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ACC/AHA GUIDELINE REVISION

ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction—Executive Summary

A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction) Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine

Jeffrey L. Anderson, MD, FACC, FAHA, Chair, Wrting Committee Member, Cynthia D. Adams, RN, PhD, FAHA, Elliott M. Antman, MD, FACC, FAHA, Charles R. Bridges, ScD, MD, FACC, FAHA^_*, Robert M. Califf, MD, MACC, Donald E. Casey, Jr, MD, MPH, MBA, FACP, William E. Chavey, II, MD, MS, Francis M. Fesmire, MD, FACEP, Judith S. Hochman, MD, FACC, FAHA, Thomas N. Levin, MD, FACC, FSCAI^||, A. Michael Lincoff, MD, FACC, Eric D. Peterson, MD, MPH, FACC, FAHA, Pierre Theroux, MD, FACC, FAHA, Nanette Kass Wenger, MD, FACC, FAHA, R. Scott Wright, MD, FACC, FAHA, Sidney C. Smith, Jr, MD, FACC, FAHA, Chair, Task Force Member, Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair, Cynthia D. Adams, RN, PhD, FAHA, Jeffrey L. Anderson, MD, FACC, FAHA, Elliot M. Antman, MD, FACC, FAHA^¶, Jonathan L. Halperin, MD, FACC, FAHA, Sharon A. Hunt, MD, FACC, FAHA, Harlan M. Krumholz, MD, FACC, FAHA, Frederick G. Kushner, MD, FACC, FAHA, Bruce W. Lytle, MD, FACC, FAHA, Rick Nishimura, MD, FACC, FAHA, Joseph P. Ornato, MD, FACC, FAHA^**, Richard L. Page, MD, FACC, FAHA and Barbara Riegel, DNSc, RN, FAHA

	Table of contents

Top Table of contents Preamble I. Introduction Recommendations II. Overview of the... III. Initial Evaluation and... IV. Early Hospital Care V. Coronary Revascularization VI. Late Hospital Care,... VII. Special Groups Appendix 1. Relationships With... Appendix 2. Relationships With... References

Preamble......654

I Introduction......655

A Organization of Committee and Evidence Review......655

B Changes Since Publication of These Guidelines in 2002......655

1 Purpose of These Guidelines......657

C Recommendations for Management of Patients With UA/NSTEMI......657

1 Identification of Patients at Risk of UA/NSTEMI......657

2 Initial Evaluation and Management......657

a Clinical Assessment......657

b Early Risk Stratification......658

c Immediate Management......658

3 Early Hospital Care......659

a Anti-Ischemic and Analgesic Therapy......659

b Antiplatelet/Anticoagulant Therapy in Patients for Whom Diagnosis of UA/NSTEMI Is Likely or Definite......660

c Initial Conservative Versus Initial Invasive Strategies......662

d Risk Stratification Before Discharge......662

4 Revascularization With PCI and CABG in Patients With UA/NSTEMI......663

a Percutaneous Coronary Intervention......663

b CABG......663

5 Late Hospital Care, Hospital Discharge, and Post-Hospital Discharge Care......664

a Medical Regimen and Use of Medications......664

b Long-Term Medical Therapy and Secondary Prevention......664

c Postdischarge Follow-Up......667

d Cardiac Rehabilitation......668

6 Special Groups......668

a Women......668

b Diabetes Mellitus......668

c Post-CABG Patients......668

d Older Adults......668

e Chronic Kidney Disease......669

f Cocaine and Methamphetamine Users......669

g Variant (Prinzmetal's) Angina......669

h Cardiovascular "Syndrome X"......669

II Overview of the Acute Coronary Syndromes......669

A Definition of Terms......669

B Pathogenesis of UA/NSTEMI......670

C Presentations of UA and NSTEMI......670

D Prevention of UA/NSTEMI......670

E Onset of UA/NSTEMI......670

1 Recognition of Symptoms by Patient......670

2 Silent and Unrecognized Events......670

III Initial Evaluation and Management......671

A Clinical Assessment......671

1 Patient Transportation and ED or Outpatient Facility Evaluation......671

B Early Risk Stratification......672

1 Estimation of the Level of Risk......672

2 History......672

3 Tools to Estimate Risk at Presentation......673

4 Electrocardiogram......673

5 Physical Examination......673

6 Noncardiac Causes of Symptoms and Secondary Causes of Myocardial Ischemia......674

7 Cardiac Biomarkers of Necrosis and the Redefinition of AMI......675

a Creatine Kinase-MB......676

b Cardiac Troponins......676

c Myoglobin......676

d Clinical Use......676

8 Other Markers and Multimarker Approaches......677

C Immediate Management......677

1 Chest Pain Units......677

IV Early Hospital Care......678

A Anti-Ischemic and Analgesic Therapy......678

1 General Care......678

2 Use of Anti-Ischemic Therapies......678

a Nitrates......678

b Morphine Sulfate......678

c Beta-Adrenergic Blockers......679

d Calcium Channel Blockers......679

e Inhibitors of the Renin-Angiotensin-Aldosterone System......679

f Intra-Aortic Balloon Counterpulsation......679

g Analgesic Therapy......679

B Antiplatelet/Anticoagulant Therapy in Patients With Likely or Definite UA/NSTEMI......679

1 Antiplatelet Therapy (Aspirin, Ticlopidine, Clopidogrel)......680

a Aspirin......680

b Adenosine Diphosphate Receptor Antagonists and Other Antiplatelet Agents......681

