ACUTE CORONARY SYNDROME(ACS)

BENITA PUTRI PERMATA

EPIDEMIOLOGI

> 6.000.000 penduduk Amerika menderita penyakit jantung koroner

Setiap tahun di Amerika Serikat 1.300.000 pasien dirawat di RS dengan UAP / NSTEMI, sedangkan 350.000 pasien Infark miokard dengan STEMI.

Sering pada pria dengan umur antara 45-65 tahun

Tidak ada perbedaan dengan wanita setelah umur 65 tahun.

 

ThrombusThrombus

PPllaatteelleettss

LumenLumen

Lipid Rich CoreLipid Rich Core

EndotheliumEndothelium

ThickThickFibrous CapFibrous Cap

UnstableUnstableStableStable

ThinThinFibrous CapFibrous Cap

Falk E et al. Falk E et al. Circulation.Circulation. 1995;92:657–671. 1995;92:657–671.

Plak Aterosklerosis

Plaque disruption (plaque cracking, fissuring, rupture – thrombosis start point)

Plaque rupture The main releasing factors

Faktor yang mempengaruhiruptur plak

Disfungsi sel endotel

komponen lipid plak

derajat inflamasi lokal

tonus arteri daerah plak yang ireguler

lokal tekanan shear stress

fungsi trombosit dan sistem koagulasi

Faktor presipitasi

Variasi sirkadian

Tekanan darah

Denyut jantung

Stress emosional

Latihan fisik

DIAGNOSIS

Keluhan : nyeri dada khas angina/infark

Keluhan tambahab : dyspnoe, palpitasi

Perubahan EKGST elevasi

ST depresi/ T inverted

BBB (bundle branch block)

Peningkatan cardiac markerTroponin I/T, CK, CK-MB, CRP, dll

NYERI DADALokasi: substernal, retrosternal, dan prekordial.

Sifat nyeri: rasa sakit, seperti ditekan, rasa terbakar, ditindih benda berat, seperti ditusuk, rasa diperas, dan dipelintir.

Penjalaran ke: biasanya ke lengan kiri, dapat juga ke leher, rahang bawah, gigi, punggung/interskapula, perut, dan dapat juga ke lengan kanan.

Nyeri membaik atau hilang dengan istirahat, atau obat nitrat.

Faktor pencetus: latihan fisik, stres emosi, udara dingin, dan sesudah makan.

Gejala yang menyertai: mual, muntah, sulit bernapas, keringat dingin, lemas dan cemas.

LOCALIZATION OF MI

Anatomic area ECG Leads w/ STE Coronary artery

Septal V1-V2 Proximal LAD

Anterior V3-V4 LAD

Apical V3-V6 Distal LAD,LCx, or RCA

Lateral I, aVL LCx

Inferior II.III.aVF RCA (-85%),LCx (-15%)

RV V1-V2 &V4R Proximal RCA

Posterior ST deppression V1-V3

RCA or LCx

EKG Perubahan Segmen ST

Acute Anterior Myocardial Infarction

Acute Anterolateral Myocardial Infarction

Acute Lateral Myocardial Infarction

Acute Inferoposterior Myocardial Infarction

0.04

CCS functional classification of Angina Pectoris

Kelas 1 : aktivitas fisik biasa/sehari-hari tidak menimbulkan angina, seperti jalan, naik tangga tidak menyebabkan angina. Angina timbul pada keadaan fisik berat, cepat, tergesa-gesa, kegiatan fisik lama dalam pekerjaan atau rekreasi

Kelas 2 : Pembatasan ringan dari kegiatan fisik biasa/sehari-hari. Angina timbul apabila jalan atau naik tangga dengan cepat, naik bukit, naik tangga atau jalan dengan emosi-stress, jalan atau naik tangga sesudah makan, udara dingin

Kelas 3 : Pembatasan bermakna dari aktivitas fisik sehari-hari. Angina sudah timbul pada jalan mendatar jarak dekat atau naik tangga pada kondisi normal

Kelas 4: aktivitas fisik selalu disertai angina. Angina dapat timbul pada keadaan istirahat

Stratifikasi ResikoResiko Rendah:Tidak mempunyai angina sebelumya

Sudah tidak ada serangan angina

Sebelumnya tidak memakai obat antiangina

EKG normal/tidak ada perubahan dari sebelumnya

Enzim jantung tidak meningkat

Usia muda

• Resiko Sedang– Angina baru dan makin berat

– Angina pada waktu istirahat

– Tidak ada perubahan segmen ST

– Enzim jantung tidak meningkat

• Resiko Tinggi– Angina waktu istirahat– Agina berlangsung

lama/angina pasca infark– Sebelumnya sudah mendapat

terapi intensif– Perubahan segmen ST yang

baru– Kenaikan troponin– Keadaan hemodinamik tidak

stabil– Usia lanjut

PENANGANAN

Unstable angina pectoris

Tindakan Umum:Perawatan di Rumah Sakit (sebaiknya di ICCU)

