Acute Coronary Syndromes Recognition, Risk Stratification, and Management
Acute Coronary Syndromes Recognition, Risk Stratification, and Management Claudia P. Hochberg, MD, FACC August 12, 2013 Topics to Cover Identification of the patient with ACS Initiation of anti-thrombotic therapy and anti-ischemic therapy Risk stratification as it relates to the decision of early invasive vs. conservative strategy Secondary prevention/risk factor modification 124 Class I recommendations 23 Class III recommendations Acute Coronary Syndrome An ischemic myocardial event that is a direct consequence of atherosclerotic plaque activation and/or local thrombus formation
May be divided into that association with ST segment elevation and that associated with ST segment depression Spectrum: UANSTEMISTEMI Acute Myocardial Infarction: Definition 1. Typical rise and fall of biochemical markers of myocardial necrosis (troponin or CK-MB) with at least one of the following: a) ischemic symptoms b) development of pathologic Q waves on EKG c) ischemic EKG changes (ST depression or elevation) d) coronary intervention 2. Pathologic findings of an acute MI Unstable Angina: Guideline Definition Three principal presentations: Rest angina >20 minutes in last week New onset angina in last 2 months Increasing angina - increased frequency,
duration, or severity Hospital Admissions for ACS: Unstable Angina/NSTEMI vs STEMI Acute Coronary Syndrome 2.3 Million Hospital Admissions ACS UA/NSTEMI STEMI 1.43 million Admissions per Year 829,000 Admissions per Year Sodnick EJ, et al. National Center for Health Statistics. 2001. Mr JS 65 yo male with h/o HTN, hyperlipidemia
Had 1st episode of chest pain (a pressure with radiation to his left shoulder) 2 weeks prior to admit, while shoveling snow. Over the 3 days prior to admit he had 4 episodes of chest pain, initially with mild exertion, and finally at rest. The pain resolved spontaneously in 3-4 minutes. Meds: atenolol, amlodipine, HCTZ, atorvastatin, aspirin BP: 136/95 HR: 92 No vascular bruits, no murmur, +S4, no congestion How can we tell if this man is having an ACS? Acute presentation Baseline Labs normal except troponin 0.15, CK: 370 Chest Pain History and Diagnosis of Acute Myocardial Infarction (AMI)
Swap, C. J. et al. JAMA 2005;294:2623-2629. Likelihood that Signs and Symptoms Represent ACS Secondary to CAD HIGH Left arm or chest pain typical of prior angina Hx of CAD or MI CHF Transient MR murmur Hypotension New ECG changes (ST
deviation > 1mm; Twave inversion in many leads) Elevated biomarkers (troponin/CK-MB) Intermediate Left arm or chest pain Age > 70 years Male Diabetes PVD,CVA Q waves on ECG ST deviation 0.5-1.0 mm, Twave inversion > 1 mm
Normal biomarkers Circulation. 2007;116:e148 e304. Likelihood that Signs and Symptoms Represent ACS Secondary to CAD Low Probable ischemic symptom in absence of intermediate risk markers Recent cocaine use Pain reproduced by palpation T wave inversion < 1 mm Normal ECG Normal biomarkers
Circulation. 2007;116:e148 e304. Initial Anti-Ischemic Therapies (Class I) Bed Rest (~ 24 hours) Oxygen Nitrates Morphine Sulfate Beta-blocker (within the 1st 24 hours in patients without contraindications) Non-dihydropyridine CCB (verapamil/dilt) in patients with contraindications to BB ACE inhibitor for HTN, low LVEF or CHF or DM Discontinue NSAIDs Circulation. 2007;116:e148
e304. What Anti-Thrombotic Therapy Should be Used in the Initial Hours of Management of ACS? The Vulnerable Plaque Images from Falk E, et al. Circulation. 1998;92:657-671. Plaque rupture Platelet adhesion Platelet activation Platelet aggregation Thrombotic occlusion Characteristics of Unstable and Stable Plaque Unstable Few SMCs
Thin fibrous cap Stable Inflammatory cells Eroded endothelium Activated macrophages More SMCs Thick fibrous cap Lack of inflammatory cells
