Langsa ACS

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    ACUTE CORONARY SYNDROME

    Dr. Zainal Safri, SpPD, SpJP

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    PATHOFISIOLOGY OFACUTE CORONARY SYNDROME

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    Endothelial

    DysfunctionFoamCells

    FattyStreak

    IntermediateLesion Atheroma

    FibrousPlaque

    ComplicatedLesion/Rupture

    Endothelial injurynitric oxideendothelin-1vasodilation

    Lipidaccumulationadhesion molecules(ICAM, VCAM)

    monocyte adhesion

    macrophage LDLuptake

    Inflammationcontinued macrophage/lipidaccumulation

    leukocyte accumulationcytokines (IL-6, TNFa, IFNg

    MMP's

    CRP(hepatic)

    oxidized LDL

    homocysteinesmokingaginghyperglycemiahypertension

    Pathophysiology of Atherosclerosis

    35-45 yrs 45-55 yrs 55-65 yrs >65 yrs

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    The Process

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    nical Manifestations of Arterial Thrombo

    UA/NSTEMI:Partially-occlusive thrombus

    (primarily platelets)

    Intra-plaque

    thrombus (plateletdominated)

    Plaque core

    STEMI:occlusive thrombus (platelets,

    red blood cells, and fibrin)

    Intra-plaquethrombus (platelet

    dominated)

    Plaque core

    SUDDEN DEATH

    Adapted from Davies MJ Circulation1990

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    Non ST Elevation MI

    90% of acute MIs are caused by thrombus formation from rupture of unstable plaques

    Ruptured Plaque

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    Occlusive Thrombus

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    ANGINA PEKTORIS

    INFARK MIOKARD

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    Stable Plaque Unstable Plaque Disrupted Plaque

    Braunwald E et al. J Am Coll Cardiol2000;36:9701062.

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    Stable versus Unstable

    Plaque

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    Mortalitas dan morbiditas tinggi , 40 %kematian terjadi sebelum sampai di rumah sakit( HARUS SEGERA DIRUJUK!!)

    Setidaknya 250.000 kematian sehubunganinfark miokard terjadi dalam 1 jam setelahonset gejala dan sebelum terapi dimulai (USA)

    DalamSATUtahun hampirsetengah kematianterjadi pada4 minggu pertamasetelahdiagnosa.

    Mengapa SKA harus segeraditangani?

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    Risk Factors Aterosklerosis

    faktor genetik/riwayat keluargakandung

    merokok dislipidemia hipertensi diabetes

    obesitas usia Dll.*Pernah infark miokard dan/atau stroke

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    DIAGNOSISACUTE CORONARY SYNDROME

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    Angina:

    Gejala angina dapat dibedakan darinyeri non jantung atau nyerikardiogenik lain, berdasarkananamnesis,

    dan k/p ditunjang pemeriksaan fisik

    EKG,dan laboratorium.

    Berkaitan dengan kejadian iskemiapada otot jantung

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    KELUHAN UTAMA SINDROM KORONER AKUT

    Sakit dada atau nyeri hulu hati yang berat, asalnya non-

    traumatik, dengan ciri-ciri tipikal iskemia miokard atauinfark:

    Dada bgn tengah/substernal rasa tertekan atau sakitseperti diremas

    Rasa sesak, berat/tertimpa beban , mencengkeram,terbakar,sakitsakit perut yg tdk dpt dijelaskan, sendawa, nyeri huluhatiPenjalaran ke leher, rahang, bahu, punggung atau 1

    atau ke 2 lenganDisertai sesakDisertai mual dan/atau muntahDisertaiberkeringat

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    Keluhan :SAKIT DADA/ANGINA

    PECTORIS

    Sifat & kualitas

    LokasiPenjalaranLamaKeluhan dan Gejala penyerta

    Anamesis harus terarah

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    Angina Pectoris Stabil

    ANGINA STABIL, ditandai nyeri dada atau rasa tidakenak sewaktu adanya beban (aktivitas, beban

    mental) dimana kebutuhan miokardium tidak dapatdipenuhi dengan suplai yang cukup.

    Angina Stabil dapat diprediksi dan dapat hilang atauberkurang dengan istirahat dan nitrogliserin.

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    Dimana Rasa Nyeri Dirasakan??

