Increased resources may be needed for reassessment, but it is anticipated that this could be performed at routine follow-up appointments with a cardiologist. Return to recommendations Rate and rhythm control for people presenting acutely Why the committee made the recommendation The committee agreed that the evidence was too limited in quality and quantity to be able to specify a preferred rate-control drug for acute atrial fibrillation. Although there was some evidence that amiodarone was better than digoxin for rate control, the committee had concerns about the quality of the evidence and the short timeframe used in 1 study, which it agreed could disadvantage digoxin. In addition, there was limited evidence available for morbidity and adverse events for this comparison and no evidence identified for other drug classes. The committee highlighted that the existing recommendations gave no guidance on acute atrial fibrillation with acute decompensated heart failure. Using their expertise and experience the committee agreed that advice on the use of beta-blockers and rate- limiting calcium-channel blockers should be included because they can lead to further deterioration in people with pulmonary oedema caused by heart failure. How the recommendation might affect practice The recommendations do not constitute a change in practice, and so are unlikely to have a resource impact. Return to recommendations Preventing postoperative atrial fibrillation Why the committee made the recommendations The committee noted that the most recent studies reviewed showed no benefit from statins in reducing atrial fibrillation after cardiothoracic surgery. This contrasted with analysis of the evidence overall, which showed a small but definite benefit from statins. The committee agreed that the evidence of no effect in the newer studies was important, because these studies were larger and of higher quality than the older studies included in the analysis.


The committee agreed that the evidence of no effect in the newer studies was important, because these studies were larger and of higher quality than the older studies included in the analysis. Although the newer studies suggested that statins did not affect the short-term risk of stroke, they did suggest a greater risk of mortality in the peri-operative period compared with placebo treatment or usual care. The committee agreed that although the additional risk of death was probably small, it was important, especially alongside the lack of convincing evidence of benefit. For these reasons, the committee decided that statins should not be given to prevent atrial fibrillation after cardiothoracic surgery. However, the committee wanted to highlight that statins have an important role in preventing cardiovascular events other than atrial fibrillation and that people already taking statins for other reasons should continue to do so. How the recommendations might affect practice The committee agreed that the recommendation would not constitute a change in practice, and that there would not be a resource impact on the NHS. Return to recommendations Managing atrial fibrillation after cardiothoracic surgery Why the committee made the recommendations The evidence on managing postoperative atrial fibrillation after cardiothoracic surgery in people without pre-existing atrial fibrillation was limited many of the studies reviewed were old and included small numbers of participants. There were few studies comparing drug classes, and the committee agreed that they could not recommend a particular class of drugs based on such limited evidence. One larger study comparing mixed rate control and rhythm control with a potassium-channel blocker (amiodarone) with or without rate control suggested little difference between the 2 groups.


One larger study comparing mixed rate control and rhythm control with a potassium-channel blocker (amiodarone) with or without rate control suggested little difference between the 2 groups. Based on this evidence and their experience, the committee decided that rhythm control could be considered but that the evidence no longer supported the stronger recommendation included in the 2014 guideline. The committee noted that postoperative atrial fibrillation often resolves naturally, meaning that rate control rather than rhythm control may be a suitable option for some people. Reducing the emphasis on rhythm-control strategies will allow rate-control strategies to be considered if appropriate for the person. The committee were also aware of the risk of adverse events if amiodarone, a rhythm control drug, is taken long-term. They highlighted that if a rhythm-control strategy is chosen, the need for rhythm control drugs should be reassessed at approximately 6 weeks, in line with current practice, and they should not be continued automatically for long periods of time. The committee agreed that 6 weeks is an appropriate time point to assess the person's recovery, including for example prosthetic valve function, and to check if sinus rhythm has been restored. The committee did not make a separate recommendation for people with pre-existing atrial fibrillation because of a lack of evidence. The committee noted that most people undergoing mitral valve surgery with pre-existing atrial fibrillation would undergo left atrial surgery to treat atrial fibrillation at the same time. How the recommendations might affect practice Rhythm control for the treatment of new-onset atrial fibrillation after cardiothoracic surgery is current practice and amiodarone is most commonly used. This can still be considered, but there may be a reduction in the use of rhythm control in this population and an increase in the use of rate-control drugs instead.