2 Anticoagulants......686

a Unfractionated Heparin......686

b Low-Molecular-Weight Heparin......686

c Direct Thrombin Inhibitors......689

d Factor Xa Inhibitors......690

e Long-Term Anticoagulation......691

3 Platelet GP IIb/IIIa Receptor Antagonists......691

C Initial Conservative Versus Initial Invasive Strategies......694

1 General Principles and Care Objectives......694

2 Rationale for the Conservative Strategy......695

3 Rationale for the Invasive Strategy......695

4 Comparison of Invasive and Conservative Strategies......695

a Subgroups......697

5 Risk Stratification Before Discharge......697

a General Principles and Care Objectives......697

b Noninvasive Test Selection......697

c Selection for Coronary Angiography......697

V Coronary Revascularization......698

A General Principles and Care Objectives......698

1 Platelet Inhibitors and PCI......699

B Surgical Revascularization......699

VI Late Hospital Care, Hospital Discharge, and Post-Hospital Discharge Care......699

A General Principles and Care Objectives......699

1 Long-Term Medical Therapy......700

B Postdischarge Risk Assessment and Follow-Up......700

C Risk Factor Modification......700

D Physical Activity......700

E Cardiac Rehabilitation......701

F Return to Work and Disability......701

G Other Activities......701

H Patient Records and Other Information Systems......701

VII Special Groups......701

A Women......701

1 Profile of UA/NSTEMI in Women......701

2 Stress Testing......701

3 Management......702

a Pharmacological Therapy......702

b Coronary Artery Revascularization......702

c Initial Invasive Versus Initial Conservative Strategy......702

B Diabetes Mellitus......702

1 Profile and Initial Management of Diabetic and Hyperglycemic Patients With UA/NSTEMI......702

2 Coronary Revascularization......702

C Post-CABG Patients......703

1 Pathological Findings......703

2 Clinical Findings and Approach......703

D Older Adults......703

1 Pharmacological Management......703

2 Functional Studies......704

3 Contemporary Revascularization Strategies in Older Patients......704

E Chronic Kidney Disease......704

F Cocaine and Methamphetamine Users......704

1 Pathophysiology and Presentation......704

2 Treatment......704

3 Methamphetamine Use and UA/NSTEMI......705

G Variant (Prinzmetal's) Angina......705

1 Clinical Picture, Pathogenesis, and Diagnosis......705

2 Treatment and Prognosis......705

H Cardiovascular "Syndrome X"......705

1 Definition and Clinical Picture......705

2 Treatment......705

Appendix 1......706

Appendix 2......711

References......716

	Preamble

Top Table of contents Preamble I. Introduction Recommendations II. Overview of the... III. Initial Evaluation and... IV. Early Hospital Care V. Coronary Revascularization VI. Late Hospital Care,... VII. Special Groups Appendix 1. Relationships With... Appendix 2. Relationships With... References

 
It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced and tested in the detection, management, or prevention of disease states. Rigorous and expert analysis of the available data documenting absolute and relative benefits and risks of those procedures and therapies can produce helpful guidelines that improve the effectiveness of care, optimize patient outcomes, and favorably affect the overall cost of care by focusing resources on the most effective strategies.

The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly engaged in the production of such guidelines in the area of cardiovascular disease since 1980. The American College of Cardiology (ACC)/AHA Task Force on Practice Guidelines, whose charge is to develop, update, or revise practice guidelines for important cardiovascular diseases and procedures, directs this effort. Writing committees are charged with the task of performing an assessment of the evidence and acting as an independent group of authors to develop, update, or revise written recommendations for clinical practice.

Experts in the subject under consideration have been selected from both organizations to examine subject-specific data and write guidelines. The process includes additional representatives from other medical practitioner and specialty groups when appropriate. Writing committees are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities and issues of patient preference that might influence the choice of particular tests or therapies are considered as well as frequency of follow-up and cost-effectiveness. When available, information from studies on cost will be considered; however, review of data on efficacy and clinical outcomes will constitute the primary basis for preparing recommendations in these guidelines.

The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflict of interest that may arise as a result of an industry relationship or personal interest of the Writing Committee. Specifically, all members of the Writing Committee, as well as peer reviewers of the document, were asked to provide disclosure statements of all such relationships that may be perceived as real or potential conflicts of interest. Writing Committee members are also strongly encouraged to declare a previous relationship with industry that might be perceived as relevant to guideline development. If a Writing Committee member develops a new relationship with industry during their tenure, they are required to notify guideline staff in writing. The continued participation of the Writing Committee member will be reviewed. These statements are reviewed by the parent task force, reported orally to all members of the Writing Committee at each meeting, and updated and reviewed by the Writing Committee as changes occur. Please refer to the methodology manual for ACC/AHA Guideline Writing Committees for further description of the relationships with industry policy, available on ACC and AHA World Wide Web sites (http://www.acc.org/clinical/manual/manual_introltr.htm and http://circ.ahajournals.org/manual/). Please see Appendix 1 for author relationships with industry and Appendix 2 for peer reviewer relationships with industry that are pertinent to these guidelines.

These practice guidelines are intended to assist health care providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management and prevention of specific diseases or conditions. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. These guidelines attempt to define practices that meet the needs of most patients in most circumstances. These guideline recommendations reflect a consensus of expert opinion after a thorough review of the available, current scientific evidence and are intended to improve patient care.

Patient adherence to prescribed and agreed upon medical regimens and lifestyles is an important aspect of treatment. Prescribed courses of treatment in accordance with these recommendations will only be effective if they are followed. Since lack of patient understanding and adherence may adversely affect treatment outcomes, physicians and other health care providers should make every effort to engage the patient in active participation with prescribed medical regimens and lifestyles.

If these guidelines are used as the basis for regulatory/payer decisions, the ultimate goal is quality of care and serving the patient's best interests. The ultimate judgment regarding care of a particular patient must be made by the health care provider and the patient in light of all of the circumstances presented by that patient. There are circumstances in which deviations from these guidelines are appropriate.