Intact endothelium Foam cells Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org. Plaque Rupture, Thrombosis, and Microembolization Marker Quiescent plaque Lipid Lipid core core Vulnerable plaque Inflammation TF Clotting Cascade Collagen platelet
activation Foam Cells MacrophagesMetalloproteinases Process Cholesterol Cholesterol Plaque Plaque formation formation LDL LDL C-Reactive C-Reactive Inflammation Inflammation Protein Protein Multiple Multiple factors factors Adhesion Adhesion
Thrombosis Thrombosis LDL LDL Platelet Platelet Activation Activation Thrombin Thrombin Courtesy of David Kandzari. D-dimer, D-dimer, Thrombus Formation and ACS Plaque Disruption/Fissure/Erosion Thrombus Formation Old Terminology: UA
New Terminology: Non-ST-Segment Elevation Acute Coronary Syndrome (ACS) NQMI QWMI ST-Segment Elevation Acute Coronary Syndrome (ACS) Plaque Fissure or Rupture Pathogenesis of Acute Coronary
Syndromes: The integral role of platelets Platelet Adhesion Platelet Activation Platelet Aggregation Thrombotic Occlusion Antiplatelet Therapy in ACS Act by inhibiting different platelet functions (aggregation, release of granule contents, platelet-mediated vascular constriction) Aspirin: blocks cyclooxygenase which mediates the first step in the biosynthesis of prostaglandins and thromboxanes from arachidonic acid P2Y12 receptor blockers:clopidogrel, ticlopidine, prasugrel, ticagrelor all block the binding of ADP
to P2Y12R-->inhibits activation of the GP IIb/IIIa complex and platelet aggregation GP IIb/IIIa inhibitors:inhibit the final common pathway of platelet aggregation (cross-bridging of platelets by fibrinogen) 20 2 0 Region of vascular injury llag Co vW F en ? Anti-vWF ? Anti-GpIb AA
TSI PGH2 TXA2 E pi ADP Fibrinogen TXA2 receptor antagonist AD P UF heparin LMWH Thrombin inhibitors Aspirin 2
TXA Th rom bin Gp Ib GPIIb/IIIa thienopyridine GpIIB/IIIA inhibitors Fibrin GPIIb/IIIa Awtry EH, Loscalzo J 2003 Aspirin
The Antithrombotic Trialists' Collaboration Aspirin (75-1500 mg daily) in 200,000 patients Antiplatelet therapy produced a significant 46% reduction in the combined end point of subsequent nonfatal myocardial infarction (MI), nonfatal stroke, or vascular death (8.0 vs 13.3%) in patients with unstable angina Textwith acute myocardial infarction 30 percent reduction in patients (10.4 vs 14.2 %) No significant difference in efficacy between lower and higher daily doses (75 to 325 versus 500 to 1500 mg)
The addition of a second antiplatelet agent (eg, dipyridamole, ticlopidine, or intravenous glycoprotein IIb/IIIa inhibitor) significantly lowered the combined end point Antithrombotic Trialists' Collaboration. BMJ 2002; 324:71. 2 2 Treatment of Unstable Angina Results of a study from the Montreal Heart Institute In multiple studies aspirin significantly reduces risk of: % Developing MI 12
10 8 - subsequent MI 6 - cardiac death 4 2 0 - overall mortality placebo aspirin Theroux P, et al. N Engl J Med. 1988;319:1105-1111. (>50% reduction)
Aspirin Class I 1. 160-325mg should be given on day one and continued indefinitely (may be decreased to 81mg daily after the acute event if no PCI, or after PCI). Class IIb 1. Other antiplatelet agents such as clopidogrel (300-600 mg po loading dose, then 75 mg QD) or prasugrel may be substituted if true aspirin allergy is present.Circulation. 2007;116:e148 e304. P2Y12 Receptor Blockers CURE trial: randomly assigned 12,562 patients who presented within 24 hours after the onset of a NSTEMI to aspirin alone (75 to 325 mg/day) or with clopidogrel (300 mg loading dose followed by 75 mg/day) for 9 to 12 months
High risk patients : electrocardiogram (ECG) changes elevated cardiac enzymes 60 % did not receive revascularization Primary endpoint: cardiovascular death, myocardial infarction, or stroke At an average follow-up of nine months, combination therapy led to a significant reduction in the combined primary endpoint (9.3 vs 11.4%), largely due to fewer MIs (5.2 vs 6.7%) Clopidogrel increased the rate of major bleeding (3.7 vs 2.7 %) but not in life-threatening bleeding or hemorrhagic stroke 2 5 Yusuf S, et al. N Engl J Med. 2001;345:494-502. CURE: Primary Composite End Point (CV Death/MI/Stroke) Placebo + Aspirin % With Event 14