This can still be considered, but there may be a reduction in the use of rhythm control in this population and an increase in the use of rate-control drugs instead. Return to recommendations Stopping anticoagulation Why the committee made the recommendations There was limited evidence on whether to continue anticoagulation or to stop it and switch to aspirin after successful treatment of atrial fibrillation by catheter ablation. The committee agreed that the evidence was insufficient and that there was too much uncertainty in the results to make a recommendation based on the evidence. The committee therefore developed research recommendations on stopping anticoagulation after ablation and stopping anticoagulation after resolution of postoperative atrial fibrillation to encourage further research. The committee was concerned about the potential withdrawal of anticoagulation in people who had not had ablation or cardiac surgery for atrial fibrillation, but in whom sinus rhythm is now present and atrial fibrillation is no longer detectable. In particular, the committee noted that paroxysmal atrial fibrillation is not always detectable. Based on their experience, the committee made a consensus-based recommendation to ensure that decisions about stopping anticoagulation in this population are based on formal risk assessment of stroke and bleeding risks and patient preference. How the recommendations might affect practice The committee felt that the recommendation would not constitute a change in practice, and that there would not be a resource impact on the NHS. Return to recommendations Context Atrial fibrillation is the most common heart rhythm disorder (affecting approximately 2% of the adult population), and estimates suggest its prevalence is increasing. Atrial fibrillation causes palpitations and breathlessness in many people but it may be silent and undetected.


Atrial fibrillation causes palpitations and breathlessness in many people but it may be silent and undetected. If left untreated it is a significant risk factor for stroke and other morbidities: it is estimated that it is responsible for approximately 20% of all strokes and is associated with increased mortality. Men are more commonly affected than women and the prevalence increases with age and in underlying heart disease, diabetes, obesity and hypertension. Atrial fibrillation is typically detected as an irregular pulse or an irregular rhythm on an electrocardiogram (ECG). This may be an incidental finding or may arise while investigating symptoms suggestive of the disease. Because atrial fibrillation can be intermittent, detection and diagnosis may be challenging. The aim of treatment is to prevent complications, particularly stroke, and alleviate symptoms. Drug treatments include anticoagulants to reduce the risk of stroke and antiarrhythmics to restore or maintain the normal heart rhythm or to slow the heart rate in people who remain in atrial fibrillation. Non-pharmacological management includes electrical cardioversion, which may be used to 'shock' the heart back to its normal rhythm, and catheter or surgical ablation to create lesions to stop the triggers that cause atrial fibrillation. These procedures can markedly reduce the symptom burden when drug therapy is ineffective or not tolerated. This update focuses on areas of new evidence and changing practice since the 2014 NICE guideline. These include methods of identifying atrial fibrillation; assessing stroke and bleeding risk; antithrombotic agents; ablation strategies; preventing recurrence; and preventing and managing postoperative atrial fibrillation. This guideline update includes recommendations on these specific issues. The recommendations apply to adults (18 years or older) with atrial fibrillation, including paroxysmal (recurrent), persistent and permanent atrial fibrillation, and atrial flutter. They do not apply to people with congenital heart disease precipitating atrial fibrillation.


