Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI

Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI Education         

SR Negeri Tabing, Padang, Tahun 1957 SMPN Kuranji, Padang, Tahun 1960 SMAN I Padang, Tahun 1963 Dokter Umum Fakultas Kedokteran Universitas Gadjah Mada; (S1) Tahun 1972 Dokter Spesialis Jantung dan Pembuluh Darah FK UI; (S2) Tahun1983 Post Graduate Course on Invasive Cardiology, Nuclear Cardiology Austin Hospital Melbourne, Australia, 1992 Post Graduate Course on Non-Invasive Cardiology Pacemaker Implantation, Royal Melbourne Hospital, Australia, 1993 Pendidikan Dokter Universitas Airlangga; (S3) Tahun 2000 Guru Besar tetap Universitas Indonesia; Tahun 2004

Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI • Staf senior, Dept. Kardiologi & Kedokteran Vaskular FKUI & Pusat Jantung Nasional Harapan Kita • Chief cardiologist, RS Medika BSD • Sekretaris Kolegium Pengurus Pusat Perhimpunan Dokter Spesialis Kardiovaskular (PP PERKI) 2008-sekarang • Fellow of Indonesian Heart Association (FIHA) • Fellow of American College of Cardiology (FACC) • Fellow of European Society of Cardiology (FESC) • Fellow of ASEAN Federation of Cardiology (FAsCC) • Fellow of Society of Cardiovascular Angiography and Intervention (FSCAI) • Head of Cardiovascular Devision Medika BSD Hospital

Cardiovascular Emergency : Focus On Acute Coronary Syndromes Roles of Primary Physicians

Idris Idham RS MEDIKA BSD

Spectrum of CV Emergency • Congenital Heart Diseases • Acute Coronary Syndrome : UAP, NSTEMI, STEMI • Acute Lung Edema • Acute Aortic Dissection • Acute Limb Ischemia • Deep Veins Thrombosis

• Hypertensive Crisis : emergency, urgency • Arrhythmia : AFRVR, SVT, VT, VF, TAVB • Cardiomyopathy : PPCM, HCM, DCM.

CARDIOVASCULAR SPECIALIST COMPETENCY ↓ FRONTLINE DOCTORS ↓

FROM PALPITATION TO CVD

Front-line medical practitioners • Play very important role in fighting cardiovascular diseases (CVD), the no.1 killer in Indonesia1 • Front liners are doctors who first encounter the patient, including family physicians • Patients will benefit from early diagnosis and prompt treatment • Competent of recognizing important signs & symptoms of CVD, e.g. chest pain 1Dept.

of Health, RI. 2002.

Chest Pain • One of the most challenging symptoms1 • Diagnosis ranges from benign esophageal reflux to fatal MCI – Failure to manage fatal conditions lead to complications including death – Over management of low risk conditions causes unnecessary burden

• Acute or escalating chronic chest discomfort is most challenging. 1Harrison’s

principles of internal medicine: McGraw-Hill, 2005.

Evaluation Aim • To assess the general clinical condition of patient • To determine the working diagnosis • To initiate immediate management plan • Should be performed rapidly yet accurately

General Clinical Assessment • Stratify patient : stable vs unstable condition; based on level of consciousness & vital signs. • Stabilize the patient first! Secure ABC (airway, breathing, circulation)

Determining Working Diagnosis • Largely a clinical work, accurate anamnesis is the key. • Characteristics of chest pain should be thoroughly explored: – Quality, duration, location, precipitating & relieving factors, other associated features.

• Based on characteristics, determine the organ(s) or system(s) causing the pain.