9 12 Follow-up (months) Yusuf S, et al. N Engl J Med. 2001;345:494-502. CURE Bleeding Complications Data from Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345:494-502. ACC/AHA Recommendations Antiplatelet Therapy for NSTE-ACS Class I Clopidogrel if ASA-allergic or intolerant Clopidogrel in addition to ASA if early invasive approach not planned (for 112 months) Clopidogrel in addition to ASA, if invasive approach is planned Clopidogrel should be withheld for 5-7 days if CABG planned Circulation. 2007;116:e148
68/655=10.4% Oler A, et al. JAMA. 1996;276:811-815. Anticoagulants Unfractionated Heparin (UFH) Most widely used antithrombotic agent Disadvantages include: Poor bioavailability No inhibition of clot-bound thrombin Dependent on antithrombin III (ATIII) cofactor Variable effects Frequent monitoring (aPTT) to ensure therapeutic levels Rebound ischemia after discontinuation Risk of heparin-induced thrombocytopenia (HIT) Anticoagulants Low-MolecularWeight Heparin (LMWH) Fraction of standard (UFH) heparin 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 Enoxaparin, dalteparin, reviparin, nadroparin, fraxiparin, others Differ in anti-Xa/anti-IIa ratios UFH vs LMWH ESSENCE Death, MI or Recurrent Angina 25% Unfractionated Heparin16.7% Enoxaparin (Lovenox) 16 20% 12
15% P = 0.02 Risk Reduction 16.2% 10% 14.2% 8 p = 0.03 Relative Risk Reduction = 15% 4 5% 0 20 Death, MI or Urgent Revascularization Unfractionated Heparin
Enoxaparin (Lovenox) 30% TIMI 11B 5 9 13 17 21 25 29 Days After Randomization Cohen M, et al. N Engl J Med. 1997;337:447-452. 0 2 4
6 8 Days 10 12 14 Antman EM, et al. Circulation. 1999;100:1593-1601. Guidelines for the Use of Enoxaparin in Patients with NSTE-ACS 1 mg/kg SQ q12 hours (actual body weight) An initial 30 mg IV dose can be considered Adjust dosing if CrCl <30 cc/min 1 mg/kg SQ q24 hours Do not follow PTT; do not adjust based on PTT Stop if platelets by 50% or below 100,000/mm3 If patient to undergo PCI: 0-8 hours since last SQ dose: no additional antithrombin therapy 8-12 hours since last SQ dose: 0.3 mg/kg IV during PCI
Low Molecular Weight Heparin in ACS Effects on Triple Endpoints Day FRIC (dalteparin; n=1482) 6 FRAXIS (nadroparin; n=2357) 14 ESSENCE (enoxaparin; n=3171) (p=0.032) 14 TIMI 11 B (enoxaparin; n=3910) (p=0.029) 14
Number of Risk Factors 6/7 Antman et al JAMA 284: 835, 2000 ACC/AHA Recommendations for Antithrombin Therapy in Patients with NSTE-ACS Class I: Anticoagulation should be added to antiplatelet therapy as soon as possible after recognition of ACS If early invasive strategy: may use UFH (60-70 U/kg to max 5000 IV followed by infusion of 12-15 U/kg/hr (initial max 1000 U/hr) titrated to aPTT 1.5-2.5 times control), enoxaparin (1 mg/kg subcutaneously q12 hr) If conservative strategy: may use UFH, enoxaparin, or fondaparinux Class IIa Enoxaparin or fondaparinux is preferable to UFH as an anticoagulant unless CABG is planned within 24
hours Circulation. 2007;116:e148 e304. ACC/AHA Recommendations for Antithrombin Therapy in Patients with NSTE-ACS Class I: Anticoagulation should be added to antiplatelet therapy as soon as possible after recognition of ACS If early invasive strategy: may use UFH (60-70 U/kg to max 5000 IV followed by infusion of 12-15 U/kg/hr ** Unfractionated heparin preferred in (initial max 1000 U/hr) titrated to aPTT 1.5-2.5 times patients
with creatinine > subcutaneously 2.0 (Cr clearance control), enoxaparin (1 mg/kg q12 hr), or direct inhibitors or <30)thrombin or weight >120(bivalirudin kg fondiparinux) If conservative strategy: may use UFH, enoxaparin, or fondaparinux Class IIa Enoxaparin or fondaparinux is preferable to UFH as an anticoagulant unless CABG is planned within 24 hours Circulation. 2007;116:e148