The guidelines will be reviewed annually by the ACC/AHA Task Force on Practice Guidelines and will be considered current unless they are updated, revised, or sunsetted and withdrawn from distribution. The executive summary and recommendations are published in the August 14, 2007, issue of the Journal of the American College of Cardiology and the August 14, 2007, issue of Circulation. The full-text guidelines are e-published in the same issue of the journals noted above, as well as posted on the ACC (www.acc.org) and AHA (www.americanheart.org) World Wide Web sites. Copies of the full text and the executive summary are available from both organizations.

Sidney C. Smith, Jr., MD, FACC, FAHAChair, ACC/AHA Task Force on Practice Guidelines

	I. Introduction

Top Table of contents Preamble I. Introduction Recommendations II. Overview of the... III. Initial Evaluation and... IV. Early Hospital Care V. Coronary Revascularization VI. Late Hospital Care,... VII. Special Groups Appendix 1. Relationships With... Appendix 2. Relationships With... References

 
A. Organization of Committee and Evidence Review.   The ACC/AHA Task Force on Practice Guidelines was formed to make recommendations regarding the diagnosis and treatment of patients with known or suspected cardiovascular disease. Coronary artery disease (CAD) is the leading cause of death in the United States. Unstable angina (UA) and the closely related condition of non–ST-segment elevation myocardial infarction (NSTEMI) are very common manifestations of this disease.

The committee members reviewed and compiled published reports through a series of computerized literature searches of the English-language literature since 2002 and a final manual search of selected articles. Details of the specific searches conducted for particular sections are provided when appropriate. Detailed evidence tables were developed whenever necessary with the specific criteria outlined in the individual sections. The recommendations made were based primarily on these published data. The weight of the evidence was ranked highest (A) to lowest (C). The final recommendations for indications for a diagnostic procedure, a particular therapy, or an intervention in patients with UA/NSTEMI summarize both clinical evidence and expert opinion.

Classification of Recommendations
The schema for classification of recommendations and level of evidence is summarized in Table 1, which also illustrates how the grading system provides an estimate of the size of the treatment effect and an estimate of the certainty of the treatment effect.

View this table: [in this window] [in a new window]   Table 1 Applying Classification of Recommendations and Level of Evidence

B. Changes Since Publication of These Guidelines in 2002.   The writing committee considered evidence published since 2002 and drafted revised recommendations to incorporate results from major clinical trials. The text has been reorganized and rewritten to reflect these developments. Greater emphasis is placed on earlier access to medical evaluation of the acute coronary syndrome (ACS) patient, including avoidance of delays inherent in patient self-medication, as well as facilitated emergency department (ED) diagnosis and triage. New imaging tests (cardiac magnetic resonance imaging and coronary computed tomographic [CT] angiography) have emerged as diagnostic options in selected patients. Troponins have become the dominant cardiac biomarker of necrosis, have redefined NSTEMI, and have changed its demographics and prognosis. B-type natriuretic peptide (BNP) now may be added to the list of biomarkers that are potentially useful in risk assessment. Clinical trials data continue to build support for an initial invasive strategy for higher-risk UA/NSTEMI patients (as assessed by troponin positivity or a formal risk score); in contrast, such a strategy is not of benefit and may be harmful in low-risk women, in whom an initially conservative strategy is recommended. Two new anticoagulants, fondaparinux and bivalirudin, have undergone favorable testing in clinical trials and are recommended as alternatives to unfractionated heparin (UFH) and low-molecular-weight heparins (LMWHs) for specific or more general applications. Support for thienopyridine use (primarily with clopidogrel) continues to grow, including higher loading-dose options, earlier (upstream) administration, and longer administration (especially after drug-eluting stent placement). The question of how best to integrate thienopyridine use with parenteral glycoprotein (GP) IIb/IIIa antagonists to provide optimal antiplatelet therapy early in the course of UA/NSTEMI therapy, including cardiac catheterization, is an evolving subject and continues to present a challenge. These guidelines incorporate changes based on recent updates for percutaneous coronary intervention (PCI) and for secondary prevention as they impact patients with UA/NSTEMI. An expanded section on special patient groups recognizes the need to highlight specific diagnostic and therapeutic considerations in patients with diverse characteristics. Care processes are highlighted as another area important to patient outcomes. These and other developments and advances also highlight important knowledge and treatment gaps, which should stimulate continued progress in UA/NSTEMI through research and clinical application.

1. Purpose of These Guidelines
These guidelines address the diagnosis and management of patients with UA and the closely related condition of NSTEMI. These potentially life-threatening disorders are a major cause of emergency medical care and hospitalization in the United States. In 2004, the National Center for Health Statistics reported 1,565,000 hospitalizations for primary or secondary diagnosis of an ACS, 669,000 for UA and 896,000 for myocardial infarction (MI) (1). These guidelines are intended to assist both cardiovascular specialists and nonspecialists in the proper evaluation and management of patients with an acute onset of symptoms suggestive of these conditions. These clinical practice guidelines also provide recommendations and supporting evidence for the continued management of patients with these conditions in both inpatient and outpatient settings.

C. Recommendations for Management of Patients With UA/NSTEMI.   Classification of recommendations and level of evidence are expressed in the ACC/AHA format as described above and in Table 1. Recommendations are evidence-based and derived primarily from published data. The reader is referred to the full-text guidelines for a complete description of the rationale and evidence supporting these recommendations.

