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ACUTE CORONARY

SYNDROME
dr. Ilham Uddin SpJP
New Paradigm Threshold

Decades Years-Months Months-Days


healthy subclinical symptomatic

Thrombus

Intima
Lumen
Media

Plaque

• Unstable angina
• Unstable plaque no narrowing
• Difficult to diagnose (IVUS, MRI)
• Frequent MI with sudden death
• Easy to prevent
Pathophysiology of Atherosclerosis
Endothelial
Dysfunction
•Foam •Fatty •Intermediate •Fibrous •Complicated
•Cells •Streak •Lesion •Atheroma •Plaque•Lesion/Rupture

•oxidized LDL
•homocystein
e
•smoking
•aging
•hyperglycemi
a
•hypertension

35-45 yrs 45-55 yrs 55-65 yrs >65 yrs


•Endothelial injury•Lipid
accumulation
•Inflammation
•nitric oxide
•continued macrophage/lipid •MMP's
•endothelin-1 •adhesion molecules accumulation •CRP
•vasodilation (ICAM, VCAM) (hepatic)
•leukocyte accumulation
•monocyte adhesion
•cytokines (IL-6, TNFa, IFNg
•macrophage LDL )
uptake
Pathophysiology

Thrombosis Mechanical
Obstruction

Dynamic > MVO2


obstruction
Inflammation/
Infection
Thrombosis Mechanical
Obstruction

Dynamic
> MVO2
obstruction
Inflammation/
Infection
Braunwald, Circulation 98:2219,1998
Acute Coronary Syndromes
 Are a continuum initiated by:
 rupture of an unstable, lipid-rich atheromatous
plaque in epicardial artery; activating platelet
adhesion, fibrin clot formation and coronary
thrombosis
ACUTE CORONARY SYNDROME

No ST Elevation ST Elevation

NSTEMI

Unstable Angina Qw Myocardial


N Qw Myocardial Infarction
Infarction
AHA Guidelines, 2000
New terminology for coronary syndromes

Adapted from Aroney C, Boyden AN, Jelinek MV, et al.


Management of unstable angina: guidelines 2000.
Med J Aust 2000;173(Suppl):S65–S88, with permission.
Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS SAKIT DADA Anamnesis & pem. fisik

Diagnosis Curiga Sindrom Koroner Akut


Kerja

Elevasi ST Tanpa Elevasi Normal atau


ECG
menetap ST menetap Tdk dpt ditentukan

Bio- Troponin Troponin ECG


chemistry CK/CKMB Troponin
2 X negative
Stratifikasi
Risiko: :Tinggi Sedang Rendah Mungkin bukan SKA
risiko

Pengobatan
Pencegahan
sekunder

Esc/EHJ 2002
KELUHAN UTAMA SINDROM KORONER AKUT
•Sakit dada atau nyeri hulu hati yang berat, asalnya
non-traumatik, dengan ciri-ciri tipikal iskemia miokard
atau infark:
Dada bgn tengah/substernal rasa tertekan atau sakit
seperti diremas
Rasa sesak, berat/tertimpa beban , mencengkeram,
terbakar,sakit
sakit perut yg tdk dpt dijelaskan, sendawa, nyeri hulu
hati
Penjalaran ke leher, rahang, bahu, punggung atau 1
atau ke 2 lengan
•Disertai sesak
•Disertai mual dan/atau muntah
•Disertai berkeringat
Patients with suspected ACS, who have chest
pain at rest > 20 minutes, syncope/presyncope,
or unstable vital signs ----refer to EMG
immediately
AFP Guideline 2005

