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on Jan 23, 2012 Says :
There is a correction guys pn slide number 30. The dividing line has to be one point down....i.e Reduced LV function is an indication for early invasive strategy.
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Slide 1 :
Unstable Angina and Non-ST Elevation Myocardial Infarction By Jaspreet Singh
Slide 2 :
Objective Definition, Pathophysiology Risk and Risk Stratification Initial Therapies and Management Platelets and Anti-Platelet Therapies Initial Invasive Strategy vs Initial Conservative strategy At Discharge Medications and Management
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Definition And Pathophysiology
Slide 4 :
Definition Unstable Angina is defined as angina pectoris with at least one of three features: (1) Occurring at rest (or minimal exertion) and usually lasting >20 minutes (if not interrupted) (2) Being severe and usually described as frank pain (3) Occurring with a crescendo pattern (pain that is more severe, prolonged, or frequent than previously)
Slide 5 :
Approximately 66 % of patients with unstable angina have evidence of myocardial necrosis on the basis of elevated cardiac serum markers (Trop I and CK-MB) and hence making a diagnosis of NSTEMI.
Slide 6 :
Pathophysiology Six pathophysiologic processes contribute to the development of UA/NSTEMI : Plaque rupture or erosion with superimposed non- occlusive thrombus (MC) Dynamic obstruction of the Coronary vasculature Severe coronary luminal narrowing caused by progressive coronary atherosclerosis or post PCI restenosis Inflammation of the coronary arteries Secondary UA ,that is, severe myocardial ischemia related to increased myocardial oxygen demand or decreased oxygen supply Coronary Artery Dissection
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Thrombus Superimposed on Atherosclerotic Plaque
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Characteristics of Unstable and Stable Plaque Thin fibrous cap Inflammatory cells Few SMCs Eroded endothelium Activated macrophages Thick fibrous cap Lack of inflammatory cells Foam cells Intact endothelium More SMCs Unstable Stable
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Plaque Rupture, Thrombosis, and Microembolization Culprit plaque Platelet-thrombin micro-emboli Plaque rupture Process Plaque formation Inflammation Multiple factors ? Infection Plaque Rupture ? Macrophages Metalloproteinases Thrombosis Platelet Activation Thrombin Markers Cholesterol LDL Hs-CRP , Adhesion Molecules Interleukin 6, TNFa, sCD-40 ligand MDA Modified LDL D-dimer, Complement, Fibrinogen, Troponin, CRP, CD40L Vulnerable plaque Macrophages Foam Cells Collagen ? platelet activation TF ? Clotting Cascade Lipid core Metalloproteinases Inflammation Courtesy of David Kandzari.
Slide 12 :
Risk and Risk Stratification
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Braunwald’s Classification of Risk for patients with NSTE-ACS
Slide 14 :
Slide 15 :
TIMI Risk Score Age >65 years >3 CAD Risk Factors Prior Coronary Stenosis >50 % ST deviation >2 Anginal events <24 hours ASA in last 7 days Elevated Cardiac Markers (CK-MB or troponin)
Slide 16 :
The TIMI Risk Score and Incidence of Adverse Ischemic Events in Patients with NSTE-ACS 4.7 8.3 13.2 19.9 26.2 40.9 0 10 20 30 40 50 0/1 2 3 4 5 6/7 Number of Risk Factors Death, MI, or Urgent Revascularization (%)
Slide 17 :
Troponin I Levels and Mortality in Patients with NSTE-ACS 0 2 4 6 8 0- <0.4 0.4- <1.0 1.0- <2.0 2.0- <5.0 5.0- <9.0 >9.0 % Mortality at 42 Days Troponin I Level
Slide 18 :
Initial Therapies and Management
Slide 19 :
SYMPTOMS SUGGESTIVE OF ACS Noncardiac Diagnosis Chronic Stable Angina Possible ACS Definite ACS Treatment as indicated by alternative diagnosis ACC/AHA Chronic Stable Angina Guidelines No ST-Elevation ST-Elevation Nondiagnostic ECG Normal initial serum cardiac biomarkers ST and/or T wave changes Ongoing pain Positive cardiac biomarkers Hemodynamic abnormalities Evaluate for reperfusion therapy ACC/AHA STEMI Guidelines Observe = 12 h from symptom onset No recurrent pain; negative follow-up studies Recurrent ischemic pain or positive follow-up studies Diagnosis of ACS confirmed Stress study to provoke ischemia Consider evaluation of LV function if ischemia is present (tests may be performed either prior to discharge or as outpatient) Negative Potential diagnoses: nonischemic discomfort; low-risk ACS Arrangements for outpatient follow-up Positive Diagnosis of ACS confirmed or highly likely Admit to hospital Manage via acute ischemia pathway Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.
