*DEFINISISuatu sindroma klinik yang menandakanadanya iskemia miokard akut, terdiri dari : Infark miokard akut Q wave (STEMI)Infark miokard akut non-Q (NSTEMI)Angina pektoris tidak stabil (UAP)

Ketiga kondisi ini sangat berkaitan erat, berbeda hanya dalam derajat beratnya iskemi dan luasnya miokard yang mengalami nekrosis.

*PATOGENESISUmumnya disebabkan oleh aterosklerosis koronerPlak aterosklerosis ruptur terbentuk trombus diatas ateroma yang secara akut menyumbat lumen koronerApabila sumbatan terjadi secara total hampir seluruh dinding ventrikel akan nekrosis

Uncontrollable

SexHereditaryRaceAgeControllableHigh blood pressureHigh blood cholesterolSmokingPhysical activityObesityDiabetesStress and angerRisk Factors

CADAtherosclerosisRisk Factors( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)The cardiovascular continuum of eventsDYSLIPIDEMIAAdapted fromDzau et al. Am Heart J. 1991;121:1244-1263Myocardial IschemiaplaqueIschemia = oxygen supply and demand imbalance

CADAtherosclerosisRisk Factors( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)The cardiovascular continuum of eventsDYSLIPIDEMIAAdapted fromDzau et al. Am Heart J. 1991;121:1244-1263Myocardial IschemiaCoronary Thrombosis

CADAtherosclerosisRisk Factors( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)The cardiovascular continuum of eventsDYSLIPIDEMIAAdapted fromDzau et al. Am Heart J. 1991;121:1244-1263Myocardial IschemiaCoronary ThrombosisACS

Stable angina

PenyempitanPembuluh darah

Clinical Spectrum of Acute Coronary SyndromeAcute Coronary SyndromeNon-ST SegmentElevationST SegmentElevationUnstableAngina PectorisNon-Q-waveQ-waveAcute Myocardial InfarctionSTEMINSTEMI

Unstable AnginaSTEMI NSTEMINon occlusive thrombus

Non specific ECG

Normal cardiac enzymes

Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis

ST depression +/- T wave inversion on ECG

Elevated cardiac enzymesComplete thrombus occlusion

ST elevations on ECG or new LBBB

Elevated cardiac enzymes

More severe symptoms

DiagnosisAnamnesisPemeriksaan FisikPemeriksaan Penunjang :1. Laboratorium2. Elektrokardiografi3. Thoraks Foto

*AnamnesisNyeri dada atau nyeri epigastrium hebat yang mengarah pada iskemia miokard :Seperti dihimpit benda beratTerasa tercekikRasa ditekan, ditinju, ditikamRasa terbakarBiasanya dirasakan dibelakang stenum seluruh dada terutama kiri, dapat ke tengkuk, rahang, bahu, punggung, lengan kiri atau kedua lengan

Terutama laki-laki > 35 tahun dan Wanita > 40 tahun

Seringkali disertai mual atau muntah, dapat pula rasa tidak enak disertai sesak nafas, lemah, penurunan kesadaran, dan keringat banyak

*Pemeriksaan Fisik

Biasanya penderita tampak cemas, gelisah, pucat, dan keringat dinginPeriksa tanda-tanda vital :Denyut nadi cepat, reguler tetapi dapat pula bradi atau tachycardia, irama iregulerTekanan darah biasanya normal bila belum terjadi komplikasi, dapat pula terjadi hipo atau hipertensiBunyi jantung dapat terdengar redup S3 dapat terdengar bila kerusakan miokard luasParu-paru dapat terdengar ronkhi basah dan atau wheezing yang menandakan terjadinya bendungan paru tergantung ada tidaknya gangguan fungsi ventrikel kiri

*Pain Patterns with Myocardial Ischemia

*Anamnesis untuk UAP

3 kategori presentasi klinik UAP:Angina saat istirahat (resting angina)Angina awitan baru (new onset angina)Angina yang bertambah berat (increasing angina)

Riwayat penyakit dahulu :Riwayat angina on effort, infark atau operasi pintasRiwayat penggunaan nitrogliserinIdentifikasi faktor-faktor risiko

*PHYSICAL EXAMINATIONGENERAL APPEARANCEAnxious, considerable distress, restless, fist on chest (Levine sign)LV failure & symp. stimulation : cold perspiration, pallor, dyspnea, cough with frothy pink or blood-streaked sputum.Shock : cool, clammy skin, facial pallor, cyanosis, confusion or disorientation

HEART RATEVariable depending on underlying rhythm and degree or ventr. failureMost commonly, HR 100 110/min; > 95% patients : VPBs within first 4 hours

*BLOOD PRESSUREMajority normotensive, but syst. BP may decline and diast. BP may rise Half of pts with inferior MI parasympathetic stimulation : hypotension, bradycardia or both (Bezold Jarisch reflex) half of pts with anterior MI, sympathetic excess : hypertension, tachycardia or both

TEMPERATURE AND RESPIRATIONMost pts with extensive MI fever within 24-48 hrs, fever resolves by 4th or 5th dayRespiration due to anxiety and pain, in LV failure : resp. rate correlates with degree of heart failure