PERKI Guideline 2003 : 10 minutes


NHFA &CSANZ Guideline 2006 : 10 minutes
European Guideline 2003 : 20 minutes
Suspicious Chest Pains
 Classic angina - dull, pressure, substernal;
arm or neck radiation; SOB, palpitations,
sweating, nausea or vomiting
 Angina Equivalent - no pain but sudden
ventricular failure or ventricular dysrhythmias
 Atypical chest pain - precordial area but with
musculoskeletal, positional, or pleuritic
features
DIAGNOSIS DIFERENSIAL
SAKIT DADA
Cardiac Gastrointestinal
 ACS : Infarct,angina •Reflux esofagus
 MVP •Ruptur esofagus
•Gall bladder disease
 Aortic Stenosis
•Peptic Ulcer
 Hypertrophic cardio-
•Pancreatitis
myopathy
 Pericarditis
Vascular
Lungs •Aortic dissection/aneurysma
 Lung Emboli
 Pnemonia Others
 Pneumothorax •Musculoskeletal
 Pleuritis •Herpes zoster
CAD Risk Stratification
 High Risk (≧1 of the following features)
 Prior MI, VT or VF or known CAD
 Definite clinical angina
 Dynamic ST changes
 Marked anterior T-wave changes
CAD Risk Stratification
 Intermediate Risk (no high-risk features
plus 1 of the following)
 Definite angina (young age)
 Probable angina (older age)
 Possible angina (DM or 3 other risk factors)
 ST depression  1 mm or T inversion  1 mm
CAD Risk Stratification
 Low Risk (no high- or intermediate-risk
features plus 1 of the following)
 Possible angina
 One risk factor (not DM)
 T-wave inversion < 1mm
 Normal ECG
Sasaran utama terapi SKA :

• Mengurangi nekrosis miokard pada pasien yg mengalami infark

• Mencegah MACE ( kematian, IMA non fatal,


kebutuhan untuk revaskularisasi segera )

• Defibrilasi segera bila terjadi VF

Stratifikasi risiko : EKG 12 lead

3 kelompok triase :

• Elevasi segmen ST
• Depresi segmen ST
• EKG non diagnostik/normal
ER Patient Care
Initial assessment (< 10 min)  Obtain initial cardiac
 Measure vital signs marker levels
 Measure SpO2  Evaluate initial
 Obtain IV access electrolyte and
coagulation studies
 Obtain 12-lead ECG
 Request, review
 Perform brief, targeted
portable chest x-ray
history and PE)
(<30 min
ER patient care
 Initial general treatment (memory aid:
“MONA” greets all patients
 Morphine, 2-4 mg repeated q 5-10 min
 Oxygen, 4 L/min; continue if SaO2 < 90%
 NTG, SL or spray, followed by IV for persistent or
recurrent discomfort
 Aspirin, 160 to 325 mg (chew and swallow)
Triage by ECG
 ST elevation or new LBBB
 ST elevation ≧1 mm in 2 or more contiguous leads
 ST depression or dynamic T-wave inversion
 ST depression > 1 mm
 Marked symmetrical T-wave inversion in multiple
precordial leads
 Dynamic ST-T changes with pain
 Nondiagnostic ECG or normal ECG
ST depresi dan perubahan gelombang T

• ST depresi dianggap bermakna bila > 1 mm di bawah garis dasar PT di titik J


• Titik J didefinisikan sebagai akhir kompleks QRS dan permulaan segmen ST

Bentuk segmen ST :

• up-sloping ( tidak spesifik )


• horizontal ( lebih spesifik untuk iskemia )
• down-sloping ( paling terpercaya untuk iskemia )

Perubahan gelombang T pada


iskemia kurang begitu spesifik

Gelombang T hiperakut
kadang2 merupakan satu-satunya
perubahan EKG yang terlihat
T Wave
Stable atherosclerotic plaque
Electrocardiography

 ECG necessary to detect ischaemic changes or


arrhythmias.

 Initial ECG has a low sensitivity for ACS, and a


normal ECG does not rule out ACS.

 However, the ECG is the sole test required to select


patients for emergency reperfusion (fibrinolytic
therapy or direct PCI).
ECG
 serial ECGs : in patients with NSTEACS w
high and intermediate risk features

The frequency of ECGs will depend on clinical


features (eg, every 10– 15 minutes during
ongoing symptoms, immediately if symptoms
change while the patient is under observation
Blood tests
Measurements should include:
• Serum troponin I or T levels ( or CK-MB if troponin is not
available).
• Full blood count.
• Serum creatinine and electrolyte levels, particularly K+
concentration,
as hypokalaemia is associated with an increased risk of arrhythmias, especially
ventricular fibrillation10 (grade B recommendation). Knowledge of kidney function
(expressed as estimated glomerular filtration rate) is strongly encouraged (grade B
recommendation) given the association between renal impairment and adverse
outcomes (evidence level III).11

Serum creatine kinase (CK) level.


