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Acute Coronary Acute Coronary Syndrome Syndrome Faculty of Medicine Faculty of Medicine University of Brawijaya University of Brawijaya

ACS ClarifyingLecture

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  • Acute Coronary SyndromeFaculty of Medicine University of Brawijaya

  • ObjectivesDefine & delineate acute coronary syndrome

    Review Management GuidelinesUnstable Angina / NSTEMISTEMI

    Review secondary prevention initiatives

  • Scope of Problem (2004 stats)CHD single leading cause of death in United States452,327 deaths in the U.S. in 2004

    1,200,000 new & recurrent coronary attacks per year

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

    Annual cost > $300 billion

  • Expanding Risk FactorsSmokingHypertensionDiabetes MellitusDyslipidemiaLow HDL < 40Elevated LDL / TGFamily Historyevent in first degree relative >55 male/65 femaleAge-- > 45 for male/55 for femaleChronic Kidney DiseaseLack of regular physical activityObesityLack of Etoh intakeLack of diet rich in fruit, veggies, fiber

  • Acute Coronary Syndromes

    Similar pathophysiology

    Similar presentation and early management rules

    STEMI requires evaluation for acute reperfusion intervention

    Unstable Angina

    Non-ST-Segment Elevation MI (NSTEMI)

    ST-Segment Elevation MI (STEMI)

  • Diagnosis of Acute MI STEMI / NSTEMIAt least 2 of the followingIschemic symptomsDiagnostic ECG changesSerum cardiac marker elevations

  • Diagnosis of AnginaTypical anginaAll three of the followingSubsternal chest discomfortOnset with exertion or emotional stressRelief with rest or nitroglycerin

    Atypical angina2 of the above criteria

    Noncardiac chest pain1 of the above

  • Diagnosis of Unstable AnginaPatients with typical angina - An episode of angina Increased in severity or durationHas onset at rest or at a low level of exertionUnrelieved by the amount of nitroglycerin or rest that had previously relieved the pain

    Patients not known to have typical anginaFirst episode with usual activity or at rest within the previous two weeksProlonged pain at rest

  • 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 enzymes

    Complete thrombus occlusion

    ST elevations on ECG or new LBBB

    Elevated cardiac enzymes

    More severe symptoms

  • Acute Management

    Initial evaluation & stabilization

    Efficient risk stratification

    Focused cardiac care

  • EvaluationEfficient & direct history Initiate stabilization interventions

    Plan for moving rapidly to indicated cardiac care

    Directed Therapies are Time Sensitive! Occurs simultaneously

  • Chest pain suggestive of ischemia

    12 lead ECGObtain initial cardiac enzymeselectrolytes, cbc lipids, bun/cr, glucose, coagsCXR

    Immediate assessment within 10 MinutesEstablish diagnosisRead ECGIdentify complicationsAssess for reperfusionInitial labsand testsEmergent careHistory & PhysicalIV accessCardiac monitoringOxygenAspirinNitrates

  • Focused HistoryAid in diagnosis and rule out other causes

    Palliative/Provocative factorsQuality of discomfortRadiationSymptoms associated with discomfortCardiac risk factorsPast medical history -especially cardiac

    Reperfusion questions

    Timing of presentationECG c/w STEMI Contraindication to fibrinolysisDegree of STEMI risk

  • Targeted PhysicalRecognize factors that increase riskHypotensionTachycardiaPulmonary rales, JVD, pulmonary edema,New murmurs/heart soundsDiminished peripheral pulsesSigns of stroke

    ExaminationVitalsCardiovascular systemRespiratory systemAbdomenNeurological status

  • ECG assessmentST Elevation or new LBBBSTEMINon-specific ECGUnstable AnginaST Depression or dynamicT wave inversionsNSTEMI

  • Normal or non-diagnostic EKG

  • ST Depression or Dynamic T wave Inversions

  • ST-Segment Elevation MI

  • New LBBBQRS > 0.12 secL Axis deviation

    Prominent S wave 1, aVL, V5-V6 with t-wave inversion

  • Cardiac markersTroponin ( T, I)

    Very specific and more sensitive than CKRises 4-8 hours after injuryMay remain elevated for up to two weeksCan provide prognostic informationTroponin T may be elevated with renal dz, poly/dermatomyositis

    CK-MB isoenzyme

    Rises 4-6 hours after injury and peaks at 24 hoursRemains elevated 36-48 hoursPositive if CK/MB > 5% of total CK and 2 times normalElevation can be predictive of mortalityFalse positives with exercise, trauma, muscle dz, DM, PE

