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Acls Fmi 2009
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Acls Fmi 2009

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    • 1. ACLS 2009 Acute Coronary Syndromes M. LaCombe MDFMR June 3, 2009
    • 2. Our first case: Chief Complaint: 30 minutes of squeezing substernal chest pain History of Present Illness: A 60-year-old hypertensive diabetic male presents to the emergency room (ER) with 30 minutes of squeezing substernal chest pain, relieved by sublingual nitroglycerin and nasal oxygen. Risk factors: positive for hypertension and diabetes mellitus
    • 3. Physical Findings: Age: 60 Gender: Male Weight: 60 kg Blood Pressure: 130/76 mm Hg Pulse: 86 bpm Head and Neck: Normal jugular venous pressure Chest and Lungs: clear Cardiac Exam: Regular rhythm, no murmurs, gallops Extremities: 2+ symmetric
    • 4. EKG:
    • 5. Labs: troponin is 4.2 (what other labs are absolutely essential in this case?)
    • 6. Stool for occult blood renal function studies
    • 7. How will you treat this patient?
    • 8. Times to remember <ul><li>10 minutes  time for ED eval </li></ul><ul><li>30 minutes  door to needle </li></ul><ul><li>90 minutes  door to balloon </li></ul><ul><li>3 hours (symptom onset)  Fibrinolytic vs. PCI therapy </li></ul><ul><li>12 hours (symptom onset)  Time limit for revascularization therapies as supported by data </li></ul>
    • 9. Initial Therapy/Recognition <ul><li>Starts in transport to ED </li></ul><ul><ul><li>O2 </li></ul></ul><ul><ul><li>Aspirin </li></ul></ul><ul><ul><li>Nitro </li></ul></ul><ul><ul><li>Morphine </li></ul></ul><ul><ul><li>Beta Blockers? </li></ul></ul><ul><ul><li>12 lead EKG </li></ul></ul>
    • 10. Therapy and recognition in ED <ul><li>12 lead EKG  Will be used to stratify patients into treatment groups </li></ul><ul><li>O2, ASA, Nitro, Morphine  MONA </li></ul><ul><li>Physical exam </li></ul><ul><li>Cardiac biomarkers  troponins </li></ul><ul><li>10 minute time frame </li></ul>
    • 11. Treatment Groups Stratification <ul><li>ST-elevation MI (STEMI)  ST-segment elevation or presumed new LBBB in 2 or more contiguous precordial or limb leads </li></ul><ul><li>UA/non-ST-elevation MI (NSTEMI )  ischemic ST-segment depression or dynamic T wave inversion with pain. Transient ST-segment elevation. </li></ul><ul><li>Normal or nondiagnostic changes with pain </li></ul>
    • 12. Copyright ©2005 American Heart Association Circulation 2005;112:IV-89-IV-110 Acute Coronary Syndromes Algorithm
    • 13. Medications to Consider for a NONSTEMI: <ul><li>Nitroglycerine </li></ul><ul><li>Beta blockers </li></ul><ul><li>Clopidogrel </li></ul><ul><li>Heparin </li></ul><ul><li>Glycoprotein IIb/IIIA inhibitors </li></ul>
    • 14. Should be managed with invasive strategy if: <ul><li>New ST-segment depression and positive troponins </li></ul><ul><li>Persistent or recurrent symptoms </li></ul><ul><li>Hemodynamic instability or VT </li></ul><ul><li>Depressed LV function (ejection fraction <40%) </li></ul><ul><li>ECG or functional study that suggests multivessel CAD </li></ul>
    • 15. ACS Risk Guided Algorithm Definite ACS Possible ACS (–) ECG; Normal biomarkers Observe; repeat ECG, markers at 4-8 h No recurrent pain; (–) follow-up studies Recurrent pain; (+) follow-up studies Stress test;  LV function if ischemia (–) test: outpatient follow-up (+) test Use 2007 NSTE ACS Guidelines ST  Use 2004 Updated MI Guidelines No ST  ST-T  ’s, def. pain,  markers Symptoms Suggestive of ACS
    • 16. Applying Classification of Recommendations Class I Benefit >>> Risk Procedure/ Treatment SHOULD be performed/ administered Class IIa Benefit >> Risk Additional studies with focused objectives needed IT IS REASONABLE to perform procedure/administer treatment Class IIb Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Procedure/Treatment MAY BE CONSIDERED Class III Risk ≥ Benefit No additional studies needed Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL should is recommended is indicated is useful/effective/ beneficial is reasonable can be useful/effective/ beneficial is probably recommended or indicated may/might be considered may/might be reasonable usefulness/effectiveness is unknown /unclear/uncertain or not well established is not recommended is not indicated should not is not useful/effective/beneficial may be harmful
    • 17. Applying Classification of Recommendations and Level of Evidence Class I Benefit >>> Risk Procedure/ Treatment SHOULD be performed/ administered Class IIa Benefit >> Risk Additional studies with focused objectives needed IT IS REASONABLE to perform procedure/administer treatment Class IIb Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Procedure/Treatment MAY BE CONSIDERED Class III Risk ≥ Benefit No additional studies needed Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effect Level B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluated Level C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated
