Curriculum Vitae

Prof dr Bambanq Irawan FIHA FAsCC FInaSIM

1981 1996 2004 2005 2006 2008 2009

Internist [ PB PAPDI ] Internist Cardiovascular Consultant [ PB PAPDI ] Cardiologist and FIHA Cardiologist Consultant Profesor in Cardiology FAsCC FinaSIM [ PP PERKI ] [ PP PERKI ] [ DIRJEN DIKTI ]

[ Asean Society of Cardiology ] [ PB PAPDI ]

Simple Guideline for Acute Coronary Syndrome (ACS)

Bambang Irawan SpPD[K], SpJP[K], FIHA, FInaSIM, FAsCC Divisi Cardiology Departement of Cardiology Faculty of Medicine Gadjah Mada University

Coronary Heart Disease

Ischemic heart disease : epidemiology

Annual incidence of angina: 213/100.000 population > 30 years old Ischemic heart disease (IHD) is the main cause of death in Europe and USA Cardiovascular mortality in patients with chronic stable angina: 1.3-10 %/year Chronic stable angina is the initial symptom of IHD

Murray CJL.,ed,Lopez AD. The Global Burden of Disease: a Comprehensive Assessment of Mortality and Disability from disease, Injurues and Risk Farctors in 1990 and projected to 2020.Cambridge, Mass:Harvard University Press;1996

Supply-Demand Mismatch

O xygen Supply - Blood Flow -O2 Carrying Capacity

O xygen Dem and - Heart rate -Contractility -W all stress

Hb Level Exercise Heart rate Afterload wall stress Heart size Contractility

O2 Saturation

O2 Content

Collaterals Coronary blood flow

O2 O2 VS Demand Supply

Vasoconstriction Spasm

Ischemic Oxygen Balance

CLINICAL CLASSIFICATION OF CHEST PAIN

Typical angina (definite) Substernal chest discomfort with a characteristic quality and duration that is provoked by exertion or emotional stress and relieved by rest or nitroglycerin

Atypical angina (probable) meets 2 of the above characteristics Noncardiac chest pain meets <=1 of the typical angina characteristics
Diamond GA. J Am Coll Cardiol 1983;1:574

CCS Classification
I : Angina occurring with strenous but not ordinary physical activity II : Slight limitation of ordinary physical activity III : Marked limitation of ordinary physical activity IV : Inability to carry on any physical activity without discomfort, symptoms may be present at rest.

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis kerja SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap ST/Tabnormalities Troponin (+) Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif
Risiko rendah

ECG 3
Biochemistry Stratifikasi risiko Diagnosis Pengobatan

Risiko tinggi

STEMI Reperfusi

NSTEMI Invasive

Angina tidak stabil Non-Invasive

Karakteristik Angina pd ACS

Terlokalisir terutama (tapi tidak selalu) di daerah prekordium Menyebar ke lengan, leher, punggung, atau epigastrium Tidak berubah dengan posisi atau pergerakan Sering terasa seperti menekan, constricting atau crushing Episode > 20 menit Diikuti sesak, pusing, mual, atau berkeringat

Possible presentation of ACS

Angina at rest, with pain episodes lasting > 20 min New onset ( within < 2 months ) exertional angina of at least CCSC III Recent increase ( < 2 months ) in anginal severity to at least CCSC III Angina post MCI

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis kerja SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap ST/Tabnormalities Troponin (+) Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif
Risiko rendah

ECG 3
Biochemistry Stratifikasi risiko Diagnosis Pengobatan

Risiko tinggi

STEMI Reperfusi

NSTEMI Invasive

Angina tidak stabil Non-Invasive

CHARACTER OF ANGINAL PAIN

Localized usually at precordium Radiate to arm, neck, shoulder, back or epicardium Feels like being pressed by heavy object, or constricting or crushing. Episode > 20 min Concomitant systemic symptoms: dyspnea, dizziness, nausea, diaphoresis

The Grip of Angina

Atherosclerosis Timeline
Foam Cells Fatty Streak Intermediate Lesion Atheroma Fibrous Plaque Complicated Lesion/Rupture

Endothelial Dysfunction From first decade From third decade From fourth decade
Growth mainly by lipid accumulation
Smooth muscle and collagen Thrombosis, hematoma

Stary HC, et al. Circulation. 1995;92:1355-74. Artery wall often gets larger with increasing plaque-Glagov NEJM 1987

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis kerja SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap ST/Tabnormalities Troponin (+) Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif
Risiko rendah

ECG 3
Biochemistry Stratifikasi risiko Diagnosis Pengobatan

Risiko tinggi

STEMI Reperfusi

NSTEMI Invasive

Angina tidak stabil Non-Invasive

ELEKTROKARDIOGRAM
EKG 12 Sandapan Pertama

TENTUKAN: Irama Elevasi SEGMENT ST ? Depresi SEGMENT ST ? LEFT BUNDLE BRANCH BLOCK (BARU)? T inverted ? Gelombang Q ? NON DIAGNOSTIK atau EKG normal

.
.

