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Acute coronary syndrome

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  • 1. Acute Coronary Syndrome (ACS) Dr. B. K. Iyer
  • 2. Goals of lecture • Definition of ACS • Diagnosis of ACS • Treatment of ACS: Antiplatelet agents; Antithrombin agents; Reperfusion therapies • Role of the emergency physician in the diagnosis and management of ACS
  • 3. ACS: definition • ACC/AHA definition: ”a group of clinical syndromes compatible with acute myocardial ischemia” • Physiologic definition: Plaque rupture leading to thrombus formation, leading to partial or complete blockage of a coronary artery with or without myocyte death. • Spectrum includes unstable angina (No ST elevation, normal biomarkers), NSTEMI (no ST elevation, abnormal biomarkers), STEMI (ST elevation, abnormal biomarkers) • Unstable angina includes: angina at rest, new angina, increasing angina • Anderson JL et al. ACC/AHA 2007 guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction. J AM Coll Cardiology 2007. 50(7); e8
  • 4. Definition & spectrum • Any constellation of clinical symptoms that are compatible with acute myocardial ischemia. It encompasses 1.AMI (ST-segment elevation and depression, Q wave and non-Q wave) as well as 2.Unstable angina. Acute Coronary Syndromes No ST elevation ST elevation Enzymes not ↑ Enzymes ↑ USA NSTEMI STEMI ECG
  • 5. Pathopysiology • Plaques: atheromatous plaques are formed in the coronary arteries and when they rupture, exposing endothelium, they trigger a cascade of events • Thrombus: thrombin is deposited as well as fibrin, as the fibrin aggregates, platelets are activated • White: platelet-rich thrombi, more often partially occlusive and associated with UA/NSTEMI • Red: fibrin-rich thrombi, more often totally occlusive and associated with STEMI • Treatment of ACS is targeted at the root causes
  • 6. Golden Hour • Maximum damage to heart muscle • Maximum efficacy of treatment seen • Survival is best if thrombolysis is given within this period “Time is muscle and muscle is time” ““Each minute of delay inEach minute of delay in the first 3 hours confers 10the first 3 hours confers 10 lost days of survival”lost days of survival”
  • 7. Process of care in emergency : 4 D’s • Timed 0: onset of symptoms • ED time 1: Door [arrival at ED] • ED time 2: Data [initial ECG] • ED time 3: Decision [to administer thrombolytics] • ED time 4: Drug [infusion of thrombolytic started Time interval 1 Time interval 2 Time interval 3 Door To Drug time
  • 8. Door to Needle time • < 30 min in 33% patients only • Adjusted odds ratio of death if Door to Needle time as observed: – 61 - 90 min = 11% – > 90 min = 23 % • 11-23 % increased the odds of developing EF<40%, if Door to Needle time was > 30 min. • Door to Ballon time > 2 hrs associated with 41-62 % increase in adjusted odds ratio of death.
  • 9. Reducing treatment delays • Heart attack awareness campaign • Excellent Emergency Management System • Ambulance transport with pre-hospital ECGs • Pre-hospital thrombolysis : only when a physician is present or if pre-hospital transport time is > 6o min
  • 10. Diagnosis of ACS • No single factor from the history is a powerful enough predictor to exclude ACS. • Increased likelihood of ACS in patients with: –Radiation of pain to the right arm (LR 4.7) –Radiation of pain to both arms (LR 4.1) – Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA 2005; 294:2623-2629.
  • 11. Diagnosis of ACS • Presentation: Classic story most often seen in younger (50-65) patients, males • Those who present atypically tend to present further on in their disease and have worse outcomes (REACT) • Typical versus Atypical • Elderly: tend to present with shortness of breath • Diabetics: vague symptoms • Women: complain of feeling fatigued • Missed Diagnosis of Acute Cardiac Ischemia in the Emergency Department. N Engl J Med. 2000. April 20; 342 (16): 1163-70.