*JUGULAR VENOUS PULSEJVP usually normalRV infarction : marked jug. venous distension

CAROTID PULSESmall pulse reduced stroke volumePulse alternans : severe LV dysfunction

*CHESTLV failure and/or LV compliance : moist ralesSevere failure : diffuse wheezing, cough + hemopthysis1967 : Killip & Kimball : prognostic classification

ClassI: patients free of rales or S3II: rales < 50% lung fields +/- S3III: rales > 50% lung fields, frequently pulm. edemaIV: cardiogenic shock

*Pemeriksaan Penunjang

Pemeriksaan EKG

Gambaran EKG infark miokard akut Q-wave (STEMI) :

Elevasi segmen ST 1 mm pada 2 sadapan extremitas

Atau 2 mm pada 2 sadapan prekordial yang berurutan

Atau gambaran LBBB baru atau diduga baru

ST-segment elevation

*Gambaran EKG infark miokard akut non-Q-wave (NSTEMI) atau angina pektoris tidak stabil (UAP) :

Depresi segment ST atau gelombang T terbalik pada 2 sadapan berurutan

Inversi gelombang T minimal 1 mm pada 2 sadapan atau lebih yang berurutan.

Perubahan segment ST saat keluhan dan kembali normal saat keluhan hilang sangat menyokong UAP

ST-segment depression

T-wave inversion

*Current-of-injury patterns with acute ischemiaELEKTROKARDIOGRAM

*Pemeriksaan Penanda Jantung/Enzim jantung (Cardiac Markers):

Yang lazim adalah CKMB, dapat pula troponin T (TnT) atau troponin I (TnI)Peningkatan marka jantung akan terlihat pada infark miokard akut Q-wave (STEMI) dan non-Q-wave (NSTEMI)

*Plot of the appearance of cardiac markers in blood versus time after onset of symptomsAmyoglobin CCK-MBBtroponinDtroponin in UA

*Diseksi aortaPerikarditisNyeri angina atipikal pada kardiomiopati hipertrofiPenyakit esofageal, GI atas atau traktus biliarisPenyakit paru-paru : pneumotoraks, emboli, pleuritisSindroma hiperventilasiGangguan dinding dada : muskuloskeletal, neurogenPsikogenDiagnosis Banding

Manajemen

ACSCoronary ThrombosisMyocardial IschemiaCADAtherosclerosisRisk Factors( , BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)Adapted fromDzau et al. Am Heart J. 1991;121:1244-1263The cardiovascular continuum of eventsDYSLIPIDEMIAArrhythmia andLoss of MuscleRemodelingVentricular DilatationCongestive Heart FailureEnd-stage Heart Disease

DELAY TO THERAPY1. From onset of symptoms to patient recognition2. Out-hospital transport3. In-hospital evaluation

ISCHEMIC CHEST PAIN ALGORYTHMChest pain suggestive of ischemia

Chest discomfort suggestive of ischemia2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90Acute coronary syndrome algorithm

Chest discomfort suggestive of ischemia2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90Acute coronary syndrome algorithm

ST elevation or new or presumably new LBBB strongly suspicious for injuryAcute coronary syndrome algorithm2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

ST-depression or dynamic T-wave inversion strongly suspicious for injuryST elevation or new or presumably new LBBB strongly suspicious for injuryAcute coronary syndrome algorithmChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

ST-depression or dynamic T-wave inversion strongly suspicious for injury (UA/NSTEMI)ST elevation or new or presumably new LBBB strongly suspicious for injury (STEMI)Acute coronary syndrome algorithmChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

Start adjunctive treatmentAcute coronary syndrome algorithmChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

Beta-adrenergic receptor blockerClopidogrelHeparin (UFH or LMWH)ADJUNCTIVE TREATMENT(Do not delay reperfusion)2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

Start adjunctive treatmentAcute coronary syndrome algorithmChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

Time from onset of symptomsReperfusion strategy: PCI (90 min) or fibrinolysis (30 min)ACE-I/ARB within 24 hours of onsetStatin 12 hoursStart adjunctive treatmentAcute coronary syndrome algorithmChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90Start adjunctive treatment

Heparin (UFH/LMWH) Glycoprotein IIb/IIIa receptor inhibitors -Adrenoreceptor blockers ClopidogrelAdjunctive treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90

Time from onset of symptomsReperfusion strategy: PCI (90 min) or fibrinolysis (30 min)ACE-I/ARB within 24 h of symptom onset)Statin 12 hoursStart adjunctive treatmentChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatment2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90Start adjunctive treatment

2005 AHA-ILCOR Guidelines for CPR and ECC. Circulation 2005;112 (Suppl):IV-90Time from onset of symptomsReperfusion strategy: PCI (90 min) or fibrinolysis (30 min)ACE-I/ARB within 24 h of symptom onset)Statin 12 hours 12 hrsStart adjunctive treatmentChest discomfort suggestive of ischemiaReview initial 12 lead ECGImmediate ED assessment and immediate ED general treatmentStart adjunctive treatmentAdmit to monitored bedAssess risk status High risk: early invasive strategy Continue ASA, heparin, ACE-I, statin

