simple guideline for acute coronary syndrome prof bambangirawan

Curriculum Vitae. Prof dr Bambanq Irawan FIHA FAsCC FInaSIM

• Internist [ PB PAPDI ] 1981 • Internist Cardiovascular Consultant [ PB PAPDI ] 1996

• Cardiologist and FIHA [ PP PERKI ] 2004• Cardiologist Consultant [ PP PERKI ] 2005

• Profesor in Cardiology [ DIRJEN DIKTI ] 2006

• FAsCC [ Asean Society of Cardiology ] 2008• FinaSIM [ PB PAPDI ] 2009

Bambang Irawan SpPD[K], SpJP[K], FIHA, FInaSIM, FAsCC

Divisi Cardiology Departement of Cardiology

Faculty of Medicine Gadjah Mada University

Simple Guideline for Acute Coronary Syndrome (ACS)

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 fromdisease, Injurues and Risk Farctors in 1990 and projected to 2020.Cambridge, Mass:Harvard University Press;1996

Supply-Demand Mismatch

Oxygen Supply -Blood Flow -O2 Carrying Capacity

Oxygen Demand -Heart rate -Contractility -Wall stress

Heart rate

Afterload

wall stress

Heart size

Contractility

Exercise

Spasm

Collaterals

O2 O2Demand Supply Vasoconstriction

Ischemic Oxygen Balance

VS

Hb Level

O2 Content

Coronary blood flow

O2 Saturation

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

Diamond GA. J Am Coll Cardiol 1983;1:574

Atypical angina (probable)meets 2 of the above characteristics

Noncardiac chest painmeets <=1 of the typical angina characteristics

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.

SAKIT DADA

Bio-chemistry

Stratifikasirisiko

Diagnosis

Pengobatan

Curiga Sindrom Koroner Akut

Elevasi STmenetap

ST/T-abnormalities

Normal atauTdk dpt ditentukan ECG

Risiko tinggi Risiko rendah

Pemeriksaan awal pada Sindrom Koroner Akut

STEMI NSTEMI Angina tidak stabil

Reperfusi Invasive Non-Invasive

Troponin (+) Troponin 2 kali negatif

Masuk RS

ECG

Diagnosis kerja

3

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

SAKIT DADA

Bio-chemistry

Stratifikasirisiko

Diagnosis

Pengobatan

Curiga Sindrom Koroner Akut

Elevasi STmenetap

ST/T-abnormalities

Normal atauTdk dpt ditentukan ECG

Risiko tinggi Risiko rendah

Pemeriksaan awal pada Sindrom Koroner Akut

STEMI NSTEMI Angina tidak stabil

Reperfusi Invasive Non-Invasive

Troponin (+) Troponin 2 kali negatif

Masuk RS

ECG

Diagnosis kerja

3

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

FoamCells

FattyStreak

IntermediateLesion Atheroma

FibrousPlaque

ComplicatedLesion/Rupture

Endothelial DysfunctionFrom first decade From third decade From fourth decade

Growth mainly by lipid accumulation Smooth muscleand collagen

Thrombosis,hematoma

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

SAKIT DADA

Bio-chemistry

Stratifikasirisiko

Diagnosis

Pengobatan

Curiga Sindrom Koroner Akut

Elevasi STmenetap

ST/T-abnormalities

Normal atauTdk dpt ditentukan ECG

Risiko tinggi Risiko rendah

Pemeriksaan awal pada Sindrom Koroner Akut

STEMI NSTEMI Angina tidak stabil

Reperfusi Invasive Non-Invasive

Troponin (+) Troponin 2 kali negatif

Masuk RS

ECG

Diagnosis kerja

3

ELEKTROKARDIOGRAMEKG 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

3

.

• .