  • 12. Symptoms • Chest pain (variously described, but classically it is pressure-like) • Shortness of breath • Nausea/Vomiting (especially in inferior MI) • Diaphoresis • Weakness • Syncope
  • 13. Signs • Not terribly helpful to rule in or out ACS, but: – JVD, S3, pulmonary edema, new heart murmur are concerning for significant myocardial damage and indicate a patient at high risk for death/MI – Diaphoresis is never a good sign and should always concern the wary clinician – Can help discern alternate causes of chest pain – Anderson JL et al. J Am Coll Card 2007. 50(7): e1-157
  • 14. Emergency Room Triage in ACS • Initial presentation • 12 Lead ECG • Cardiac Enzymes
  • 15. Ischemic Chest Discomfort ST Elevation or New LBBB ECG s/o Ischemia ST dep, T inversion Non-diagnostic or Normal ECG Assess initial ECG Aspirin Baseline CK, CK-MB Assess C/I to thrombolysis Anti-ischemic therapy Reperfusion therapy thrombolyse or Primary PTCA ] Admit Anti-ischemic therapy Serial cardiac markers 2D Echo E/o ischemia / MI NoYes DischargeAdmit Goal 10 minutes Goal < 30 min for STK or < 60 min for arrival in Cath Lab for PTCA Triage of ACS
  • 16. ↑ Biomarkers + ≥ of the following Pathological findings of AMI Typical symptoms of AMI + one of the following Procedural myocardial damage Typical symptoms of myocardial ischemia No other findings required ST segment elevation in the ECG ↑ cardiac biomarkers to prespecified levels; symptoms may be absent; ECG changes absent/nonspecific Q waves in the ECG Increased levels of cardiac biomarkers ST segment elevation or depression in the ECG Modified from Alpert J, Thygesen K, et al: Towards a new definition of myocardial infarction for the 21st century. J Am Coll Cardiol 2000 Criteria For The Diagnosis Of Acute Myocardial Infarction (AMI)
  • 17. Initial Presentation
  • 18. Common symptom history in acute MI – Location • Usually substernal – Quality • Crushing or squeezing – Radiation • Either Arm, Neck, Jaw, Epigastrium, or between Scapulae – Duration • Generally 30 minutes to several hours • Anginal Pain Equivalents • Dyspnoea • Marked weakness • Syncope • Accompanied diaphoresis, nausea, vomiting • Chest Pain
  • 19. No pain ; No gain • In a lot of cases with proven acute MI, chest pain was absent at initial presentation [33%] • These pts – were at least 70 years older; – Higher proportion were women[49% vs 38%]; diabetics; had h/o prior heart failure – Had longer delay before hospital admission; – Were less likely to receive thrombolysis or primary PTCA; b-blockers, aspirin or heparin – Had higher in-hospital mortality [23.3% vs 9.3%]
  • 20. Recognition of high risk cases • Demographic and historical factors associated with poor prognosis – Age > 70 years – Female gender – History of Diabetes mellitus – Prior angina pectoris – Previous MI Peterson ED et al. Ann Intern Med 126:561-582,1997
  • 21. Electrocardiogram “standard of care”
  • 22. ECG • Very specific and a good test, particularly helpful if positive: – Should be done within 10 minutes of arrival on anyone with suspected ACS – Serial ECGs in the ED are a must when looking for changes, especially if the patient is initially pain-free or has atypical symptoms – Can have a normal ECG with significant disease, particularly if the patient is pain free – Tells us the most likely artery affected and area of myocardium affected – Kumar, Amit, et al. Acute Coronary Syndromes: Diagnosis and Management, Part 1. Mayo Clin Proc. October 2009;84(10):917-938