They do not apply to people with congenital heart disease precipitating atrial fibrillation. Finding more information and committee details To find NICE guidance on related topics, including guidance in development, see the NICE webpage on heart rhythm conditions. For full details of the evidence and the guideline committee's discussions, see the evidence reviews. You can also find information about how the guideline was developed, including details of the committee. NICE has produced tools and resources to help you put this guideline into practice. For general help and advice on putting our guidelines into practice, see resources to help you put NICE guidance into practice. Update information 30 June 2021: We further corrected recommendation 1.2.2 on using the ORBIT score to assess bleeding risk to reinstate the link to the previous calculation tool, which was amended in error on 10 June. The tool includes the full criteria, including options for reduced haemoglobin and reduced haematocrit which are available once the patient's sex has been selected. 10 June 2021: We amended recommendation 1.2.2 on using the ORBIT score to assess bleeding risk so that it links to a calculation tool that includes the full list of criteria, including reduced haemoglobin, reduced haematocrit and history of anaemia. We deleted a paragraph of text from the rationale and impact section for recommendation 1.8.3 that was included incorrectly. April 2021: We have reviewed the evidence and made new recommendations on diagnosis and assessment, assessment of stroke and bleeding risks, preventing stroke, rate and rhythm control, preventing recurrence, and preventing and managing postoperative atrial fibrillation. These recommendations are marked [2021]. Recommendations marked [2014] and [2006] last had an evidence review in 2014 and 2006 respectively.


Recommendations marked [2014] and [2006] last had an evidence review in 2014 and 2006 respectively. In some cases, minor changes have been made to the wording for clarity and to bring the language and style up to date, without changing the meaning. Minor changes since publication January 2022: Minor changes to redirect NICE Pathways links. October 2021: We added a link to NICE's shared decision making guideline in recommendation 1.4.2. Accreditation


Practice Guideline 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons WRITING COMMITTEE MEMBERS* Stephan D. Fihn, MD, MPH, Chair ; Julius M. Gardin, MD, Vice Chair* ; Jonathan Abrams, MD ; Kathleen Berra, MSN, ANP* ; James C. Blankenship, MD*\; Apostolos P. Dallas, MD* ; Pamela S. Douglas, MD* ; JoAnne M. Foody, MD* ; Thomas C. Gerber, MD, PhD ; Alan L. Hinderliter, MD ; Spencer B. King III, MD* ; Paul D. Kligfield, MD ; Harlan M. Krumholz, MD ; Raymond Y.K. Kwong, MD ; Michael J. Lim, MD*\; Jane A. Linderbaum, MS, CNP-BC ; Michael J. Mack, MD*#; Mark A. Munger, PharmD* ; Richard L. Prager, MD#; Joseph F. Sabik, MD***; Leslee J. Shaw, PhD* ; Joanna D. Sikkema, MSN, ANP-BC* ; Craig R. Smith, Jr, MD**; Sidney C. Smith, Jr, MD* ; John A. Spertus, MD, MPH* ; Sankey V. Williams, MD* The writing committee gratefully acknowledges the memory of James T. Dove, MD, who died during the development of this document but contributed immensely to our understanding of stable ischemic heart disease. *Writing committee members are required to recuse themselves from voting on sections to which their specific relationship could apply; see Appendix 1 for detailed information. ACP Representative. ACCF/AHA Representative. PCNA Representative. ||SCAI Representative. Critical care nursing expertise. #STS Representative. **AATS Representative. ACCF/AHA Task Force on Practice Guidelines Liaison. ACCF/AHA Task Force on Performance Measures Liaison. Former Task Force member during this writing effort.


ACCF/AHA Task Force on Performance Measures Liaison. Former Task Force member during this writing effort. This document was approved by the American College of Cardiology Foundation Board of Trustees, American Heart Association Science Advisory and Coordinating Committee, American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons in July 2012. The American Heart Association requests that this document be cited as follows: Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas P, Douglas PS, Foody JM, Gerber TC, Hinderliter AL, King SB III, Kligfield PD, Krumholz HM, Kwong RYK, Lim MJ, Linderbaum JA, Mack MJ, Munger MA, Prager RL, Sabik JF, Shaw LJ, Sikkema JD, Smith CR Jr, Smith SC Jr, Spertus JA, Williams SV. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2012;126:e354 e471. This article is copublished in the Journal of the American College of Cardiology and the Annals of Internal Medicine. Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.cardiosource.org) and the American Heart Association (my.americanheart.org). A copy of the document is available at http://smy.americanheart.org/statements by selecting either the By Topic link or the By Publication Date link. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com. Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://my.americanheart.org/statements and select the Policies and Development link.