Determining Working Diagnosis • Consider anatomical structure of thorax & adjacent abdominal organs ; each organ has typical characteristics • Important : features may not always present ; several features may occur simultaneously

Anatomy of Thoracic Cavity

I.I. - ’09 / PDKI Pekanbaru

Features of Major Causes of Chest Pain • Angina: sensation of pressure, tightness, squeezing, heaviness, burning ; located retrosternal, often radiate (detailed later) • Aortic dissection : abrupt onset of tearing or ripping sensation, knife-like pain in anterior chest, often radiate to back • Pleuritis : pleuritic pain, influenced by breathing ; accompanied by cough, fever. 1Harrison’s

principles of internal medicine: McGraw-Hill, 2005.

Features of Major Causes of Chest Pain • Esophageal reflux : burning, substernal or epigastric pain, relieved by antacids • Musculoskeletal : aching, worsened by movement, may be reproduced by localized pressure • Herpes zoster : sharp, burning, dermatomal distribution, with vesicular rash

Differential Diagnosis of Chest Pain Cardiac

Gastrointestinal

• • • •

•Esophageal reflux •Esophageal rupture •Gall bladder disease •Peptic Ulcer •Pancreatitis

ACS: infarct,angina MVP Aortic Stenosis Hypertrophic cardiomyopathy • Pericarditis

Vascular •Aortic dissection/aneurysm

Lungs • • • •

Lung Emboli Pneumonia Pneumothorax Pleuritis

Others •Musculoskeletal •Herpes zoster

General Approach for First liners • Targetted anamnesis and thorough physical exams • Consider most likely diagnoses If more than one, consider the worst one

• Closely monitor vital signs • Administer essential first-line drugs • Refer to higher facility if required, after patient is reasonably stabilized

Focus on:

Acute Coronary Syndromes


DEFINITION A spectrum of clinical syndromes due to sudden, significantly compromised coronary circulation ranging from unstable angina to NSTEMI and STEMI. Further stages of stable angina pectoris

Topol EJ, ed. Textbook of cardiovascular medicine 2007.

PATHOPHYSIOLOGY

Atherosclerosis Timeline Foam Cells

Fatty Streak

Intermediate Atheroma Lesion

Fibrous Plaque

Complicated Lesion/Rupture

Endothelial Dysfunction From first decade

From third decade

Growth mainly by lipid accumulation

From fourth decade Smooth muscle and collagen

Thrombosis, hematoma

Stary HC et al. Circulation 1995;92:1355-1374.

DIAGNOSIS

Presentation (Clinical, Initial ECG)

Working diagnosis

ST-Seg Elevation Myocardial Infarction

Non-STSeg Elevation Acute Coronary Syndr

Time

Evolution of ECG & Biomarkers Final diagnosis

Biomarker (+)

ST-Seg Elevation MCI

Non-ST-segElevation MCI

Biomarker (-)

Unstable Angina

National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006 I.I. - ’09 / PDKI Pekanbaru

Algorithm in Acute Coronary Syndrome CHEST PAIN

Working diagnosis

Suspected ACS

ECG

Biochemistry

Persistent ST elevation

No persistent ST elevation

Troponin, CKMB (+)

Troponin, CKMB (+)

Risk Stratification

Risk: high / low

Management

Initial management, ± revascularization

Secondary prevention

Medical therapy, coronary angiography

{on serial ECG}

Performed in 10 min

Admission

- ACS unlikely - NSTEMI - STEMI

Modified from ESC 2007

Clinical Classification of Angina 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

UA/NSTEMI THREE PRINCIPAL PRESENTATIONS • Rest Angina*

Angina occurring at rest and prolonged, usually > 20 minutes

• New-onset Angina

New-onset angina of at least CCS Class III severity

• Increasing Angina

Previously diagnosed angina that has become distinctly more frequent, Longer in duration, or lower in threshold (i.e., increased by > 1 CCS) class to at least CCS Class III severity


Working diagnosis

Suspected ACS

ECG

Biochemistry

Persistent ST elevation Troponin, CKMB (+)

No persistent ST elevation Troponin, CKMB (+)