Inferior Wall MI

Anterior Wall MI

New LBBB

T inverted

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis kerja SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap ST/Tabnormalities Troponin (+) Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif
Risiko rendah

ECG 3
Biochemistry Stratifikasi risiko Diagnosis Pengobatan

Risiko tinggi

STEMI Reperfusi

NSTEMI Invasive

Angina tidak stabil Non-Invasive

SPEKTRUM KLINIS SKA

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis kerja SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap ST/Tabnormalities Troponin (+) Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif
Risiko rendah

ECG 3
Biochemistry Stratifikasi risiko Diagnosis Pengobatan

Risiko tinggi

STEMI Reperfusi

NSTEMI Invasive

Angina tidak stabil Non-Invasive

TIMI Risk Score UA / NSTEMI

HISTORICAL Age 65 3 CAD risk factors POINTS 1 1 1
RISK OF CARDIAC EVENTS (%) BY 14 DAYS IN TIMI 11B*
RISK SCORE DEATH OR MI DEATH, MI OR URGENT REVASC

(FHx, HTN, chol, DM, active smoker)

Known CAD (stenosis 50%) 1 ASA use in past 7 days PRESENTATION Recent ( 24H) severe angina 1 cardiac markers 1 1 ST deviation 0.5 mm RISK SCORE = Total Points (0 - 7)
Low = 0-2 points, Medium = 3-4 points High = 5-7 points

0/1 2 3 4 5 6/7

3 3 5 7 12 19

5 8 13 20 26 41

*Entry criteria:UA or NSTEMI defined as ischemic pain at rest within past 24H, with evidence of CAD (ST segment deviation or +marker)

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis kerja SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap ST/Tabnormalities Troponin (+) Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif
Risiko rendah

ECG 3
Biochemistry Stratifikasi risiko Diagnosis Pengobatan

Risiko tinggi

STEMI Reperfusi

NSTEMI Invasive

Angina tidak stabil Non-Invasive

Elevation of oxygen supply

Reduction of the extravasal coronary resistance Nitro vasodilatators ACE-I In case of HF

Prolongation of the diastolic interval B Blockers CCBs

Dissolution or Prevention Of Intravasal obstruction Inhibitor of pletelet Aggregation Thrombvolytic agents

Providing relief for the ischemic heart

Nitro compounds Reduction of Preload CCBs ACE-I B Blockers CCBs

Reduction of afterload

Reduction of contractility

Reduction of Heart rate

Reduction of the oxygen demand

Treatment Delayed is Treatment Denied

Symptom Recognition

Call to Medical System

PreHospital

ER

Cath Lab

Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy

Immediate Assessment in ER
Vital signs, including blood pressure Oxygen saturation IV access 12-leads ECG < 10 minutes Brief, targeted history and physical exam (to identify reperfusion candidates) Fibrinolytic check list; check contraindications Obtain initial cardiac markers

Immediate Assessment in ER
Portable Chest X-ray < 30 min Assess for the following : -Heart rate > 100 bpm and SBP < 100 mmHg -Pulmonary edema/rales or -Signs of shock If any of these conditions is present, consider triage to a facility capable of cardiac catheterization and revascularization

TERAPI PADA SINDROMA KORONER AKUT

PERAWATAN DI RUMAH SAKIT 1. Antiplatelet (Aspirin 160 mg) 2. Pain killer (morfin) M 3. Suplemen O2 O 4. Terapi anti iskemia Nitrat N 5. Antiplatelet dan antikoagulan A Clopidogrel 300 mg, Ticlopidine Heparin atau Low Molecular Weight Heparin Hirudin 5. a. STEMI : tentukan segera pilihan revaskularisasi ( Fibrinolitik Vs PCI) b. Non STEMI : segera lakukan stratifikasi risiko