    • 18. Acute Evaluation of ACS ST-segment Elevation Chest pain or Short of Breath NSTEMI ST-segment Depression – + + Presentation ECG Diagnosis Normal Markers STEMI – + Rule-Out Adapted from: Anderson JL. J Am Coll Cardiol 2007;50:e1-157
    • 19. Initial Evaluation - Risk Stratification <ul><li>12-lead ECG within 10 min for all patients with chest pain or symptoms suggestive of ACS </li></ul><ul><li>Early risk stratification by symptoms, physical findings, ECG, cardiac markers </li></ul><ul><li>Cardiac markers, Troponins and CK-MB, for initial assessment </li></ul><ul><li>Use of risk stratification models (TIMI, PURSUIT, GRACE) can be useful to assist in decision making for treatment options </li></ul>JACC 2007. I IIa IIb III
    • 20. Anti-Ischemic Therapy <ul><li>It is reasonable to administer intravenous beta blockers at the time of presentation for hypertension to UA/NSTEMI patients who do not have 1 or more of the following: 1) signs of HF, 2) evidence of a low-output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 s, second or third degree heart block, active asthma, or reactive airway disease). </li></ul>*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60, increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B I -> IIa
    • 21. Anti-Ischemic Therapy <ul><li>It may be harmful to administer intravenous beta blockers to UA/NSTEMI patients who have contraindications to beta blockade, signs of HF or low-output state, or other risk factors* for cardiogenic shock. </li></ul>*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60, increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A New
    • 22. Anti-Ischemic Therapy <ul><li>Oral beta-blocker therapy should be initiated within the first 24 h for patients who do not have 1 or more of the following: 1) signs of HF, 2) evidence of a low-output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 s, second or third degree heart block, active asthma, or reactive airway disease). </li></ul>*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60, increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B Major Change
    • 23. Alert: Avoid beta blockers in ACS if there is impending cardiogenic shock! Cardiogenic Shock: Current Concepts and Improving Outcomes Reynolds HR, Hochman JS
 Circulation. 2008;117:686-697 Cardiogenic Shock: Basics and Clinical Considerations Gowda RM, Fox JT, Khan IA 
Int J Cardiol. 2008;123:221-228
    • 24. Cardiogenic shock (CS) is defined as a state of tissue hypoperfusion resulting from cardiac failure. Hypoperfusion may manifest as systemic hypotension, peripheral vasoconstriction and diminished pulses, decreased urine output, decreased mental status, or significantly reduced cardiac indices (cardiac index) despite correction of preload.
 CS occurs in 5% to 10% of patients hospitalized with MI (ST-segment elevated MI) and is a common cause of death in this group. An unknown additional number of prehospital patients die from CS, making the exact incidence uncertain.
 Risk factors for development of post-MI CS include older age, anterior location of MI, hypertension, diabetes, multivessel occlusions, left bundle branch block, and prior history of cardiac disease or heart failure.
 Tachycardia and/or hypotension at admission predict CS in patients with MI.

    • 25. Anti-Ischemic Therapy <ul><li>Because of the increased risks of mortality, reinfarction, hypertension, HF, and myocardial rupture associated with their use, nonsteroidal anti-inflammatory drugs (NSAIDs), except for ASA, whether nonselective or cyclooxygenase (COX)-2–selective agents, should be discontinued at the time a patient presents with UA/NSTEMI. </li></ul>The selective COX-2 inhibitors and other nonselective NSAIDs have been associated with increased cardiovascular risk. An AHA scientific statement on the use of NSAIDs concluded that the risk of cardiovascular events is proportional to COX-2 selectivity and the underlying risk to the patient (Antman EM, et al. Use of nonsteroidal antiinflammatory drugs. An update for clinicians. A scientific statement from the American Heart Association. Circulation 2007;115:1634–42. Further discussion can be found in Anderson JL, et al. J Am Coll Cardiol 2007;50:e1 – e157 and in the Secondary Prevention Section of this slide set. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III C New
    • 26. Antiplatelet Therapy <ul><li>Aspirin should be administered to UA/NSTEMI patients as soon as possible after hospital presentation and continued indefinitely in patients not known to be intolerant of that medication. </li></ul><ul><li>Clopidogrel (loading dose [LD] followed by daily maintenance dose)* should be administered to UA/NSTEMI patients who are unable to take ASA because of hypersensitivity or major gastrointestinal intolerance. </li></ul>*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive clinical efficacy and the safety of higher oral loading doses have not been rigorously established. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A LD added
