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

2. 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

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


Idris Idham
RS MEDIKA BSD

4. 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

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

6. CARDIOVASCULAR SPECIALIST
COMPETENCY
↓
FRONTLINE DOCTORS
↓

FROM PALPITATION TO CVD

7. Front-line medical practitioners

•Play very important role in fighting
cardiovascular diseases (CVD), the no.1 killer
in Indonesia
1

•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

1
Dept. of Health, RI. 2002.

8. Chest Pain
•One of the most challenging symptoms
1

•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.

1
Harrison’s principles of internal medicine: McGraw-Hill, 2005.

9. 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

10. 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)

11. 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.

12. 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

13. Anatomy of Thoracic Cavity
I.I. - ’09 / PDKI Pekanbaru

14. 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.
1
Harrison’s principles of internal medicine: McGraw-Hill, 2005.

15. 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

16. Differential Diagnosis of
Chest Pain
Cardiac
•ACS: infarct,angina
•MVP
•Aortic Stenosis
•Hypertrophic cardio-
myopathy
•Pericarditis

Lungs
•Lung Emboli
•Pneumonia
•Pneumothorax
•Pleuritis
Gastrointestinal
•Esophageal reflux
•Esophageal rupture
•Gall bladder disease
•Peptic Ulcer
•Pancreatitis

Vascular
•Aortic dissection/aneurysm

Others
•Musculoskeletal
•Herpes zoster

17. 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

18. Focus on:
Acute Coronary Syndromes
I.I. - ’09 / PDKI Pekanbaru

19. 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.
DEFINITION

20. PATHOPHYSIOLOGY

21. Foam
Cells
Fatty
Streak
Intermediate
Lesion Atheroma
Fibrous
Plaque
Complicated
Lesion/Rupture
Endothelial Dysfunction
Smooth muscle
and collagen
From first decade From third decade From fourth decade
Growth mainly by lipid accumulation
Thrombosis,
hematoma
Stary HC et al. Circulation 1995;92:1355-1374.
Atherosclerosis Timeline

24. DIAGNOSIS

25. Presentation
(Clinical, Initial ECG)
ST-Seg Elevation
Myocardial Infarction
Non-STSeg Elevation
Acute Coronary Syndr
ST-Seg Elevation
MCI
Non-ST-seg-
Elevation MCI
Unstable
Angina
Working
diagnosis
Time

Evolution of
ECG &
Biomarkers
Final
diagnosis
National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
Biomarker (-) Biomarker (+)
I.I. - ’09 / PDKI Pekanbaru

26. CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management, ±
revascularization
Medical therapy,
coronary angiography
Performed in 10 min

{on serial
ECG}
Troponin,
CKMB (+)

27. 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

28. 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

29. CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
±revascularization
Medical therapy,
coronary angiography
Performed in 10 min

{on serial
ECG}
Troponin,
CKMB (+)

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

31. CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management, ±
revascularization
Medical therapy,
coronary angiography
Performed in 10 min

{on serial
ECG}
Troponin,
CKMB (±)

32. 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)

34. 0 1 2 3 4 5 6 7 8
50
20
10
5
2
1
Early release myoglobin of
CKMB isoform
Cardiac troponin after “classical”
myocardial infarction
CK-MB after myocardial infarction
Cardiac troponin after “microinfarction”
Multiple of the AMI cutoff limit

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
Biomarkers

35. CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
±revascularization
Medical therapy,
coronary angiography
Performed in 10 min

{on serial
ECG}
Troponin,
CKMB (±)
I.I. - ’09 / PDKI Pekanbaru

36. 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

37. 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

38. CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management, ±
reperfusion
Medical therapy,
coronary angiography
Performed in 10 min

{on serial
ECG}
Troponin,
CKMB (±)

39. 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

40. 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

41. 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

42. Algorithm in ACLS
I.I. - ’09 / PDKI Pekanbaru

43. CHEST PAIN
Admission
Working
diagnosis
Bio-
chemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely
- NSTEMI
- STEMI
ECG
Initial management,
±revascularization
Medical therapy,
coronary angiography
Performed in 10 min