Slide 20 :
Acute Ischemic Pathway
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Slide 22 :
ACC/AHA Class I Recommendations for Initial Management and Anti-Ischemic Therapy Bed/Chair Rest Continuous ECG Monitoring Supplemental O2 if SaO2 <90% Nitroglycerine (IV or PO as indicated clinically) Beta-blockers (PO) when hemodynamically Stable CCB’s If Beta-blockers Contraindicated Ace Inhibitors in the presence of LV Dysfunction
Slide 23 :
Platelets and Antiplatelet Therapy
Slide 24 :
Pathogenesis of Acute Coronary Syndromes: The integral role of platelets Plaque Fissure or Rupture Platelet Aggregation Platelet Activation Platelet Adhesion Thrombotic Occlusion
Slide 25 :
Adhesion The Role of Platelets in Atherothrombosis Aggregation 3 Reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org. 1 Activation 2
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Slide 27 :
Platelet Inhibition With GP IIb/IIIa Inhibitors Reproduced with permission from Yeghiazarians Y, Braunstein JB, Askari A, et al. Unstable angina pectoris. N Engl J Med. 2000;342:101-114. Copyright © 2000, Massachusetts Medical Society. All rights reserved.
Slide 28 :
Aspirin (Loading dose followed by daily maintenance dose) should be given as soon as possible Clopidogrel (Loading dose 300mg and followed by daily maintenance dose of 75 mg) Glycoprotein IIb IIIa inhibitors have been shown to reduce mortality if PCI is indicated ? Upstream GP IIb IIIa inhibitors in patients selected for invasive strategy is reasonable to use.
Slide 29 :
Initial Invasive v/s conservative strategy
Slide 30 :
Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy
Slide 31 :
Initial Invasive Strategy
Slide 32 :
Diagnosis of UA/NSTEMI is Likely or Definite ASA (Class I, LOE: A) Clopidogrel if ASA intolerant (Class I, LOE: B) Select Management Strategy Initial Conservative Strategy or Unknown Invasive Strategy† Initiate anticoagulant therapy (Class I, LOE: A) Acceptable options include • Enoxaparin or UFH (Class I, LOE: A) • Fondaparinux (Class I, LOE: B)* • Enoxaparin or fondaparinux preferred over UFH (Class IIa, LOE: B) Initiate clopidogrel (Class I, LOE: B) Initiate anticoagulant therapy (Class I, LOE: A)* Acceptable options include • Enoxaparin or UFH (Class I, LOE: A) • Bivalirudin (Class I, LOE: B) CABG: Maintenance ASA (Class I, LOE: A) Medical Therapy: D/C GP IIb/IIIa inhibitors if begun and give clopidogrel per conservative strategy Precatheterization: Add second antiplatelet agent (Class I, LOE: A)‡ • Clopidogrel (Class I, LOE: B) or • GP IIb/IIIa inhibitor (Class I, LOE: A) • (IV eptifibatide or tirofiban preferred) Next step per triage decision at angiography PCI: Class I: • Clopidogrel (if not begun precatheterization) (LOE: A) or • Prasugrel (LOE: B) or • Selectively, a GP IIb/IIIa inhibitor (if not begun precatheterization) (LOE: A) Wright RS, et al. J Am Coll Cardiol. 2011;57(19):1920-59. Revised 2011 *If fondaparinux is used with an invasive strategy (Class I, LOE: B), it must be coadministered with another anticoagulant with Factor IIa activity, i.e., UFH.) †Timing of invasive strategy generally is assumed to be 4 to 48 hours. If immediate angiography is selected, see STEMI guidelines. ‡Precatheterization triple antiplatelet therapy (ASA, clopidogrel, GP inhibitors) is a Class IIb, LOE: B rec for selected high-risk patients.
Slide 33 :
Initial Invasive Strategy: Anticoagulant Therapy Anticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI patients as soon as possible after presentation. 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.
Slide 34 :
Initial Conservative Strategy: Antiplatelet Therapy 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 aspirin and anticoagulant therapy as soon as possible after admission and administered for at least 1 month and ideally up to 1 year.
Slide 35 :
Slide 36 :
Aspirin Clopidogrel Nitrates Beta Blockers Statins Ace Inhibitors if LV Dysfunction , Diabetes Mellitus , Hypertension present CCB’s if Beta Blockers Contraindicated or anti anginal effect not delivered by maximal anti-ischemic treatment.
Slide 37 :
Long-Term Antithrombotic Therapy at Hospital Discharge after UA/NSTEMI Medical Therapy without Stent Bare Metal Stent Group Drug Eluting Stent Group aspirin 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? aspirin 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) aspirin 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
Slide 38 :
Pathophysiology of C...
Unstable Angina and ...
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