  • Prognosis with Troponin

  • Risk Stratification UA or NSTEMI- Evaluate for Invasive vs. conservative treatment- Directed medical therapyBased on initialEvaluation, ECG, andCardiac markers- Assess for reperfusion- Select & implement reperfusion therapy- Directed medical therapySTEMI Patient?YESNO

  • Cardiac Care Goals

    Decrease amount of myocardial necrosisPreserve LV functionPrevent major adverse cardiac events Treat life threatening complications

  • STEMI cardiac care STEP 1: AssessmentTime since onset of symptoms90 min for PCI / 12 hours for fibrinolysis

    Is this high risk STEMI?KILLIP classificationIf higher risk may manage with more invasive rx

    Determine if fibrinolysis candidateMeets criteria with no contraindications

    Determine if PCI candidateBased on availability and time to balloon rx

  • Fibrinolysis indicationsST segment elevation >1mm in two contiguous leadsNew LBBBSymptoms consistent with ischemiaSymptom onset less than 12 hrs prior to presentation

  • Absolute contraindications for fibrinolysis therapy in patients with acute STEMI

    Any prior ICH (intracerebral hemorrhage)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 hoursSuspected aortic dissectionActive bleeding or bleeding diathesis (excluding menses)Significant closed-head or facial trauma within 3 months

  • Relative contraindications for fibrinolysis therapy in patients with acute STEMI History of chronic, severe, poorly controlled hypertensionSevere uncontrolled hypertension on presentation (SBP greater than 180 mm Hg or DBP greater than 110 mmHg) History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindicationsTraumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks)Recent (within 2-4 weeks) internal bleedingNoncompressible vascular puncturesFor streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior allergic reaction to these agentsPregnancyActive peptic ulcerCurrent use of anticoagulants: the higher the INR, the higher the risk of bleeding

  • STEMI cardiac careSTEP 2: Determine preferred reperfusion strategy Fibrinolysis preferred if: 90mindoor to balloon minus door to needle > 1hrDoor to needle goal 3 hrHigh risk STEMIKillup 3 or higherSTEMI dx in doubt

  • Comparing outcomes

  • Comparing outcomes

  • Medical Therapy

    Morphine (class I, level C)AnalgesiaReduce pain/anxietydecrease sympathetic tone, systemic vascular resistance and oxygen demandCareful with hypotension, hypovolemia, respiratory depression

    Oxygen (2-4 liters/minute) (class I, level C)Up to 70% of ACS patient demonstrate hypoxemiaMay limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation

  • Nitroglycerin (class I, level B)Analgesiatitrate infusion to keep patient pain freeDilates coronary vesselsincrease blood flowReduces systemic vascular resistance and preloadCareful with recent ED (erectile dysfunction) meds, hypotension, bradycardia, tachycardia, RV infarction

    Aspirin (160-325mg chewed & swallowed) (class I, level A)Irreversible inhibition of platelet aggregationStabilize plaque and arrest thrombusReduce mortality in patients with STEMICareful with active gastrointestinal bleeding, hypersensitivity, bleeding disorders

  • Beta-Blockers (class I, level A)14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMIApproximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptomsBe aware of contraindications (CHF, Heart block, Hypotension)Reassess for therapy as contraindications resolve

    ACE-Inhibitors / ARB (class I, level A)Start in patients with anterior MI, pulmonary congestion, LVEF < 40% in absence of contraindication/hypotensionStart in first 24 hoursARB as substitute for patients unable to use ACE-I

  • Heparin (class I, level C to class IIa, level C)LMWH or UFH (max 4000u bolus, 1000u/hr)Indirect inhibitor of thrombin less supporting evidence of benefit in era of reperfusionAdjunct to surgical revascularization and thrombolytic / PCI reperfusion24-48 hours of treatmentCoordinate with PCI team (UFH preferred)Used in combo with aspirin and/or other platelet inhibitorsChanging from one to the other not recommended

  • Additional medication therapyClopidodrel (class I, level B)Irreversible inhibition of platelet aggregationUsed in support of cath / PCI intervention or if unable to take aspirin3 to 12 month duration depending on scenario

    Glycoprotein IIb/IIIa inhibitors (class IIa, level B)Inhibition of platelet aggregation at final common pathwayIn support of PCI intervention as early as possible prior to PCI

  • Additional medication therapyAldosterone blockers (class I, level A)Post-STEMI patients no significant renal failure (cr < 2.5 men or 2.0 for women)No hyperkalemis > 5.0LVEF < 40%Symptomatic CHF or DM

