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Acute coronaire syndromen

Prof dr M ClaeysUZ Antwerpen

Universiteit Antwerpen

TRIADE VAN ACS

AnamneseCardiac enzymes

Surface ECG

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Anamnese

• Klachtenpatroon Stabiel AP ACS

– aard: drukkend, beklemmend

– localisatie retrosternaal, li schouder/hals

– uitlokkende factoren inspanning los van inspanning

– duur <20 minuten > 20 minuten

– reproduceerdbaarheid ja niet altijd

– begeleidende symptomen neen vaak

– (zweten, malaise, nausea)

– reactie op nitraten ja niet altijd (MI)

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Voorwandinfarct: grootste infarct? A of B

Proximal LAD Occlusion

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Distal LAD Occlusiondistal to both S1 and D1

ST- Elevation: in II > III and aVF

ST- Elevation: in lead V5-V6

Proximal LAD Occlusion Distal LAD Occlusion

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KEY POINT: Anterior infarction

DIAGNOSIS of anterior wall infarction

ST-elevation in the precordial leads V1 to V4

SITE of OCCLUSION in the LAD and AREA at RISKcan be recognized in the frontal leads

Inferior infarct

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From “ECG uit of in het hoofd” Andries E, Stroobandt R, De Cock N et al., Garant, 2006

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ST- Elevation: in lead III > II ST- Elevation: in II > III

Proximal occlusion RCA ST-elevation > 1 mmpositive T-wave

Distal occlusion RCA No ST-elevationpositive T-wave

Occlusion LCX Negative T-wave

Right Ventricular Myocardial Infarction V4R

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ACS zonder ST elevatie: hoofdstamstenose of 3VD

ST- Depression: in > 8 leads (most pronounced in V4)

ST- Elevation: in lead aVR and V1

Kritische Proximal LAD Stenosis (Wellens Syndrome)

CAVE:

Bij pijnaanval

Pseudonormalisatie !!!

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VROEGE DIAGNOSE:BIOCHEMISCHE MERKERS

snel duur gevoelig specifiekCK MB +++ kort +++ +++

Myoglobine ++++ kort+ ++++ -

Troponine + lang+ ++++ ++++

SGOT + lang ++ ++

LDH - lang+ ++ ++

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High sensitivity-Troponine

1x HsTrop + ≠ ACS

Giannitsis, ClinChem, 201020,2 ng/l � 55,3 ng/l (n=13, p=0,02) 4,3 ng/l � 2,9 ng/l (n=31, p=0,87)

Hs-Trop en ACS

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Acute coronair syndroom

Zonder ST-segment elevatie

Onstabiele Angor

Non-STEMI

met ST-segment elevatie

STEMI

Onstabiele

angor pectoris

Non Q-golf

myocardinfarct

Q-golf

myocardinfarct

* absolute ∆ hs trop of 50%ULN

∆ (0-3h) hs trop*

BELEID VAN ACS

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MCCU: early diagnosis

• Rhytm monitoring

• 12 lead ECG registration

+ wireless data transfer!

Early-in-hospital Management

1. Check vital signs2. Establish ECG monitoring + defibrillator 3. Give oxygen (3-5 lit/min) indien O²sat<90%

4. Establish IV access5. Take 12-lead ECG6. Obtain serum cardiac markers

7. Cardiological assessment:ST elevation AMI ACS without ST elevationACS doubtful or non cardiac pathology

< 3‘

< 10‘

< 20‘

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Acute coronary syndrome without ST elevation

1. Check intake ASA 2. Check intake nitrates SL3. Start heparin

(Fondaparinux sc* or LMWH sc** orunfractionated IV)

4. Start nitrate IV (if bloodpressure > 100 mmHg)

5. Start Beta-Blockers6. OralP2Y12 inhibitors

(clopidogrel/prasugrel/ticagrelor)

* Fondaparinux: 2.5mg 1/d subcutaan

** LMWH: vb enoxaparine (R/clexane 1mg/kg 2x/d subcutaan)

Anti-trombotica

Prasugrel

Ticagrelor

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GP = glycoprotein; ADP = adenosine diphosphate; PAR = protease-activated receptor; AA = arachidonic acid; Tx = thromboxane.

Adapted from Brogan. Ann Emerg Med. 2002;9:1029.

