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    ANTITHROMBOTIC THERAPY IN ACUTE CORONARY

    SYNDROME

    BY:

    Topan Binawan

    Supervisor :

    Prof.DR.dr.Moch.Fathoni,SpJP(K),FIHA,FAsCC,FAPSC

    CARDIOLOGY PAPERS

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    introduction

    Coronary heart disease : a disability premature deathsworldwide

    Each year : 1,300,000 non-Qmyocardial infarction,350,000 Q wave myocardial infarction

    in the US

    Antithrombotic proper handling during myocardial ischemiaacute, cardiac care to help provide safe and effective

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    Impact of bleeding ACSpatient outcomesPCIhighlight the importance of

    antithrombotic doses,especially vulnerable

    populations such as womenand the elderly

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    Acute Coronary Syndrome (ACS)

    Manifestation of spectrum acute and hard is an

    emergency condition of coronary because of

    imbalance oxygen myocard need & blood

    flow.

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    Classification

    Based on ECG andcardiac enzymes,ACS is classified

    into:

    STEMI: STelevation, elevatedcardiac enzymes

    NSTEMI: STdepression, T-wave

    inversion, elevatedcardiac enzymes

    Unstable Angina:Non specific EKG

    changes, normalcardiac enzymes

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    Pathogenesis

    UnstableAngina

    Plaque Rupture

    Thrombosis &

    platelet aggregation

    Vasospasme

    Plaque erotionwithout rupture.

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    STEMIInfark : plaque becomefissure and rupture,

    thrombogenesismuralthrombus on location ofruptureocclution of

    coronary artery.

    Location of plaquerupture, agonis

    activation of plateletstromboxan A2the

    receptor glycoprotein IIb/ IIIa.

    The receptor has a highaffinity amino acid

    sequence : bind to twodifferent platelets,

    platelet aggregation

    Tissue factorCoagulation cascade

    endothelial cells :damaged.

    Activated fo VII and X,conversion of

    prothrombin -thrombin,then converts

    fibrinogen- fibrin.

    Undergo coronaryartery occlusionby a

    thrombus composed ofplatelets and fibrin

    aggregates

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    NSTEMI

    Acute thrombosis occurs NSTEMI / processescoronary vasoconstriction.

    Acute thrombosis in coronary artery plaquerupture begins with an unstable

    This unstable plaque has a large lipid core, alow density of smooth muscle, thin fibrous cap

    and a high concentration of tissue factor.

    Location of plaque rupture in macrophage and

    lymphocyte cell encounteredinflammation ;TNF , and IL-6.

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    Therapy antithrombotic in ACS

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    Non Stable Angina/NSTEMI

    The intensity of medical therapy based risk

    doctor assessment ischemia and bleeding

    events.

    This factor combined approach physicians to

    the most appropriate strategy risk assessment

    early invasive versus early conservative.

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    TIMI : Trombolysis risk score in Myocardial

    Infarction, GRACE : risk score Global Registry of Acute

    Coronary Events, and risk models Platelet

    glycoprotein IIb / IIIa in Unstable angina

    PURSUIT : Receptor Suppression Using Integrilin

    Therapy.

    To help formulate management better strategies

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    High risk scoreearly invasive.

    Low risk scoreinitial conservative.

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    Antiplatelet Strategy on unstable angina / NSTEMI

    ACC / AHA, ESC, and ACCP : the highest

    aspirin immediately on non-stable angina /

    NSTEMI. Start ; > 160 mg, the long-termmaintenance : aspirin

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    Antiplatelet Strategy on unstable angina / NSTEMI

    Guidelines ACC / AHA and ACCP

    recommends Class I / class 1A, consecutive

    use of aspirin and clopidogrel, whilelowering the therapeutic use of GP IIb / IIIa

    inhibitors (ACC / AHA Class IIb, LOE; B;

    ACCP class 2B) : initial conservative

    strategy.

    The option to use a replacement bivalirudinGP IIb / IIIa inhibitor-treated patients with

    invasive : thiopyridine early (

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    Selection of Anticoagulants: early conservative

    strategies in unstable angina / NSTEMI

    Guidelines ACC / AHA recommendationof UFH or enoxaparin (Class I, LOE: A)or fondaparinux (Class I, LOE: B) withenoxaparin / fondaparinux are preferred(Class IIa, LOE: B).

    Similarly, the ESC guidelinesrecommendation fondaparinux (Class 1,LOE: A) or UFH (Class 1, LOE C) in aconservative, but also loweredrecommendation for enoxaparin (ClassIIa, LOE: B)

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    The Fifth Organization to Assess Strategies in

    Acute Ischemic Syndromes (OASIS-5)

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    Guideline recommendations and level of evidence

    for anticoagulation in non-ST elevation ACS

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    Selection of anticoagulants: an early invasive strategy in

    unstable angina / NSTEMI

    Anticoagulants are one of the 4 currently available > than norecommended for the treatment of non-ST elevation ACS : (ACC / AHAClass I, LOE: A], ESC [Class I, LOE: A], and ACCP [Class 1A]).

    Invasive strategy guidelines : the ACC / AHA recommendation UFH orenoxaparin (Class I, LOE: A) or bivalirudin or fondaparinux (Class I,

    LOE: B).

