1

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

Birth : 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.

CURRICULUM VITAE

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 SyndromeSLIDE 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

• Age

• Sex

• Race

• Heredity

Major Controllable

Smoking

Hypertension

Dyslipidemia

Diabetes

Minor Controllable

Obesity

Lack of exercise

Stress

Personality

PathophysiologySLIDE 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 ELECTROCARDIOGRAMINFARCT 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

SLIDE 14

Inferior STEMI

Which Part of the Heart is Affected?

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

SLIDE 16

Anterior STEMI

Which Part of the Heart is Affected?

Which Part of the Heart is Affected? SLIDE 17

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Anteroseptal Wall

ECG Correlations to Arteries

SLIDE 18

Lateral STEMI

Which Part of the Heart is Affected?

Which Part of the Heart is Affected? SLIDE 19

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Lateral Wall

ECG Correlations to Arteries

ATHEROSCLEROTIC / ISCHAEMIC HEART DISEASE

Cardiac enzyme Marker

Cardiac

enzyme

Marker

Initial

elevation

after AMI

Mean time

to peak

elevations

Time to

return to

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 TherapySLIDE 28

1

2

3 Preventing heart failure

4 Limiting other cardiovascular complication

Reduce the amount of myocardial necrosis that occurs in patients with acute myocardial infarction (AMI)

Preserving left ventricular (LV) function

ACS AlgorithmSLIDE 29American Heart Association

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 LAKSANATindakan 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 Therapy1. ASA (Class I; LOE: A)

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

· Ticagrelor

3. Anticoagulant:· UFH (Class I; LOE: B) or

· Enoxaparin (Class I; LOE: A) or

· Fondaparinux (Class I; LOE: B)

Initiate DAPT and Anticoagulant Therapy1. ASA (Class I; LOE: A)

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

· Ticagrelor

3. Anticoagulant:· UFH (Class I; LOE: B) or

· Enoxaparin (Class I; LOE: A) or

· Fondaparinux† (Class I; LOE: B) or

· Bivalirudin (Class I; LOE: B)

Medical therapy chosen based on cath

findings

PCI With StentingInitiate/continue antiplatelet and anticoagulant

therapy1. 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)

CABGInitiate/continue ASA therapy and

discontinue P2Y12 and/or GPI therapy1. 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 Care1. 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)

Can consider GPI in addition to ASA and P2Y12 inhibitor in high-risk (e.g., troponin positive) pts (Class IIb; LOE: B)

· Eptifibatide

· Tirofiban

TherapyIneffective

TherapyEffective

NSTE-ACS: Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy1. ASA (Class I; LOE: A)

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

· Ticagrelor

3. Anticoagulant:· UFH (Class I; LOE: B) or

· Enoxaparin (Class I; LOE: A) or

· Fondaparinux (Class I; LOE: B)

Initiate DAPT and Anticoagulant Therapy1. ASA (Class I; LOE: A)

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

· Ticagrelor

3. Anticoagulant:· UFH (Class I; LOE: B) or

· Enoxaparin (Class I; LOE: A) or

· Fondaparinux† (Class I; LOE: B) or

· Bivalirudin (Class I; LOE: B)

Medical therapy chosen based on cath

findings

PCI With StentingInitiate/continue antiplatelet and anticoagulant

therapy1. 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)

CABGInitiate/continue ASA therapy and

discontinue P2Y12 and/or GPI therapy1. 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 Care1. 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)

Can consider GPI in addition to ASA and P2Y12 inhibitor in high-risk (e.g., troponin positive) pts (Class IIb; LOE: B)

· Eptifibatide

· Tirofiban

TherapyIneffective

TherapyEffective

†In patients 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.

PENEGAKAN DIAGNOSIS

Evolusi EKG pada SKA