  • 23. ECG: watch for • Inferior: II, III, AVf • Anterior: V1-V6 • Lateral: I, AVL, V5, V6 • Posterior: depression V1-V3 with tall R waves • Right ventricular infarct: right sided leads • Wellens (indicates significant LAD disease): T wave inversions V2-V4 without pain • NSTEMI: ST depressions; T wave inversions
  • 24. ECG Patterns In Acute Chest Pain In unstable angina TIMI IIIb Investigators, Circulation 1994;89Hamm et al. NEJM 1997;337 23% 18% 11% 10% 30% 0% 5% 10% 15% 20% 25% 30% T-wave inversion ST- depression ST- elevation LBBB Normal 13% 57% 17% 12% 0% 10% 20% 30% 40% 50% 60% T-wave inversion ST- depression ST- elevation Normal
  • 25. Prognostication through ECG • ST elevation • decisive role regarding thrombolytic therapy • Worse prognosis / Increase mortality in • Anterior MI > Inferior MI • RVMI complicating IWMI • Multiple leads with ST elevation & high sum of ST elevation • Persistent advanced heart block • New IVCD (Bifascicular / trifascicular) • Persistent ST depression / Q waves in many leads • ST depression in anterior leads in IWMI NEJM 330:1211-1217, 1994 , Ann Intern Med 126:556;1997
  • 26. Risk of MI/ death during 1 year follow up based on admission-ECG 0 5 10 15 20 25 30 60 120 180 240 300 360 Follow Up ( Days) MIorDeath(%) ST Elev + Dep ST Dep ST Elev T Inv NO ST/T Changes The RISC Study Group . J.Intern.Med.1993;234
  • 27. Time of ECG and outcomes
  • 28. Limitations of ECG • It provides a snapshot view of a highly dynamic process. • Lack of perfect detection in areas of myocardium it supplies. • Small areas of ischemia or infarction may not be detected. • Conventional leads do not directly examine right ventricle, posterior basal or lateral walls very well. • Baseline changes like BBBs, early repolarization, LVH, & arrhythmias make interpretation difficult. • AMI in LCx territory are likely to have non-diagnostic ECG. • ECG is not very sensitive test & should always be considered a supplement to, rather than a substitute for, physician judgment.
  • 29. Pseudo-infarction on ECG • LVH • Conduction disturbance • Pre-excitation • Primary myocardial disease • Traumatic heart disease • Pericarditis • Early repolarization • Pneumothorax • Pulmonary embolism • I/C hemorrhage • Hyperkalemia • Amyloidosis • Sarcoid cardiac involvement
  • 30. Inferior MI
  • 31. Right Ventricular MI
  • 32. Lateral MI
  • 33. Wellen’s Syndrome
  • 34. NSTEMI
  • 35. Cardiac Markers
  • 36. hFABP=heart fatty acid binding proteins; MLC=myosin light chain; cTnI=cardiac troponin I; cTnT=cardiac troponin T; MB-CK=MB isoenzyme of creatinine kinase (CK); MM-CK=MM isoenzyme of CK; LD=lactate dehydrogenase; MHC=myosin heavy chain; CP=chest pain Markers, MW, Time to initial elevation, Mean time to peak, Time to return to normal, Common sampling schedule
  • 37. Appearance of cardiac markers in blood versus time after onset of symptoms • Peak A: Myoglobin or CK-MB isoforms post AMI • Peak B: cardiac troponin post AMI • Peak C: CK-MB post AMI • Peak D: cardiac troponin after unstable angina.
  • 38. Predictive value of troponin rapid testing Predischarge TMT + Troponin • If Both Normal – 1 % risk of Death /MI at 5 Months • If both Abnormal – 50 % risk of death/MI at 5 Months
  • 39. Troponins • 30% patients with rest pain without ST- elevation and were diagnosed as unstable angina based on CPK_MB results are found to have elevated troponins, converting these to NSTEMI.
