Tatalaksana Awal

Sindroma Koroner Akut

(SKA )

Siska Suridanda Danny

RS Jantung Nasional Harapan Kita Jakarta
2015

siskadanny@yahoo.com
 Penyakit Arteri
Koroner

Sindroma Angina
Koroner Akut Stabil

Unstable
STEMI NSTEMI
Angina
 Tata laksana SKA
ACS with persistent ACS without persistent
STEMI
ST segment elevation UAP/NSTEMI
ST segment elevation

PROMPT DIAGNOSIS and EARLY MANAGEMENT and

REVASCULARIZATION offers RISK STRATIFICATION
greatest benefit for myocardial reduces adverse events and
salvage in the first hours of improves outcome
STEMI

O’Connor RE et al. Circulation. 2010;122[suppl ]:S787–S817.)

PROFIL PASIEN

Perempuan, 62 tahun

Faktor Risiko PJK

•  Hipertensi > 10 thn, kontrol dan minum obat tidak rutin
•  Menopause
•  Riwayat kolesterol tinggi
•  Diabetes
•  Obesitas

Riwayat Penyakit Sekarang

•  Sejak + 3 hr terakhir mengeluhkan rasa berat di dada dan ulu
hati, hilang timbul, yang dianggap pasien sebagai ‘maag yang
kambuh’
•  Nyeri dada hebat disertai sesak nafas, mual-muntah dan
keringat dingin 4 jam sebelumnya
Algoritma pendekatan terhadap SKA

5
Hamm CW, et al. European Heart Journal (2011) 32, 2999–3054
 ANGINA
•  Sakit dada (sakit, nyeri, rasa tertimpa beban, rasa
terbakar) di belakang tulang dada
•  Dipicu oleh aktivitas atau stres emosional à
menghilang dengan istirahat atau nitrat
•  Dapat menjalar ke punggung, bahu, rahang atau
lengan.
•  Disertai rasa lemah, keringat dingin, rasa cemas dan
bahkan bisa pingsan.
 Presentasi Angina pada SKA

•  Angina berat yang timbul saat istirahat dengan durasi

lebih dari 20 menit
•  Angina new onset (dalam 1 bulan terakhir), dengan
derajat CCS III (angina muncul dengan aktivitas
ringan sehari-hari)
•  Angina progresif (dirasakan lebih berat, lebih lama,
atau dicetuskan oleh aktivitas yang lebih ringan
dibandingkan biasanya)

Braunwald, et al. JACC 2000;36:3

ELEKTROKARDIOGRAM

• EKG 12 Sandapan
• Dalam 10 menit !!
• Membuat dan menganalisa EKG
• Tentukan:
•  Irama
•  Elevasi segmen ST ?
•  Depresi segmen ST ?
•  LBBB (BARU )?
•  Gelombang Q ?
•  Non diagnostik/EKG normal
•  Dapat diulang dalam 3-6 jam atau
jika pasien melaporkan keluhan lagi
 ELEKTROKARDIOGRAM YANG NORMAL
TIDAK MENGEKSKLUSI ADANYA SINDROMA
KORONER AKUT

ANGINA TIDAK STABIL (UAP/APTS) ADALAH

DIAGNOSIS BERDASARKAN ANAMNESIS
Contoh perlepasan penanda jantung pada pasien
NSTE-ACS
(ESC 2007)
EKG dan BioMarker

•  Rhythm ?
•  Segmen ST elevation ?
•  Segmen ST depresssion?
•  LBBB (new )?
•  Q Wave?

TEST RESULT REMARKS

Hs Troponin T 585 ug/L (<14 ug/L) Elevated consistent with myocardial
damage
DIAGNOSIS?
TATA LAKSANA?
 SINDROMA KORONER AKUT

Non ST Elevasi ST Elevasi

TATA LAKSANA AWAL YANG HAMPIR

SAMA

Validasi diagnosis Terapi reperfusi

dan Stratifikasi risiko secepatnya
 Gejala dan Tanda sesuai dengan SKA
Pemeriksaan awal
•  Tanda Vital
•  Akses intravena
•  EKG 12 lead
•  Riwayat penyakit terfokus
•  Pemeriksaan fisik terfokus
•  Ambil sampel darah untuk
pemeriksaan biomarker
kardiak, ditambah dengan
darah rutin, fungsi ginjal dan
elektrolit
•  Chest X-Ray(<30 min)
•  Checklist fibrinolitik
Penanganan awal
•  Oksigen 4 L/menit jika
saturasi <95%
•  Morphine iv jika nyeri dada
hebat dan tidak berkurang
dengan nitrat
•  Nitroglycerin / Nitrat
Sublingual, spray atau IV. Hati-
hati pada TDS < 90 mmHg
•  Aspirin 160 to 325 mg
•  Clopidogrel 600 mg ATAU
Ticagrelor 180 mg
NSTEACS Management strategy