Platelet activation - aggregation

Variation in platelet respons on clopidogrel

ACC 2008;52:1052-9

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Schomig A. N Engl J Med 2009;361:1108-1111

Biotransformation and Mode of Action of Clopidogrel , Prasugrel, and Ticagrelor

Pharmokinetic new P2Y12 inhibitors

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Mortality in PCI for STEMI 0.78 (0.66-0.93) .004

Major Bleed in STEMI 0.98 (0.85-1.13) .76

Mortality in any PCI for ACS 0.83 (0.73-0.93) < .001

AnyMajor Bleed 1.23 (1.04-1.46) 0.01

Risk Ratio

(95% CI)P value

0.5 1.0 1.5

ClopidogrelNew P2Y12

A class effect of novel P2Y12 inh.A metanalysis of clopidogrel vs. new comers (n=48599 pts)

J Am Coll Cardiol 2010;56:000–0

Giugliano et al, NEJM 2009

Delayed Provisional GPIIbIIIa:

- Same Ischemic benefit

- Lower bleeding risk

N=9492

Upstream GP blokker in non-STEMI ACS: EARLY ACS

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Mehta et al. NEJM 2009 - TIMACS Study

Early (≤24 h, median=14h) or delayed intervention ( ≥36 h, median=50h)

Death, >MI, Refractory AnginaDeath, MI, Stroke

N=3031

GRACE>140

Acute coronary syndrome without ST elevation

Aspirin - Nitrate - Beta-blocker

P2Y12 inhibitor # -Anticoagulation *

*Anticoagulation : Fondaparinux (+UHF in case of PCI) / Enoxaparine / U FH

# P2Y12 inhibotor: Ticagrelor / Prasugrel (reimbursement only in diabetic patients with PCI )

clopidogrel (high bleeding risk or low risk ACS)

HIGH RISK

Recurrent severe ischemia Elevated troponin

Hemodynamic instability Early post infarct angina

Major arrhythmias (VF, VT) Diabetes mellitus

Coronarography:

Urgent (<2h) Elective (<72h)(< 24h if Grace score>140)

consider IIB -IIIA antagonist + hep or bivaluridin

LOW RISK

No recurrent ischemia

No rise in trop

No diabetes

Non-invasive testing

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Early-in-hospital Management

1. Check vital signs2. Establish ECG monitoring + defibrillator 3. Give oxygen (3-5 lit/min) indien O²sat<90%

4. Establish IV access5. Take 12-lead ECG6. Obtain serum cardiac markers

7. Cardiological assessment:ACS without ST elevation ST elevation AMI ACS doubtful or non cardiac pathology

< 3‘

< 10‘

< 20‘

ST- Elevation AMI : management

1. Check intake ASA / nitrates SL2. Prasugrel/Ticagrelor/clopidogrel

4. Initiate Reperfusion therapy

Thrombolyse PTCA

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The 90 Minute Wall:The 90 Minute Wall: Rates of TIMI Grade 3 FlowRates of TIMI Grade 3 Flow

% T

IMI 3

Flo

w%

TIM

I 3 F

low

Primary PCI vs. thrombolytic therapy

Keeley Lancet 2003;361:13

Death Death excl.

Shock

Nonfatal MI

Recurrent ischemia

Total CVA

Hemorr. CVA

Major bleeds

Death/ CVA/AMI

p=0.0002

p=0.0003 p<0.0001

p<0.0001

p=0.0004

p<0.0001

p=0.032

p<0.0001

Fre

quen

cy (

%)

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De Luca, Circulation 2004

Primary PCI and timePrimary PCI and timePrimary PCI and timePrimary PCI and time

30 minutes delay increases 1-year mortality by 7.5%

Europese richtlijnen reperfusietijden: PCI

<90-120min

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ST elevation MI (<12 h after onset of pain)

Admission in

PCI-center

Primary PCI

• Thrombus aspiration

• Bivalirudin( IIB-IIIa antagonists for bail-out)

Admission in non-PCI-center OR

1st medical contact outside hospital

• Transfer time to PCI center < 90 min

(transfer time<60 if ischemic time<2h)

• Hemodynamic instability

(shock / cardiac failure/ malignant arrhythmias)

• Contra-indication thrombolysis

Thrombolysis

YES

NO

• PPCI: UFH and Prasugrel 60 mg/ Ticagrelor 180mg

•Trombolysis: Enoxaparin and clopidogrel 300mg (adjus ted dose if >75y)