e304. IIb/IIIa Inhibitors in ACS PURSUIT PRISM PRISM PLUS Theroux PARAGON B PARAGON A COMBINED 1998 (n = 23,967) 0.88 (0.79-0.97) 0.25 0.50 1.0 2.0 Odds Ratio for 30-day Death or MI Relative to Control
4.0 ACC/AHA Recommendations Antiplatelet Therapy for NSTE-ACS Class I Clopidogrel OR GP IIb/IIIa inhibitor, in addition to ASA, if invasive approach is planned Class IIa GP IIb/IIIa inhibitor in patients with high-risk features if invasive strategy not planned GP IIb/IIIa inhibitor in patients receiving clopidogrel if cardiac cath and PCI planned Class IIb GP IIb/IIIa inhibitor in patients without high-risk features and PCI not planned Available at: www.acc.org/clinical/guidelines/unstable/unstable.pdf. GP IIb/IIIa Dosing and Administration for Up-Front Therapy in Patients with NSTE-ACS Dosing: Integrilin: 180 mcg/kg bolus (over 1-2 min), then 2 mcg/kg/min
continuous infusion Aggrastat: Initial 0.4 mcg/kg/min for 30 min, then continuous infusion at 0.1 mcg/kg/min Always also treat with ASA and some form of heparin (UFH or LMWH) Patients most commonly treated 2-4 days Follow platelet count qD and D/C for significant fall Adjust doses for renal insufficiency: Integrilin: For creatinine 2-4 mg/dL, decrease infusion to 1 mcg/kg/min; avoid if creatinine >4 mg/dL Aggrastat: For CrCl < 30 mL/min, cut all doses in 1/2 Contraindications to GP IIb/IIIa Rx Active or recent bleeding (4-6 weeks) Severe hypertension (SBP >180-200 mm Hg; DBP >110 mm Hg) Any hemorrhagic CVA (+/- intracranial neoplasm, AVM, or aneurysm) Any CVA within 30 days2 years Major surgery or trauma within 4-6 weeks Thrombocytopenia ( <100,000/mm3 ) Bleeding diathesis/warfarin with elevated INR
IIb/IIIa Inhibitors in ACS PURSUIT PRISM PRISM PLUS Theroux PARAGON B PARAGON A COMBINED 1998 (n = 23,967) ACUITY Timing 0.88 (0.79-0.97) EARLY ACS EARLY ACS + ACUITY 0.92 (0.82-1.01) COMBINED 2009 (n = 42,666) 0.89 (0.84-0.95)
0.25 0.50 1.0 2.0 Odds Ratio for 30-day Death or MI Relative to Control 4.0 Early ACS - Conclusions Among high-risk NSTE ACS patients, a strategy of routine, early eptifibatide compared with delayed, provisional eptifibatide at PCI did not significantly reduce the primary composite of death, MI; resulted in a trend toward reduction in death or MI at 30 days, but no difference in 30-day mortality; resulted in higher rates of non-life-threatening bleeding and transfusions The results of EARLY ACS do not support a strategy of routine early eptifibatide use in high-risk NSTE
ACS patients managed with an invasive strategy NEJM on line March 30, 2009 How Best to Risk Stratify Patients with ACS? Risk Stratification Based on validated risk prediction models that include the most important predictors of outcomes Certain patients that are such high risk that they need not be risk stratified: cardiogenic shock overt CHF or LV dysfunction Rest angina despite max medical therapy Hemodynamic instability, mechanical complications Unstable ventricular arrythmias 43 4 5 TIMI Risk Score for UA/NSTEMI
Age >65 years 3 or more CAD risk factors HTN, DM, Hyperlipidemia, smoking, + family hx Prior CAD (cath stenosis>50%) ASA in last 7 days 2 or more anginal events in last 24 hours ST deviation on admission ECG Elevated cardiac markers (troponin/CK-MB) Antman EM, et al. JAMA.. 2000;284:835-842. 14 day Death, MI, or Urgent Revascularization (%) The TIMI Risk Score and Incidence of Adverse Ischemic Events in
2 3 4 5 # of Risk Factors 6/7 Antman EM, et al. JAMA.. 2000;284:835842. Download at: http://www.timi.org/ TIMI Risk Score for UA/NSTEMI Higher TIMI risk scores correlated with more severe angiographic disease