    • 27. Select Management Strategy: Initial Invasive Versus Initial Conservative Strategy Major Changes New Trial Data
    • 28. Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy Invasive Recurrent angina/ischemia at rest with low-level activities despite intensive medical therapy Elevated cardiac biomarkers (TnT or TnI) New/presumably new ST-segment depression Signs/symptoms of heart failure or new/worsening mitral regurgitation High-risk findings from noninvasive testing Hemodynamic instability Sustained ventricular tachycardia PCI within 6 months Prior CABG High risk score (e.g., TIMI, GRACE) Reduced left ventricular function (LVEF < 40%) Conservative Low risk score (e.g., TIMI, GRACE) Patient/physician presence in the absence of high-risk features
    • 29. Risk Scores Antman EM, et al. JAMA 2000;284:835–42. Eagle KA, et al. JAMA 2004;291:2727–33. GRACE = Global Registry of Acute Coronary Events; TIMI = Thrombolysis in Myocardial Infarction. TIMI GRACE History Age Hypertension Diabetes Smoking ↑ Cholesterol Family history History of CAD Age Presentation Severe angina Aspirin within 7 days Elevated markers ST-segment deviation Heart rate Systolic BP Elevated creatinine Heart failure Cardiac arrest Elevated markers ST-segment deviation
    • 30. Algorithm for Patients with UA/NSTEMI Managed by an Initial Invasive Strategy Proceed to Diagnostic Angiography ASA (Class I, LOE: A) Clopidogrel if ASA intolerant (Class I, LOE: A) Diagnosis of UA/NSTEMI is Likely or Definite Invasive Strategy Init ACT (Class I, LOE: A) Acceptable options: enoxaparin or UFH (Class I, LOE: A) bivalirudin or fondaparinux (Class I, LOE: B) Select Management Strategy Proceed with an Initial Conservative Strategy Anderson JL, et al. J Am Coll Cardiol . 2007;50:e1-e157, Figure 7. ACT = anticoagulation therapy; LOE = level of evidence. Prior to Angiography Init at least one (Class I, LOE: A) or both (Class IIa, LOE: B) of the following: Clopidogrel IV GP IIb/IIIa inhibitor Factors favoring admin of both clopidogrel and GP IIb/IIIa inhibitor include: Delay to Angiography High Risk Features Early recurrent ischemic discomfort
    • 31. Initial Invasive Strategy: Antiplatelet Therapy <ul><li>For UA/NSTEMI patients in whom an initial invasive strategy is selected, antiplatelet therapy in addition to ASA should be initiated before diagnostic angiography (upstream) with either clopidogrel (loading dose followed by daily maintenance dose)* or an IV GP IIb/IIIa inhibitor. </li></ul><ul><li>Abciximab as the choice for upstream GP IIb/IIIa therapy is indicated only if there is no appreciable delay to angiography and PCI is likely to be performed; otherwise, IV eptifibatide or tirofiban is the preferred choice of GP IIb/IIIa inhibitor.† </li></ul>*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive clinical efficacy and the safety of higher oral loading doses have not been rigorously established; †Factors favoring administration of both clopidogrel and a GP IIb/IIIa inhibitor include: delay to angiography, high-risk features, and early ischemic discomfort. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B
    • 32. Clopidogrel in Unstable angina to prevent Recurrent ischemic Events (CURE) <ul><li>12,562 patients within 24 h UA/NSTEMI </li></ul><ul><li>Placebo vs clopidogrel (LD 300 mg -> 75 mg qd) </li></ul><ul><li>Other meds: ASA </li></ul><ul><li>↓ CV death, MI, or stroke, rate of recurrent ischemia & revasc with clopidogrel </li></ul><ul><li>↑ Major (non–life-threatening) bleeding with clopidogrel </li></ul><ul><li>No routine inv strategy, 23% revasc during initial admission </li></ul><ul><li>Although well tolerated, < 10% GP IIb/IIIa + ASA + clopidogrel + heparin use in study patients </li></ul>Yusuf S, et al. N Engl J Med 2001;345:494–502.
    • 33. Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using InTegrilin (PURSUIT) <ul><li>10,948 patients within 24 h UA/NSTEMI </li></ul><ul><li>Low-dose eptifibatide (n=1,487) vs high-dose eptifibatide (n=4,722) vs placebo (n=4,739) </li></ul><ul><li>Other meds: ASA, heparin </li></ul><ul><li>↓ Death/MI @ 96 hours, 7 d, 30 d with eptifibatide </li></ul><ul><li>― 1.5% ARR 4–30 d </li></ul><ul><li>― ↑ major bleeding </li></ul><ul><li>― no diff stroke </li></ul><ul><li>↑ Event rate in 11% of patients not treated with concomitant heparin </li></ul>The PURSUIT Trial Investigators. N Engl J Med 1998;339:436–43. Boersma E, et al. Circulation 2000;101:2557–67. ARR= absolute risk reduction.
    • 34. Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) <ul><li>1,915 patients within 12 h UA/NSTEMI </li></ul><ul><li>Tirofiban alone, UFH alone, or both for 48–108 h. </li></ul><ul><li>Tirofiban-alone arm discontinued d/t ↑ mortality rate. </li></ul><ul><li>↓ Death, MI, or refractory ischemia at 7 d, 30 d & 6 mo by tirofiban + heparin </li></ul><ul><li>High rate of angio could have contributed to important ↓ in event rates </li></ul><ul><li>Recommend: Tirofiban + heparin for medical rx or during PCI </li></ul>PRISM-PLUS Study Investigators. N Engl J Med 1998;338:1488–97.