ASA- Morphine - Heparin* - P2Y12 inhibitor *

Failed

Rescue PCI

Succes

Coronaro/

PCI 3-24h*

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Voorkamerfibrillatie

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VKF

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Doel Behandeling VKF

• Controle kamerfrequentie

• Preventie van embolie

• Herstel van sinusritme

– Medicamenteus

– Electrische cardioversie

– Ablatie

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Stabilisatie Hartritme

Betablokkers CAVE bronchospasme, cardiodepressie

Calcium-antagonist: verapamil/diltiazem

CAVE: WPW, HOCM, cardiodepressie

Digitalis: vooral bij hartfalen

CAVE: WPW, HOCM

Amiodarone IV: bij hartfalen

bij refractaire tachycardie

Cardioversie en Cardiale Embolen

Risico cardiale embolen

VKF> 2 d: 5-8 %

VKF< 2d: <1%

ANTICO indien VKF > 2 dagen !! of TEE

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Onregelmatig kamerritme > 100/min + onregelmatige o f zaagtand basislijn

ECG, bloeddrukmonitoring, O 2

IV lijn, 12-afleidingen ECG

Hemodynamische evaluatie

ONSTABIEL* STABIEL

Synchrone cardioversie

Start Heparine IV/SC

Start Heparine IV/SC

Evaluatie: slechte hartfunctie

>of<48 h?

Goede hartfct Duur < 48u

Goede hartfctDuur > 48u

Slechte hartfctDuur < 48u

Digoxine

(Amiodarone)

+

synchrcardioversie na 4 weken antico

(INR 2-3) **

Digoxine

Amiodarone

En/of

Synchrone Cardioversie

Slechte hartfctDuur > 48 u

Bètablokker

Verapamil of Diltiazem

+

synchr cardioversie

na 4 weken antico

(INR 2-3) **

Bètablokker

Verapamil of Diltiazem

+

Flecaïnide of Propafenone of

Amiodarone of

Synchr. cardioversie

TACHYCARDIE tgv ATRIALE FIBRILLATIE/FLUTTER

** of TEE

Geleid

C—CHF 1

H—Hypertension 1

A2—Age >75 2

D—Diabetes mellitus 1

S2—TIA/stroke 2

Risk Factors for Stroke in Non-valvular AF (ESC guidelines 2010)

Overall Yearly Risk of Stroke in Non-valvular AF is 5%Camm et al, European Heart Journal 2010

0

2

4

6

8

10

12

14

16

1,3 2,2 3,24.0

6.7

9,8 9,6

6,7

15,2

Stroke rate (% per year)

0

0 1 2 3 4 5 6 7 8 9

V—Vascular 1

A—Age >65 1

S— Sex 1

CHA2DS2-VASc Score

48

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NEW ORAL ANTICOAGULANS (NOAC)

Minstens even effectief dan OAC

Korter half leven (12-16h)

Minder IC bloedingen

Geen INR controle

Vb dabigratan (pradaxa)

rivoraxabam (xarelto)

apixabam (eliquis)

Monitoring of NOAC

• Dabigratan en aPTT

Normaal APTT wijst op minimale ontstolling!!!

>2 wijst op verhoogd bloedingsrisico

Douxfill et al, Thromb and hemost. 2012

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Monitoring en NOAC

• Rivoroxabam en PT

Normaal PT wijst op minimale ontstolling!!!

>2 wijst op verhoogd bloedingsrisico

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Dosis aanpassing - interacties

Dabigratan® pradaxa

Rivoraxabam® xarelto

Apixabam® Eliquis

Standaard dosis 2x150mg/d 20mg/d 2x5mg/d

Dosisaanpassing GFR<50 ml/min GFR<50ml/min GFR <30ml/min

Aangepast dosis 2x110mg/d 15mg/d 2x2.5mg/d

Niet aanbevolen GFR <30 ml/min GFR<15 ml/min GFR <15ml/min

Niet te associeren(cf CYP3A4)

Antifungal(Ketoconazole, )HIV protease inh

Antifungal(Ketoconazole, )HIV protease inh(fluconazole wel)

Antifungal(Ketoconazole, )HIV protease inh

Referenties

• European Task force report on management of AMI. EHJ 2012

• European Task force report on management of ACS without persistent ST elevation. EHJ 2011

• European Task force report onrevascularisation, EHJ 2010