Inferior Wall MI

Anterior Wall MI

New LBBB

T inverted

SAKIT DADA

Bio-chemistry

Stratifikasirisiko

Diagnosis

Pengobatan

Curiga Sindrom Koroner Akut

Elevasi STmenetap

ST/T-abnormalities

Normal atauTdk dpt ditentukan ECG

Risiko tinggi Risiko rendah

Pemeriksaan awal pada Sindrom Koroner Akut

STEMI NSTEMI Angina tidak stabil

Reperfusi Invasive Non-Invasive

Troponin (+) Troponin 2 kali negatif

Masuk RS

ECG

Diagnosis kerja

3

SPEKTRUM KLINIS SKA4

SAKIT DADA

Bio-chemistry

Stratifikasirisiko

Diagnosis

Pengobatan

Curiga Sindrom Koroner Akut

Elevasi STmenetap

ST/T-abnormalities

Normal atauTdk dpt ditentukan ECG

Risiko tinggi Risiko rendah

Pemeriksaan awal pada Sindrom Koroner Akut

STEMI NSTEMI Angina tidak stabil

Reperfusi Invasive Non-Invasive

Troponin (+) Troponin 2 kali negatif

Masuk RS

ECG

Diagnosis kerja

3

TIMI Risk Score UA / NSTEMI

Age ≥ 65≥ 3 CAD risk factors(FHx, HTN, ↑ chol, DM, active smoker)

ST deviation ≥ 0.5 mm↑ cardiac markersRecent (≤ 24H) severe angina

HISTORICAL

PRESENTATION

RISK SCORE = Total Points (0 - 7)

Known CAD (stenosis ≥ 50%)ASA use in past 7 days

1

1

11

11

POINTS

0/12345

6/7

RISKSCORE

RISK OF CARDIAC EVENTS (%)BY 14 DAYS IN TIMI 11B*

33571219

DEATH OR MI

DEATH, MI ORURGENT REVASC

5813202641

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

1

Low = 0-2 points, Medium = 3-4 pointsHigh = 5-7 points

5

SAKIT DADA

Bio-chemistry

Stratifikasirisiko

Diagnosis

Pengobatan

Curiga Sindrom Koroner Akut

Elevasi STmenetap

ST/T-abnormalities

Normal atauTdk dpt ditentukan ECG

Risiko tinggi Risiko rendah

Pemeriksaan awal pada Sindrom Koroner Akut

STEMI NSTEMI Angina tidak stabil

Reperfusi Invasive Non-Invasive

Troponin (+) Troponin 2 kali negatif

Masuk RS

ECG

Diagnosis kerja

3

Providing relief for the ischemic heart

Reduction ofPreload

Reduction ofafterload

Reduction ofcontractility

Reduction ofHeart rate

Reduction of the oxygen demand

Elevation of oxygen supply

Reduction of the extravasalcoronary resistance

Prolongation of thediastolic interval

Dissolution or Prevention Of Intravasal obstruction

Nitrocompounds

CCBsACE-I B Blockers CCBs

Nitro vasodilatatorsACE-IIn case of HF

B BlockersCCBs

Inhibitor of pleteletAggregationThrombvolytic agents

Symptom Recognition

Call to Medical System

ER Cath LabPreHospital

Delay in Initiation of Reperfusion Therapy

Increasing Loss of Myocytes

Treatment Delayed is Treatment Denied

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)3. Suplemen O2 4. Terapi anti iskemia

Nitrat5. Antiplatelet dan antikoagulan

Clopidogrel 300 mg, TiclopidineHeparin atau Low Molecular Weight HeparinHirudin

Tranquilizer5. a. STEMI : tentukan segera pilihan revaskularisasi

( Fibrinolitik Vs PCI)b. Non STEMI : segera lakukan stratifikasi risiko

MONA

• Morfin:2.5mg-5 mg IV perlahanHati –hati pada : inferior MCI,asthma, bradikardia

• Pethidin : 12.5-25 mg IV pelan

PAIN KILLER

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

LMWHEnoxaparineFondaparinux

• 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)

• 1mg/kg, SC , bid (5 hari)• 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 jam2. 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 jam2. Presentasi < 3 jam namun terdapat

kontraindikasi fibrinolitik3. 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 RISIKOpada 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)

Extension / Ischemia

Complications of Acute MI

Acute MI

Arrhythmia

Heart Failure

Expansion / Aneurysm RV Infarct

Pericarditis

Mechanical Mural Thrombus

Komplikasi awal :

Aritmia Disfungsi LV dan gagal jantungRuptur ventrikel Regurgitasi mitral akut Gagal fungsi RV Syok kardiogenik

Komplikasi lambat :

Trombosis mural dan Emboli sistemikAneurisma LV DVT Emboli paru Sindrome Dressler

How to reduce plaque formationIntervention on risk fact

How to reduce the risk of plaque rupture

KESIMPULAN1. 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.