acute coronary syndrome

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Acute Coronary Syndrome In Clinical Practice Firman B. Leksmono

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  • Acute Coronary SyndromeIn Clinical PracticeFirman B. Leksmono

  • Acute Coronary SyndromeAcute coronary syndrome(ACS) refers to any group ofsymptoms attributed toobstruction of the coronaryarteries.

  • Coronary Anatomy

  • Acute Coronary Syndrome

  • Acute Coronary Syndrome

  • Epidemiology CHD single leading cause of death in United

    States 452,327 deaths in the U.S. in 2004

    1,200,000 new & recurrent coronaryattacks per year

    38% of those who with coronary attack diewithin a year of having it

    Annual cost > $300 billion

    CHD single leading cause of death in UnitedStates 452,327 deaths in the U.S. in 2004

    1,200,000 new & recurrent coronaryattacks per year

    38% of those who with coronary attack diewithin a year of having it

    Annual cost > $300 billion

  • Epidemiology

    Acute coronary syndrome1,5 million hospital addmision - ACS

    UA/ NSTEMIUA/ NSTEMI

    1,24 millionadmission per

    year

    STEMI

    0,33 millionadmission per

    year

    Heart disease and stroke statistic 2007 update. Circulation 2007 , 155 : 69 171

  • Epidemiology

    Guideline for the Management of STEMI. JACC 2013

  • Risk FactorNon- Modifiable Modifiable

    Gender Men > WomenAge Men, increased risk after age 45 Women, increased risk after age 55Family History Heart disease diagnosed before age 55 in father

    or brother Heart disease diagnosed before age 65 in mother

    or sister Race

    Hypertension Diabetes Mellitus Dyslipidemia Obesity Cigarette Smoking Lack of physical activity Diet (high fat and high

    carbohidrat) Stress Novel Factors :

    Hiperhomocysteinemia, CRP, Lipoprotein (a)

    Gender Men > WomenAge Men, increased risk after age 45 Women, increased risk after age 55Family History Heart disease diagnosed before age 55 in father

    or brother Heart disease diagnosed before age 65 in mother

    or sister Race

    Hypertension Diabetes Mellitus Dyslipidemia Obesity Cigarette Smoking Lack of physical activity Diet (high fat and high

    carbohidrat) Stress Novel Factors :

    Hiperhomocysteinemia, CRP, Lipoprotein (a)

  • At least 2 of the following (WHO criteria):At least 2 of the following (WHO criteria):

    Diagnosis

    1. Ischemic Symptoms

    2. Diagnostic ECG Changes

    3. Serum Cardiac Marker

  • Diagnosis

    Hamm CW et al. European Heart Journal 2011

  • ST-Elevation Myocardial Infarction There is a transmural infarction of the myocardium. Entire thickness

    of the myocardium has undergone necrosis.

    Usually occurs when blood flow of artery coronary suddenlydecreased after occlusive thrombus on atherosclerotic plaque.

    Coronary plaques tend to rupture if it has a thin fibrous cap and alipid-rich core.

    Classical pathological picture consists of rich red fibrin thrombus,which is believed to be the basis of so STEMI response tothrombolytic therapy.

    There is a transmural infarction of the myocardium. Entire thicknessof the myocardium has undergone necrosis.

    Usually occurs when blood flow of artery coronary suddenlydecreased after occlusive thrombus on atherosclerotic plaque.

    Coronary plaques tend to rupture if it has a thin fibrous cap and alipid-rich core.

    Classical pathological picture consists of rich red fibrin thrombus,which is believed to be the basis of so STEMI response tothrombolytic therapy.

  • NSTEMI and Unstable Angina UA or NSTEMI is when there is a partial dynamicblock to coronary arteries (non-occlusive thrombus).

    There will be no ST elevation or Q waves on ECG, astransmural infarction is not seen.

    The main difference between NSTEMI and unstableangina is that in NSTEMI the severity of ischemia issufficient to cause cardiac enzyme elevation.

    UA or NSTEMI is when there is a partial dynamicblock to coronary arteries (non-occlusive thrombus).

    There will be no ST elevation or Q waves on ECG, astransmural infarction is not seen.

    The main difference between NSTEMI and unstableangina is that in NSTEMI the severity of ischemia issufficient to cause cardiac enzyme elevation.