Tranquilizer

PAIN KILLER
Morfin: 2.5mg-5 mg IV perlahan Hati hati pada : inferior MCI, asthma, bradikardia Pethidin : 12.5-25 mg IV pelan

OKSIGEN
Pemberian suplemen O2 diberikan pada pasien dengan desaturasi O2 (SaO2 <90%) Suplemen O2 mungkin membatasi injury miokard atau bahkan mengurangi elevasi ST Pemberian suplemen O2 rutin > 6 jam pertama pd kasus tanpa komplikasi

ACC/AHA Guideline of STEMI 2004

ANTI ISKEMIK
NITRAT B BLOKER (jika tidak ada kontraindikasi) ANTAGONIS KALSIUM (UAP/NSTEMI)

VASODILATOR
INHIBITOR ACE (EF < 40%, anterior MCI, HF) NITRAT IV (jika AHF)

ANTITROMBOTIK DAN ANTIKOAGULAN

Heparin ( Unfractionated Heparin) Low Molecular Weight Heparin Anti Xa

DOSIS YANG DIREKOMENDASIKAN

UFH
Initial I.V BOLUS 60 UI/Kg max 4000 UI Infus :12-15 UI/kg BB/jam max 1000 UI/jam Monitor APTT : 3, 6, 12, 24 jam setelah mulai terapi Target APTT 50-70 msec (1,5 -2 x kontrol)

LMWH
Enoxaparine 1mg/kg, SC , bid (5 hari) Fondaparinux 2,5 cc , satu kali sehari (5 hari)

REVASKULARISASI PADA STEMI < 12 jam Apa pilihan kita?

FIBRINOLITIK VS PCI

Fibrinolitik lebih dianjurkan jika: ( 3 Point)

1. Presentasi STEMI akut 3 jam 2. Jika presentasi STEMI > 3 jam namun tindakan PCI tidak bisa dikerjakan atau akan terlambat dikerjakan;
Waktu antara pasien tiba sampai dengan inflasi balon >90 menit

3. Tidak ada kontraindikasi fibrinolitik

Catatan: Fibrinolitik harus dikerjakan dalam waktu < 30 mnt (Door to Needle time < 30 menit)

PCI primer lebih dianjurkan jika: ( 5 Point )

1. Presentasi 3 jam 2. Presentasi < 3 jam namun terdapat kontraindikasi fibrinolitik 3. Tersedia fasilitas PCI dan waktu kontak antara pasien tiba sampai dengan inflasi balon <90 menit 4. STEMI akut dengan risiko tinggi ( gagal jantung Killip 3 dan syok kardiogenikl) 5. Diagnosis STEMI masih diragukan

STRATIFIKASI RISIKO pada Non-STEMI / UAP

MENENTUKAN STRATEGI TATALAKSANA NON STEMI/UAP

Strategi Invasif (angiografi akan dilakukan dalam 48 jam) VS Strategi Konservatif (angiografi tidak akan dilakukan/direncanakan elektif)

Complications of Acute MI
Extension / Ischemia Arrhythmia Pericarditis

Expansion / Aneurysm

Acute MI

RV Infarct

Mechanical

Heart Failure

Mural Thrombus

Komplikasi awal :
Aritmia Disfungsi LV dan gagal jantung Ruptur ventrikel Regurgitasi mitral akut Gagal fungsi RV Syok kardiogenik

Komplikasi lambat :
Trombosis mural dan Emboli sistemik Aneurisma LV DVT Emboli paru Sindrome Dressler

How to reduce plaque formation Intervention on risk fact

How to reduce the risk of plaque rupture

KESIMPULAN
1. Tatalaksana STEMI dimana tersedia fasilitas PCI adalah PCI primer. Jika sarana PCI tidak tersedia diberikan trombolitik sesuai indikasi dan kontraindikasi. 2. Tatalaksana NSTEMI meliputi strategi invasif dini dan strategi konservatif sesuai stratifikasi risiko. 3. Klopidogrel direkomendasikan sebagai antiplatelet (klas 1) untuk penanganan ACS baik STEMI maupun UA/NSTEMII dan diberikan bersama ASA. Clopidogrel diberikan tunggal jika terdapat kontraindikasi ASA (ACC-AHA / ESC Guideline). 4. GPIIb-IIIa inhibitor diberikan pada pasien yang menjalani PCI primer. 5. Fondaparinux dan Enoksaparin efektif pada SKA.