Risk Stratification

Risk: high / low

Management

Initial management, ±revascularization



{on serial ECG}

Performed in 10 min

Admission



ECG pattern • Ischemia : ST ↓, tall T, inverted T • Injury : ST ↑ • Infarction : pathologic Q EVOLVING ECG A. Normal ECG B. Tall or peaked T waves C. ST ↑ D. & E. ST ↑ with inverted T waves F. Abnormal Q


Working diagnosis

Suspected ACS

ECG

Biochemistry



Troponin, CKMB (+)

Troponin, CKMB (±)

Risk Stratification

Risk: high / low

Management

Initial management, ± revascularization



{on serial ECG}

Performed in 10 min

Admission



Biomarkers • Recommendation : CK, CKMB & Troponin upon admission and serial in 6-12 hours • LDH, SGOT/SGPT and other enzymes not recommended • Increase of plasma CK plasma & CK-MB happens early, but less specific • Increase of TnI & TnT are more specific in diagnosing marker MI ; its level corresponds with prognosis (higher value, worse prognosis)

Multiple of the AMI cutoff limit

Biomarkers

Early release myoglobin of CKMB isoform

50

Cardiac troponin after “classical” myocardial infarction

20

CK-MB after myocardial infarction

10

Cardiac troponin after “microinfarction”

5 2

1 0

1

2

3

4

5

6

7

8

Day after onset of AMI Time-course of the different cardiac biochemical markers. From Wu AH et al. Clin Chem 1999 ; 45 : 1104, with permission


Working diagnosis

Suspected ACS

ECG

Biochemistry



Troponin, CKMB (+)

Troponin, CKMB (±)

Risk Stratification

Risk: high / low

Management

Initial management, ±revascularization

Secondary prevention I.I. - ’09 / PDKI Pekanbaru


{on serial ECG}

Performed in 10 min

Admission



High Risk • Repetitive or prolonged (> 10 minutes) pain • Elevated level of cardiac biomarker (troponin or creatine kinase-MB isoenzyme); • Persistent or dynamic ST depression 0.5 mm or new T-wave inversion • Transient ST-segment elevation (0.5 mm) in more than two contiguous leads • Haemodynamic compromise

Guideline ACS 2006 National Heart Foundation Australia

High Risk • • • • • •

Sustained ventricular tachycardia Syncope LV systolic dysfunction (ejection fraction <40%); Prior PCI or CABG within 6 months or prior Diabetes Chronic kidney disease (estimated GFR< 60 mL/min)

Guideline ACS 2006 National Heart Foundation Australia

Algorithm in Acute Coronary Syndrome Admission

ECG

Biochemistry Risk Stratification Management Secondary prevention

Suspected ACS Persistent ST elevation


Troponin, CKMB (+)

Troponin, CKMB (±)

{on serial ECG}

Performed in 10 min

Working diagnosis

CHEST PAIN


Risk: high / low Initial management, ± reperfusion Medical therapy, coronary angiography


Initial Management • • • •

Monitor and support ABCs Check vital signs, including O2 saturation Establish IV access Administer – – – – –

Oxygen 4L/min Aspirin 160-325 mg chewed Clopidogrel loading dose 300 mg ISDN 5 mg sublingual, nitroglycerine iv if necessary Morphine if pain not relieved with NTG

• Caution: hemodynamic instability due to pump failure &/ malignant arrhythmia

Anticoagulation & Reperfusion • Heparin administration (LMWH or UFH) • Reperfusion in STEMI – Fibrinolysis or primary percutaneous coronary intervention (PCI). GPs should be trained to give fibrinolytic – Assess onset (≤12 hours) and contraindication (bleeding, etc) – Door to needle time: 30 min – Door to balloon time: 90 min

Fibrinolytic Absolute Contraindication • • • • • • • •

Hemorrhagic stroke, or stroke of unknown origin Ischemic stroke in preceding 6 months Central nervous system trauma or neoplasm Recent major trauma/surgery/head injury (within preceding 3 weeks) Gastro-intestinal bleeding within the last month Known bleeding disorder Aortic dissection Non-compressible punctures (e.g liver biopsy, lumbar puncture) ESC Guidelines of STEMI, 2008