	Recommendations

Top Table of contents Preamble I. Introduction Recommendations II. Overview of the... III. Initial Evaluation and... IV. Early Hospital Care V. Coronary Revascularization VI. Late Hospital Care,... VII. Special Groups Appendix 1. Relationships With... Appendix 2. Relationships With... References

 
1. Identification of Patients at Risk of UA/NSTEMI.   Class I

1 Primary care providers should evaluate the presence and status of control of major risk factors for coronary heart disease (CHD) for all patients at regular intervals (approximately every 3 to 5 years). (Level of Evidence: C)

2 Ten-year risk (National Cholesterol Education Program global risk) of developing symptomatic CHD should be calculated for all patients who have 2 or more major risk factors to assess the need for primary prevention strategies (2,3). (Level of Evidence: B)

3 Patients with established CHD should be identified for secondary prevention efforts, and patients with a CHD risk equivalent (e.g., atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or 10-year risk greater than 20% as calculated by Framingham equations) should receive equally intensive risk factor intervention as those with clinically apparent CHD. (Level of Evidence: A)

2. Initial Evaluation and Management.   a. Clinical Assessment
Class I

1 Patients with symptoms that may represent ACS (Table 2) should not be evaluated solely over the telephone but should be referred to a facility that allows evaluation by a physician and the recording of a 12-lead ECG and biomarker determination (e.g., an ED or other acute care facility). (Level of Evidence: C)

2 Patients with symptoms of ACS (chest discomfort with or without radiation to the arm[s], back, neck, jaw, or epigastrium; shortness of breath; weakness; diaphoresis; nausea; lightheadedness) should be instructed to call 9-1-1 and should be transported to the hospital by ambulance rather than by friends or relatives. (Level of Evidence: B)

3 Health care providers should actively address the following issues regarding ACS with patients with or at risk for CHD and their families or other responsible caregivers:

a The patient's heart attack risk; (Level of Evidence: C)

b How to recognize symptoms of ACS; (Level of Evidence: C)

c The advisability of calling 9-1-1 if symptoms are unimproved or worsening after 5 min, despite feelings of uncertainty about the symptoms and fear of potential embarrassment; (Level of Evidence: C)

d A plan for appropriate recognition and response to a potential acute cardiac event, including the phone number to access emergency medical services (EMS), generally 9-1-1 (4). (Level of Evidence: C)

4 Prehospital EMS providers should administer 162 to 325 mg of aspirin (ASA; chewed) to chest pain patients suspected of having ACS unless contraindicated or already taken by the patient. Although some trials have used enteric-coated ASA for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations. (Level of Evidence: C)

5 Health care providers should instruct patients with suspected ACS for whom nitroglycerin (NTG) has been prescribed previously to take not more than 1 dose of NTG sublingually in response to chest discomfort/pain. If chest discomfort/pain is unimproved or is worsening 5 min after 1 NTG dose has been taken, it is recommended that the patient or family member/friend/caregiver call 9-1-1 immediately to access EMS before taking additional NTG. In patients with chronic stable angina, if symptoms are significantly improved by 1 dose of NTG, it is appropriate to instruct the patient or family member/friend/caregiver to repeat NTG every 5 min for a maximum of 3 doses and call 9-1-1 if symptoms have not resolved completely. (Level of Evidence: C)

6 Patients with a suspected ACS with chest discomfort or other ischemic symptoms at rest for greater than 20 min, hemodynamic instability, or recent syncope or presyncope should be referred immediately to an ED. Other patients with a suspected ACS who are experiencing less severe symptoms and who have none of the above high-risk features, including those who respond to an NTG dose, may be seen initially in an ED or an outpatient facility able to provide an acute evaluation. (Level of Evidence: C)

1 It is reasonable for health care providers and 9-1-1 dispatchers to advise patients without a history of ASA allergy who have symptoms of ACS to chew ASA (162 to 325 mg) while awaiting arrival of prehospital EMS providers. Although some trials have used enteric-coated ASA for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations. (Level of Evidence: B)

2 It is reasonable for health care providers and 9-1-1 dispatchers to advise patients who tolerate NTG to repeat NTG every 5 min for a maximum of 3 doses while awaiting ambulance arrival. (Level of Evidence: C)

3 It is reasonable that all prehospital EMS providers perform and evaluate 12-lead electrocardiograms (ECGs) in the field (if available) on chest pain patients suspected of ACS to assist in triage decisions. Electrocardiographs with validated computer-generated interpretation algorithms are recommended for this purpose. (Level of Evidence: B)

4 If the 12-lead ECG shows evidence of acute injury or ischemia, it is reasonable that prehospital ACLS providers relay the ECG to a predetermined medical control facility and/or receiving hospital. (Level of Evidence: B)

b. Early Risk Stratification
Class I

1 A rapid clinical determination of the likelihood risk of obstructive CAD (i.e., high, intermediate, or low) should be made in all patients with chest discomfort or other symptoms suggestive of an ACS and considered in patient management. (Level of Evidence: C)

2 Patients who present with chest discomfort or other ischemic symptoms should undergo early risk stratification for the risk of cardiovascular events (e.g., death or [re]MI) that focuses on history, including anginal symptoms, physical findings, ECG findings, and biomarkers of cardiac injury and results should be considered in patient management. (Level of Evidence: C)

3 A 12-lead ECG should be performed and shown to an experienced emergency physician as soon as possible after ED arrival, with a goal of within 10 min of ED arrival for all patients with chest discomfort (or anginal equivalent) or other symptoms suggestive of ACS. (Level of Evidence: B)

4 If the initial ECG is not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs, initially at 15- to 30-min intervals, should be performed to detect the potential for development of ST-segment elevation or depression. (Level of Evidence: B)

5 Cardiac biomarkers should be measured in all patients who present with chest discomfort consistent with ACS. (Level of Evidence: B)

6 A cardiac-specific troponin is the preferred marker, and if available, it should be measured in all patients who present with chest discomfort consistent with ACS. (Level of Evidence: B)

7 Patients with negative cardiac biomarkers within 6 h of the onset of symptoms consistent with ACS should have biomarkers remeasured in the time frame of 8 to 12 h after symptom onset. (The exact timing of serum marker measurement should take into account the uncertainties often present with the exact timing of onset of pain and the sensitivity, precision, and institutional norms of the assay being utilized as well as the release kinetics of the marker being measured.) (Level of Evidence: B)

8 The initial evaluation of the patient with suspected ACS should include the consideration of noncoronary causes for the development of unexplained symptoms. (Level of Evidence: C)