PRISM-PLUS: Increasing TIMI risk scores from 0-2 (low risk) to 5-7 (high risk) were associated with increases in the frequency of high-risk angiographic findings: >70 % culprit stenosis (from 58 to 81%) multivessel disease (43 to 80%) visible thrombus (30 to 41%) left main disease The TIMI risk score can also identify patients most likely to benefit from particular therapies: In TACTICS-TIMI 18, only patients with score 3 benefited from early invasive strategy The degree of troponin elevation and magnitude of ST segment deviation were independent predictors of an adverse outcome and of benefit from an early invasive strategy In TIMI 11B and ESSENCE, enoxaparin was associated with better 14-day and six-week post-discharge outcomes compared to UFH; these benefits were primarily seen in high-risk patients with risk scores 4 and 5, respectively GRACE Risk Calculator Estimates the risk of in-hospital and six-month mortality among all patients with an ACS This end point is different from the composite end point in the TIMI risk score of all-cause mortality,
new or recurrent MI, or severe recurrent ischemia requiring revascularization While the GRACE prediction model is well validated and its use is recommended by multiple guideline organizations, its complexity makes it somewhat difficult to use in some clinical settings 47 4 9 GRACE Risk Calculator 6 month mortality after ACS Eagle et al. JAMA 2004;291:2727 GRACE Risk Calculator 6 month mortality after ACS 55 14 32%
14 11 3 15 112 4% Eagle et al. JAMA 2004;291:272733. Download at: http://www.outcomes-umassmed.org/grace Prognostic Value of Troponin T or I in ACS: A Meta-Analysis Neg Pos (Trop I + T) 25 RR 3.8 (2.6-5.5) 20.8 20 15
RR 3.9 % (2.9-5.3) 10 5 6.4 6.7 1.9 0 Death Death/MI Heidenreich PA, et al. JACC. 2001;38:478-485.
Troponin I Levels and Mortality in Patients with NSTE-ACS % Mortality at 42 Days 8 6 4 2 0 0<0.4 0.4<1.0 1.0<2.0 2.0<5.0 Troponin I Level 5.0<9.0
>9.0 Adapted with permission from Antman EA, Tanasijevic MJ, Thompson B, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med. 1996;335:1342-1349. Copyright 1996, Massachusetts Medical Society. All rights reserved. B-type Natriuretic Peptide (BNP) and Mortality in ACS Patients Quartile 4 (n=630) 10 Mortality (%) >138 pg/ml P<.001 8 6
250 300 Days After Randomization Lemos JA,, et al. N Engl J Med. 2001;345:1014-1021. Predictive Value of hs-CRP for Mortality from ACS in FRISC Substudy CRP >10mg/l (n=309) Cumulative Probability of Death (%) 20 CRP 2-10mg/l (n=294) 10
Lindahl B, et al.. N Engl J Med. 2000;343:1139-1147. Therapeutic Approaches Invasive vs Conservative Invasive vs Conservative Strategy for UA/NSTEMI 2003 VANQWISH ISARCOOL RITA-3 MATE VINO TIMI IIIB
TRUCS TACTICSTIMI 18 FRISC II Conservative Invasive UA indicates unstable angina, NSTEMI, nonST-segment myocardial infarction; ISAR, Intracoronary Stenting and Antithrombic Regimen Trial; RITA, Randomized Intervention Treatment of Angina; VANQWISH, Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital study; MATE, Medicine vs Angioplasty for Thrombolytic Exclusions trial; TACTICS-TIMI18, Treat Angina with Aggrastat and Determine Cost of Therapy with Invasive or Conservative Strategy; and FRISC, Fragmin during InStability in Coronary artery disease. Slide reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org. TACTICS TIMI 18 Patients (%) 20%
19.4% Initial Medical Rx 16% 15.9% 12% Early Cath + PTCA 8% 4% 1 2 3 4 Months 5
6 Cumulative Incidence of the Primary Endpoint of Death, Nonfatal MI, rehospitalization for an ACS within 6 months Cannon CP, et al. N Engl J Med. 2001;344:1879-1887. TACTICS Trial Results Based on Troponin Initial Medical Rx Early Cath + PTCA P<0.001 25% 20% P=NS 15% 10% 5% Negative Troponin
Positive Troponin Cannon CP, et al. N Engl J Med. 2001;344:1879-1887. Benefit of Invasive Strategy by Troponin and ST Changes Death, MI, or Rehospitalization for ACS at 6 Months 30 CV Events (%) 25 Conservative Invasive P=NS P<.001 30 25.0*
10 10 5 5 0 0 TnT P=NS TnT + No ST change ST change Morrow DA, et al. JAMA. 2001;286:2405-2412 and Cannon CP, et al. N Engl J Med. 2001;344:1879-1887.