  • STEMI care CCUMonitor for complications: recurrent ischemia, cardiogenic shock, ICH, arrhythmias

    Review guidelines for specific management of complications & other specific clinical scenariosPCI after fibrinolysis, emergent CABG, etc

    Decision making for risk stratification at hospital discharge and/or need for CABG

  • Unstable angina/NSTEMI cardiac careEvaluate for conservative vs. invasive therapy based upon:Risk of actual ACSTIMI risk scoreACS risk categories per AHA guidelines

    LowIntermediateHigh

  • Risk Stratification to Determine the Likelihood of Acute Coronary Syndrome

    AssessmentFindings indicating HIGH likelihood of ACSFindings indicating INTERMEDIATE likelihood of ACS in absence of high-likelihood findingsFindings indicating LOW likelihood of ACS in absence of high- or intermediate-likelihood findingsHistoryChest or left arm pain or discomfort as chief symptomReproduction of previous documented anginaKnown history of coronary artery disease, including myocardial infarctionChest or left arm pain or discomfort as chief symptomAge > 50 yearsProbable ischemic symptomsRecent cocaine usePhysical examinationNew transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or ralesExtracardiac vascular diseaseChest discomfort reproduced by palpationECGNew or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptomsFixed Q wavesAbnormal ST segments or T waves not documented to be newT-wave flattening or inversion of T waves in leads with dominant R wavesNormal ECGSerum cardiac markersElevated cardiac troponin T or I, or elevated CK-MBNormal Normal

  • TIMI Risk ScorePredicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days

  • ACS risk criteriaLow Risk ACS

    No intermediate or high risk factors

    10 minutes rest pain, now resolved

    T-wave inversion > 2mm

    Slightly elevated cardiac markers

  • High Risk ACS

    Elevated cardiac markersNew or presumed new ST depressionRecurrent ischemia despite therapyRecurrent ischemia with heart failureHigh risk findings on non-invasive stress testDepressed systolic left ventricular functionHemodynamic instabilitySustained Ventricular tachycardiaPCI with 6 monthsPrior Bypass surgery

  • Low riskHigh riskConservative therapyInvasive therapyChest Pain centerIntermediate risk

  • Invasive therapy option UA/NSTEMICoronary angiography and revascularization within 12 to 48 hours after presentation to EDFor high risk ACS (class I, level A)MONA + Anticoagulant (UFH)Clopidogrel20% reduction death/MI/Stroke CURE trial1 month minimum duration and possibly up to 9 monthsGlycoprotein IIb/IIIa inhibitors

  • Conservative Therapy for UA/NSTEMIEarly revascularization or PCI not plannedMONA + Anticoagulant (LMWH or UFH)ClopidogrelGlycoprotein IIb/IIIa inhibitorsOnly in certain circumstances (planning PCI, elevated TnI/T)Surveillence in hospitalSerial ECGsSerial Markers

  • Secondary PreventionDiseaseHipertension, DM, Dyslipidemia

    Behavioralsmoking, diet, physical activity, weight

    Cognitive Education, cardiac rehab program

  • Secondary Preventiondisease managementBlood PressureGoals < 140/90 or 500; consider omega-3 fatty acids

    DiabetesA1c < 7%

  • Secondary preventionbehavioral interventionSmoking cessationCessation-class, medications, counseling

    Physical ActivityGoal 30 - 60 minutes dailyRisk assessment prior to initiation

    DietDASH diet, fiber, omega-3 fatty acids

  • Thinking outside the box

  • Secondary preventioncognitivePatient educationIn-hospital discharge outpatient clinic/rehab

    Monitor psychosocial impactDepression/anxiety assessment & treatmentSocial support system

  • Medication Checklist after ACSAntiplatelet agentAspirin* and/or Clopidorgrel

    Lipid lowering agentStatin*Fibrate / Niacin / Omega-3

    Antihypertensive agentBeta blocker*ACE-I*/ARBAldactone (as appropriate)

  • Prevention newsFrom 1994 to 2004 the death rate from coronary heart disease declined33%...

    But the actual number of deaths declined only18%Getting better with treatment

    But more patients developing disease need for primary prevention focus

  • SummaryACS includes UA, NSTEMI, and STEMI

    Management guideline focusImmediate assessment/intervention (MONA+BAH)Risk stratification (UA/NSTEMI vs. STEMI)RAPID reperfusion for STEMI (PCI vs. Thrombolytics)Conservative vs Invasive therapy for UA/NSTEMI

    Aggressive attention to secondary prevention initiatives for ACS patients Beta blocker, ASA, ACE-I, Statin