Tatalaksana Awal Sindroma Koroner Akut (SKA )

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Tatalaksana Awal

Sindroma Koroner Akut (SKA )

Siska Suridanda Danny

RS Jantung Nasional Harapan Kita Jakarta 2015

[email protected]

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Penyakit Arteri Koroner

Sindroma Koroner Akut

STEMI NSTEMI Unstable

Angina Angina

Stabil

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Tata laksana SKA

PROMPT DIAGNOSIS and REVASCULARIZATION offers greatest benefit for myocardial

salvage in the first hours of STEMI

EARLY MANAGEMENT and RISK STRATIFICATION reduces adverse events and

improves outcome ACS with persistent

ST segment elevation ACS without persistent

ST segment elevation

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

STEMI UAP/NSTEMI

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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

PROFIL PASIEN

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Algoritma pendekatan terhadap SKA

5 Hamm CW, et al. European Heart Journal (2011) 32, 2999–3054

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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.

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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

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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

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ELEKTROKARDIOGRAM YANG NORMAL TIDAK MENGEKSKLUSI ADANYA SINDROMA

KORONER AKUT

ANGINA TIDAK STABIL (UAP/APTS) ADALAH DIAGNOSIS BERDASARKAN ANAMNESIS

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Contoh perlepasan penanda jantung pada pasien NSTE-ACS

(ESC 2007)

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EKG dan BioMarker

TEST RESULT REMARKS

Hs Troponin T 585 ug/L (<14 ug/L) Elevated consistent with myocardial damage

•  Rhythm ?

•  Segmen ST elevation ?

•  Segmen ST depresssion?

•  LBBB (new )?

•  Q Wave?

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DIAGNOSIS?

TATA LAKSANA?

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SINDROMA KORONER AKUT

Non ST Elevasi ST Elevasi

TATA LAKSANA AWAL YANG HAMPIR SAMA

Terapi reperfusi secepatnya Validasi diagnosis

dan Stratifikasi risiko

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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

Gejala dan Tanda sesuai dengan SKA

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NSTEACS Management strategy

Step 1. initial evaluation

Step 2. Diagnosis validation and risk assessment

Step 3. invasive strategy

Step 5. hospital discharge and post-discharge management Step 4. revascularization modalities

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

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Risk Stratification is important in NSTE-ACS Management

TIMI SCORE GRACE SCORE

recommended as the preferred classification to apply on admission

and at discharge in daily clinical routine practice

Less accurate in predicting events but its simplicity makes it useful and

widely accepted

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

CLINICAL CONDITION

1

2 3

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Clinical condition

PRIMARY

• Relevant rise or fall in troponin

• Dynamic ST- or T-wave changes (symptomatic or silent)

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

HIGH RISK VERY HIGH RISK

•  Refractory angina

•  Severe heart failure

•  Life-threatening ventricular arrhythmias, or Hemodynamic instability

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TIMI SCORE

Age 65 years or older?

At least 3 risk factors for CAD?

Prior coronary stenosis of 50% or more?

ST-segment deviation on ECG 0.5mm?

Use of aspirin in prior 7 days

At least 2 anginal events in prior 24 hours?

Elevated serum cardiac markers?

Risk Score

TIMI risk score for developing at least 1 component of the primary

end point through 14 days after randomization.¹

0-1 4.7%

2 8.3%

3 13.2%

4 19.9%

5 26.2%

6- 7 40.9%

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

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GRACE SCORE

Predictor Score Age, years

< 40 0

40 - 49 18

50 - 59 36

60 - 69 55

70 - 79 73

80 91

Predictor Score Heart Rate , beats/min

< 70 0

70-89 7

90-109 13

110 - 149 23

150 - 199 36

> 200 46

Predictor Score

Systolic Blood Pressure (mmHg)

< 80 63

80 – 99 58

100 - 119 47

120 - 139 37

140 - 159 26

160 - 199 11

> 200 0

Predictor Score

Creatinine (µmol/L)

0 - 34 2

35 – 70 5

71 – 105 8

106 – 140 11

141 – 176 14

177 – 353 23

≥ 354 31

Predictor Score Killip class

I 0

II 21

III 43

IV 64

Predictor Score Cardiac

arrest at admission

43

Elevated cardiac markers

15

ST Segment deviation

30

Khalill R et al. Exp Clin Cardiol.2009; 14(2): e25 – e30

Risk category (tertile)