Step 1. initial evaluation

Step 2. Diagnosis validation and risk

assessment

Step 3. invasive strategy

Step 4. revascularization modalities

Step 5. hospital discharge

and post-discharge management

Hamm CW et al. Eur Heart J 2011;32:2999 – 3054

 Risk Stratification is important in NSTE-ACS
Management

1 CLINICAL CONDITION

2 3
TIMI SCORE GRACE SCORE

Less accurate in predicting events but recommended as the preferred

its simplicity makes it useful and classification to apply on admission
widely accepted and at discharge in daily clinical
routine practice

Hamm W et al. European Heart Journal 2007; 28:1598–1660; Hamm CW et al. Eur Heart J 2011;32:2999 – 3054
 Clinical condition

HIGH RISK VERY HIGH RISK

PRIMARY •  Refractory angina
• Relevant rise or fall in troponin •  Severe heart failure
• Dynamic ST- or T-wave changes •  Life-threatening ventricular
(symptomatic or silent) arrhythmias, or Hemodynamic
instability
SECONDARY
•  Diabetes mellitus
• Renal insufficiency
(eGFR <60 mL/min/1.73 m²)
• Reduced LV function (EF <40%)
• Early post infarction angina
• Recent PCI
• Prior CABG
• Intermediate to high GRACE risk score

Hamm CW et al. Eur Heart J 2011;32:2999 – 3054

TIMI SCORE

Age 65 years or older? Risk TIMI risk score for developing at

Score least 1 component of the primary
end point through 14 days after
At least 3 risk factors for CAD? randomization.1
0-1 4.7%
Prior coronary stenosis of 50% or more?
2 8.3%

ST-segment deviation on ECG 0.5mm? 3 13.2%

4 19.9%
Use of aspirin in prior 7 days
5 26.2%
At least 2 anginal events in prior 24 hours?
6- 7 40.9%

Elevated serum cardiac markers?

Hamm W et al. European Heart Journal 2007;28:1598–1660

GRACE SCORE

Predictor Score Predictor Score Predictor Score

Age, years Systolic Blood Pressure (mmHg) Killip class
< 40 0 < 80 63 I 0
40 - 49 18 80 – 99 58 II 21
50 - 59 36 100 - 119 47 III 43
60 - 69 55 120 - 139 37 IV 64
70 - 79 73 140 - 159 26
Predictor Score
80 91 160 - 199 11
Cardiac 43
> 200 0 arrest at
admission
Predictor Score Predictor Score Elevated 15
Heart Rate , beats/min Creatinine (µmol/L) cardiac
markers
< 70 0 0 - 34 2
ST Segment 30
70-89 7 35 – 70 5 deviation
90-109 13 71 – 105 8
110 - 149 23 106 – 140 11 Risk GRACE In-hospital
150 - 199 36 141 – 176 14 category Risk Score death
(tertile) (%)
> 200 46 177 – 353 23
Low ≤ 108 <1
≥ 354 31
Intermediate 109 - 140 1-3

Khalill R et al. Exp Clin Cardiol.2009; 14(2): e25 – e30 High > 140 >3
Initial Treatment

Initial Therapeutic Measures Checklist of treatments when an ACS

diagnosis appears likely

Hamm CW et al. Eur Heart J 2011;32:2999 – 3054

 Activated platelets are central to thrombus
formation in ACS
•  Platelets do 3 things that promote thrombus formaton
-  Adhesion
-  Activation Activated platelets aggregate
-  Aggregation and assemble a critical mass
3 of activated, pro-thrombotic
platelet membrane at the site
of injury

Adherent platelet become activated

2

1
Plaque rupture leads
to platelet adhesion
to the exposed
subendothelium

Vorchheimer DA, et al. Mayo Clin Proc. 2006;81:59-68; Davies MJ. Heart. 2000;83:361-366.
 Antiplatelet recommendation in
Updated ACS Guidelines

Aspirin should be given to all patients without

contraindications at an initial loading dose of 150–300 mg,
and at a maintenance dose of 75–100 mg daily long-term
regardless of treatment strategy.

A P2Y12 inhibitor should be added to aspirin as soon as

possible and maintained over 12 months, unless there are
contraindications such as excessive risk of bleeding.

Clopidogrel Ticagrelor Prasugrel*

1.Kolh P et al. Eur Heart J August 29 2014; DOI:10.1093/eurheart/ehu278 [Epub ahead of

print]
*Not yet approved and
2.Steg PG et al. Eur Heart J 2012;33:2569–2619; 3.Hamm CW et al. Eur Heart J available in Indonesia
2011;32:2999 – 3054. 4. Amsterdam EA et al. J Am Coll Cardiol Sept 23, 2014 Epub ahead
of print. DOI:10.1016/j.jack.2014.09.017
 Profile P2Y12 inhibitor

*Prasugrel is not yet approved and available in Indonesia

Adapted from Hamm CW et al. Eur Heart J 2011;32:2999 – 3054
 Metabolism P2Y12 inhibitor
(Pro drug vs active drug)

No in vivo
Active compound biotransformation
Intermediate metabolite
Pro-drug
CYP-dependent
oxidation
CYP3A4/5
Ticagrelor CYP2B6
(Active Drug) CYP2C19
Hydrolysis CYP2C9 Binding
by esterase CYP2D6
Prasugrel* Platelet
(Prodrug)