    • 35. GP IIb/IIIa Inhibition for Non – ST-Elevation ACS 30-Day Death or Nonfatal MI Risk Ratio and 95% CI Placebo Better GP IIb/IIIa Inhibitor Better Trial Pooled 11.5% Placebo GP IIb/IIIa Inhibitor 10.7% 29,855 n 0.92 (0.86, 0.995) P =.037 PRISM-PLUS 11.9% 10.2% 1,915 PURSUIT 15.7% 14.2% 9,461 PARAGON A 11.7% 11.3% 2,282 7.1% PRISM 5.8% 3,232 0.5 1.0 1.5 PARAGON B 11.4% 10.5% 5,165 GUSTO-IV ACS 8.0% 8.7% 7,800 Boersma E, et al. Lancet. 2002;359:189-198. CI = confidence interval.
    • 36. Benefits of GP IIb/IIIa by Troponin Status in Clinical Trials Newby KL, et al. Circulation . 2001;103:2891-2896. TnT-Negative TnT-Positive PARAGON-B PRISM CAPTURE Combined 0.125 1 2 0.5 0.125 1 2 0.5 GP IIb/IIIa Better GP IIb/IIIa Worse GP IIb/IIIa Better GP IIb/IIIa Worse
    • 37. ISAR-REACT 2: Cumulative Incidence of Death, MI, or Urgent TVR in Subsets With and Without Elevated Troponin levels (>0.03 µg/L) ISAR-REACT 2 = Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment 2. Adapted with permission from Kastrati A, et al. JAMA . 2006;295:1531-1538. 0 5 10 15 20 25 30 Days After Randomization Cumulative Rate of Primary End Point, % Placebo Group (n=1010) Abciximab Group (n=1012) Troponin >0.03 µg/L Log-Rank P =.02 Troponin < 0.03 µg/L Log-Rank P =.98 20 15 10 5 0
    • 38. The Bottom Line for IV GP IIb IIIa Inhibitors <ul><li>Consider starting upfront (ED) when patients at highest risk undergoing early invasive </li></ul><ul><li>Consider in lab if PCI and not started upfront </li></ul><ul><li>Clopidogrel complementary, not competitor </li></ul><ul><li>Dose appropriately for renal function </li></ul>
    • 39. Initial Invasive Strategy: Anticoagulant Therapy <ul><li>Anticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI patients as soon as possible after presentation. </li></ul><ul><li>For patients in whom an invasive strategy is selected, regimens with established efficacy at a Level of Evidence: A include enoxaparin and unfractionated heparin (UFH), and those with established efficacy at a Level of Evidence: B include bivalirudin and fondaparinux. </li></ul>I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A New Drugs
    • 40. Initial Conservative Strategy <ul><li>Major Changes </li></ul><ul><li>New Drugs </li></ul><ul><li>Longer Duration of Rx </li></ul><ul><li>Revised Algorithm </li></ul>
    • 41. Init clopidogrel (Class I, LOE: A) Consider adding IV eptifibatide or tirofiban (Class IIb, LOE: B) Conservative Strategy Init anticoagulant therapy (Class I, LOE: A): Acceptable options: enoxaparin or UFH (Class I, LOE: A) or fondaparinux (Class I, LOE: B), but enoxaparin or fondaparinux are preferable (Class IIa, LOE: B) Select Management Strategy ASA (Class I, LOE: A) Clopidogrel if ASA intolerant (Class I, LOE: A) Diagnosis of UA/NSTEMI is Likely or Definite Algorithm for Patients with UA/NSTEMI Managed by an Initial Conservative Strategy Proceed with Invasive Strategy (Continued) Anderson JL, et al. J Am Coll Cardiol . 2007;50:e1-e157, Figure 8. ACT = anticoagulation therapy; LOE = level of evidence.