Bed rest

Penenang

Oksigen

Morfin/petidin

UA/NSTEMI (NSTE ACS) Anti-ischemic and other treatment

Nitrates (SL, PO, topical, or IV)

Anginal sx, no in mortality

β – blocker PO; IV if ongoing pain, HTN or HR (w/o s/s CHF)Eg, metoprolol 5mg IV q5 min x 3Then 25-50 mg PO q6hTitrate to HR 50-60

13% in priggression to MI Controindicated if HR <50, SPB <90Moderate or severe CHF,severe bronchospasm

CCB (nondihydropyridines) If cannot tolerate β B bronchospasm

ACEI or ARB Especially if CHF or EF <0,040 and if SBP>100

Morphine Consider if persistent sx or pulmonary edema should not be used to mask persistent CP

Oxygen Use if necessary to keep S2O2>90%

Antiplatelet Therapy

Aspirin162-325 mg x 1Then 75-325 mg/d

50-70% D/MIIf ASA allergy, use clopidogrel instead(and desensitize to ASA)

Clopidogrel (ADP reseptor blocker)300mg x 1 75 mg/d600mgx 1 150 mg/dx7d may

Give in addition to ASA, 20% CVD/MI/stroke but need to wait >5 d ater d/c clopi prior to CABG

Prasugrel (ADO reseptor blocker)180mgx1 10mg/dreversible

More rapid (~30min) and potent plt inhib c/w clopi. 19% CVD/MI/stroke in ACS w/ planned PCI vs clopi, but bleedingParticullary efficacious in DMAvoid if>75 y

Ticagrelor(ADP reseptor blocker)180 mg x 1 90mg bidReversible

More rapid (~30min) and potent plt inhib c/w clopi. 16% CVD/MI/stroke and 22%death c/w planned PCI vs clopi but with non CABG bleeding frequency of dyspnea.

GP IIb/Iia inhibitors (GPI)Abciximab;eptifibatide;tirofiban

Ma be given in addition to oral antiplt Rx(s)No clear benegit for starting GPI prior to PCI and risk of bleeding

Anticoagulant Therapy

UFH60 U/kg IVB (max 4000 U)12 U/kg/h (max 1000 U/H)

24% D/MITitrate to aPTT 1,5-2x

Enoxaparin (low molecular weight heparin)

Consider instead to UFH ~10% D/MIBenefit greatest if conservative strategy. Can perform PCI on enixaparin

Bivalirudin (direct thrombin inhibitor)

Use instead of heparin for pts w? HIT. With invasive strategy, bival alone noninferior to heparin+GPI

Fondaparinux (Xa inhibitor) C/w enox, 17% mortality & 38% bleeding by 30 d, however risk of cath thromb

STEMI

ANTIPLATELET THERAPY

Aspirin 162-325mg 23% in death

ADP receptor blockerClopidogrel 600mg pre-PCI,300mgIf lysis (not if>75 y) 75mg/dPrasugrel & ticagrelor as above

Lysis:clopidogrel 41% in patency, 7% mort

GP IIb/Iia inhibitorAbciximab, tirofiban

Lysis; no indication

Anticoagulant therapy

UFH60 U/Kg IVB12 U/Kg

No demonstrated mortality benefitPatency with fibrin-spesific lysisTitrate to aPTT 1,5-2

Enoxaparin30 mg IVBx1 1 mg/kg SC bid(>75 y: no bolus, o,75 mg/kg SC bid)(CrCl <30 mL/min: 1 mg?kg SC qd)

Lysis 17%D/Miw/ ENOX x 7

Bivalirudin0,75 mg/kg IVB 1,75 mg/kg/hr IV

PCI : death 7 bleeding but acute stent thrombosis c/w heparin+GPI

Fondaparinux Lysis : superior to placebo & to UFH with less bleeding

Immediate adjuntive therapy

Β blockersEg. Metoprolol 25mg POTitrate ti HR 55-60IV only if HTN & no s/s CHF

-20% arrhytmic death or reMI, 30% cardiogenic shock&no overall mortallity when given to Pts inc. those w/mod CHFContraindic. If HR <60 or>110

NitratesSL or IV

?-50% mortallityUse to relief of sx, control of BP or Rx of CHF contraindic in hipovolemia

Oxygen Use if necessary to keep S2O2>90%

Morphine Reliefe pain anxiety, venodilation preload

ACE inhibitorsEg. Captopril 6,25 tidTitrate up as tolerate

`10% mortality greatest benefit in ant MI, EF<40% or prior MIContraindication in severe hypotension or renal failure

ARBs Appear~ACEI

insulin Treat hyperglycemia >180 mg/dl while avoiding hypoglicemia, no clear benefit for intensive control