  • 40. Clinical Status GISSI-1 (%) Killip Definition Incidence Control Lytic Class Mortality Mortality I No CHF 71 7.3 5.9 II S3 gallop or 23 19.9 16.1 basilar rales III Pulmonary edema 4 39.0 33.0 (rales >1/2 up) IV Cardiogenic shock 2 70.1 69.9 Killip T et al. Am J Cardiol 20:457;1967 GISSI. Lancet 1”397-401, 1986
  • 41. Hospital Phase
  • 42. Hospital Phase : Tools • Risk stratification in ICU is done by: – Clinical findings – ECG monitoring – Invasive hemodynamic monitoring – LV Function • Most important determinant of hospital mortality – Echocardiography • LVEF, diastolic function, hemodynamics, degree of MR, mechanical complications
  • 43. Hemodynamic Classification Subset Definition PCWP CI Mortality I Normal hemodynamics <18 >2.2 3% II Pulmonary Congestion >18 >2.2 9% III Peripheral hypoperfusion <18 <2.2 23% IV Pulmonary congestion & Peripheral hypoperfusion >18 <2.2 51% Forrester J et al. NEJM 295:1356:1976 PCWP = pulmonary capillary wedge pressure
  • 44. Inpatient stratification
  • 45. Risk Stratification • GRACE (Global Registry of Acute Coronary Events) risk score and PURSUIT (Platelet G IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) risk score: too time consuming and complex for regular use in the emergency department. Better for in-patient risk stratification. • TIMI (Thrombolysis in Myocardial Infarction) score (1 point for each): – Age > 65 – Aspirin use in the last 7 days – 3 or more conventional cardiac risk factors – Severe angina (> 2 episodes in 24 hours) – Positive cardiac markers – ST changes > 0.5 mm – > 3 TIMI score is high risk for ACS • Hoekstra J, et al. Management of patients with unstable angina/non-ST- elevation myocardial infarction: a critical review of the 2007 ACC/AHA guidelines. Int J Clin Pract, April 2009, 63, 4, 642-655
  • 46. Echocardiography • Identification of location of infarction • Estimation of infarct size • Assessment of diastolic function • Degree of MR • Recognition of mechanical complications • Determination of LVEF – LVEF < 40% within 72 hrs of onset of AMI is associated with increase risk of death Berning et al. Am J Cardiol 69:1538-44;1992
  • 47. Echocardiography • Greater number of WMA [wall motion abnormalities] correlated with – Higher Killip class, – Lower pO2, – Higher CPK levels and – Larger number of Q waves on ECG • Romano et al • 30 day mortality – WMA < 3 segments= 3.5% – WMA 4-6 segments= 12.9% – WMA 7-9 segments= 18.3% – WMA > 9 segments= 37.8% Am J Cardiol 81(12A):13G-16G;1998
  • 48. Mitral inflow patterns • Worse is the flow pattern, worse is the prognosis • A deceleration time < 130 msec indicates future development of CHF Normal Relaxation Defect Pseudo- Normalization Restrictive pattern A E Poulsen et al , Eur Heart J 1997;18:1882
  • 49. Complications • LV systolic dysfunction • Rupture Free Wall VSD Papillary muscle rupture Subepicardial aneurysm MRCARDIAC RUPTURE VSD LV ANEURYSMLV ANEURYSM
  • 50. Complications • Mitral regurgitation LV dilatation Papillary muscle dysfunction Papillary muscle rupture LV thrombus Pericardial effusion/ tamponade RV infarct LV outflow tract obstruction
  • 51. Echo: value in ACS • Echo provides new and useful information in 29% of the patients admitted to ICU • Decision about reperfusion strategy • ACE-I therapy (SAVE trial) • Unrecognized prior MI • Titrating beta-blockers • Need for invasive monitoring • Standby IABP support