  • Patophysiology

  • Patophysiology

  • Patophysiology

  • Clinical ManifestationIschemic symptoms Prolonged pain (usually >20 mins), constricting,

    crushing, squeezing Usually retrosternal location, radiating to left

    chest, left arm, can be epigastric Dyspnea Diaphoresis Palpitations Nausea/vomiting Light headedness

    Ischemic symptoms Prolonged pain (usually >20 mins), constricting,

    crushing, squeezing Usually retrosternal location, radiating to left

    chest, left arm, can be epigastric Dyspnea Diaphoresis Palpitations Nausea/vomiting Light headedness

  • Clinical Manifestation

    Duration :Variable, often more than 30 minutes.Quality : Feels squeezing, pressurelike, tightness, heaviness, and burning.Location : Retrosternal, often with radiation to or isolated discomfort in neck, jaw, shoulders, orarms frequently on left.Associated features : Not relieve with rest or nitrat

  • Electrocardiography

    STEMI NSTEMI/UAP

  • Electrocardiography

  • Whole Anterior STEMI

    Inferior STEMI

  • Biomarker

  • Biomarker

  • BiomarkerBiochemical marker for detection of myocardial necrosis

    Enzyme Normal value First rise afterAMI

    Peak afterAMI

    Return tonormal

    CK-MB < 5.0 ng/ml 4 h 24 h 72 hMyoglobin < 82 ng/ml 2 h 6-8 h 24 hTroponin T Negatif 4 h 24 - 48 h 5 21 daysTroponin T Negatif 4 h 24 - 48 h 5 21 daysTroponin I Detection Limit = 0.5 ng/ml

    Abnormal > 2.0 ng/mlBorderline - Not detected

    3-4 h 24 36 h 5 14 days

  • Decission Making of ACS

  • Cardiac Care Goals Decrease amount of myocardial necrosis Preserve LV function Prevent major adverse cardiac events Treat life threatening complications

  • Chest pain suggestive of ischemia

    12 lead ECG Obtain initial cardiac

    enzymes Electrolytes, cbc

    lipids, bun/cr, glucose,coagulation

    CXR

    Immediate assessment within 10 Minutes

    Establish diagnosis Read ECG Identify

    complications Assess for

    reperfusion

    InitialInitial LabsLabsandandTestsTests

    EmergentEmergentCareCare

    History &History &PhysicalPhysical

    IV access Cardiac monitoring Oxygen Aspirin and CPG Nitrates Morphin

    12 lead ECG Obtain initial cardiac

    enzymes Electrolytes, cbc

    lipids, bun/cr, glucose,coagulation

    CXR

    Establish diagnosis Read ECG Identify

    complications Assess for

    reperfusion

    IV access Cardiac monitoring Oxygen Aspirin and CPG Nitrates Morphin

  • Basic Treatment

  • Basic Treatment

  • Invasive Strategy for UA-NSTEMI

    Hamm CW et al. European Heart Journal 2011

  • Reperfussion Therapy of STEMI

    Guideline for the Management of STEMI. JACC 2013

  • Reperfussion Therapy of STEMI

    Guideline for the Management of STEMI. JACC 2013

  • Trombolytic vs Primary PCI

  • Trombolytic vs Primary PCI

  • Trombolytic Streptokinase 1.5 million iu infusion over 30-60 minin 100 ml D5w or 0,9% saline.

    rTPA Accelerated infusion over 1.5 hrs - 15mg IVbolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr.

    Streptokinase 1.5 million iu infusion over 30-60 minin 100 ml D5w or 0,9% saline.

    rTPA Accelerated infusion over 1.5 hrs - 15mg IVbolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr.

    Contraindication Any prior ICH Known structural cerebral vascular lesion (e.g., AVM) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months

  • Primary PCI

  • Routine Medical Therapy

  • Routine Medical Therapy

    Guideline for the Management of STEMI. JACC 2013

  • Class Description Mortality Rate (%)I No clinical signs of heart failure 6II Rales or crackles in the lungs, an S3, and

    elevated jugular venous pressure17

    KILLIP Classification For STEMI

    Prognosis

    Rales or crackles in the lungs, an S3, andelevated jugular venous pressure

    III Acute pulmonary edema 30 - 40IV Cardiogenic shock or hypotension (systolic

    BP < 90 mmHg), and evidence of peripheralvasoconstriction

    60 80

  • TIMI Score for STEMI

  • TIMI Score for UA-NSTEMI

    TIMI RISK SCORE Increase in mortality with increasing score ~40% all causemortality at 14 days for patients requiring urgent revascularisation.

  • GRACE Score

  • Sudden Death

    Arrhythmia (VT/VF)

    Ventricular Dysfunction (Heart Failure)

    Interventricular septum and myocardial wall rupture

    Hemodynamic Disturbances

    Cardiogenic shock

    Pericarditis

    Complication

    Sudden Death

    Arrhythmia (VT/VF)

    Ventricular Dysfunction (Heart Failure)

    Interventricular septum and myocardial wall rupture

    Hemodynamic Disturbances

    Cardiogenic shock

    Pericarditis

  • Secondary Prevention Disease

    Hypertension, DiabetesMellitus, Dislipidemia

    Behavioral Smoking, diet, physical activity,

    weight

    Cognitive Education, cardiac rehab

    program

    Disease Hypertension, Diabetes

    Mellitus, Dislipidemia

    Behavioral Smoking, diet, physical activity,

    weight

    Cognitive Education, cardiac rehab

    program