Curriculum Vitae .
Prof dr Bambanq Irawan FIHA FAsCC FInaSIM
• •
Internist [ PB PAPDI ] Internist Cardiovascular Consultant [ PB PAPDI ]
1981 1996
• •
Cardiologist and FIHA Cardiologist Consultant
2004 2005
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Profesor in Cardiology
• •
FAsCC FinaSIM
[ PP PERKI ] [ PP PERKI ] [ DIRJEN DIKTI ]
[ Asean Society of Cardiology ] [ PB PAPDI ]
2006 2008 2009
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
O2 Saturation
O2 Content
Heart rate Afterload
Collaterals
wall stress
Coronary blood flow
Heart size Contractility
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 SAKIT DADA
Masuk RS Diagnosis kerja
ECG 3
Curiga Sindrom Koroner Akut Elevasi ST menetap
ST/Tabnormalities
Biochemistry
Troponin (+)
Stratifikasi risiko
Risiko tinggi
Diagnosis
STEMI
Pengobatan
Reperfusi
NSTEMI Invasive
Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif Risiko rendah
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 SAKIT DADA
Masuk RS Diagnosis kerja
ECG 3
Curiga Sindrom Koroner Akut Elevasi ST menetap
ST/Tabnormalities
Biochemistry
Troponin (+)
Stratifikasi risiko
Risiko tinggi
Diagnosis
STEMI
Pengobatan
Reperfusi
NSTEMI Invasive
Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif Risiko rendah
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 SAKIT DADA
Masuk RS Diagnosis kerja
ECG 3
Curiga Sindrom Koroner Akut Elevasi ST menetap
ST/Tabnormalities
Biochemistry
Troponin (+)
Stratifikasi risiko
Risiko tinggi
Diagnosis
STEMI
Pengobatan
Reperfusi
NSTEMI Invasive
Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif Risiko rendah
Angina tidak stabil Non-Invasive
3
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 SAKIT DADA
Masuk RS Diagnosis kerja
ECG 3
Curiga Sindrom Koroner Akut Elevasi ST menetap
ST/Tabnormalities
Biochemistry
Troponin (+)
Stratifikasi risiko
Risiko tinggi
Diagnosis
STEMI
Pengobatan
Reperfusi
NSTEMI Invasive
Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif Risiko rendah
Angina tidak stabil Non-Invasive
4
SPEKTRUM KLINIS SKA
Pemeriksaan awal pada Sindrom Koroner Akut SAKIT DADA
Masuk RS Diagnosis kerja
ECG 3
Curiga Sindrom Koroner Akut Elevasi ST menetap
ST/Tabnormalities
Biochemistry
Troponin (+)
Stratifikasi risiko
Risiko tinggi
Diagnosis
STEMI
Pengobatan
Reperfusi
NSTEMI Invasive
Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif Risiko rendah
Angina tidak stabil Non-Invasive
5
TIMI Risk Score UA / NSTEMI HISTORICAL Age ≥ 65 ≥ 3 CAD risk factors
(FHx, HTN, ↑ chol, DM, active smoker)
POINTS 1 1
Known CAD (stenosis ≥ 50%) 1 ASA use in past 7 days
1
PRESENTATION Recent (≤ 24H) severe angina 1 ↑ cardiac markers 1 1 ST deviation ≥ 0.5 mm
RISK OF CARDIAC EVENTS (%) BY 14 DAYS IN TIMI 11B* RISK SCORE
0/1 2 3 4 5 6/7
DEATH OR MI
DEATH, MI OR URGENT REVASC
3 3 5 7 12 19
5 8 13 20 26 41
RISK SCORE = Total Points (0 - 7) Low = 0-2 points, Medium = 3-4 points High = 5-7 points
*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 SAKIT DADA
Masuk RS Diagnosis kerja
ECG 3
Curiga Sindrom Koroner Akut Elevasi ST menetap
ST/Tabnormalities
Biochemistry
Troponin (+)
Stratifikasi risiko
Risiko tinggi
Diagnosis
STEMI
Pengobatan
Reperfusi
NSTEMI Invasive
Normal atau Tdk dpt ditentukan ECG Troponin 2 kali negatif Risiko rendah
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
Dissolution or Prevention Of Intravasal obstruction
B Blockers CCBs
Inhibitor of pletelet Aggregation Thrombvolytic agents
Providing relief for the ischemic heart Nitro compounds Reduction of Preload
CCBs ACE-I
Reduction of afterload
B Blockers
Reduction of contractility
CCBs
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
Tranquilizer
5. a. STEMI : tentukan segera pilihan revaskularisasi ( Fibrinolitik Vs PCI) b. Non STEMI : segera lakukan stratifikasi risiko
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
Expansion / Aneurysm
Mechanical
Arrhythmia Pericarditis
Acute MI
Heart Failure
RV Infarct
Mural Thrombus
Komplikasi awal : 9Aritmia 9Disfungsi LV dan gagal jantung 9Ruptur ventrikel 9Regurgitasi mitral akut 9Gagal fungsi RV 9Syok kardiogenik
Komplikasi lambat : 9Trombosis mural dan 9Emboli sistemik 9Aneurisma LV 9DVT 9Emboli paru 9Sindrome 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.