• Serum lipid levels (fasting levels of total cholesterol, lowdensity-
lipoprotein cholesterol, high-density-lipoprotein cholesterol and
triglycerides) within 24 hours.
• Blood glucose level.
Recommendations on Cardiac Biomaker
Cardiac Troponin
•On arrival -------- Troponin indicates myonecrosis
--high feature in NSTEACS
-------- 1/3 pts high Troponin but normal CK
& CKMB will develop adverse outcome

•Not repeated if positif --- not useful for identifying ealy


reinfarction
•If initial negative --- repeat > 8 hours after last episode
of chest pain or other symptoms

•Serial troponin ----in pts NSTEACS suspected to be at high


risk.Rise indicates more aggressive thx.
Recommendations on Cardiac Biomarkers

CK-MB Level
•Measured in All pts with an ACS if Troponin assay
unavailable
( if Trop unavailable, CK-MB is more spesific than
CK for myocardial injury. CK-MB may be used
to confirm a re-infarction)

Total CK Level
•Serial measurements for 48 hrs in MCI
•Remeasurement if reinfarction suspected
Chest x-ray

 A chest x-ray is useful for assessing cardiac


size, evidence of heart failure and other
abnormalities (grade D recommendation), but
should not delay reperfusion treatment where
indicated.
Kriteria infark miokard akut
Kriteria infark miokard akut adalah terdapat 2
dari 3 kriteria dibawah ini :
 Nyeri khas infark
 Perubahan serial EKG
 Peningkatan diikuti dengan penurunan serum
cardiac marker.
Penanganan Khusus

Terapi reperfusi, dengan sasaran:

• Fibrinolitik : door-to-needle < 30 menit


• Primary PTCA: door-to-dilatation < 90 menit

Terapi Conjunctive ( kombinasi dengan obat fibrinolitik )

• Aspirin
• Heparin ( khususnya dengan TPA )

Terapi Tambahan

•  blocker oral , bila memungkinkan


• Nitrogliserin iv ( iskemik menetap, kontrol hipertensif dan udem paru )
• ACE Inhibitor ( IMA anterior, LVEF < 40%,
gagal jantung tanpa hipotensi - TD sistolik > 100 mmHg )
Terapi Fibrinolitik

Tissue Plasminogen Activator ( tPA )


Diberikan pada AMI yang luas, datang dini dan kemungkinan
komplikasi pendarahan kecil

Diberikan dengan dosis bertahap


• 15 mg bolus iv
• 0.75 mg/kg - jangan > 50 mg, 30 menit
• 0.50 mg/kg - jangan > 35 mg, 60 menit

Streptokinase
Diberikan pada pasien IMA yang kemungkinan komplikasi
perdarahan otak tinggi, datang lambat dan infarknya tak luas

• 1.5 juta unit dalam 1 jam


Terapi Fibrinolitik

Reteplase (rPA)
10 U + 10 U iv bolus selang 30’

Tenecteplase (TNK-tPA)
Single iv bolus
• 30 mg = < 60 kg
• 35 mg = 60-70 kg
• 40 mg = 70-80 kg
• 45 mg = 80-90 kg
• 50 mg = > 90 kg
Heparin IV ( U F H ) AHA, 2004

Direkomendasikan untuk :

• Pasien yang strategi reperfusinya menggunakan PTCA / CABG


• Pasien yang diberi TPA, Reteplase atau Tenecteplase
• Pasien yang diberi Streptokinase, Anistreplase atau Urokinase
dengan risiko tromboemboli ( IMA anterior / luas, AF,
riwayat emboli atau diketahui Trombus LV )
• Trombosit harus diperiksa setiap hari

Perhatian :
Kontraindikasi seperti pada terapi fibrinolitik

LMWH ( Enoxaparin )

30 mg bolus iv, diikuti 1 mg / kg / sc tiap 12 jam


ST-Elevation

ASA Beta
Blocker

<12h >12h

Eligible for Thrombolytic Not a


thrombolytic therapy Candidate for Persistent
therapy contraindicated reperfusion Symptoms
therapi