Algorithm in ACLS



Working diagnosis

Suspected ACS

ECG

Biochemistry Risk Stratification

Management Secondary prevention



Troponin, CKMB (+)

Troponin, CKMB (±)

{on serial ECG}

Performed in 10 min

Admission


Risk: high / low Initial management, ±revascularization Medical therapy, coronary angiography


Secondary Prevention Strategy A

Aspirin and Anticoagulants

B

Beta blockers and Blood Pressure

C

Cholesterol and Cigarettes

D

Diet and Diabetes

E

Education and Exercise

F

Fun and Faith

Invasive Strategy As secondary prevention • Early catheterization (before discharge): for patients with moderate-high risk not receiving primary percutaneous coronary intervention • Later catheterization: for low risk patients

Summary • Acute Coronary Syndrome as one of potentially fatal cardiovascular emergency should be recognized immediately • Early diagnosis and prompt treatment should be managed to overcome good results and avoid myocardial damage (Time is muscle)

Thank You

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, belum terdapat landasan ilmiah yang kuat.

ACC/AHA Guideline of STEMI 2004 I.I. - ’09 / PDKI Pekanbaru

ANTIPLATELET •ASPIRIN •CLOPIDOGREL •TICLOPIDINE •Gp IIb / IIIa inhibitor


Aspirin • MANFAAT : menurunkan angka reinfark 50% dalam 30hari ; 20% penurunan mortaliti dlm 2 tahun • Dosis 81-325 mg P.O. • Trials: ISIS (88), Antiplatelet Trialist Group (94), HART (90)

•Aspirin kunyah segera diberikan meskipun belum ada hasil EKG (non coated/slow released) I.I. - ’09 / PDKI Pekanbaru

Adenosine Diphosphate Inhibitors • ADP disekresi oleh platelet (aktivasi dan agregasi platelet) • P2T cell surface receptors • Ticlodipine • Clopidogrel • Efek samping : Neutropenia, trombositopenia


Synergistic Mode of Action with Clopidogrel and ASA1 CLOPIDOGREL

C

ADP ADP

GPllb/llla

Activation

(Fibrinogen receptor)

ASA ASA

COX

TXA COX (cyclo-oxygenase) ADP (adenosine diphosphate) TXA2 (thromboxane A2) 1. Schafer AI. Am J Med 1996; 101: 199–209.


2

Collagen thrombin TXA 2

Clopidogrel • Gol Thienopyridine yg memblok P2Y reseptor ADP • Menghambat aktivasi platelet

•Digunakan pada pasien UA/NSTEMI : Diberikan pada semua pasien Bukan kandidat CABG Pasien yg direncanakan kateterisasi dlm 24-36 jam stlh masuk I.I. - ’09 / PDKI Pekanbaru

Glycoprotein IIb/IIIa Inhibitors • • • •

50,000 receptors per platelet Aggregation final common pathway “Passivation”; stops deposition Abciximab (Reopro); tirofiban (Aggrastat); eptifibatide (Integrilin) and lamifiban (Canada) • Pre-PCI/ Procedural Coronary Intervention


Anti Ischemia •NITRAT •B BLOKER •ANTAGONIS KALSIUM


Nitrat • Indikasi : pada Anterior MI, iskemja persisten, CHF, hipertensi • Manfaat: dapat memperbaiki perfusi koroner • Hati-hati pd: inferior MI dengan perluasan atau keterlibatan RV • Trials: GISSI-3 (94), ACC/AHA (96) •Pemberian Sublingual •Pemberian per IV Dosis awal 5Ug/mnt ditingkatkan tiap 5 menit disesuaikan dengan gejala klinis dan EKG I.I. - ’09 / PDKI Pekanbaru

Beta-bloker • Effektif untuk pengobatan simtomatik dan pencegahan infark miokard. • Vasokonstriktor moderat – Dipilih obat yang kardio-selektif

