CURRICULUM VITAE

Name : Dr Syamsu Indra, SpPD, K-KV FINASIM, MARS, PhD.

Birth
Curriculum Vitae
: Plaju, 28 Januari 1964
Education : 1990 - GP FK UNSRI
2002 - Internist FK UNSRI
2010 - Konsultan Kardiovascular FK UNSRI
2012 - MARS Universitas Respati Indonesia
2019 – PhD, Management Science University, Shah Alam,
Kuala Lumpur, Malaysia.

Experiences : 1992 – 1995 : Head of Public Health Centre Pagar Dewa,

Mesuji, OKI, Sumsel
1995 – 1996 : Doctor on duty, Tanah Merah Conoco Warim
B.V Marauke, Irian Jaya
1996 – 2002 : Internal Medicine Recident
2002 – 2004 : Staff Department of Internal Medicinepart, Prof WZ
Johannes Hospital, Kupang, NTT
2005 – Now : Staff Cardiologi Division Dement of Internal
Medicine, dr Moh Hoesin General Hospital.
2012 – 2016 : Head of Brain Heart Centre, dr Moh Hoesin
General Hospital.
2017 – Now : Head of National Referral Hospital, dr Moh
General Hoesin Hospital.
1
Diagnosis dan tatalaksana
terkini sindrom koroner
akut

Dr.
Syamsu Indra, SpPD, K-KV, FINASIM, MARS,PhD
Divisi Kardiologi, Departemen Ilmu Penyakit Dalam
RSMH/FK UNSRI Palembang
Acute Coronary Syndrome
SLIDE 3

• Acute Coronary Syndrome (ACS) refers to a spectrum of clinical

presentations ranging from those for ST-segment elevation
myocardial infarction (STEMI) to presentations found in non ST-
segment elevation myocardial infarction (NSTEMI) or in unstable
angina.

• It is almost always associated with rupture of an atherosclerotic

plaque and partial or complete thrombosis of the infarct-related
artery, resulting in decreased oxygen supply to the heart muscle.
ACUTE CORONARY
SYNDROMES
Cardiovascular Disease Risk Factors
Major Uncontrollable  Major Controllable
• Age  Smoking
• Sex
 Hypertension
• Race
• Heredity  Dyslipidemia
 Diabetes
 Minor Controllable
 Obesity
 Lack of exercise
 Stress
 Personality
Pathophysiology
SLIDE 7
 Symptoms
Angina Pectoris
• Substernal
• Squeezing, Heaviness
• May radiate to arms, shoulders,
jaw, upper back, upper
abdomen.
• May be associated with
shortness of breath, nausea,
sweating

8
Symptoms
Great anxiety/Fear
Pale or livid face
Dyspnea (SOB)
BP usually up during attack
Disritmia may be present

9
Forms of Angina Pectoris
Unstable Angina
• More frequent/severe
• Can occur during rest
• Requires immediate treatment and
transport to appropriate facility

10
THE ELECTROCARDIOGRAM

12 lead EKG
• Cornerstone of initial evaluation
• Within 10 minutes of presentation
Previous EKG tracings
• Compare
Serial EKGs
• Essential
THE ELECTROCARDIOGRAM
1. ST segment elevation 2mm (2 contiguous
leads), new LBBB
STEMI

2. ST depression >1mm, marked symmetrical T

wave inversions >2 mm, dynamic ST-T changes
with pain
UA/NSTEMI LIKELY

3. Non-diagnostic or normal ECG

 THE ELECTROCARDIOGRAM
INFARCT LOCATION

• II, III, AVF : Inferior

• V1 - V4 : Anterosept
• I, aVL, V5-V6 : Lateral
• I,aVL, V1-V6 : Extensive
anterior
• V1-V2 tall R, ST depression:True posterior
Which Part of the Heart is
Affected? SLIDE 14

Inferior STEMI
Which Part of the Heart is
Affected? SLIDE 15

ECG Correlations to Arteries

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6

Inferior Wall
Which Part of the Heart is
Affected? SLIDE 16

Anterior STEMI
Which Part of the Heart is
Affected? SLIDE 17

ECG Correlations to Arteries

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6

Anteroseptal Wall
Which Part of the Heart is
Affected? SLIDE 18

Lateral STEMI
Which Part of the Heart is
Affected? SLIDE 19

ECG Correlations to Arteries

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6

Lateral Wall
ATHEROSCLEROTIC / ISCHAEMIC
HEART DISEASE
Cardiac enzyme Marker

Cardiac Initial Mean time Time to

enzyme elevation to peak return to
Marker after AMI elevations baseline
Myoglobin 1-4hr 6-7hr 18-24hr
CTnI 3-12hr 10-24hr 3-10 day
CTnT 3-12hr 12-48hr 5-14 day

CKMB 4-12 hr 10-24hr 2-3day

TCK 2-6 hr 4.7hr(3-5) 72hr(50-96)
CARDIAC ENZYME
DIAGNOSIS
Differential Diagnosis
Diagnosis of
ACS
Management of ACS
Primary Goals of Therapy
SLIDE 28

1 Reduce the amount of myocardial necrosis that occurs in

patients with acute myocardial infarction (AMI)