  • 52. Management • Goals • Immediate relief of ischemia • Prevention of serious adverse outcomes • Approach • Anti-ischemic therapy • Anti-platelet therapy • Anti-coagulant therapy & Reperfusion therapies • Ongoing risk stratification • Invasive procedures • Adjunctive anti-ischemic therapies: Beta-blockers, Nitrates, Morphine, Calcium channel blockers, O2, ACE inhibitors Match treatment to risk: More aggressive treatment in higher risk & unstable patients
  • 53. Management – initial medical therapy • Unstable Angina guidelines: Class 1 recommendations for antithrombotic therapy Braunwald E et al , J. Am coll Cardiol 2000; 36:970-1002
  • 54. Anti-Ischemic therapy for continuing ischemia • Bed rest with ECG monitoring • O2 to maintain SaO2 >90% • NTG IV • Beta-blockers • Morphine • IABP if ischemia or hemodynamic instability persists • ACE I for control of hypertension or LV dysfunction, after MI Class-I Recommendations, ACC/AHA practice guidelines
  • 55. Anti Ischemic Therapy • Nitrates • Beta Blockers • Calcium Channel Blockers
  • 56. Nitrates in ACS No. Of Pts. Mortality (%)Study Year Tt Control GISSI 3 94 18895 6.5 6.9 ISIS-4 95 58050 7.3 7.5
  • 57. Beta blockers in ACS Mortality Study Year n Tt C MIAMI * 1985 5578 4.3 4.9 ISIS-1# 1986 16027 3.9 4.6 * Eur H Journal 1985;6 # Lancet 1986;ii
  • 58. Calcium Channel Blockers in ACS MortalityStudy Yr N Tt C Meta analysis 1989 7351 5.9 5.2 Salim Yusuf, BMJ 1989; 299
  • 59. Antiplatelet and Anticoagulation Therapy • Oral Antiplatelet therapy • Aspirin – Thienopyridines Ticlopidine Clopidogrel • Heparins – UFH – LMWH • IV Antiplatelet therapy • Abciximab • Eptifibatide • Tirofiban
  • 60. Role of Anticoagulants in ACS Mortality %Study Yr N Tt c UFH [Meta-analysis] 1994 1353 6.5 6.9 LMWH [FRISC 1] 1996 1506 1.8 3.8
  • 61. New Anti-coagulants in ACS
  • 62. Anticoagulants - Unfractionated Heparin (UFH) • Most widely used antithrombotic agent • Recommendation is based on documented efficacy in many trials of moderate size • Meta-analyses of 6 trials showed a 33% risk reduction in MI and death, but with a 2-fold increase in major bleeding
  • 63. Anticoagulants - Unfractionated Heparin (UFH) • Disadvantages include: – Poor bioavailability – No inhibition of clot-bound thrombin – Dependent on antithrombin III (ATIII) cofactor – Frequent monitoring (aPTT) to ensure therapeutic levels – Rebound ischemia after discontinuation – Risk of heparin-induced thrombocytopenia (HIT)
  • 64. Anticoagulants - Low-Molecular-Weight Heparin (LMWH) • Fraction of standard (UFH) heparin • Enoxaparin, dalteparin, reviparin, nadroparin, fraxiparin • Advantages over UFH: – Greater bioavailability – No need to closely monitor – Resistant to inhibition by activated platelets – Lower incidence of HIT Enhanced anti-factor Xa activity – Effective subcutaneous administration
  • 65. ESSENCE Trial: (Efficacy and Safety of Subcutaneous Enoxaparin in non-Q-Wave Coronary Events Study) • LMWH (enoxaparin)+ASA vs UFH+ASA • Patients: – angina at rest or non-Q-wave MI; • n = 3,171 • Composite triple endpoint: – death/nonfatal MI/RA
  • 66. 0 5 10 15 20 25 0 5 10 15 20 25 heparin enoxaparin Heparin enoxaparin n=1564 n=1607 n=1564 n=1607 19.8% 16.6% P=0.019 23.3% 19.8% P=0.016 Day 14 Day 30 N Eng J Med 1997;337:447-452 ESSENCE Trial - Incidence of death, MI, or recurrent angina
  • 67. AntiThrombotic Therapy for ACS • Anticoagulants – Heparin • UFH • LMW – Hirudin – Coumarins • Antiplatelets – Aspirin – Ticlopidine – Gp IIb/IIIA Inhibitors • Thrombolytics