GRACE Risk Score

In-hospital death (%)

Low ≤ 108 < 1

Intermediate 109 - 140 1-3

High > 140 > 3

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Initial Treatment

Initial Therapeutic Measures Checklist of treatments when an ACS diagnosis appears likely

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Activated platelets are central to thrombus formation in ACS

•  Platelets do 3 things that promote thrombus formaton -  Adhesion

-  Activation -  Aggregation

Plaque rupture leads to platelet adhesion to the exposed

subendothelium

Adherent platelet become activated

Activated platelets aggregate and assemble a critical mass of activated, pro-thrombotic platelet membrane at the site of injury

2 1

3

Vorchheimer DA, et al. Mayo Clin Proc. 2006;81:59-68; Davies MJ. Heart. 2000;83:361-366.

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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*

*Not yet approved and available in Indonesia

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

2.Steg PG et al. Eur Heart J 2012;33:2569–2619; 3.Hamm CW et al. Eur Heart J

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

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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

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Metabolism P2Y12 inhibitor (Pro drug vs active drug)

*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.

Binding

P2Y₁₂

Platelet

No in vivo biotransformation

Ticagrelor (Active Drug) Prasugrel*

(Prodrug)

Clopidogrel (Prodrug)

CYP-dependent oxidation CYP3A4/5

CYP2B6 CYP2C19

CYP2C9 CYP2D6 Hydrolysis

by esterase

CYP-dependent oxidation

CYP1A2 CYP2B6 CYP2C19

CYP-dependent oxidation CYP2C19 CYP3A4/5

CYP2B6

Active compound

Intermediate metabolite Pro-drug

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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

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

Both groups included aspirin.

*NNT at one year.

Ticagrelor : PLATO study (efficacy)

No. at risk

Clopidogrel Ticagrelor

9,291 9,333

Months After Randomization

8,521 8,628

8,362 8,460

8,124 6,650 6,743

5,096 5,161

4,047 4,147 8,219

0 2 4 6 8 10 12

12 11 10 9 8 7 6 5 4 3 2 1 0 13

Cumulative Incidence (%) 11.7 Clopidogrel

9.8 Ticagrelor

ARR=0.6%

RRR=12%

P=0.045

HR: 0.88 (95% CI, 0.77−1.00)

0–30 Days

4.8 5.4

Clopidogrel

Ticagrelor

ARR=1.9%

RRR=16%

NNT=54*

P<0.001

HR: 0.84 (95% CI, 0.77–0.92)

0–12 Months

Ticagrelor : PLATO study (efficacy)

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11,6

5,8 5,3

7,9 11,2 11,4

5,8 5,2

7,7

10,9

0 2 4 6 8 10 12 14 16 18 20

Total Major Major Fatal/Life-

Threatening Other Major TIMI Major TIMI Major+Minor Ticagrelor Clopidogrel

PLATO bleeding criteria TIMI bleeding criteria

HR=1.03 (P=0.70) HR=1.04

(P=0.43)

HR=0.87 (P=0.6553)

HR=1.03 (P=0.57)

HR=1.05 (P=0.33)

K-Mestimated rate (% per year)

Both groups included aspirin

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

Ticagrelor : PLATO study (safety)

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ONSET Ticagrelor vs high dose clopidogrel

Onset

100 90 80 70 60 50 40 30 20 10 0

IPA %

//

Ticagrelor (n=54) Clopidogrel (n=50)

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

Maintenance Offset

Time (Hours) Loading

Dose 180 mg 600 mg

*

* * * *

‡

†

* * _†

Last Maintenance

Dose 90 mg bid 75 mg qd

//

*

//

* P<0.0001

† P<0.005

‡ P<0.05

Time (Hours)

Adapted from Gurbel PA, et al. Circulation. 2009;120:2577–2585.

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ACS PERKI GUIDELINE - NSTEACS

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ACS PERKI GUIDELINE - STEMI

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P2Y12 Di Dalam Addendum 2 FORNAS 2015

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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

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

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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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