    ESCurgent invasive UFH (Class I, LOE: C), enoxaparin (Class IIa,LOE: B), bivalirudin (Class I, LOE: B) recommendation.

    ESC : urgent invasive no recommendation Fondaparinux

    Early invasive strategy ACCP recommendations UFH with GP IIb /

    IIIa inhibitor IV use in than LMWH (enoxaparin) or fondaparinux (Class1B). 19

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    Superior Yield of the New Strategy of Enoxaparin,

    Revascularization and Glycoprotein IIb/IIIa inhibitors

    (SYNERGY)

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    Guideline recommendations and level of evidence for

    anticoagulation in non-ST elevation ACS

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    Antiplatelet drugs in patients with STEMI

    All the guidelines, a starting dose of nonenteric-aspirin 150-325 mg, daily dose > lowthereafter ( Low high risk for bleeding(Class IIa, LOE: C).

    STEMI post-PCI recommendations for 1 yearclopidrogel after drug elution stents and 1month to 1 year bare metal stents (Class I,LOE: B)

    ACC / AHA STEMIsupport the addition ofclopidogrel + aspirin STEMI (initiation ofclopidogrel 300 mg

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    The selection of anti thrombotic patients with a fibrinolysis

    ACC / AHA recommendations fibrinolysisanticoagulant treated patients at least 48 hours

    (Class I, LOE: C), continued up to 8 days or untilthe patients home (Class I, LOE: A).

    UFH (Class I, LOE: C) enoxaparin (Class I, LOE:A), / fondaparinux (Class I, LOE: B)

    recommendation on fibrinolysis

    ACCP recommendations antithrombin therapy than

    no antithrombin therapy (Class 1A).Regarding the use of LMWH, ACCP >

    recommendation reviparin than no treatment(Class 1B).

    ESC for co-STEMI anticoagulant therapy inpatients with fibrinolysis (non-streptokinase)

    include enoxaparin and UFH (Class I, LOE: A).Patients with streptokinase, fondaparinux or

    enoxaparin (Class IIa, LOE: B) or UFH (Class IIa,LOE: C) recommendation.

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    R d ti f ti l ti STEMI

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    Recommendations for anticoagulation on STEMI

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    The selection of the antithrombotic primary PCI

    ACC / AHA supports thecontinuation of anticoagulants onthe scope of peri-PCI (Class I)

    primary PCI of STEMI.Recommendations include UFH

    (Class I, LOE: C) with the option ofswitching to bivalirudin (Class I,LOE: C) for the previous UFH.Enoxaparin (Class I, LOE: B) /

    fondaparinux (Class I, LOE: C) isreceived anticoagulant STEMI with

    PCI

    ACCP and strong ESCrecommendation fondaparinux on

    primary PCI.

    ACCP supports the use of UFH

    dosing based on the weight(Class1B) and abciximab (inhibitor of GPIIb / IIIa) IV during primary PCI

    (Class 1B) for STEMI.ESC Guidelines recommendationUFH (Class I, LOE: C) / bivalirudin

    (Class IIa, LOE: B)

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    T iti t P t ACS A ti Th b ti Th f

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    Transition to Post-ACS Anti Thrombotic Therapy ofChronic

    The guidelines continue to support

    low-dose aspirin, ideally 100 mg /day.

    Patients in-stent acute coronarysyndrome, the dose of aspirin (162-

    325 mg) can be used for the firstmonth of bare metal stents, and for

    3-6 months of drug-eluting stents.

    Clopidogrel is recommended at least

    one month at a bare metal stent andideally for at least 1 year drug-elutingstents.

    Oral anticoagulants + dualantiplatelet no recommendation for

    secondary prevention in the absence

    of a clear indication (ie AF, DVT).

    Warfarin may be considered inpatients with a high risk of ischemia

    and bleeding risk is low if notintolerant of clopidogrel (Class IIb,

    LOE: B).

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    RESUME

    Using anti-platelet therapy and anti-coagulants on

    ACS clinical outcomes associated development ofshort-term and long-term, depending onconservative treatment or acute coronaryrevascularization.

    Selecting anti-thrombotic therapy lowers the riskof ischemic while minimizing the risk of bleedingfrom various subtype ACS.

    Selecting of appropriate antithrombotic during the

    transition from the phase of the sub-acute andchronic secondary prevention can be worthattention

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    Thank you

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    Karakteristik pasien strategi invasif awal pedoman

    ACC/AHA dan ESC.

    Pedoman ACC/AHA dan ESC

    Angina menetap /kambuhan meskipun ada

    terapi medis intensif, tanpa menghiraukan

    perubahan gelombang ST atau T

    Troponin meningkat

    Perubahan gelombang ST atau T dinamis,

    tanpa menghiraukan gejalanya.

    Fraksi ejeksi < 40%

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    Tanda-tanda atau gejala kegagalan jantung /

    regurgitasi mitral baru

    Ketidakstabilan hemodinamik

    VT atau VF berkelanjutan

    PCI dalam 6 bulan

    CABG sebelumnya

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    Pedoman ACC/AHA

    Temuan beresiko tinggi pengujian non-invasif Skor resiko iskemia tinggi

    Pedoman ESC

    DM

    Disfungsi ginjal (eGFR < 60 ml/menit/1,73

    m2)

    MI sebelumnya

    Skor resiko GRACE menengah hingga tinggi

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