  • 68. Anti Platelet Therapy in ACS • Aspirin – Inhibits cyclo-oxygenase in platelets • Ticlopidine – Inhibits the ADP receptor on the platelet surface • Gp iib/iiia receptor antagonist
  • 69. Aspirin Advantages • In AMI, ASA reduced the risk of death by 20- 25% • In UA, ASA reduced the risk of fatal or nonfatal MI by – 71% during the acute phase, – 60% at 3 months, and – 52% at 2 years Disadvantages • Not Perfect • Patients on ASA may present with ACS • ASA non-responders 20-30% • Not adequate alone for stent implantation • Side effects
  • 70. Incidence of Ischemic Events 0 2 4 6 8 10 12 14 16 No aspirin (early 1980s) Aspirin Aspirin + Heparin 16% 12% 9% Incidence of death and MI
  • 71. Thienopyridines • Ticlopidine • Clopidogrel – Block ADP receptor resulting in inhibition of transformation of GP IIb/IIIa into its high affinity state
  • 72. Aspirin & Ticlopidine in ACS
  • 73. IV Anti-platelet Therapy • GP IIb/IIIa inhibitors • abciximab (monoclonal antibody) • eptifibatide (peptide inhibitor) • lamifiban and tirofiban (non-peptides)
  • 74. Recommendations for Antiplatelet & Anticoagulation Therapy • Class 1: – Antiplatelet therapy should be initiated promptly. Aspirin is the first choice and is administered as soon as possible after presentation and is continued indefinitely. (Level of Evidence: A) – Clopidogrel should be administered to patients who are unable to take ASA because of hypersensitivity or major gastrointestinal intolerance. (Evidence Level: A) – In hospitalized patients in whom an early noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month (Level of Evidence : A) and for upto 9 months (Evidence Level: B)
  • 75. Recommendations for Antiplatelet & Anticoagulation Therapy • Class 1: – In hospitalized patients for whom a PCI is planned, clopidogrel should be started and continued for at least 1 month (Level of Evidence : A) and for up to 9 months in patients who are not at high risk for bleeding (Level of Evidence : B) – In patients taking clopidogrel in whom CABG is planned, if possible the drug should be withheld for at least 5 days, and preferably for 7 days. (Level of Evidence :B) – Anticoagulation with subcutaneous LMWH or intravenous UFH should be added to antiplatelet therapy with ASA and/or clopidogrel. (Level of Evidence : A) – A platelet GP IIb/IIIa receptor antagonist should be administered, in addition to ASA and heparin, to patients in whom catheterization and PCI are planned. The GP IIb/IIIa antagonist may also be administered just prior to PCI (Level of Evidence: A)
  • 76. Early Conservative vs Invasive Strategies - Recommendations Class I • An early invasive strategy in patients with UA/NSTE- MI and any of the following high risk indicators. (Level A) – Recurrent angina/ischemia at rest or with low-level activities despite intensive anti-ischemic therapy – Elevated TnT or TnI – New or presumably new ST-segment depression – Recurrent angina/ischemia with CHF symptoms, an S3 gallop, pulmonary edema, worsening rales, or new or worsening MR – High-risk findings on noninvasive stress testing – Depressed LV systolic function (EF < 0.40) – Hemodynamic instability – PCI within 6 months – Prior CABG
  • 77. Early Conservative vs Invasive Strategies - Recommendations Class I • In the absence of these findings, either an early conservative or an early invasive strategy in hospitalized patients without contraindications for revascularization (Level of Evidence: B)
  • 78. Indications of primary PTCA • Cardiogenic Shock • Large area of myocardium at risk • Thrombolysis contraindicated • Alternative to thrombolysis