2 Preserving left ventricular (LV) function

3 Preventing heart failure

4 Limiting other cardiovascular complication

ACS Algorithm
American Heart Association
SLIDE 29
SLIDE 30
TREATMENT
STEMI
That’s all. Thank you very much!
PENEGAKAN DIAGNOSIS
Enzim Jantung
• Kreatinin kinase-MB (CK-MB) atau troponin I/T  marka
nekrosis miosit jantung dan menjadi marka untuk diagnosis
infark miokard.
• Troponin I/T  marka nekrosis jantung mempunyai sensitivitas
dan spesifisitas lebih tinggi dari CK-MB.
• Troponin I/T juga dapat meningkat oleh sebab kelainan
kardiak nonkoroner  takiaritmia, trauma kardiak, gagal
jantung, HVK, miokarditis/perikarditis.
• Keadaan nonkardiak yang dapat meningkatkan kadar troponin
I/T  sepsis, luka bakar, gagal napas, penyakit neurologik
akut, emboli paru, hipertensi pulmoner, kemoterapi, dan
insufisiensi ginjal
TATA LAKSANA
Tindakan Umum dan Langkah Awal

• Tirah Baring
• Oksigen
• Aspirin
• Penghambat reseptor ADP
• Nitrogliserin/Isosorbid dinitrat
• Morfin
TATA LAKSANA
• Menilai stratifikasi resiko dgn TIMI score, Grace score, atau Crusade score 
strategi invasive atau konservatif, dan waktu pelaksanaan revaskularisasi
• Waktu pelaksanaan angiografi menjadi 4 kategori:
1. Strategi invasif segera (<2 jam, urgent). Dilakukan bila pasien memenuhi
salah satu kriteria risiko sangat tinggi (very high risk)
2. Strategi invasif awal (early) dalam 24 jam. Dilakukan bila pasien
memiliki skor GRACE >140 atau dengan salah satu kriteria risiko tinggi (high
risk) primer.
3. Strategi invasif awal (early) dalam 72 jam. Dilakukan bila pasien
memenuhi salah satu kriteria risiko tinggi (high risk) atau dengan gejala
berulang
4. Strategi konservatif (tidak dilakukan angiografi) atau angiografi
elektif
Skor TIMI untuk UAP & NSTEMI
Skor GRACE

(dikutip dari Killip T, Kimball JT (Oct 1967). “Treatment of

myocardial infarction in a coronary care unit. A two year
experience with 250 patients”. Am J Cardiol. 20 (4): 457–64.)
Skor risiko perdarahan CRUSADE
KLASIFIKASI
Algorithm for Management of Patients With Definite or Likely NSTE-ACS
NSTE-ACS:
Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy Initiate DAPT and Anticoagulant Therapy
1. ASA (Class I; LOE: A) 1. ASA (Class I; LOE: A)

2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) : 2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):
· Clopidogrel or · Clopidogrel or
· Ticagrelor · Ticagrelor

3. Anticoagulant: 3. Anticoagulant:
· UFH (Class I; LOE: B) or · UFH (Class I; LOE: B) or
· Enoxaparin (Class I; LOE: A) or · Enoxaparin (Class I; LOE: A) or
· Fondaparinux (Class I; LOE: B) · Fondaparinux† (Class I; LOE: B) or
· Bivalirudin (Class I; LOE: B)
Can consider GPI in addition to ASA and P2Y12 inhibitor
in high-risk (e.g., troponin positive) pts
(Class IIb; LOE: B)
· Eptifibatide
· Tirofiban

Medical therapy
chosen based on cath
findings

Therapy Therapy
Effective Ineffective
 Therapy Therapy
Effective Ineffective
PCI With Stenting
Initiate/continue antiplatelet and anticoagulant
therapy
1. ASA (Class I; LOE: B)
2. P2Y12 Inhibitor (in addition to ASA) :
· Clopidogrel (Class I; LOE: B) or
· Prasugrel (Class I; LOE: B) or
· Ticagrelor (Class I; LOE: B)
3. GPI (if not treated with bivalirudin at time of PCI)
· High-risk features, not adequately pretreated
with clopidogrel (Class I; LOE: A)
· High-risk features adequately pretreated with
clopidogrel (Class IIa; LOE: B)
4. Anticoagulant:
· Enoxaparin (Class I; LOE: A) or
· Bivalirudin (Class I; LOE: B) or
· Fondaparinux† as the sole anticoagulant (Class
III: Harm; LOE: B) or
· UFH (Class I; LOE: B)
†Inpatients who have been treated with fondaparinux (as upfront therapy) who are
undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at
the time of PCI because of the risk of catheter thrombosis.
CABG
Initiate/continue ASA therapy and
discontinue P2Y12 and/or GPI therapy
1. ASA (Class I; LOE: B)
2. Discontinue clopidogrel/ticagrelor 5 d
before, and prasugrel at least 7 d before
elective CABG
3. Discontinue clopidogrel/ticagrelor up to
24 h before urgent CABG (Class I; LOE: B).
May perform urgent CABG <5 d after
clopidogrel/ticagrelor and <7 d after
prasugrel discontinued
4. Discontinue eptifibatide/tirofiban at
least 2-4 h before, and abciximab ≥12 h
before CABG (Class I; LOE: B)
Late Hospital/Posthospital Care
1. ASA indefinitely (Class I; LOE: A)
2. P2Y12 inhibitor (clopidogrel or
ticagrelor), in addition to ASA, up
to 12 mo if medically treated
(Class I; LOE: B)
3. P2Y12 inhibitor (clopidogrel,
prasugrel, or ticagrelor), in
addition to ASA, at least 12 mo if
treated with coronary stenting
(Class I; LOE: B)
PENEGAKAN DIAGNOSIS
Evolusi EKG pada SKA