AntiiskemiaNitrat, beta bloker, Ca antagonis

Antiagregasi trombositAspirin, Clopidogrel, glikoprotein IIB/IIIA inhibitor

AntitrombinUFH, LMWH, Direct thrombin inhibitors

Tindakan revaskularisasi pembuluh koroner

Reperfusi

Memperpendek lama oklusi koroner

Meminimalkan derajat disfungsi dan dilatasi ventrikel

Mencegah STEMI berkembang menjadi pump failure/takiaritmia maligna

Terapi Reperfusi

Sequence of Events from Unstable Atherosclerotic Plaque to Death

Sequence of Events from Unstable Atherosclerotic Plaque to Death

UNSABLE PLAQUEUNSABLE PLAQUE

Coronary occlusion

Infarction

LV Dilatation

Death

Late Reperfusion

LV Remodeling

Electrical InstabilityPump FailurePump Failure

LV Dysfunction

Early Reperfusion

Limit Infarction

X

X

Circulation 1993;88:2426-36 Circulation 1993;88:2426-36

ACS

Coronary Thrombosis

Myocardial Ischemia

CAD

Atherosclerosis

Risk Factors( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)

Adapted fromDzau et al. Am Heart J. 1991;121:1244-1263

The cardiovascular continuum of events

DYSLIPIDEMIA

Arrhythmia andLoss of Muscle

Remodeling

Ventricular Dilatation

Congestive Heart Failure

End-stage Heart Disease

Atherosclerosis

PROGNOSIS

pola nyeri

Usia

Perubahan segmen ST

Peningkatan troponin T

CRP and other inflammatory markers

DAFTAR PUSTAKAHamm CW, Bertrand M, Braunwald E. Acute coronary syndrome without ST elevation : implementation of new guidelines. Lancet 2001; 358: 1533-8.

Antman EM, Fox KM. Guidelines for the diagnosis and management of unstable angina and non Q wave myocardial infarction. Proposed revisions. Am Heart J 2000; 139:461-75.

Patrono C, Renda G. Platelet activation and inhibition in unstable coronary syndromes. Am J Cardiol 1997; 80(5A): 17E-20E.

Hamm CW, Braunwald E. A Classification of unstable angina revisited. Circulation 2000; 102:118-22.

Lincoff MA. GUSTO IV: Expanding therapeutic options in acute coronary syndrome. Am Heart J 2000; 140: S103-14.

Trisnohadi HB. Angina Pektoris Tak Stabil. Dalam: Sudoyo A, Setiyohadi B, Alwi I, K Simadibrata M, Setiati S, editor. Buku Ajar Ilmu Penyakit Dalam. Jilid III. Edisi IV. Jakarta: Pusat Penerbitan Departemen Ilmu Penyakit Dalam FKUI, 2006. hal. 1621-3.

Alwi I. Tatalaksana Infark Miokard Akut Dengan Elevasi ST. Dalam: Sudoyo A, Setiyohadi B, Alwi I, K Simadibrata M, Setiati S, editor. Buku Ajar Ilmu Penyakit Dalam. Jilid III. Edisi IV. Jakarta: Pusat Penerbitan Departemen Ilmu Penyakit Dalam FKUI, 2006. hal. 1630-9.

Alwi I, Harun S. Infark Miokard Akut Tanpa Elevasi ST. Dalam: Sudoyo A, Setiyohadi B, Alwi I, K Simadibrata M, Setiati S, editor. Buku Ajar Ilmu Penyakit Dalam. Jilid III. Edisi IV. Jakarta: Pusat Penerbitan Departemen Ilmu Penyakit Dalam FKUI, 2006. hal. 1641-7.

Brown CT. Penyakit Aterosklerosis Koroner. Dalam: Price SA, Wilson LM. Patofisiologi. Konsep Klinis Proses-Proses Penyakit. Edisi 6. Volume 1. Jakarta: ECG, 2006. hal. 577-88.

Scottish Intercollegiate Guidelines Network. Acute Coronary Syndromes, a National Clinical Guideline.Myocardial Infarction. Tersedia pada situs: http://www.sign.ac.uk. Diperbaharui pada bulan Februari 2007. Diunduh pada bulan Mei 2010.

Circulation Journal of The American Heart Association. ACC/AHA Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation): Developed in Collaboration with the American College of Emergency Physicians, the Society of Thoracic Surgeons: Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. Tersedia pada situs: http://circ.ahajornals.org. Diperbaharui pada tahun 2007. Diunduh pada tanggal 28 Mei 2010.

Circulation Journal of The American Heart Association. 2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 207 Focused Update): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practical Guidelines. . Tersedia pada situs: http://circ.ahajornals.org. Diperbaharui pada tahun 2007. Diunduh pada tanggal 28 Mei 2010.