P2Y12
Clopidogrel
(Prodrug) CYP-dependent CYP-dependent
oxidation oxidation
CYP1A2 CYP2C19
CYP2B6 CYP3A4/5
CYP2C19 CYP2B6

*Prasugrel is not yet approved and available in Indonesia

Figure adapted from Schömig A (2009). CYP, cytochrome P450.
Schömig A. N Engl J Med 2009;361:1108–1111.
 Limitation of clopidogrel
•  Dual antiplatelet therapy (DAPT) with aspirin & clopidogrel
is the current standard treatment in patients with ACS1
-  With or without ST segment elevation1
•  Poor platelet inhibition response to clopidogrel is seen in
approximately 5% - 40% of patients2
-  Contribute to residual high risk of recurrent results
•  Clopidogrel has slow onset of action1
-  Prodrug that requires conversion to active metabolite1
•  Variable metabolism results in interindividual variability in
inhibition of platelet agregation1

1.  Bassand JP . European Heart Journal Supplements 2008; 10 : Supplement D, D3–D11;

2.  Gurbel PA, Tantry US. Thrombosis Research. 2007;120: 311–321
 Ticagrelor
Ticagrelor: PLATO study
: PLATO (efficacy)
study (efficacy)

13 0–30 Days 0–12 Months

12 11.7 Clopidogrel
Cumulative Incidence (%)

11
10 9.8 Ticagrelor
9 Clopidogrel
8 5.4
7
6
5
4 ARR=0.6% ARR=1.9%
4.8
RRR=12% RRR=16%
3 Ticagrelor
P=0.045 NNT=54*
2 HR: 0.88 (95% CI, 0.77−1.00) P<0.001
1 HR: 0.84 (95% CI, 0.77–0.92)
0
0 2 4 6 8 10 12
No. at risk Months After Randomization
Ticagrelor 9,333 8,628 8,460 8,219 6,743 5,161 4,147

Clopidogrel 9,291 8,521 8,362 8,124 6,650 5,096 4,047

Both groups included aspirin.
*NNT at one year.

Wallentin L, et al. N Engl J Med. 2009;361:1045–1057.

 Ticagrelor : PLATO study (safety)

Ticagrelor Clopidogrel

20
PLATO bleeding criteria TIMI bleeding criteria
K-M estimated rate (% per year)

18
16 HR=1.04 HR=1.05
14 (P=0.43) (P=0.33)
11,6 11,2 11,4 10,9
12 HR=1.03
10 HR=1.03 (P=0.57)
HR=0.87 7,9
8 (P=0.70) 7,7
5,8 5,8 (P=0.6553)
6 5,3 5,2

4
2
0
Total Major Major Fatal/Life- Other Major TIMI Major TIMI Major+Minor
Threatening

Both groups included aspirin

Wallentin L, et al. N Engl J Med. 2009;361:1045–1057.

 ONSET Ticagrelor vs high dose clopidogrel
Last
Maintenance
Dose
Loading 90 mg bid
100 Ticagrelor (n=54)
Dose 75 mg qd
90
* * * * * †
180 mg
600 mg
* * Clopidogrel (n=50)
80
// * * P<0.0001
70 † P<0.005
‡ P<0.05
IPA %

60

50
* //
40
‡
30
†
20

10

0
//
0 0.5 1 2 4 8 24 6 weeks 0 2 4 8 24 48 72 120 168 240

Onset Maintenance Offset

Time (Hours) Time (Hours)
Adapted from Gurbel PA, et al. Circulation. 2009;120:2577–2585.
ACS PERKI GUIDELINE - NSTEACS
ACS PERKI GUIDELINE - STEMI
P2Y12 Di Dalam Addendum 2 FORNAS 2015
 Updated Guidelines 2014

STEMI Primary PCI and NSTEACS PCI1

A P2Y12 inhibitor is recommended in addition to ASA, and

maintained over 12 months unless there are contraindications
such as excessive risk of bleeding.

NSTE-ACS
Early invasive or ischemia-guided strategy2

A P2Y12 inhibitor (either clopidogrel or ticagrelor) in addition

to aspirin should be administered for up to 12 months to all
patients without contraindications

33 1. Windecker S et al. European Heart Journal / doi:10.1093/eurheartj/ehu278; 2. Amsterdam EA et al. J

Am Coll Cardiol Sept 23, 2014 Epub ahead of print. DOI: 10.1016/j.jack.2014.09.017
 OUR PATIENT:

•  Pasien klinis perbaikan dengan pemberian anti platelet, anti

iskemia dan anti koagulan
•  Dilakukan tindakan PCI pada hari ke-3 perawatan dengan
hasil CAD 1 VD dan dipasang 1 stent di LCx
•  Pasien pulang pada hari ke-5 dalam kondisi baik, dengan
terapi:
–  Aspirin 1x80 mg
–  Ticagrelor 2x90 mg
–  Rosuvastatin 1x20 mg
–  Ramipril 1x5 mg
–  Bisoprolol 1x5 mg

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