Class IIa

1 Use of risk-stratification models, such as the Thrombolysis In Myocardial Infarction (TIMI) or Global Registry of Acute Coronary Events (GRACE) risk score or the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) risk model, can be useful to assist in decision making with regard to treatment options in patients with suspected ACS. (Level of Evidence: B)

2 It is reasonable to remeasure positive biomarkers at 6- to 8-h intervals 2 to 3 times or until levels have peaked, as an index of infarct size and dynamics of necrosis. (Level of Evidence: B)

3 It is reasonable to obtain supplemental ECG leads V₇ through V₉ in patients whose initial ECG is nondiagnostic to rule out MI due to left circumflex occlusion. (Level of Evidence: B)

4 Continuous 12-lead ECG monitoring is a reasonable alternative to serial 12-lead recordings in patients whose initial ECG is nondiagnostic. (Level of Evidence: B)

Class IIb

1 For patients who present within 6 h of the onset of symptoms consistent with ACS, assessment of an early marker of cardiac injury (e.g., myoglobin) in conjunction with a late marker (e.g., troponin) may be considered. (Level of Evidence: B)

2 For patients who present within 6 h of symptoms suggestive of ACS, a 2-h delta CK-MB mass in conjunction with 2-h delta troponin may be considered. (Level of Evidence: B)

3 For patients who present within 6 h of symptoms suggestive of ACS, myoglobin in conjunction with CK-MB mass or troponin when measured at baseline and 90 min may be considered. (Level of Evidence: B)

4 Measurement of BNP or NT-pro-BNP may be considered to supplement assessment of global risk in patients with suspected ACS. (Level of Evidence: B)

Class III
Total CK (without MB), aspartate aminotransferase (AST, SGOT), alanine transaminase, beta-hydroxybutyric dehydrogenase, and/or lactate dehydrogenase should not be utilized as primary tests for the detection of myocardial injury in patients with chest discomfort suggestive of ACS. (Level of Evidence: C)

c. Immediate Management
Class I

1 The history, physical examination, 12-lead ECG, and initial cardiac biomarker tests should be integrated to assign patients with chest pain into 1 of 4 categories: a noncardiac diagnosis, chronic stable angina, possible ACS, and definite ACS. (Level of Evidence: C)

2 Patients with probable or possible ACS but whose initial 12-lead ECG and cardiac biomarker levels are normal should be observed in a facility with cardiac monitoring (e.g., chest pain unit or hospital telemetry ward), and repeat ECG (or continuous 12-lead ECG monitoring) and repeat cardiac biomarker measurement(s) should be obtained at predetermined, specified time intervals (see Section III.B). (Level of Evidence: B)

3 In patients with suspected ACS in whom ischemic heart disease is present or suspected, if the follow-up 12-lead ECG and cardiac biomarkers measurements are normal, a stress test (exercise or pharmacological) to provoke ischemia should be performed in the ED, in a chest pain unit, or on an outpatient basis in a timely fashion (within 72 h) as an alternative to inpatient admission. Low-risk patients with a negative diagnostic test can be managed as outpatients. (Level of Evidence: C)

4 In low-risk patients who are referred for outpatient stress testing (see above), precautionary appropriate pharmacotherapy (e.g., ASA, sublingual NTG, and/or beta blockers) should be given while awaiting results of the stress test. (Level of Evidence: C)

5 Patients with definite ACS and ongoing ischemic symptoms, positive cardiac biomarkers, new ST-segment deviations, new deep T-wave inversions, hemodynamic abnormalities, or a positive stress test should be admitted to the hospital for further management. Admission to the critical care unit is recommended for those with active, ongoing ischemia/injury and hemodynamic or electrical instability. Otherwise, a telemetry step-down unit is reasonable. (Level of Evidence: C)

6 Patients with possible ACS and negative cardiac biomarkers who are unable to exercise or who have an abnormal resting ECG should undergo a pharmacological stress test. (Level of Evidence: B)

7 Patients with definite ACS and ST-segment elevation in leads V₇ to V₉ due to left circumflex should be evaluated for immediate reperfusion therapy. (Level of Evidence: A)

8 Patients discharged from the ED or chest pain unit should be given specific instructions for activity, medications, additional testing, and follow-up with a personal physician. (Level of Evidence: C)

Class IIa
In patients with suspected ACS with a low or intermediate probability of CAD, in whom the follow-up 12-lead ECG and cardiac biomarker measurements are normal, performance of a noninvasive coronary imaging test (i.e., coronary CT angiography) is reasonable as an alternative to stress testing. (Level of Evidence: B)

3. Early Hospital Care
   a. Anti-Ischemic and Analgesic Therapy
   Class I

1 Bed/chair rest with continuous ECG monitoring is recommended for all UA/NSTEMI patients during the early hospital phase. (Level of Evidence: C)

2 Supplemental oxygen should be administered to patients with UA/NSTEMI with an arterial saturation less than 90%, respiratory distress, or other high-risk features for hypoxemia. (Pulse oximetry is useful for continuous measurement of SaO₂.) (Level of Evidence: B)

3 Patients with UA/NSTEMI with ongoing ischemic discomfort should receive sublingual NTG (0. 4 mg) every 5 min for a total of 3 doses, after which assessment should be made about the need for intravenous NTG, if not contraindicated. (Level of Evidence: C)

4 Intravenous NTG is indicated in the first 48 h after UA/NSTEMI for treatment of persistent ischemia, heart failure (HF), or hypertension. The decision to administer intravenous NTG and the dose used should not preclude therapy with other proven mortality-reducing interventions such as beta blockers or angiotensin-converting enzyme (ACE) inhibitors. (Level of Evidence: B)

5 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). (Level of Evidence: B)

6 In UA/NSTEMI patients with continuing or frequently recurring ischemia and in whom beta blockers are contraindicated, a nondihydropyridine calcium channel blocker (e.g., verapamil or diltiazem) should be given as initial therapy in the absence of clinically significant left ventricular (LV) dysfunction or other contraindications. (Level of Evidence: B)