    • 42. Any subsequent events necessitating angiography? EF greater than 40% Evaluate LVEF Low Risk Cont ASA (Class I, LOE A) Cont clopidogrel (Class I, LOE A) and ideally up to 1 yr (Class I, LOE B) DC IV GP IIb/IIIa if started previously (Class I, LOE A) DC ACT (Class I, LOE A) (Class I, LOE: B) Proceed to Dx Angiography Yes EF 40% or less Stress Test (Class I, LOE: A) No Not Low Risk (Class IIa, LOE: B) Algorithm for Patients with UA/NSTEMI Managed by an Initial Conservative Strategy (Continued) Anderson JL, et al. J Am Coll Cardiol . 2007;50:e1-e157, Figure 8. ACT = anticoagulation therapy; LOE = level of evidence. (Class I, LOE: A) (Class IIa, LOE: B) (Class I, LOE: B) (Class I, LOE: A)
    • 43. Initial Conservative Strategy: Antiplatelet Therapy <ul><li>For UA/NSTEMI patients in whom an initial conservative (i.e., noninvasive) strategy is selected, clopidogrel (loading dose followed by daily maintenance dose)* should be added to ASA and anticoagulant therapy as soon as possible after admission and administered for at least 1 month (Level of Evidence: A) and ideally up to 1 year. (Level of Evidence: B) </li></ul>*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive clinical efficacy and the safety of higher oral loading doses have not been rigorously established. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B
    • 44. Initial Conservative Strategy: Antiplatelet Therapy <ul><li>For UA/NSTEMI patients in whom an initial conservative (i.e., noninvasive) strategy is selected, it may be reasonable to add eptifibatide or tirofiban to anticoagulant and oral antiplatelet therapy. </li></ul><ul><li>Abciximab should not be administered to patients in whom PCI is not planned. </li></ul>I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A
    • 45. Initial Conservative Strategy: Anticoagulant Therapy <ul><li>Anticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI patients as soon as possible after presentation. </li></ul><ul><li>For patients in whom a conservative strategy is selected, regimens using either enoxaparin* or UFH (Level of Evidence: A) or fondaparinux (Level of Evidence: B) have established efficacy. </li></ul><ul><li>In patients in whom a conservative strategy is selected and who have an increased risk of bleeding, fondaparinux is preferable. </li></ul>B *Limited data are available for the use of other low-molecular-weight heparins (LMWHs), e.g., dalteparin. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A New Drugs
    • 46. Initial Conservative Strategy: Anticoagulant Therapy <ul><li>For UA/NSTEMI patients in whom an initial conservative strategy is selected, enoxaparin* or fondaparinux is preferable to UFH as anticoagulant therapy, unless CABG is planned within 24 h. </li></ul>*Limited data are available for the use of other low-molecular-weight heparins (LMWHs), e.g., dalteparin. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B
    • 47. Initial Conservative Strategy: Additional Management Considerations <ul><li>b. If, after stress testing, the patient is classified as being at low risk, the instructions noted below should be followed in preparation for discharge: </li></ul><ul><li>1. Continue ASA indefinitely. (Level of Evidence: A) </li></ul><ul><li>2. Continue clopidogrel for at least 1 month (Level of Evidence: A) and ideally up to 1 year. (Level of Evidence: B) </li></ul><ul><li>3. Discontinue IV GP IIb/IIIa inhibitor if started previously. (Level of Evidence: A) </li></ul><ul><li>4. Continue UFH for 48 h or administer enoxaparin or fondaparinux for the duration of hospitalization, up to 8 d, and then discontinue anticoagulant therapy. (Level of Evidence: A) </li></ul>I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A
    • 48. Long-Term Antithrombotic Therapy at Hospital Discharge after UA/NSTEMI Medical Therapy without Stent Bare Metal Stent Group Drug Eluting Stent Group ASA 162 to 325 mg/d for at least 1 month, then 75 to 162 mg/d indefinitely (Class I, LOE: A) & Clopidogrel 75 mg/d for at least 1 month and up to 1 year (Class I, LOE:B) Add: Warfarin (INR 2.0 to 2.5) (Class IIb, LOE: B) Continue with dual antiplatelet therapy as above Yes No Indication for Anticoagulation? ASA 75 to 162 mg/d indefinitely (Class I, LOE: A) & Clopidogrel 75 mg/d at least 1 month (Class I, LOE: A) and up to 1 year (Class I, LOE: B) ASA 162 to 325 mg/d for at least 3 to 6 months, then 75 to 162 mg/d indefinitely (Class I, LOE: A) & Clopidogrel 75 mg/d for at least 1 year (Class I, LOE: B) Anderson JL, et al. J Am Coll Cardiol 2007;50:e1 – e157, Figure 11. INR = international normalized ratio; LOE = level of evidence. UA/NSTEMI Patient Groups at Discharge New
    • 49. Beta Blockers <ul><li>Beta blockers are indicated for all patients recovering from UA/NSTEMI unless contraindicated. (For those at low risk, see Class IIa on the next slide). Treatment should begin within a few days of the event, if not initiated acutely, and should be continued indefinitely. </li></ul><ul><li>Patients recovering from UA/NSTEMI with moderate or severe LV failure should receive beta-blocker therapy with a gradual titration scheme. </li></ul>New I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B
    • 50. Inhibition of the Renin-Angiotensin-Aldosterone System <ul><li>ACE inhibitors are reasonable for patients recovering from UA/NSTEMI in the absence of LV dysfunction, hypertension, or diabetes mellitus unless contraindicated. </li></ul><ul><li>ACE inhibitors are reasonable for patients </li></ul><ul><li>with HF and LVEF > 0.40. </li></ul><ul><li>In UA/NSTEMI patients who do not tolerate ACE inhibitors, an ARB can be useful as an alternative to ACE inhibitors in long-term management provided there are either clinical or radiological signs of HF and LVEF < 40%. </li></ul>New I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B New
    • 51. Lipid Management <ul><li>Lipid management should include assessment of a fasting lipid profile for all patients, within 24 h of hospitalization. </li></ul><ul><li>Hydroxymethyl glutaryl-coenzyme A reductase inhibitors (statins), in the absence of contraindications, regardless of baseline LDL-C and diet modification, should be given to post-UA/ </li></ul><ul><li>NSTEMI patients, including postrevascularization patients. </li></ul><ul><li>For hospitalized patients, lipid-lowering medications should be initiated before discharge. </li></ul>I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III C I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A Major Changes
    • 52. Heart Protection Study (HPS) <ul><li>20,536 patients with CHD </li></ul><ul><li>Simvastatin (40 mg qd) vs placebo </li></ul><ul><li>↓ Total mortality by simvastatin </li></ul><ul><li>― ↓ Total CHD, total stroke, revascularization </li></ul><ul><li>― ↑ Benefit over time, irrespective of initial cholesterol level and in broad spectrum of patients (e.g., women, elderly & patients with diabetes) </li></ul><ul><li>Recommend: Statin in all patients at discharge regardless of baseline LDL-C ( Class I, LOE: A ) </li></ul>Heart Protection Collaborative Group. Lancet 2002;360:7–22. LOE = level of evidence.