– Berhubungan dengan nitrat. • Kontraindikasi:vasospastik angina, blok SV derajat II atau III, asma, gagal jantung dlm dekompensasi,penyakit arteri perifer yg berat I.I. - ’09 / PDKI Pekanbaru

Beta-bloker Metoprolol Metoprolol Atenolol Propranolol oral Bisoprolol Carvedilol


IV oral oral oral oral

5 – 15 mg 2 x 25 – 100 mg 1 x 25 – 100 mg 3 x 20 – 80 mg 1 x 5 – 10 mg 1 x 25 mg

Antagonis kalsium • Pd UAP atau NSTEMI bila ada indikasi kontra Bbloker • Tidak ada bukti manfaatnya pada pencegahan infark miokard. • Memberikan hasil yang baik dalam jangka pendek pada episode iskemik. I.I. - ’09 / PDKI Pekanbaru

Antagonis kalsium Diltiazem

Lepas cepat :30 -120 mg 3x/hr Lepas lambat: 100-360 mg 1x/hr

Verapamil

Lepas cepat : 40 – 160 mg/hr Lepas lambat: 120-480 mg 1x/hr


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


ANTITROMBOTIK DAN ANTIKOAGULAN •Heparin ( Unfractionated Heparin) •Low Molecular Weight Heparin


Heparin (UFH) • Terikat pada AT III (anti-thrombin III) ,menginaktivasi trombin • Tidak ada efek pada Factor Xa • Hospitalization/ PTT/ bleeding • “Benefit” in UA/ rebound effect • Anti-Xa: Anti-thrombin 1:1 • Memperpanjang APTT I.I. - ’09 / PDKI Pekanbaru

Low Molecular Weight Heparin • Depolimerasi dari UFH standar dengan berat molekul lebih kecil dari pada UFH • SQ injections/ 90% bioavailable/predictable • Anti-Xa: Anti-thrombin 2-4:1 • FDA menyetujui pemakaian enoxaparin/ dalteparin untuk SKA I.I. - ’09 / PDKI Pekanbaru

UFH

LMWH


KELEMAHAN UFH • Bioavailability kurang baik • Tidak dapat menghambat trombin yang terikat pada bekuan (clot-bound thrombin) • Tergantung pada kofaktor AT III • Efek variabel • Monitor APTT berkala untuk mendapatkan kadar terapeutik • Rebound iskemia setelah penghentian • Risiko heparin-induced thrombocytopenia (HIT) Panduan Terapi SKA tanpa ST Elevasi PERKI 2004 I.I. - ’09 / PDKI Pekanbaru

KEUNGGULAN DARI LMWH • • • •

Mengurangi ikatan pada protein pengikat heparin Efek yang dapat diprediksi lebih baik Tidak memerlukan pengukuran APTT Pemakaian subkutan,menghindari kesulitan dalam pemakaian secara IV • Berkaitan dengan kejadian perdarahan yang kecil, namun bukan perdarahan besar • Stimulasi trombosit kurang dari UFH dan jarang menimbulkan HIT • Penghematan biaya perawatan (dari studi ESSENCE)

Panduan Terapi SKA tanpa ST Elevasi PERKI 2004 I.I. - ’09 / PDKI Pekanbaru

TEHNIK INJEKSI LMWH SUBKUTAN


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 • 1mg/kg, SC , bid Enoxaparine • 0,1 ml/10 kg , SC , bid Nadroparine • 2.5 mg Fondaparinux I.I. - ’09 / PDKI Pekanbaru

ACC/AHA 2007 Guidelines Update for UA and NSTEMI1 Class I Recommendations for Antithrombotic Therapy*

Possible ACS

Aspirin

†

Likely/Definite ACS

Definite ACS with continuing ischemia or other high-risk features or planned PCI

SC LMWH or IV heparin

Aspirin† + IV heparin/SC LMWH‡ + IV GP IIb/IIIa antagonist

+ Clopidogrel

+ Clopidogrel

Aspirin†

+

*During hospital

care Clopidogrel should be administered to hospitalized patients who are unable to take ASA because of hypersensitivity or major GI intolerance ‡Class IIa: enoxaparin preferred over unfractionated heparin, unless CABG is planned within 24 hours †

1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA) 6/12/2011 Guidelines, USA: ACC/AHA; 2007.


