-obat yang diberikan

1. Analgetik
▶ Morfin 2,0-2,5 mg iv, titrasi
2. Nitrat
a. Sublingual dilanjutkan peroral/ intravena
b. Efek venodilatasi
▶ Menurunkan venous return
▶ Menurunkan preload
c. Efek dilatasi koroner
3. Aspirin
▶ Menurunkan angka kematian
 3. INFARK MIOKARD AKUT

Obat-obat yang diberikan

4. Beta blocker
5. ACE-inhibitor

Obat-obat lain
6. laxantia
7. Diit
8. Modifikasi faktor resiko
 3. INFARK MIOKARD AKUT
▶ Terapi trombolitik (bila onset < 12 jam)
a. Streptokinase
b. r-TPA
▶ (recombinant tissue plasminogen activator complex)
c. Urokinase
d. ASPAC
▶ (Anisolated plasminogen streptokinase activator)
e. Scu-PA
▶ (single chain urokinase-type plasminogen activator)
3. INFARK MIOKARD AKUT

Komplikasi
1. Gagal jantung akut
2. Edema paru akut
3. Aritmia
4. Ruptur dinding ventrikel, septum (IVS)
5. Regurgitasi mitral akut
6. Syok kardiogenik
7. kematian
 Revascularizations

Percutaneous coronary intervention (

Coronary artery bypass grafting (CABG)
Terima Kasih