    • 53. Lipid Management <ul><li>For UA/NSTEMI patients with elevated LDL-C (≥ 100 mg per dL), cholesterol-lowering therapy should be initiated or intensified to achieve an LDL-C < 100 mg per dL. </li></ul><ul><li>Further titration to less than 70 mg per dL is reasonable. ( Class IIa, Level of Evidence: A ) </li></ul><ul><li>Therapeutic options to reduce non–HDL-C* are recommended, including more intense LDL-C–lowering therapy. </li></ul>*Non-HDL-C = total cholesterol minus HDL-C I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B New Lower LDL-C Goal
    • 54. PRavastatin Or atorVastatin Evaluation and Infection Therapy–Thrombolysis In Myocardial Infarction 22 (PROVE-IT TIMI 22) <ul><li>4,162 patients within 10 d of ACS </li></ul><ul><li>40 mg pravastatin vs 80 mg atorvastatin daily </li></ul><ul><li>↓ All-cause death, MI, UA requiring hosp, revasc & stroke @ 2 y by atorvastatin </li></ul><ul><li>― Median LDL-C ↓ (62 vs 95 mg/dL) </li></ul>Cannon CP, et al. N Engl J Med 2004;350:1495–504.
    • 55. Lipid Management <ul><li>Further reduction of LDL-C to < 70 mg per dL is reasonable. </li></ul><ul><li>If baseline LDL cholesterol is 70 to 100 mg per dL, it is reasonable to treat LDL-C to < 70 mg per dL. </li></ul><ul><li>Further reduction of non-HDL-C* to < 100 mg per dL is reasonable; if TG are 200 to 499 mg per dL, non- HDL-C target is < 130 mg per dL. </li></ul><ul><li>Therapeutic options to reduce non-HDL-C* (after LDL-C lowering) include niacin† or fibrate‡ therapy. </li></ul>*Non-HDL-C = total cholesterol minus HDL-C. † The combination of high-dose statin plus fibrate can increase risk for severe myopathy. Statin doses should be kept relatively low with this combination. Dietary supplement niacin must not be used as a substitute for prescription niacin. ‡ Patients with very high triglycerides should not consume alcohol. The use of bile acid sequestrants is relatively contraindicated when triglycerides are greater than 200 mg per dL. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III A I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III B
    • 56. Next Case: Chief Complaint: Subxiphoid burning sensation and dyspnea History of Present Illness: A 48-year-old female who smokes two packs per day presents with 1 hour of a subxiphoid burning sensation with dyspnea and diaphoresis, which are ongoing. She denies any prior cardiovascular or gastrointestinal history. Risk factor: positive family history of premature coronary artery disease
    • 57. Age: 48 Gender: Female Blood Pressure: 170/95 mm Hg Pulse: 96 bpm Head and Neck: Jugular venous pressure, 10 Chest and Lungs: Clear Cardiac Exam: Regular rhythm, normal S 1 /S 2 ; S 4 present Extremities: 2+ pulses, no edema
    • 58. Her EKG:
    • 59. Copyright ©2005 American Heart Association Circulation 2005;112:IV-89-IV-110 Acute Coronary Syndromes Algorithm
    • 60. Initial Therapy/Recognition <ul><li>Starts in transport to ED </li></ul><ul><ul><li>O2 </li></ul></ul><ul><ul><li>Aspirin </li></ul></ul><ul><ul><li>Nitro </li></ul></ul><ul><ul><li>Morphine </li></ul></ul><ul><ul><li>Beta Blockers? </li></ul></ul><ul><ul><li>12 lead EKG </li></ul></ul>
    • 61. Therapy and recognition in ED <ul><li>12 lead EKG  Will be used to stratify patients into treatment groups </li></ul><ul><li>O2, ASA, Nitro, Morphine  MONA </li></ul><ul><li>Physical exam </li></ul><ul><li>Cardiac biomarkers  troponins </li></ul><ul><li>10 minute time frame </li></ul>
    • 62. Treatment Groups Stratification <ul><li>ST-elevation MI (STEMI)  ST-segment elevation or presumed new LBBB in 2 or more contiguous precordial or limb leads </li></ul><ul><li>UA/non-ST-elevation MI (NSTEMI )  ischemic ST-segment depression or dynamic T wave inversion with pain. Transient ST-segment elevation. </li></ul><ul><li>Normal or nondiagnostic changes with pain </li></ul>
    • 63. ED Evaluation of Patients With STEMI 1. Airway, Breathing, Circulation (ABC) 2. Vital signs, general observation 3. Presence or absence of jugular venous distension 4. Pulmonary auscultation for rales 5. Cardiac auscultation for murmurs and gallops 6. Presence or absence of stroke 7. Presence or absence of pulses 8. Presence or absence of systemic hypoperfusion (cool, clammy, pale, ashen) Brief Physical Examination in the ED