OBAT-OBATAN LAINNYA • Tranquilizer e,g diazepam 5mg bid • Stool softener


TERAPI FIBRINOLITIK


Fibrinolitik : Indikasi • Sakit dada khas IMA ≤ 12 jam

• EKG : ≥ 1 mm elevasi seg ST pada ≥ 2 sandapan yg bersebelahan ≥ 2mm elevasi seg ST pada ≥ 2 sandapan prekordial Bundle branch block yg baru • Syok kardiogenik pd IMA ( bila kateterisasi dan revaskularisasi tdk dapat dilakukan ) • Fibrinolitik door to needle time < 30 menit !! • PCI pada IMA lebih unggul bila dpt dilakukan dlm 90 ± 30 menit I.I. - ’09 / PDKI Pekanbaru

Fibrinolitik : indikasi kontra Absolut • Riwayat stroke hemoragik,kapanpun terjadinya • Riwayat stroke iskemik dalam 3 bulan kecuali stroke iskemik dengan onset < 3 jam • Neoplasma intrakranial • Perdarahan internal aktif(tidak termasuk menstruasi) • Kecurigaan suatu diseksi aorta • Luka kepala tertutup yg signifikan atau trauma facial dalam 3 bulan • Kelainan struktural atau pembuluh darah cerebral

ACC/AHA guideline of STEMI 2004 I.I. - ’09 / PDKI Pekanbaru

Fibrinolitik :indikasi kontra relatif Hipertensi berat saat datang ke unit emergency yaitu BP> 180 / 110 mmHg Pungsi vaskuler yg tak dapat dikompresi Perdarahan internal 2 – 4 mgg sebelumnya Konsumsi antikoagulan oral prolonged CPR ( > 10 minutes) or operasi mayor dlm jangka waktu 2-4 minggu Untuk Streptokinase : pemberian sebelumnya ( 5 hari-2 tahun) atau riwayat reaksi alergi Kehamilan Active peptic ulcer Riwayat hipertensi kronis yg tak terkontrol Riwayat stroke iskemik lebih dari 3 bulan,demensia atau patologi serebral lainnya yg blm tercantum dalam indikasi kontra ACC/AHA guideline of STEMI 2004 I.I. - ’09 / PDKI Pekanbaru

Perbandingan terapi trombolitik dengan terapi standar pada IMA Mulai trombolisis

Tambahan Jiwa yg diselamatkan per 1000 pasien yg diobati ------------------------------------------------------------------•Pd jam pertama •Pd jam kedua •Pd jam ketiga •Antara jam ke 3-6 •Antara jam 6-12 •Antara jam 12-24 I.I. - ’09 / PDKI Pekanbaru

65 37 29 26 18 9

AGEN FIBRINOLITIK • • • •

Streptokinase (SK) Actylase (tPA) Reteplase (r-PA) Tenecteplase (TNK-tPA)


Skema sistem fibrinolitik Plasminogen Activators (t-PA, u-PA) Plasminogen Activator Inhibitors (PA1, PA2, TAFI)

Plasminogen

Plasmin α2-Antiplasmin

Fibrin I.I. - ’09 / PDKI Pekanbaru

Fibrin degradation Product Braunwald, A Textbook of Cardiovascular Medicine. 6th ed

SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK • • • •


Streptokinase  Actylase (tPA)  Reteplase(r-PA) Tenecteplase  (TNK-tPA)

