Acute coronaire syndromen

Acute coronaire syndromen
Prof dr M Claeys
UZ Antwerpen
Universiteit Antwerpen
TRIADE VAN ACS
Anamnese
Cardiac enzymes
Surface ECG
1
Anamnese
• Klachtenpatroon
–
–
–
–
–
–
–
–
aard:
localisatie
uitlokkende factoren
duur
reproduceerdbaarheid
begeleidende symptomen
(zweten, malaise, nausea)
reactie op nitraten
Stabiel AP
ACS
drukkend, beklemmend
retrosternaal, li schouder/hals
inspanning
los van inspanning
<20 minuten
> 20 minuten
ja
niet altijd
neen
vaak
ja
niet altijd (MI)
2
Voorwandinfarct: grootste infarct? A of B
Proximal LAD Occlusion
3
Distal LAD Occlusion
distal to both S1 and D1
ST- Elevation: in II > III and aVF
ST- Elevation: in lead V5-V6
Proximal LAD Occlusion
Distal LAD Occlusion
4
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 RISK
can be recognized in the frontal leads
Inferior infarct
5
From “ECG uit of in het hoofd” Andries E, Stroobandt R, De Cock N et al., Garant, 2006
6
ST- Elevation: in lead III > II
Right Ventricular Myocardial Infarction
Proximal occlusion RCA
ST- Elevation: in II > III
V4R
ST-elevation > 1 mm
positive T-wave
Distal occlusion RCA
No ST-elevation
positive T-wave
Occlusion LCX
Negative T-wave
7
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 !!!
8
VROEGE DIAGNOSE:
BIOCHEMISCHE MERKERS
CK MB
snel
+++
duur
kort
gevoelig
+++
specifiek
+++
Myoglobine
++++
kort+
++++
-
Troponine
+
lang+
++++
++++
SGOT
+
lang
++
++
LDH
-
lang+
++
++
9
High sensitivity-Troponine
1x HsTrop + ≠
ACS
Hs-Trop en ACS
20,2 ng/l
55,3 ng/l (n=13, p=0,02)
4,3 ng/l
2,9 ng/l (n=31, p=0,87)
Giannitsis, ClinChem, 2010
10
Acute coronair syndroom
Zonder ST-segment elevatie
met ST-segment elevatie
Onstabiele Angor
STEMI
Non-STEMI
∆ (0-3h) hs trop*
Onstabiele
angor pectoris
* absolute
Non Q-golf
myocardinfarct
Q-golf
myocardinfarct
∆ hs trop of 50%ULN
BELEID VAN ACS
11
MCCU: early diagnosis
• Rhytm monitoring
• 12 lead ECG registration
+ wireless data transfer!
Early-in-hospital Management
1. Check vital signs
2. Establish ECG monitoring + defibrillator
3. Give oxygen (3-5 lit/min) indien O²sat<90%
4. Establish IV access
5. Take 12-lead ECG
6. Obtain serum cardiac markers
7. Cardiological assessment:
ST elevation AMI
ACS without ST elevation
ACS doubtful or non cardiac pathology
< 3‘
< 10‘
< 20‘
12
Acute coronary syndrome
without ST elevation
1. Check intake ASA
2. Check intake nitrates SL
3. Start heparin
(Fondaparinux sc* or LMWH sc** or
unfractionated IV)
4. Start nitrate IV
(if bloodpressure > 100 mmHg)
5. Start Beta-Blockers
6. Oral P2Y12 inhibitors
(clopidogrel/prasugrel/ticagrelor)
* Fondaparinux: 2.5mg 1/d subcutaan
** LMWH: vb enoxaparine (R/clexane 1mg/kg 2x/d subcutaan)
Anti-trombotica
Prasugrel
Ticagrelor
13
Platelet activation - aggregation
GP = glycoprotein; ADP = adenosine diphosphate; PAR = protease-activated
receptor; AA = arachidonic acid; Tx = thromboxane.
Adapted from Brogan. Ann Emerg Med. 2002;9:1029.
Variation in platelet respons on clopidogrel
ACC 2008;52:1052-9
14
Biotransformation and Mode of Action of Clopidogrel, Prasugrel, and Ticagrelor
Schomig A. N Engl J Med 2009;361:1108-1111
Pharmokinetic new P2Y12 inhibitors
15
A class effect of novel P2Y12 inh.