7 An ACE inhibitor should be administered orally within the first 24 h to UA/NSTEMI patients with pulmonary congestion or LV ejection fraction (LVEF) less than or equal to 0.40, in the absence of hypotension (systolic blood pressure less than 100 mm Hg or less than 30 mm Hg below baseline) or known contraindications to that class of medications. (Level of Evidence: A)

8 An angiotensin receptor blocker should be administered to UA/NSTEMI patients who are intolerant of ACE inhibitors and have either clinical or radiological signs of HF or LVEF less than or equal to 0.40. (Level of Evidence: A)

9 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. (Level of Evidence: C)

   Class IIa

1 It is reasonable to administer supplemental oxygen to all patients with UA/NSTEMI during the first 6 h after presentation. (Level of Evidence: C)

2 In the absence of contradictions to its use, it is reasonable to administer morphine sulfate intravenously to UA/NSTEMI patients if there is uncontrolled ischemic chest discomfort despite NTG, provided that additional therapy is used to manage the underlying ischemia. (Level of Evidence: B)

3 It is reasonable to administer intravenous (IV) 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). (Level of Evidence: B)

4 Oral long-acting nondihydropyridine calcium antagonists are reasonable for use in UA/NSTEMI patients for recurrent ischemia in the absence of contraindications after beta blockers and nitrates have been fully used. (Level of Evidence: C)

5 An ACE inhibitor administered orally within the first 24 h of UA/NSTEMI can be useful in patients without pulmonary congestion or LVEF less than or equal to 0.40 in the absence of hypotension (systolic blood pressure less than 100 mm Hg or less than 30 mm Hg below baseline) or known contraindications to that class of medications. (Level of Evidence: B)

6 Intra-aortic balloon pump counterpulsation is reasonable in UA/NSTEMI patients for severe ischemia that is continuing or recurs frequently despite intensive medical therapy, for hemodynamic instability in patients before or after coronary angiography, and for mechanical complications of MI. (Level of Evidence: C)

   Class IIb

1 The use of extended-release forms of nondihydropyridine calcium antagonists instead of a beta blocker may be considered in patients with UA/NSTEMI. (Level of Evidence: B)

2 Immediate-release dihydropyridine calcium antagonists in the presence of adequate beta blockade may be considered in patients with UA/NSTEMI with ongoing ischemic symptoms or hypertension. (Level of Evidence: B)

   Class III

1 Nitrates should not be administered to UA/NSTEMI patients with systolic blood pressure less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, severe bradycardia (less than 50 beats per min), tachycardia (more than 100 beats per min) in the absence of symptomatic HF, or right ventricular infarction. (Level of Evidence: C)

2 Nitroglycerin or other nitrates should not be administered to patients with UA/NSTEMI who had received a phosphodiesterase inhibitor for erectile dysfunction within 24 h of sildenafil or 48 h of tadalafil use. The suitable time for the administration of nitrates after vardenafil has not been determined. (Level of Evidence: C)

3 Immediate-release dihydropyridine calcium antagonists should not be administered to patients with UA/NSTEMI in the absence of a beta blocker. (Level of Evidence: A)

4 An intravenous ACE inhibitor should not be given to patients within the first 24 h of UA/NSTEMI because of the increased risk of hypotension. (A possible exception may be patients with refractory hypertension.) (Level of Evidence: B)

5 It may be harmful to administer IV 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. (Level of Evidence: A)

6 Nonsteroidal anti-inflammatory drugs (except for ASA), whether nonselective or COX-2--selective agents, should not be administered during hospitalization for UA/NSTEMI because of the increased risks of mortality, reinfarction, hypertension, HF, and myocardial rupture associated with their use. (Level of Evidence: C)

   b. Antiplatelet/Anticoagulant Therapy in Patients for Whom Diagnosis of UA/NSTEMI Is Likely or Definite
Recommendations are written as the reader follows through the algorithm for Antiplatelet/Anticoagulant Therapy and Triage for Angiography (Figs. 6, 7, and 8). Letters after recommendations refer to the specific box in the algorithm. See Table 6 for dosing recommendations.

View larger version (31K): [in this window] [in a new window] [Download PPT slide]   Figure 6 Algorithm for Patients With UA/NSTEMI Managed by an Initial Invasive Strategy When multiple drugs are listed, they are in alphabetical order and not in order of preference (e.g., Boxes B, B1, and B2).*See dosing Table 6. See Table 5 for selection of management strategy. Evidence exists that GP IIb/IIIa inhibitors may not be necessary if the patient received a preloading dose of at least 300 mg of clopidogrel at least 6 h earlier (Class I, Level of Evidence B for clopidogrel administration) and bivalirudin is selected as the anticoagulant (Class IIa, Level of Evidence B). ASA = aspirin; GP = glycoprotein; IV = intravenous; LOE = level of evidence; UA/NSTEMI= unstable angina/non–ST-elevation myocardial infarction; UFH = unfractionated heparin.