The Primary Composite Ischemic End Point in RITA-3 Fox KA, Poole-Wilson PA, Henderson RA, et al. Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Lancet. 2002;360:743-751. Meta-Analysis of Trials of Early Cardiac Cath and Revascularization Versus Initial Medical Therapy Alone in Patients with NSTE-ACS Fox KA, Poole-Wilson PA, Henderson RA, et al. Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Lancet. 2002;360:743-751. TACTICS-TIMI18: Rates of Death, Nonfatal MI, or Rehospitalization for an ACS at Six Months, According to Base-Line Characteristics Cannon C et al. N Engl J Med 2001;344:1879- Early Invasive Therapy:
Class I Recommendations Recurrent angina despite rx* Elevated cardiac markers* New ST-segment depression* Positive stress test* the absence of any theMR above high-risk InSymptoms of ischemic CHF,ofrales, indicators, EF < 40% either an early conservative or an early invasive strategy is appropriate Sustained VT Hypotension/hemodynamic instability PCI within 6 mos, prior CABG High risk score (TIMI, GRACE) Circulation. 2007;116:e148 e304. Patient Up Date
Treated with aspirin, clopidogrel, heparin Beta-blocker titrated to resting HR ~ 60-70 bpm High dose statin given Cardiac catheterization performed. Cath PCI What About After Discharge? Secondary Prevention - Risk Factor Modification
Smoking Cessation Achieve optimal weight Increase physical activity level, cardiac rehab AHA diet HTN control to BP <130/85 mm Hg Statin with goal LDL< 70 Tight glycemic control in diabetics ** Consider referral to cardiac rehab program Circulation. 2007;116:e148 e304. Long-Term Medical Therapy: Class I Indications Aspirin 81 mg/day Clopidogrel 75 mg QD when ASA intolerant Combination ASA and clopidogrel/ticagrelor/prasugrel for 12 months after UA/NSTEMI/STEMI, 1 month BMS and 12 months DES Beta-blocker Lipid-lowering and diet (if LDL>100)
ACE Inhibitor if CHF, LV EF < 40%, HTN, DM NTG prn with clear instructions on use Circulation. 2007;116:e148 Guideline Compliance and Outcomes Tricoci P Et al. Am J Cardiol 2006;98:S30-S35. Summary Thrombosis is central in the pathophysiology of ACS and mandates antithrombotic and antiplatelet therapy All patients with ACS should be treated with aspirin and heparin. Consider treatment with Clopidogrel in patients who will be treated conservatively or those likely to undergo PCI Use of the TIMI risk score helps identify those patients that benefit from invasive therapies Improved adherence to guidelines results in improved outcomes
Recommended Strategy in ACS: Boston Medical Center Guidelines UA/ NSTEMI Aspirin Nitrates Beta-blockers UFH/LMWH ? Clopidogrel High Risk Elevated Troponin Recurrent Ischemia Dynamic EKG changes TIMI score > 3 Coronary Angiography PCI/CABG Low Risk Normal Troponin on
admission and at 12 h TIMI score <2 Stress Test Pre-dc
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