A metanalysis of clopidogrel vs. new comers (n=48599 pts)
Risk Ratio
(95% CI)
P value
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)
0.5
New P2Y12
1.0
0.01
1.5
Clopidogrel
J Am Coll Cardiol 2010;56:000–0
Upstream GP blokker in non-STEMI ACS: EARLY ACS
Delayed Provisional GPIIbIIIa:
- Same Ischemic benefit
- Lower bleeding risk
N=9492
Giugliano et al, NEJM 2009
16
Early (≤24 h, median=14h) or delayed intervention ( ≥36 h, median=50h)
N=3031
Death, >MI, Refractory Angina
Death, MI, Stroke
GRACE>140
Mehta et al. NEJM 2009 - TIMACS Study
Acute coronary syndrome without ST elevation
Aspirin - Nitrate - Beta-blocker
P2Y12 inhibitor #
-Anticoagulation *
LOW RISK
HIGH RISK
Recurrent severe ischemia
Elevated troponin
Hemodynamic
Early post infarct angina
instability
Major arrhythmias (VF, VT)
Diabetes mellitus
No recurrent ischemia
No rise in trop
No diabetes
Coronarography:
Urgent (<2h)
Elective (<72h)
Non-invasive testing
(< 24h if Grace score>140)
consider IIB -IIIA antagonist + hep or bivaluridin
*Anticoagulation: Fondaparinux (+UHF in case of PCI) / Enoxaparine / UFH
# P2Y12 inhibotor: Ticagrelor / Prasugrel (reimbursement only in diabetic patients with PCI )
clopidogrel (high bleeding risk or low risk ACS)
17
Early-in-hospital Management
1. Check vital signs
2. Establish ECG monitoring + defibrillator
3. Give oxygen (3-5 lit/min) indien O²sat<90%
4. Establish IV access
5. Take 12-lead ECG
6. Obtain serum cardiac markers
< 3‘
< 10‘
7. Cardiological assessment:
ACS without ST elevation
ST elevation AMI
ACS doubtful or non cardiac pathology
< 20‘
ST- Elevation AMI : management
1. Check intake ASA / nitrates SL
2. Prasugrel/Ticagrelor/clopidogrel
4. Initiate Reperfusion therapy
Thrombolyse
PTCA
18
Rates of TIMI
Grade 3 Flow
% TIMI 3 Flow
The 90 Minute Wall:
Primary PCI vs. thrombolytic therapy
Frequency (%)
p<0.0001
p<0.0001
p=0.0002
p=0.0003
p=0.032
p<0.0001
p=0.0004
p<0.0001
Death
Death
excl.
Shock
Nonfatal Recurrent
MI
ischemia
Total
CVA
Hemorr.
CVA
Major
bleeds
Death/
CVA/AMI
Keeley Lancet 2003;361:13
19
Primary PCI and time
30 minutes delay increases 1-year mortality by 7.5%
De Luca, Circulation 2004
Europese richtlijnen reperfusietijden: PCI
<90-120min
20
ST elevation MI (<12 h after onset of pain)
ASA- Morphine - Heparin* - P2Y12 inhibitor *
Admission in non-PCI-center OR
Admission in
1st
PCI-center
medical contact outside hospital
•
Transfer time to PCI center < 90 min
•
Hemodynamic instability
•
Contra-indication thrombolysis
(transfer time<60 if ischemic time<2h)
YES
(shock / cardiac failure/ malignant arrhythmias)
NO
Thrombolysis
Primary PCI
• Thrombus aspiration
Failed
Succes
• Bivalirudin
( IIB-IIIa antagonists for bail-out)
Rescue PCI
Coronaro/
* • PPCI: UFH and Prasugrel 60 mg/ Ticagrelor 180mg
PCI 3-24h
•Trombolysis: Enoxaparin and clopidogrel 300mg (adjusted dose if >75y)
Voorkamerfibrillatie
42
21
VKF
43
Doel Behandeling VKF
• Controle kamerfrequentie
• Preventie van embolie
• Herstel van sinusritme
– Medicamenteus
– Electrische cardioversie
– Ablatie
44
22
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
23
TACHYCARDIE tgv ATRIALE FIBRILLATIE/FLUTTER
Onregelmatig kamerritme > 100/min + onregelmatige of zaagtand basislijn
ECG, bloeddrukmonitoring, O2
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?
Slechte hartfct
Duur < 48u
Slechte hartfct
Duur > 48 u
Goede hartfct
Duur > 48u
Goede hartfct
Duur < 48u
Digoxine
Digoxine
Bètablokker
Bètablokker
Amiodarone
(Amiodarone)
Verapamil of
Diltiazem
Verapamil of Diltiazem
+
Synchrone
Cardioversie
+
+
synchr
cardioversie na 4
weken antico
En/of
Flecaïnide of Propafenone of
synchr cardioversie
na 4 weken antico
(INR 2-3) **
Amiodarone47
of
** of TEE
Geleid
Synchr. cardioversie
(INR 2-3) **
CHA2DS2-VASc Score
Risk Factors for Stroke in Non-valvular AF (ESC guidelines 2010)
C—CHF
Stroke rate (% per year) H—Hypertension
A2—Age >75
16
1
V—Vascular
1
1
A—Age >65
1
2
S— Sex
14
D—Diabetes mellitus
1
12
S2—TIA/stroke
29,8
10
1
9,6
6,7
6.7
8
15,2
6
4.0
4
2
1,3
2,2
3,2
1
2
3
0
0
0
4
5
6
7
8
9
Overall Yearly Risk of Stroke in Non-valvular AF is 5%
Camm et al, European Heart Journal 2010
48
24
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
Douxfill et al, Thromb and hemost. 2012
Normaal APTT wijst op minimale ontstolling!!!
>2 wijst op verhoogd bloedingsrisico
25
Monitoring en NOAC
• Rivoroxabam en PT
Normaal PT wijst op minimale ontstolling!!!
>2 wijst op verhoogd bloedingsrisico
26
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
Antifungal
(Ketoconazole, )
HIV protease inh
(fluconazole wel)
Antifungal
(Ketoconazole, )
HIV protease inh
Niet te associeren Antifungal
(cf CYP3A4)
(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 on
revascularisation, EHJ 2010
27

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