{on serial
ECG}
Troponin,
CKMB (±)

44. 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
Secondary Prevention Strategy

45. 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

46. 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)

47. Thank You

48. 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

49. ANTIPLATELET

•ASPIRIN
•CLOPIDOGREL
•TICLOPIDINE
•Gp IIb / IIIa inhibitor
I.I. - ’09 / PDKI Pekanbaru

50. 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

51. Adenosine Diphosphate
Inhibitors
•ADP disekresi oleh platelet (aktivasi dan
agregasi platelet)
•P2T cell surface receptors
•Ticlodipine
•Clopidogrel
•Efek samping : Neutropenia, trombositopenia
I.I. - ’09 / PDKI Pekanbaru

52. COX (cyclo-oxygenase)
ADP (adenosine diphosphate)
TXA
2 (thromboxane A
2)
CLOPIDOGREL
ASA COX
ADP
ADP
C
GPllb/llla
(Fibrinogen receptor)
Collagen thrombin
TXA
2
Activation
TXA
2

ASA

Synergistic Mode of Action with
Clopidogrel and ASA
1
1. Schafer AI. Am J Med 1996; 101: 199–209.
I.I. - ’09 / PDKI Pekanbaru

53. 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

54. 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
I.I. - ’09 / PDKI Pekanbaru

55. Anti Ischemia

•NITRAT
•B BLOKER
•ANTAGONIS KALSIUM
I.I. - ’09 / PDKI Pekanbaru

56. 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

57. 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

58. Beta-bloker

Metoprolol IV
Metoprolol oral
Atenolol oral
Propranolol oral
Bisoprolol oral
Carvedilol 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
I.I. - ’09 / PDKI Pekanbaru

59. Antagonis kalsium
•Pd UAP atau NSTEMI bila ada indikasi kontra B-
bloker

•Tidak ada bukti manfaatnya pada pencegahan
infark miokard.

•Memberikan hasil yang baik dalam jangka pendek
pada episode iskemik.


I.I. - ’09 / PDKI Pekanbaru

60. Antagonis kalsium

Diltiazem


Verapamil

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

Lepas cepat : 40 – 160 mg/hr
Lepas lambat: 120-480 mg 1x/hr
I.I. - ’09 / PDKI Pekanbaru

61. •Morfin:
2.5mg-5 mg IV pelan.
Hati –hati pada : inferior MCI,
asthma , bradikardia

•Pethidin : 12.5-25 mg IV pelan
PAIN KILLER
I.I. - ’09 / PDKI Pekanbaru

62. ANTITROMBOTIK DAN
ANTIKOAGULAN
•Heparin ( Unfractionated Heparin)
•Low Molecular Weight Heparin
I.I. - ’09 / PDKI Pekanbaru

63. 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

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

65. UFH
LMWH
I.I. - ’09 / PDKI Pekanbaru

66. 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

67. 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

68. TEHNIK INJEKSI LMWH SUBKUTAN
I.I. - ’09 / PDKI Pekanbaru

69. DOSIS YANG DIREKOMENDASIKAN
UFH




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

70. 6/12/2011
Definite ACS with continuing
ischemia or other high-risk
features or planned PCI
Aspirin
†
+
IV heparin/SC LMWH
‡
+
IV GP IIb/IIIa antagonist

Possible ACS
Aspirin
†
Likely/Definite ACS
Aspirin
†
+
SC LMWH
or
IV heparin
ACC/AHA 2007 Guidelines Update
for UA and NSTEMI
1
+ Clopidogrel + Clopidogrel
*
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
Class I Recommendations for Antithrombotic Therapy
*
1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA)
Guidelines, USA: ACC/AHA; 2007. I.I. - ’09 / PDKI Pekanbaru

