DAFTAR ISI

Daftar Isi................................................................................................................... i

Daftar Gambar…………………………………………………………………….iii

Daftar Tabel………………………………………………………………………. iv

Daftar Singkatan…………………………………………………………………. v

Bab I Latar Belakang.............................................................................................. 1

Bab II Tinjauan Pustaka......................................................................................... 3

2.1 Metabolisme sel-sel miokard pada keadaan normal dan iskemia ……...…..... 3

2.1.1 Metabolisme Miokard Pada Keadaan Normal……………………………... 3

2.1.2. Metabolisme Miokard Pada Keadaan Iskemia……………………………. 9

2.2. Perubahan Metabolik pada Infark Miokard Akut……………………………….. 14

2.2.1. Peningkatan Kadar Katekolamin Plasma………………………………….. 15

2.2.2. Peningkatan Asam lemak bebas Sirkukasi………………………………16

2.2.2.1. Efek Buruk Peningkatan Asam Lemak Bebas pada Infark Miokard 20

2.2.3. Hiperglikemia………………………………………………………………….. 22

2.2.3.1. Efek Hiperglikemia Terhadap Kardiovaskular………………………. 23

2.2.5. Perubahan Asam Basa………………………………………………………… 31

2.2.6. Gangguan Keseimbangan Elektrolit………………………………………… 33

2.3. Perubahan Asam Basa pada Infark Miokard Akut dan Efek Buruknya........ 11

2.4. Perubahan Keseimbangan Elektrolit pada Infark Miokard Akut dan

efek buruknya……………………………………………………………………… 33
2.5. Terapi Mencegah Penambahan Ukuran Infark terkait Gangguan Metabolik
padaIskemia Miokard……………...………………………………………………36

Bab III Kesimpulan..................................................................................................47

i
Daftar Pustaka.......................................................................................................... 26

ii
 DAFTAR GAMBAR

Gambar 1. Substrat Energi untuk Metabolisme Miokard………………………….. 4

Gambar 2. Metabolisme sel otot jantung pada kondisi normal……………………..5
Gambar 3. Siklus oksidasi Asam Lemak dan Glukosa pada Metabolisme Energi
Miokard……………………………………………………………………………. 6
Gambar 4. Perubahan metabolisme Glukosa dan Asam Lemak saat Iskemia 11
Gambar 5. Perubahan metabolisme Glukosa dan FFA saat Reperfusi 13
Gambar 6. Skema Metabolik oleh karena penurunan aliran darah miokard akibat
Iskemia …………………………………………………………………………….. 14
Gambar 7. Perubahan Metabolik yang terjadi pada Infark Miokard Akut………….
15
Gambar 8. Jalur lipolisis pada sel adipose…..……………………………………... 17
.Gambar 9. Bagan lipolisis klasik…………………………………………………., 18
Gambar 10. Jalur lipolisis pada sel otot skelet 19
Gambar 11. Efek hiperglikemia terhadap jantung pada fase akut infark miokard 24
Gambar 12. Mekanisme Hiperaktivasi Platelet pada Hiperglikemia 26
Gambar 13. Faktor-faktor yang Bertanggung Jawab terhadap Hiperaktivtias Platelet
pada Diabetes Melitus Tipe 2…………………………………………...…………. 27
Gambar 14. Ukuran Infark pada akhir 40 menit iskemia dan 120 menit reperfusi pada
kelompok DM dan kelompok
control……………………………………………………………………………… 29
Gambar 15. Mekanisme Hiponatremia pada Gagal Jantung……………………… 34

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 DAFTAR TABEL

Tabel 1. Pedoman Manajemen Hiperglikemia pada Sindrom Koroner

Akut …………………………… 39
Tabel 2. Trial Terapi insulin pada hiperglikemia untuk Sindrom Koroner
Akut ……………………………. 40

iv
 DAFTAR SINGKATAN

AC : Adenylate Cyclase
ADA : American Diabetic Association
AMPK :Monophosphate Activated Protein Kinase
ASDR : age-standardized death rate
ATP : Adenosine Triphosphate
cAMP : Cyclic Adenosine Monophosphate
CPT : Carnitine Palmitoyl Transferase
ETC : electron transport chain
ESC : European Society of Cardiology
FABP : Fatty Acid Binding Protein
FADH : Flavin Adenine Dinucleotide Hydrogen
FFA : Free Fatty Acid
GLUT : Glucose Transporter
HSL : Hormone sensitive Lipase
IMA : Infark Miokard Akut
IPC : Ischemic Preconditioning
LDH : Lactate Dehydrogenase
MCD : Malonyl CoA Decarboxylase
MACE : Major Adverse Cardiovasular Event
M-CPT-2 : Muscle Form Of Carnitine-Palmitoyl Transferase-2
NAD : Nicotinamide Adenine Dinucleotide
NADH : Nicotinamide Adenine Dinucleotide Hydrogen
NSTEMI : Non ST Elevasi Miokard Infark
OXPHOS : Oxidative Phosphorilation
PI3K : Phosphatidylinositol-3-phosphate–dependent kinase
PAI-1 : Plasminogen Acticator Inhibitor
PDH : Pyruvate Dehydrogenase
PCI : Percutaneous Coronary Intervention
PFK-1 : 6-phosphofructo-1-kinase
PKC : Protein Kinase C
PDC : pyruvate decarboxylase
PDH : Pyruvate Dehydrogenase
SR : Sarkoplasmik Retikulum
SAS : Siklus Asam Sitrat
SGLT : Sodium Glucose Linked Transport
STEMI : ST Elevasi Miokard Infark
TXA2 : Thromboxan A2

v
 Referat II

METABOLIC DISTURBANCE IN ACUTE MYOCARDIAL INFARCTION

Oleh :
dr. Dwi Widya Puji Astuti

Pembimbing:

1. Prof dr. Peter Kabo PhD, Sp.FK, Sp.JP (K)

2. dr. Akhtar Fajar Muzakkir Sp.JP (K)

Departemen Kardiologi Dan Kedokteran Vaskular

Fakultas Kedokteran Universitas Hasanuddin
Rumah Sakit Wahidin Sudirohusodo
Makassar
2020

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Infarction Using GC-MS-Based Tissue Metabolomics. Int Heart J 2017; 58: 441-446)

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EFEK BURUK PERUBAHAN METABOLISME ENERGI PADA OTOT JANTUNG

Sebagai konsekwensi dari perubahan metabolisme energetik sel otot jantung, dapat terjadi
beberapa efek buruk yang mengancam pertahanan miosit. Penggunaan FFA sebagai
substrat energi saat iskemia, menghasilkan beberapa efek merugikan antara lain
1. dddddd
2. 2…..
3. dddd
4. tttt

In addition, the plasma

glucose level on admission is predictive of in-hospital mortality after acute STelevation
myocardial infarction (STEMI). Thisalgprtih manajemen hiperglkemami

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