  • 79. Interventions in ACS Rationale • Prognosis of ACS is worse than Stable angina • Inhospital death / Reinf. = 5 - 10 % • Ist Mo Death / Reinf. = 5 - 10 %
  • 80. Casualty protocol for acute chest pain
  • 81. AMI: Parameters influencing prognosis Acute MI At Presentation In Hospital At Discharge Size of infarct Recurrent ischemia LV systolic dysfunction Diastolic dysfunction Mechanical complications Residual ischemia LV dysfunction Risk of arrhythmia Age Gender ECG features Concomitant Risk factors Clinical status
  • 82. TIMI myocardial perfusion grade and mortality
  • 83. TIMI myocardial perfusion grade and mortality
  • 84. TIMI Risk Score for STEMI for predicting 30-day mortality
  • 85. The GUSTO Pyramid: 30 Day Mortality Model Age (31%)Age (31%) Systolic Blood Pressure (24%)Systolic Blood Pressure (24%) Killip Class (15%)Killip Class (15%) Heart Rate (12%)Heart Rate (12%) MI Location (6%)MI Location (6%) Prior MI (3%)Prior MI (3%) Age x Killip (1.3%)Age x Killip (1.3%) Height (1.1%)Height (1.1%) Diabetes (1%)Diabetes (1%) Time-to-Rx (1%)Time-to-Rx (1%) Smoker (0.8%)Smoker (0.8%) Weight (0.8%)Weight (0.8%) Accel t-PA (0.8%)Accel t-PA (0.8%) Prior CABG (0.8%)Prior CABG (0.8%) HTN (0.6%)HTN (0.6%) H/oH/o CV DCV D (0.4%)(0.4%) Lee et al. Circulation 1995;91:1659- 1668 Influence of Clinical characteristics on 30 day mortality in thrombolyzed Initial Presentation : Clinical
  • 86. Summary
  • 87. Treatment of ACS • All patients receive aspirin • Clopidogrel is also favored as an adenosine-mediated platelet blocker, particularly in patients with aspirin allergy. • ESSENCE trial (Efficacy and Safety of Subcutaneous Enoxaparin in Non– Q Wave Coronary Events) has suggested a preference for LMWH specifically, enoxaparin (Lovenox) over unfractionated heparin in ACS • Finally, a platelet glycoprotein IIb/IIIa inhibitor is needed. • Glycoprotein IIb/IIIa receptor blockers have been studied with simultaneous use of unfractionated heparin and aspirin. Most of the trials with these agents have involved coronary interventions and have shown significant benefit. • If no intervention is planned, abciximab is not indicated. • Currently, tirofiban and eptifibatide are useful in patients with continuing ischemia when no percutaneous intervention is planned. These latter two medications are also indicated in patients with continuing ischemia or other high-risk features in whom a percutaneous intervention is planned.
  • 88. Rx of ACS • TACTICS trial and TIMI-18 compared an early invasive and a conservative strategy in patients treated with the tirofiban & showed that an early invasive strategy reduces the incidence of major cardiac events. • The data for high-risk AMI and non–Q wave MI suggest that angiography should be part of the early plan. • The data for unstable angina with no elevation in biochemical markers are less clear. • Because of cost considerations, abciximab with coronary intervention is recommended in high-risk patients. • In intermediate-risk patients, regardless of whether they are candidates for coronary intervention, tirofiban or eptifibatide is recommended. • Low-risk patients may not require either of these agents, but they should receive heparin, probably low molecular-weight heparin, aspirin, and clopidogrel at a dose of 300 mg to start and then 75 mg/d for at least 30 days. • In addition, a “statin” should be started in that hospitalization (MIRACL) if LDL cholesterol is greater than 130 mg/dL.