71. OBAT-OBATAN LAINNYA
•Tranquilizer e,g diazepam 5mg bid
•Stool softener
I.I. - ’09 / PDKI Pekanbaru

72. TERAPI FIBRINOLITIK
I.I. - ’09 / PDKI Pekanbaru

73. 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

74. 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

75. 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
Fibrinolitik :indikasi kontra relatif
ACC/AHA guideline of STEMI 2004
I.I. - ’09 / PDKI Pekanbaru

76. Perbandingan terapi trombolitik
dengan terapi standar pada IMA
Mulai trombolisis Tambahan Jiwa yg
diselamatkan per 1000
pasien yg diobati
-------------------------------------------------------------------

•Pd jam pertama 65
•Pd jam kedua 37
•Pd jam ketiga 29
•Antara jam ke 3-6 26
•Antara jam 6-12 18
•Antara jam 12-24 9
I.I. - ’09 / PDKI Pekanbaru

77. AGEN FIBRINOLITIK
•Streptokinase (SK)
•Actylase (tPA)
•Reteplase (r-PA)
•Tenecteplase (TNK-tPA)
I.I. - ’09 / PDKI Pekanbaru

78. Plasminogen Activators
(t-PA, u-PA)
Skema sistem fibrinolitik
Plasminogen Plasmin
α
2-Antiplasmin
Fibrin
Fibrin
degradation
Product
Plasminogen Activator
Inhibitors (PA1, PA2, TAFI)
Braunwald, A Textbook of Cardiovascular Medicine. 6th ed I.I. - ’09 / PDKI Pekanbaru

79. SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK
•Streptokinase 
•Actylase (tPA) 
•Reteplase(r-PA)
•Tenecteplase 
(TNK-tPA)
Rendah
Tinggi
Sedang
Sangat tinggi
I.I. - ’09 / PDKI Pekanbaru

80. 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
I.I. - ’09 / PDKI Pekanbaru

81. 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)
I.I. - ’09 / PDKI Pekanbaru

82. 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)
I.I. - ’09 / PDKI Pekanbaru

83. Extension / Ischemia
Complications of Acute MI
Acute MI
Arrhythmia
Heart Failure
Expansion / Aneurysm
RV Infarct
Pericarditis
Mechanical Mural Thrombus
I.I. - ’09 / PDKI Pekanbaru

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

I.I. - ’09 / PDKI Pekanbaru

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

I.I. - ’09 / PDKI Pekanbaru

86. SAKIT DADA Masuk RS
Diagnosis
Kerja
ECG
Bio-
chemistry
Stratifikasi
risiko
Pengobatan
Pencegahan
sekunder
Curiga Sindrom Koroner Akut
Elevasi ST
menetap
Tanpa Elevasi
ST menetap
Normal atau
Tdk dpt ditentukan
Troponin
(CKMB)
Troponin
ECG
Troponin
2 X negative
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
Esc/EHJ 2002
Mungkin bukan SKA
I.I. - ’09 / PDKI Pekanbaru

87. TERAPI INTERVENSI
PADA SINDROMA
KORONER AKUT
I.I. - ’09 / PDKI Pekanbaru

88. 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 : 30 - 40 %
era stent : 15-20%
Drug eluting stent : almost 0%
I.I. - ’09 / PDKI Pekanbaru

89. 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)
I.I. - ’09 / PDKI Pekanbaru

90. I.I. - ’09 / PDKI Pekanbaru

91. Symptom
Recognition
Call to
Medical System
ED
Cath Lab
PreHospital
Delay in Initiation of Reperfusion Therapy
Increasing Loss of Myocytes
Treatment Delayed is Treatment Denied
I.I. - ’09 / PDKI Pekanbaru

92. • 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
Primary PCI
Noninvasive Risk
Stratification
Late
Hospital Care
and Secondary
Prevention
PCI or CABG
Not
PCI Capable
PCI Capable
Rescue Ischemia
driven
Options for Transport of Patients With STEMI and Initial
Reperfusion Treatment
I.I. - ’09 / PDKI Pekanbaru

93. I.I. - ’09 / PDKI Pekanbaru

94. 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

95. Thank you
I.I. - ’09 / PDKI Pekanbaru