*Obat-obat untuk mengontrol keluhan iskemia harus dilanjutkanAspirinBeta-blockerACE inhibitorPengobatan Pasca PerawatanBerhenti merokokPertahankan BB optimalAktivitas fisik sesuai dengan hasil treadmillDietRendah lemak jenuh dengan kolesterol, bila perlu dengan target LDL < 100 mg/dLPengendalian hipertensiPengendalian ketat gula darah pada penderita DMModifikasi Faktor Risiko

Get regular medical checkups.Control your blood pressure.Check your cholesterol.Dont smoke.Exercise regularly.Maintain a healthy weight.Eat a heart-healthy diet.Manage stress.

************Public education campaigns increase public awareness and knowledge of symptoms of heart attack but have only transient effects (Blohm M, Herlitz J, Schroder U et al. Reaction to a media campaign focusing on delay in acute myocardial infarction. Heart Lung 1991;20:661-6). Half of the patients who die of AMI do so before reaching the hospital. VF or pulseless VT is the precipitating rhythm in most of the cases (Cohen MC, Rohtla EM, Lavery CE, Muller JE, Mittleman MA. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997;79:1512-16 and Colquhoun MC, Julien DG. Sudden Death in the community: the arrhythmias causing cardiac arrest and result of immediate resuscitation. Resuscitation 1992;24:177A) and in most cases developed during the first 4 hours after the onset of symptoms (Campbell RW, Murray A, Julian DG. Ventricular arrhythmias in first 12 hours of acute myocardial infarction: natural history study. Br Heart J 1981;46: 351-7 and Chiriboga D, Yarzebski J, Goldberg RJ, Gore JM, Alpert JS. Temporal trends (1975 through 1990) in the incidence and case-fatality rate of primary ventricular fibrillation complicating acute myocardial infarction: a community perspective. Circulation 1994;89:998-1003). The activation of the emergency medical services (EMS) system and prompt respond to out-hospital cardiac arrest by the community and emergency medical team is therefore necessary to be developed.ACC/AHA guidelines recommend that the patient or family members activate the EMS system rather than call their physician or driving to the hospital if chest discomfort is unimproved if chest discomfort is unimproved or worsening 5 minutes after taking 1 nitroglycerin tablet or using nitroglycerin spray (Antman EM, Anbe DT, Amstrong PW et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarctionexecutive summary: a report of the American College of Cardiology/American Heart Association ask Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction. Circulation 2004;110:558-636). Physician should also tell the patient to take aspirin.**Early recognition of symptoms of STEMI by the patient or someone with the patient is the first step that must occur before evaluation and life-saving treatment can be obtained. Although many lay persons are generally aware that chest pain is a presenting symptom of STEMI, they are unaware of the common associated symptoms, such as arm pain, lower jaw pain, shortness of breath, and diaphoresis (Goff DC, Sellers DE, McGovern PG, et al. Knowledge of heart attack symptoms in a population survey in the United States: the REACT Trial. Rapid Early Action for Coronary Treatment. Arch Intern Med 1998;158:2329-38). The average patient with STEMI does not seek medical care for approximately 2 hours after symptom onset, and this pattern appears unchanged over the last decade ( [1] Goldberg RJ, Yarzebski J, Lessard D, Gore JM. A two-decades (1975 to 1995) long experience in the incidence, in-hospital and long-term case-fatality rates of acute myocardial infarction: a community-wide perspective. J Am Coll Cardiol 1999;33:1533-9, [2] Goff DC, Sellers DE, McGovern PG, et al. Knowledge of heart attack symptoms in a population survey in the United States: the REACT Trial. Rapid Early Action for Coronary Treatment. Arch Intern Med 1998;158:2329-38. [3] Welsh RC, Ornato J, Armstrong PW. Prehospital management of acute ST-elevation myocardial infarction: a time for reappraisal in North America. Am Heart J 2003;145:1-8.). Average and median delays for patients with STEMI were 4.7 and 2.3 hours, respectively, from the 14-country Global Registry of Acute Coronary Events (GRACE) project. Half of the patients who die of AMI do so before reaching the hospital. VF or pulseless VT is the precipitating rhythm in most of the cases (Cohen MC, Rohtla EM, Lavery CE, Muller JE, Mittleman MA. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997;79:1512-16 and Colquhoun MC, Julien DG. Sudden Death in the community: the arrhythmias causing cardiac arrest and result of immediate resuscitation. Resuscitation 1992;24:177A) and in most cases developed during the first 4 hours after the onset of symptoms (Campbell RW, Murray A, Julian DG. Ventricular arrhythmias in first 12 hours of acute myocardial infarction: natural history study. Br Heart J 1981;46: 351-7 and Chiriboga D, Yarzebski J, Goldberg RJ, Gore JM, Alpert JS. Temporal trends (1975 through 1990) in the incidence and case-fatality rate of primary ventricular fibrillation complicating acute myocardial infarction: a community perspective. Circulation 1994;89:998-1003). ****