Rendah Tinggi Sedang Sangat tinggi

CARA PEMBERIAN FIBRINOLITK • Streptokinase ( Streptase ) 1.5 million Unit in 100 ml D5W or 0.9% saline selama 30-60 mnt without heparin : Inferior MCI with heparin : anterior MCI • tPA 15 mg IV bolus kemudian 0.75 mg/Kg selama 30 mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt berikutnya


Streptokinase (SK, Streptase) • Keuntungan : lebih baik pada anterior MCI, age <75; lebih murah • Komplikasi: antigenic, perdarahan intraserebral pada studi GUSTO 0.6% • Trials: GISSI-1, ISIS-2 (88)


TPA Alteplase, rTPA • Keuntungan : clot specific, baik pada anterior MCI • Komplikasi : 1% perdarahan intrakranal • Biaya: lebih mahal dari SK • Trials: ASSENT, GUSTO (93) TIMI-IIIB (94)


Complications of Acute MI

Extension / Ischemia

Expansion / Aneurysm

Mechanical I.I. - ’09 / PDKI Pekanbaru

Arrhythmia Pericarditis

Acute MI

Heart Failure

RV Infarct

Mural Thrombus

• Komplikasi awal : -aritmia -disfungsi LV dan gagal jantung -ruptur ventrikel -regurgitasi mitral akut -gagal fungsi RV -syok kardiogenik


• Komplikasi akhir : -trombosis mural dan emboli sistemik -aneurisma LV -DVT -emboli paru -sindrome Dressler


Pemeriksaan awal pada Sindrom Koroner Akut Masuk RS

Diagnosis Kerja

SAKIT DADA Curiga Sindrom Koroner Akut

ECG

Elevasi ST menetap

Tanpa Elevasi ST menetap

Biochemistry

Troponin (CKMB)

Troponin

Stratifikasi risiko

Normal atau Tdk dpt ditentukan ECG Troponin 2 X negative

Risiko tinggi Risiko rendah

Mungkin bukan SKA

Pengobatan Pencegahan sekunder Esc/EHJ 2002 I.I. - ’09 / PDKI Pekanbaru

TERAPI INTERVENSI PADA SINDROMA KORONER AKUT


Angioplasty • Keberhasilan Primer

:

85 - 95 %

• Kematian

:

0.3 - 1.3 %

• Infark Miokard

:

1.6 - 6.3 %

• Operasi By-pass darura

:

1 -7%

• Stenosis lebih lanjut sblm era stent era stent Drug eluting stent I.I. - ’09 / PDKI Pekanbaru

: 30 - 40 % : 15-20% : almost 0%

Primary PTCA/PCI • Keunggulan: ICH 0%, • Syarat : jumlah tindakan primary PCI>100 kasus/th/operator ;>600/yr/rumah sakit • Mortaliti: reinfark 5 vs 12% untuk TPA; 30 hari sama dengan TPA; namun pada AMI Anterior ; age>70 pulse >100 angka 2% vs 10% for TPA • Trials: RITA, PAMI (93); MITI (96)



Treatment Delayed is Treatment Denied

Symptom Recognition

Call to Medical System

PreHospital

ED

Increasing Loss of Myocytes Delay in Initiation of Reperfusion Therapy


Cath Lab

Options for Transport of Patients With STEMI and Initial Reperfusion Treatment

•

Patients receiving fibrinolysis should be risk-stratified to identify need for further revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG).

•

All patients should receive late hospital care and secondary prevention of STEMI. Fibrinolysis Not PCI Capable

Noninvasive Risk Stratification Rescue

Ischemia driven

PCI Capable PCI or CABG

Primary PCI


Late Hospital Care and Secondary Prevention


Chest pain: focus on acute coronary syndromes What doctor’s should know

IDRIS IDHAM Department of Cardiology and Vascular Medicine Fakultas of Medicine University of Indonesia National Cardiovascular Center Harapan Kita I.I. - ’09 / PDKI Pekanbaru

Thank you


Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI

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