1 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. (Level of Evidence: A) (Figs. 6 and 7; Box A)

2 Clopidogrel (loading dose 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. (Level of Evidence: A) (Figs. 6 and 7; Box A)

3 In UA/NSTEMI patients with a history of gastrointestinal bleeding, when ASA and clopidogrel are administered alone or in combination, drugs to minimize the risk of recurrent gastrointestinal bleeding (e.g., proton-pump inhibitors) should be prescribed concomitantly. (Level of Evidence: B)

4 For UA/NSTEMI patients in whom an initial invasive strategy is selected, antiplatelet therapy in addition to aspirin should be initiated before diagnostic angiography (upstream) with either clopidogrel (loading dose followed by daily maintenance dose) or an IV GP IIb/IIIa inhibitor. (Level of Evidence: A) 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. (Level of Evidence: B)

5 For UA/NSTEMI patients in whom an initial conservative (i.e., noninvasive) strategy is selected (see Section IV.C), 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) (Fig. 7; Box C2)

6 For UA/NSTEMI patients in whom an initial conservative strategy is selected, if recurrent symptoms/ischemia, HF, or serious arrhythmias subsequently appear, then diagnostic angiography should be performed (Level of Evidence: A) (Fig. 7; Box D). Either an IV GP IIb/IIIa inhibitor (eptifibatide or tirofiban; Level of Evidence: A) or clopidogrel (loading dose followed by daily maintenance dose; Level of Evidence: A) should be added to ASA and anticoagulant therapy before diagnostic angiography (upstream). (Level of Evidence: C)

View larger version (43K): [in this window] [in a new window] [Download PPT slide]   Figure 7 Algorithm for Patients With UA/NSTEMI Managed by an Initial Conservative Strategy When multiple drugs are listed, they are in alphabetical order and not in order of preference (e.g., Boxes C1, and C2). *See dosing Table 6. See Table 5 for selection of management strategy. Recurrent symptoms/ischemia, heart failure, serious arrhythmia. ASA = aspirin; EF = ejection fraction; GP = glycoprotein; IV = intravenous; LOE = level of evidence; LVEF = left ventricular ejection fraction; UA/NSTEMI = unstable angina/non–ST-elevation myocardial infarction; UFH = unfractionated heparin.

1 For UA/NSTEMI patients in whom an initial conservative strategy is selected and who have recurrent ischemic discomfort with clopidogrel, ASA, and anticoagulant therapy, it is reasonable to add a GP IIb/IIIa antagonist before diagnostic angiography. (Level of Evidence: C)

2 For UA/NSTEMI patients in whom an initial invasive strategy is selected, it is reasonable to initiate antiplatelet therapy with both clopidogrel (loading dose followed by daily maintenance dose) and an IV GP IIb/IIIa inhibitor (Level of Evidence: B). 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. (Level of Evidence: B)

3 For UA/NSTEMI patients in whom an initial invasive strategy is selected, it is reasonable to omit upstream administration of an IV GP IIb/IIIa antagonist before diagnostic angiography if bivalirudin is selected as the anticoagulant and at least 300 mg of clopidogrel was administered at least 6 h earlier than planned catheterization or PCI. (Level of Evidence: B)

   Class IIb
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. (Level of Evidence: B) (Fig. 7; Box C2)

   Class III
Abciximab should not be administered to patients in whom PCI is not planned. (Level of Evidence: A)

   ii. Anticoagulant Therapy
Recommendations are written as the reader follows through the algorithm for Antiplatelet/Anticoagulant Therapy and Triage for Angiography (Figs. 6, 7, and 8). Letters after recommendations refer to the specific box in the algorithm. See Table 6 for dosing recommendations.

   Class I
Anticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI patients as soon as possible after presentation.

a For patients in whom an invasive strategy is selected, regimens with established efficacy at a Level of Evidence: A include enoxaparin and UFH (Fig. 6; Box B1), and those with established efficacy at a Level of Evidence: B include bivalirudin and fondaparinux (Fig. 7; Box B1).

b 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. (Fig. 8; Box C1)* See also Class IIa recommendation below.

c In patients in whom a conservative strategy is selected and who have an increased risk of bleeding, fondaparinux is preferable. (Level of Evidence: B) (Fig. 7; Box C1)

View larger version (35K): [in this window] [in a new window] [Download PPT slide]   Figure 8 Management After Diagnostic Angiography in Patients With UA/NSTEMI *See dosing Table 6. Evidence exists that GP IIb/IIIa inhibitors may not be necessary if the patient received a preloading dose of at least 300 mg of clopidogrel at least 6 h earlier (Class I, Level of Evidence B for clopidogrel administration) and bivalirudin is selected as the anticoagulant (Class IIa, Level of Evidence B). Additional bolus of UFH is recommended if fondaparinux is selected as the anticoagulant (see dosing Table 6). For patients in whom the clinician believes coronary atherosclerosis is present, albeit without any significant, flow-limiting stenoses, long-term treatment with antiplatelet agents and other secondary prevention measures should be considered. ASA = aspirin; CABG = coronary artery bypass graft; CAD = coronary artery disease; GP = glycoprotein; IV = intravenous; LD = loading dose; PCI = percutaneous coronary intervention; pre angio = before angiography; UA/NSTEMI = unstable angina/non–ST-elevation myocardial infarction; UFH = unfractionated heparin.

   iii. Additional Management Considerations for Antiplatelet and Anticoagulant Therapy
Recommendations are written as the reader follows through the algorithm for Antiplatelet/Anticoagulant Therapy and Triage for Angiography (Figs. 6, 7, and 8). Letters after recommendations refer to the specific box in the algorithm. See Table 6 for dosing recommendations.

   Class I

1 For UA/NSTEMI patients in whom an initial conservative strategy is selected and no subsequent features appear that would necessitate diagnostic angiography (recurrent symptoms/ischemia, HF, or serious arrhythmias), a stress test should be performed. (Level of Evidence: B) (Fig. 7; Box O)

a If, after stress testing, the patient is classified as not at low risk, diagnostic angiography should be performed. (Level of Evidence: A) (Fig. 7; Box E1)

b If, after stress testing, the patient is classified as being at low risk (Fig. 7; Box E2), the instructions noted below should be followed in preparation for discharge (Fig. 7; Box K) (Level of Evidence: A):

1 Continue ASA indefinitely. (Level of Evidence: A)

2 Continue clopidogrel for at least 1 month (Level of Evidence: A) and ideally up to 1 year. (Level of Evidence: B)

3 Discontinue IV GP IIb/IIIa inhibitor if started previously. (Level of Evidence: A)

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)

2 For UA/NSTEMI patients in whom CABG is selected as a postangiography management strategy, the instructions noted below should be followed (Fig. 8; Box G).

