Tatalaksana Awal Sindroma Koroner Akut

(SKA )

Siska Suridanda Danny RS Jantung Nasional Harapan Kita Jakarta

2015

siskadanny@yahoo.com

Penyakit Arteri Koroner

Sindroma Koroner Akut

STEMI NSTEMI Unstable Angina

Angina Stabil

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

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

PROFILPASIEN

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)

EKGdanBioMarker

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?

DIAGNOSIS? TATA LAKSANA?

SINDROMA KORONER AKUT

Non ST Elevasi ST Elevasi

TATA LAKSANA AWAL YANG HAMPIR SAMA

Terapi reperfusi secepatnya

Validasi diagnosis dan Stratifikasi risiko

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

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

HammCWetal.EurHeartJ2011;32:2999–3054

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

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

HammCWetal.EurHeartJ2011;32:2999–3054

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

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

Initial Treatment

HammCWetal.EurHeartJ2011;32:2999–3054

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

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.

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

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)

*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

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

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

Cum

ulat

ive

Inci

denc

e (%

) 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)

11,6

5,8 5,3

7,9

11,411,2

5,8 5,2

7,7

10,9

02468

101214161820

Total Major Major Fatal/Life-Threatening

Other Major TIMI Major TIMI Major+Minor

Ticagrelor ClopidogrelPLATO 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-M

est

imat

ed ra

te (%

per

yea

r)

Both groups included aspirin

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

Ticagrelor : PLATO study (safety)

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.

ACS PERKI GUIDELINE - NSTEACS

ACS PERKI GUIDELINE - STEMI

P2Y12 Di Dalam Addendum 2 FORNAS 2015

33

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

34

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