    • 64. ED Evaluation of Patients With STEMI Aortic dissection Pulmonary embolus Perforating ulcer Tension pneumothorax Boerhaave syndrome (esophageal rupture with mediastinitis) Differential Diagnosis of STEMI: Life-Threatening
    • 65. ED Evaluation of Patients With STEMI Pericarditis Atypical angina Early repolarization Wolff-Parkinson-White syndrome Deeply inverted T-waves suggestive of a central nervous system lesion or apical hypertrophic cardiomyopathy LV hypertrophy with strain Brugada syndrome Myocarditis Hyperkalemia Bundle-branch blocks Vasospastic angina Hypertrophic cardiomyopathy Differential Diagnosis of STEMI: Other Cardiovascular and Nonischemic
    • 66. Gastroesophageal reflux (GERD) and spasm Chest-wall pain Pleurisy Peptic ulcer disease Panic attack Cervical disc or neuropathic pain Biliary or pancreatic pain Somatization and psychogenic pain disorder ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Other Noncardiac
    • 67. Electrocardiogram Show 12-lead ECG results to emergency physician within 10 minutes of ED arrival in all patients with chest discomfort (or anginal equivalent) or other symptoms of STEMI. In patients with inferior STEMI, ECG leads should also be obtained to screen for right ventricular infarction.
    • 68. Right Ventricular Infarction Clinical findings: Shock with clear lungs, elevated JVP Kussmaul sign Hemodynamics: Increased RA pressure (y descent) Square root sign in RV tracing ECG: ST elevation in R sided leads Echo: Depressed RV function Rx: Maintain RV preload Lower RV afterload (PA---PCW) Inotropic support Reperfusion V 4 R Modified from Wellens. N Engl J Med 1999;340:381.
    • 69. Biomarkers of Cardiac Damage Cardiac-specific troponins should be used as the optimum biomarkers for the evaluation of patients with STEMI who have coexistent skeletal muscle injury. For patients with ST elevation on the 12-lead ECG and symptoms of STEMI, reperfusion therapy should be initiated as soon as possible and is not contingent on a biomarker assay.
    • 70. Cardiac Biomarkers in STEMI 0 1 2 3 4 5 6 7 8 Cardiac troponin-no reperfusion Days After Onset of STEMI Multiples of the URL Upper reference limit 1 2 5 10 20 50 URL = 99th %tile of Reference Control Group 100 Cardiac troponin- reperfusion CKMB-no reperfusion CKMB- reperfusion Alpert et al. J Am Coll Cardiol 2000;36:959. Wu et al. Clin Chem 1999;45:1104.
    • 71. STEMI ST-segment elevation or presumed new LBBB in 2 or more contiguous precordial or limb leads
    • 72. STEMI <ul><li>Immediate reperfusion therapy indicated </li></ul><ul><ul><li>Fibrinolytics </li></ul></ul><ul><ul><li>PCI </li></ul></ul>
    • 73.  
    • 74. Medications for STEMI <ul><li>Clopidogrel </li></ul><ul><li>Beta blockers </li></ul><ul><li>Heparin </li></ul><ul><li>fibrinolytics </li></ul>
    • 75. Fibrinolysis In the absence of contraindications, fibrinolytic therapy should be administered to STEMI patients with symptom onset within the prior 12 hours. In the absence of contraindications, fibrinolytic therapy should be administered to STEMI patients with symptom onset within the prior 12 hours and new or presumably new left bundle branch block (LBBB).
    • 76. Fibrinolysis In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to STEMI patients with symptom onset within the prior 12 hours and 12-lead ECG findings consistent with a true posterior MI. In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to patients with symptoms of STEMI beginning in the prior 12 to 24 hours who have continuing ischemic symptoms and ST elevation > 0.1 mV in ≥ 2 contiguous precordial leads or ≥ 2 adjacent limb leads.
    • 77. Fibrinolysis Fibrinolytic therapy should not be administered to asymptomatic patients whose initial symptoms of STEMI began more than 24 hours earlier. Fibrinolytic therapy should not be administered to patients whose 12-lead ECG shows only ST-segment depression, except if a true posterior MI is suspected.