Thrombolytic Primary PTCA


therapy From or CABG No Yes
loaded t-PA or SK

Other medical Consider


therapy: ACE Reperfusion
inhibitor ? Nitrates Therapy

1999 Updated ACC/AHA AMI Guidelines


(Web Version:March 22, 2002)
Benefit of Thrombolytics

Time Lives saved/1000


< 1h 65
1-2 h 37
2-3 h 29
3-6 h 26
6-12 18
12-24 9
Thrombolytics and Stroke
 Risk factors:  Strokes
 > 65 years  no risks = 0.25%
 BW < 70 Kg  3 risks = 2.5%

 BP > 180/110

 on anticoagulants
Fibrinolytic Use in Myocardial Infarction ( AHA 2004 )
Absolute Contraindications Cautions/Relative Contraindications

• Previous hemorrhagic • Severe uncontrolled HT on presentation


stroke at any time (BP >180/110 mm Hg)

• Ischemic strokes 3 mo • History of prior CV accident or known intra-


( except 3 hrs ) cerebral pathology not covered in CI

• Known intracranial • Current use of anticoagulants (INR ≥2-3);


malignant neoplasm known bleeding diathesis

• Active internal bleeding • Recent trauma ( 2-4 wks ), head trauma


/ bleeding diasthesis
( not include menses ) • Noncompressible vascular punctures
• Recent ( 2-4 wks ) internal bleeding
• Suspected aortic dissection • For streptokinase : prior exposure
( within 5d-2y ) or prior allergic rx
• Head / facial trauma • Pregnancy
within 3 mo • Active peptic ulcer
• History of chronic HT
Absolute contraindications

• Haemorrhagic stroke or stroke of unknown origin at any time


• Ischaemic stroke in preceding 6 months
• Central nervous system damage or neoplasms
• Recent major trauma/surgery/head injury ( within 3 weeks )
• Gastro-intestinal bleeding within the last month
• Known bleeding disorder
• Aortic dissection
Relative contraindications

• Transient ischaemic attack in 6 months


• Oral anticoagulant therapy
• Pregnancy or within 1 week post partum
• Non-compressible punctures
• Traumatic resuscitation
• Refractory hypertension ( SBP >180 mm Hg )
• Advanced liver disease
• Infective endocarditis
• Active peptic ulcer
High risk for progression to MI or death

• recurrent ischaemia / dynamic ST-segment changes


( in particular STsegment depression,
or transient ST-segment elevation )
• early post-infarction unstable angina
• elevated troponin levels
• haemodynamic instability within observation period
• major arrhythmias ( repetitive VT, VF )
• DM
• with an ECG pattern which precludes assessment of
ST-segment changes

ESC, 2002
High Risk Unstable Angina Pectoris ( TIMI Risk Score )

• Usia > 65 tahun


• Angina > 2x dalam 24 jam
• 3 faktor resiko CAD
• Aspirin dalam 7 hari terakhir
• CAD ( stenosis > 50%, CABG, PTCA, MI )
• ST changes
• Troponin +

Risk Factors for CAD


• Family history of premature CAD
• Hypertension
• Hypercholesterol
• DM
• Smoker
Anatomi Koroner dan EKG 12 sandapan

• Sandapan V1 dan V2 menghadap septal area ventrikel kiri

• Sandapan V3 dan V4 menghadap dinding anterior ventrikel kiri

• Sandapan V5 dan V6 ( ditambah I dan avL ) menghadap


dinding lateral ventrikel kiri

• Sandapan II, III dan avF menghadap dinding inferior ventrikel kiri
ECG demonstrates large anterior infarction
A: Proximal large RCA occlusion

B: ST elevation in leads II, III, aVF


A : Small inferior distal RCA occlusion

B : ECG changes in leads II, III, and aVF


Unstable angina
Acute anterolateral myocardial infarction
Lateral myocardial infarction.
ST segment elevation in leads I and aVL
Acute inferior myocardial infarction
Acute inferoposterior myocardial infarction.
ST segment elevation in II, III and aVF
with ST depression in leads V1 and V2
Subendocardial ischemia.
Anterolateral ST-segment depression
RBBB + Anterior Infarction

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