a Continue ASA. (Level of Evidence: A)

b Discontinue clopidogrel 5 to 7 d before elective CABG. (Level of Evidence: B) More urgent surgery, if necessary, may be performed by experienced surgeons if the incremental bleeding risk is considered acceptable. (Level of Evidence: C)

c Discontinue IV GP IIb/IIIa inhibitor (eptifibatide or tirofiban) 4 h before CABG. (Level of Evidence: B)

d Anticoagulant therapy should be managed as follows:

1 Continue UFH. (Level of Evidence: B)

2 Discontinue enoxaparin* 12 to 24 h before CABG and dose with UFH per institutional practice. (Level of Evidence: B)

3 Discontinue fondaparinux 24 h before CABG and dose with UFH per institutional practice. (Level of Evidence: B)

4 Discontinue bivalirudin 3 h before CABG and dose with UFH per institutional practice. (Level of Evidence: B)

3 For UA/NSTEMI patients in whom PCI has been selected as a postangiography management strategy, the instructions noted below should be followed (Fig. 8 C; Box H):

a Continue ASA. (Level of Evidence: A)

b Administer a loading dose of clopidogrel if not started before diagnostic angiography. (Level of Evidence: A)

c Administer an IV GP IIb/IIIa inhibitor (abciximab, eptifibatide, or tirofiban) if not started before diagnostic angiography for troponin-positive and other high-risk patients. (Level of Evidence: A) See Class IIa recommendation below if bivalirudin was selected as the anticoagulant.

d Discontinue anticoagulant therapy after PCI for uncomplicated cases. (Level of Evidence: B)

4 For UA/NSTEMI patients in whom medical therapy is selected as a postangiography management strategy and in whom no significant obstructive CAD on angiography was found, antiplatelet and anticoagulant therapy should be administered at the discretion of the clinician. (Level of Evidence: C) For patients in whom evidence of coronary atherosclerosis is present (e.g., luminal irregularities or intravascular ultrasound--demonstrated lesions), albeit without flow-limiting stenoses, long-term treatment with ASA and other secondary prevention measures should be prescribed. (Fig. 8; Box I) (Level of Evidence: C)

5 For UA/NSTEMI patients in whom medical therapy is selected as a postangiography management strategy and in whom CAD was found on angiography, the following approach is recommended (Fig. 8; Box J):

a Continue ASA. (Level of Evidence: A)

b Administer a loading dose of clopidogrel if not given before diagnostic angiography. (Level of Evidence: A)

c Discontinue IV GP IIb/IIIa inhibitor if started previously. (Level of Evidence: B)

d Anticoagulant therapy should be managed as follows:

1 Continue IV UFH for at least 48 h or until discharge if given before diagnostic angiography. (Level of Evidence: A)

2 Continue enoxaparin for duration of hospitalization, up to 8 d, if given before diagnostic angiography. (Level of Evidence: A)

3 Continue fondaparinux for duration of hospitalization, up to 8 d, if given before diagnostic angiography. (Level of Evidence: B)

4 Either discontinue bivalirudin or continue at a dose of 0.25 mg per kg per h for up to 72 h at the physician's discretion, if given before diagnostic angiography. (Level of Evidence: B)

6 For UA/NSTEMI patients in whom a conservative strategy is selected and who do not undergo angiography or stress testing, the instructions noted below should be followed (Fig. 7; Box K):

a Continue ASA indefinitely. (Level of Evidence: A)

b Continue clopidogrel for at least 1 month (Level of Evidence: A) and ideally up to 1 year. (Level of Evidence: B)

c Discontinue IV GP IIb/IIIa inhibitor it started previously. (Level of Evidence: A)

d 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)

7 For UA/NSTEMI patients in whom an initial conservative strategy is selected and in whom no subsequent features appear that would necessitate diagnostic angiography (recurrent symptoms/ischemia, HF, or serious arrhythmias), LVEF should be measured. (Level of Evidence: B) (Fig. 7; Box L)

Class IIa

1 For UA/NSTEMI patients in whom PCI is selected as a postangiography management strategy, it is reasonable to omit administration of an IV GP IIb/IIIa antagonist if bivalirudin was selected as the anticoagulant and at least 300 mg of clopidogrel was administered at least 6 h earlier. (Level of Evidence: B) (Fig. 8)

2 If LVEF is less than or equal to 0.40, it is reasonable to perform diagnostic angiography. (Level of Evidence: B) (Fig. 7; Box M)

3 If LVEF is greater than 0.40, it is reasonable to perform a stress test. (Level of Evidence: B) (Fig. 7; Box N)

Class IIb
For UA/NSTEMI patients in whom PCI is selected as a postangiography management strategy, it may be reasonable to omit an IV GP IIb/IIIa inhibitor if not started before diagnostic angiography for troponin-negative patients without other clinical or angiographic high-risk features. (Level of Evidence: C)

Class III
Intravenous fibrinolytic therapy is not indicated in patients without acute ST-segment elevation, a true posterior MI, or a presumed new left bundle-branch block. (Level of Evidence: A)

c. Initial Conservative Versus Initial Invasive Strategies
   Class I

1 An early invasive strategy (i.e., diagnostic angiography with intent to perform revascularization) is indicated in UA/NSTEMI patients who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures). (Level of Evidence: B)

2 An early invasive strategy (i.e., diagnostic angiography with intent to perform revascularization) is indicated in initially stabilized UA/NSTEMI patients (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events (see Table 5 and Sections III.B and IV.C.5). (Level of Evidence: A)

   Class IIb

1 In initially stabilized patients, an initially conservative (i.e. a selectively invasive) strategy may be considered as a treatment strategy for UA/NSTEMI patients (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events (see Table 5 and Sections III.B and IV.C.5) including those who are troponin positive. (Level of Evidence: B) The decision to implement an initial conservative (vs. initial invasive) strategy in these patients may be made by consider