    • 78. Assessment of Reperfusion <ul><li>It is reasonable to monitor the pattern of ST elevation, </li></ul><ul><li>cardiac rhythm and clinical symptoms over the 60 to 180 </li></ul><ul><li>minutes after initiation of fibrinolytic therapy. </li></ul><ul><li>Noninvasive findings suggestive of reperfusion include: </li></ul><ul><li>Relief of symptoms </li></ul><ul><li>Maintenance and restoration of hemodynamic and/or electrical instability </li></ul><ul><li>Reduction of ≥ 50% of the initial ST-segment elevation pattern on follow-up ECG 60 to 90 minutes after initiation of therapy. </li></ul>
    • 79. Ancillary Therapy to Reperfusion <ul><li>Unfractionated heparin (UFH) should be given </li></ul><ul><li>intravenously in: </li></ul><ul><li>Patients undergoing PCI or surgical revascularization </li></ul><ul><li>After alteplase, reteplase, tenecteplase </li></ul><ul><li>After streptokinase, anistreplase, urokinase in patients at high risk for systemic emboli. </li></ul>
    • 80. Thienopyridines In patients taking clopidogrel in whom CABG is planned, the drug should be withheld for at least 5 days, and preferably for 7 days, unless the urgency for revascularization outweighs the risk of excessive bleeding. NOTE: Surgeons at MMC will take a patient to the OR for bypass even if given a loading dose of Plavix that day. This represents a change.
    • 81. ACE/ARB: Within 24 Hours <ul><li>An ACE inhibitor should be administered orally </li></ul><ul><li>within the first 24 hours of STEMI to the following </li></ul><ul><li>patients without hypotension or known class of </li></ul><ul><li>contraindications: </li></ul><ul><li>Anterior infarction </li></ul><ul><li>Pulmonary congestion </li></ul><ul><li>LVEF < 0.40 </li></ul>An ARB should be given to ACE-intolerant patients with either clinical or radiological signs of HF or LVEF < 0.40.
    • 82. All-Cause Mortality Years Probability of Event ACE-I 2995 2250 1617 892 223 Placebo 2971 2184 1521 853 138 Flather MD, et al. Lancet . 2000;355:1575–1581 OR: 0.74 (0.66–0.83) ACE-I: 702/2995 (23.4%) Placebo: 866/2971 (29.1%) TRACE Echocardiographic EF  35% AIRE Clinical and/or radiographic signs of HF SAVE Radionuclide EF  40% 0 0.05 0.1 0.15 0.2 0.25 0.3 0 1 2 3 0.35 0.4 4 ACE-I Placebo
    • 83. Last Case: A 58 y.o. man presents to the ER with a complaint of chest pain. His EKG and initial troponin are both normal. How will you proceed?
    • 84. First, characterize the chest pain <ul><li>Where is its location? </li></ul><ul><li>What provokes it? </li></ul><ul><li>What relieves it? </li></ul>
    • 85. Typical or classical angina: <ul><li>Is located in the center of the chest and may have textbook radiation to the arm, neck, or jaw </li></ul><ul><li>Is provoked by exercise or emotion </li></ul><ul><li>Is relieved by rest or nitroglycerine </li></ul>
    • 86. To establish the likelihood of your patient having an acute coronary syndrome, first determine whether: <ul><li>All three characteristics are present, and therefore the patient has typical angina </li></ul><ul><li>Two of three are present, i.e. this is atypical angina </li></ul><ul><li>One or none are present, i.e. this is non-anginal chest pain </li></ul>
    • 87. Then, use the medical literature:
    • 88. Diamond and Forrester: New England Journal of Medicine 1979; 300 (24): 1350 300 (24): 1350- -1358
    • 89. Diamond and Forrester: New England Journal of Medicine 1979; 300 (24): 1350 300 (24): 1350- -1358
    • 90. And to these probabilities, add some history: <ul><li>Family history of premature coronary disease? </li></ul><ul><li>Lipid profile known? </li></ul><ul><li>History of HTN? </li></ul><ul><li>Of diabetes? </li></ul><ul><li>Smoking? </li></ul>
    • 91. Now, you need to use Bayes’ Theorem… that is of course unless you are like me and want a short-cut. Here’s a short cut: It’s called the Fagan nomogram:
    • 92.  
    • 93. … together with your pretest probability you have estimated for your patient. And the likelihood ratios… for mibis, the +LR is about 2.4 and the –LR is about .2
    • 94. But look at the nomogram again! Are you convinced that stress testing is most helpful for the patient with intermediate pretest probability?
    • 95. Remember, central to the ACS algorithm is the 12-lead EKG. Which of these are acute MI’s?
    • 96.  
    • 97.  
    • 98.  
    • 99.  
    • 100.  
    • 101.  
    • 102. And which of these is V. Tach?
    • 103.  
    • 104.  
    • 105.  
    • 106.  
    • 107. cho đến tuần lễ sau 直到下个星期 hanggang kasunod linggo حتى الاسبوع المقبل поки ще не наступного тижня अगले सप्ताह तक

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