  • 89. Antithrombotic Drug Therapy Abciximab (ReoPro) with unfractionated heparin & aspirin 0.25-mg/kg intravenous bolus followed by an infusion of 0.125 μg/kg/min for 12–24 h up to 10 mg/min Eptifibatide (Integrilin) with unfractionated heparin & aspirin 180-μg/kg bolus followed by an infusion of 2 μg/kg/min up to 72 h for intervention. Max 15 mg/h Tirofiban (Aggrastat) with unfractionated heparin & aspirin 0.4 μg/kg/min × 30 min 0.1-μg/kg/min infusion × 48 h up to 108 h (PRISM-Plus) Enoxparin (clexane) 1 mg/kg q12 h Clopidogrel (Plavix) 300 mg initially, followed by 75 mg/d
  • 90. Findings in High-Risk Patients • Recurrent ischemia at rest or low levels of activity with medical management • High-risk noninvasive stress testing with depressed ejection fractions, • Extensive wall motion abnormalities • Hemodynamic instability • Sustained ventricular tachycardia • Recent revascularization with coronary intervention or coronary bypass graft surgery
  • 91. Post discharge Care “ABCDE” • A – Antiplatelets & Antianginals • B – Beta blocker, Blood pressure control • C – Cholesterol lowering, Cigarettes cessation • D – Diabetes control, Diet • E – Education & Exercise
  • 92. Invasive therapy • Percutaneous Coronary Intervention (PCI) – Confers benefit in highest risk UA/NSTEMI patients – Multiple trials done over the last 20 years with pendulum swinging from invasive to conservative and back
  • 93. Treatment of STEMI • Many of the same anti-platelet and anti- thrombin therapies used • Fibrinolytics are indicated in STEMI but not in UA/NSTEMI • Emergency physicians in the United States are held to multiple benchmarks for STEMI (door to ECG, door to medications, door to balloon time)
  • 94. Fibrinolytics • Indications: – ST segment elevation of at least 1mm in two or more contiguous leads – Pain for < 12 hours – Symptoms consistent with acute myocardial infarction – No contraindications • Fibrinolytics are particularly effective within the first six hours after pain onset and in those with new left bundle branch block and anterior wall myocardial infarctions • Kumar, Amit and Christopher Cannon. Acute Coronary Syndrome: Diagnosis and Management, Part II. Mayo Clin Proc. November 2009;84(11):1021-36
  • 95. Fibrinolytics • Absolute Contraindications: – Any previous ICH – Known structural cerebrovascular lesions – Known malignant intracranial neoplasm – Ischemic stroke within 3 months, except for acute ischemic stroke within 3 hours – Suspected aortic dissection – Active bleeding or bleeding diathesis (excluding menses) – Severe closed head or facial trauma within 3 months
  • 96. Fibrinolytics • Streptokinase: reduces mortality significantly (ISIS-1), lowest cost • Retevase: no difference between Retevase and tPA (GUSTO III) but easy dosing for ER (10 mg bolus 30 minutes apart) • Alteplase (tPA):GISSI-2, ISIS-3, GUSTO showed likely more favorable outcome than streptokinase; tPA slightly more likely to cause intracranial hemorrhage • Tenecteplase (TNK): equivalent to tPA, weight based dosing may make it more difficult for
  • 97. PCI in STEMI • Coronary angioplasty with or without stenting • Preferred at centers where available as some studies point to better outcomes than fibrinolytics (GUSTOIIb). • Depends on whether it is available at your facility and how quickly the patient can get to the cath lab
  • 98. Newer Modalities • Coronary CT angiogram to diagnose CAD and/or ACS • Bivalirudin: ACUITY trial showed similar 30 day rates of death, MI or unplanned revascularisation with lower bleeding rates in the bivalirudin alone arm. • Stone, GW et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med 2006; 355: 2203-16
  • 99. Role of emergency physician • No single historical or physical exam factor can rule out ACS • Diabetics, elderly and women present atypically – Less common risk factors such as lupus or Kawasaki’s disease • Serial ECGs are extremely important in detecting on-going ACS
  • 100. Role of emergency physician • First line for diagnosis and treatment • Earlier treatment = better outcomes • Aspirin for everyone unless contraindicated • We will miss some people with ACS, but we can minimize it by being aware of the incorrect assumptions
  • 101. Thank you!

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