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    3 Kemungkinan penampilan: Nyeri/angina wkt istirahat ( biasanya terus

    > 20 minutes)

    Angina baru-New Onset (

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    *PENILAIAN AWAL1.ANAMNESIS ( yang terarah) Nyeri dada ariwayat nyeri dada

    angina pectoris Faktor risiko Penyakti penyerta lain Obat-obat

    2.TANDA VITAL & Pemeriksaan FisikTerfokus

    3. ELEKTROCARDIOGRAM : 12 sandapan

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    ELECTROCARDIOGRAM

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    Acute anteroseptal myocardial infarction.Hyperacute T-wave changes are noted

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    Acute Anterior MI

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    ST Depresi

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    T Inverted

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    RECCOMANDATION

    Pada pasien yg dicurigai penyakit jantung iskemik akut

    1. Harus diperiksa Troponin T atau I waktu masuk dan ,bila normal,diulangi 6-12 jam lagi

    2. Mioglobin dan/atau CKMB mass boleh diperiksa pada pasienkeluhan yang baru ( < 6 jam ) sebagai petanda dini infarkmiokard akut dan pada pasien dengan iskemia berulangsetelah 2 minggu infark untuk mendeteksi infark yg lebih

    lanjut

    Level of evidence : A

    ESC/ EHJ 2002

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    Creatinine Phosphokinase

    Positif 4-12 jam

    Iso forms CK-MB1 danCK-MB 2

    CK-MB1/CK-MB 2

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    Troponin T and I

    Tropomyosin complex

    MicroinfarctionPertama terdeteksi dlm 2-

    4 jam

    Nilai Prognostik

    Cut-off pointTnT 0.01

    ng/ml

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    *INITIAL ASSESMENT1.ANAMNESIS/Targeted history

    Chest pain / history of chest pain/angina pectoris

    Risk factors Other disease ( concomitant disease )

    Medications

    2.VITAL SIGNS & Focused PHYSICALEXAMINATION

    3. ELECTROCARDIOGRAM : 12 Leads

    *BIOCHEMICAL MARKERS

    *Chest X-Ray

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    Penatalaksanaan ACS

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    Presentation(Clinical, Initial ECG)

    ST-Seg ElevationMyocardial Infarction Non-STSeg ElevationAcute Coronary Syndr

    ST-Seg ElevationMCI

    Non-ST-seg-Elevation MCI

    UnstableAngina

    Workingdiagnosis

    Time

    Evolution ofECG &

    Biomarkers

    Finaldiagnosis

    National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006

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    Recommendation for anti ischemic therapy

    Class I1. Bed rest, continuous ECG monitoring ( C )2. NTG s.l. or spray followed by IV adm. ( C )3. Oxygen ( C)4. Morphine sulphate IV if symptoms not relieved by NTG (C)5. Beta blocker,if there is ongoing chest pain (( B)6. Calcium Channel blocker if BB if contraindicated (B)

    7. ACE inhibitor when hypertension persists despite treatment with NTGand a BB in pts with LV systolic dysfunction or CHF and inPts with diabetes (B)

    Class IIa1. Oral long acting CCB for recurrent ischemia in the absence of contra

    indication and when BB and nitrates are fully used (C)2. An ACI for all post ACS patients ( level evidence B )3. IABP for severe ischemia that is continuing or recurs frequently

    despite intensive medical Tx or for hemodynamically instabibilityin pts before or after coronary angiography

    ACC Task Force 2002

    P th t Th b i

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    Pathway to Thrombosis

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    Platelet Activation Pathways

    Platelet Aggregation

    Fibrinogen

    Fibrinogen Binding Site

    Thrombin

    Platelet

    Herbert. Exp Opin Invest Drugs 1994;3:449-455.

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    Aspirin

    Benefits: decrease 50% reinfarction @30dys; two-year mortality 20%reduction

    Doses 81-325 mg P.O. Trials: ISIS (88), Antiplatelet Trialist

    Group (94), HART (90)

    Aspirin kunyah 160-325 mg segera diberikanmeskipun belum ada hasil EKG

    (non coated/slow released)

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    Clopidogrel

    Diberikan pada ACS loading 300mg ( 4 tablet) class 1A, Trials:

    CURE

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    Nitrat

    Vasodilator

    Mengurangi konsumsi Oksigen danmenurunkan jumlah episode iskemik.

    Digunakan secara luas

    Pemberian per IV

    1mg /jam

    Disesuaikan dengan gejala klinis dan EKGNitrate sublingual

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    Morfin /Beta-blocker/CCB/ Acei

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    Coagulation Cascade

    XIIa

    XIa

    IXa

    Intrinsic Pathway

    (surface contact)

    Xa

    Extrinsic Pathway

    (tissue factor)

    VIIa

    Thrombin(IIa)

    Thrombin-FibrinClot

    aPTT

    PT

    Heparin / LMWH(AT-III dependent)

    Hirudin/Hirulog(direct antithrombin)

    Courtesy of VTI

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    HEPARIN:Mechanism of

    Action Both UH and LMWH exert their

    anticoagulation activity by catalyzing

    antithrombin (AT or AT III) catalyzed AT is accelerated in its

    inactivation of the coagulationenzymes thrombin (factor IIa) andfactor Xa.

    prolongs aP