Acute coronaire syndromen Prof dr M Claeys UZ Antwerpen Universiteit Antwerpen TRIADE VAN ACS Anamnese Cardiac enzymes Surface ECG 1
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) 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 ST- Elevation: in II > III Right Ventricular Myocardial Infarction V4R Proximal occlusion RCA 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 snel duur gevoelig specifiek CK MB +++ kort +++ +++ 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 Onstabiele Angor Non-STEMI met ST-segment elevatie STEMI Onstabiele angor pectoris (0-3h) hs trop* Non Q-golf myocardinfarct Q-golf myocardinfarct * absolute 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. OralP2Y 12 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 P2Y 12 inhibitors 15
A class effect of novel P2Y 12 inh. A metanalysis of clopidogrel vs. new comers (n=48599 pts) Risk Ratio P value (95% CI) 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 0.5 1.0 1.5 New P2Y12 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, Stroke Death, >MI, Refractory Angina GRACE>140 Mehta et al. NEJM 2009 - TIMACS Study Acute coronary syndrome without ST elevation Aspirin - Nitrate - Beta-blocker P2Y 12 inhibitor # -Anticoagulation * HIGH RISK Recurrent severe ischemia Elevated troponin Hemodynamic instability Early post infarct angina Major arrhythmias (VF, VT) Diabetes mellitus LOW RISK No recurrent ischemia No rise in trop No diabetes Urgent (<2h) Coronarography: Elective (<72h) (< 24h if Grace score>140) consider IIB -IIIA antagonist + hep or bivaluridin Non-invasive testing *Anticoagulation: Fondaparinux (+UHF in case of PCI) / Enoxaparine / UFH # P2Y 12 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 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 SL 2. Prasugrel/Ticagrelor/clopidogrel 4. Initiate Reperfusion therapy Thrombolyse PTCA 18
The 90 Minute Wall: Rates of TIMI Grade 3 Flow % TIMI 3 Flow Primary PCI vs. thrombolytic therapy p<0.0001 Frequency (%) p=0.0002 p=0.0003 p<0.0001 p=0.032 p<0.0001 p=0.0004 p<0.0001 Death Death excl. Shock Nonfatal MI Recurrent 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* -P2Y 12 inhibitor * Admission in PCI-center Admission in non-pci-center OR 1 st medical contact outside hospital Transfer time to PCI center < 90 min YES (transfer time<60 if ischemic time<2h) Hemodynamic instability (shock / cardiac failure/ malignant arrhythmias) Contra-indication thrombolysis NO Primary PCI Thrombolysis Thrombus aspiration Failed Bivalirudin ( IIB-IIIa antagonists for bail-out) * PPCI: UFH and Prasugrel 60 mg/ Ticagrelor 180mg Rescue PCI Trombolysis: Enoxaparin and clopidogrel 300mg (adjusted dose if >75y) Succes Coronaro/ PCI 3-24h 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 Hemodynamische evaluatie ECG, bloeddrukmonitoring, O 2 IV lijn, 12-afleidingen ECG 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 En/of Synchrone Cardioversie (Amiodarone) + synchr cardioversie na 4 weken antico (INR 2-3) ** Verapamil of Diltiazem + synchr cardioversie na 4 weken antico (INR 2-3) ** Verapamil of Diltiazem + Flecaïnide of Propafenone of Amiodarone47 of Synchr. cardioversie ** of TEE Geleid Risk Factors for Stroke in Non-valvular AF (ESC guidelines 2010) C CHF 1 Stroke rate (% per year) H Hypertension 1 A 2 Age >75 16 2 D Diabetes mellitus 1 14 12 10 8 6 4 2 0 0 CHA 2 DS 2- VASc Score S 2 TIA/stroke 2 6.7 6,7 4.0 1,3 2,2 3,2 0 1 2 3 4 5 6 7 8 9 Overall Yearly Risk of Stroke in Non-valvularAF is 5% Camm et al, European Heart Journal 2010 9,8 9,6 V Vascular 1 A Age >65 1 S Sex 1 15,2 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 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 on revascularisation, EHJ 2010 27