For more on AHA statements and guidelines development, visit http://my.americanheart.org/statements and select the Policies and Development link. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/ Copyright-Permission-Guidelines_UCM_300404_Article.jsp. A link to the Copyright Permissions Request Form appears on the right side of the page. 2012 by the American College of Cardiology Foundation and the American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIR.0b013e318277d6a0 ACCF/AHA TASK FORCE MEMBERS Jeffrey L. Anderson, MD, FACC, FAHA, Chair; Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect; Alice K. Jacobs, MD, FACC, FAHA, Immediate Past Chair 2009 2011 ; Sidney C. Smith, Jr, MD, FACC, FAHA, Past Chair 2006 2008 ; Cynthia D. Adams, MSN, APRN-BC, FAHA ; Nancy M. Albert, PhD, CCNS, CCRN, FAHA; Ralph G. Brindis, MD, MPH, MACC; Christopher E. Buller, MD, FACC ; Mark A. Creager, MD, FACC, FAHA; David DeMets, PhD; Steven M. Ettinger, MD, FACC ; Robert A. Guyton, MD, FACC; Judith S. Hochman, MD, FACC, FAHA; Sharon Ann Hunt, MD, FACC, FAHA ; Richard J. Kovacs, MD, FACC, FAHA; Frederick G. Kushner, MD, FACC, FAHA ; Bruce W. Lytle, MD, FACC, FAHA ; Rick A. Nishimura, MD, FACC, FAHA ; E. Magnus Ohman, MD, FACC; Richard L. Page, MD, FACC, FAHA ; Barbara Riegel, DNSc, RN, FAHA ; William G. Stevenson, MD, FACC, FAHA; Lynn G. Tarkington, RN ; Clyde W. Yancy, MD, FACC, FAHA Table of Contents Preamble e357 1. Introduction e359 1.1. Methodology and Evidence Overview e359 1.2. Organization of the Writing Committee e360 1.3. Document Review and Approval e360 1.4. Scope of the Guideline e360 1.5. General Approach and Overlap With Other Guidelines or Statements e362 1.6. Magnitude of the Problem e363 1.7.


General Approach and Overlap With Other Guidelines or Statements e362 1.6. Magnitude of the Problem e363 1.7. Organization of the Guideline e364 1.8. Vital Importance of Involvement by an Informed Patient: Recommendation e364 2. Diagnosis of SIHD e367 2.1. Clinical Evaluation of Patients With Chest Pain e367 2.1.1. Clinical Evaluation in the Initial Diagnosis of SIHD in Patients With Chest Pain: Recommendations e367 2.1.2. History e367 2.1.3. Physical Examination e368 2.1.4. Electrocardiography e368 2.1.4.1. Resting Electrocardiography to Assess Risk: Recommendation e369 2.1.5. Differential Diagnosis e370 2.1.6. Developing the Probability Estimate e370 2.2. Noninvasive Testing for Diagnosis of IHD e371 2.2.1. Approach to the Selection of Diagnostic Tests to Diagnose SIHD e371 2.2.1.1. Assessing Diagnostic Test Characteristics e372 2.2.1.2. Safety and Other Considerations Potentially Affecting Test Selection e373 2.2.1.3. Exercise Versus Pharmacological Testing e374 2.2.1.4. Concomitant Diagnosis of SIHD and Assessment of Risk e374 2.2.1.5. Cost-Effectiveness e375 2.2.2. Stress Testing and Advanced Imaging for Initial Diagnosis in Patients With Suspected SIHD Who Require Noninvasive Testing: Recommendations e375 2.2.2.1. Able to Exercise e375 2.2.2.2. Unable to Exercise e376 2.2.2.3. Other e377 2.2.3. Diagnostic Accuracy of Nonimaging and Imaging Stress Testing for the Initial Diagnosis of Suspected SIHD e377 2.2.3.1. Exercise ECG e377 2.2.3.2. Exercise and Pharmacological Stress Echocardiography e377 2.2.3.3. Exercise and Pharmacological Stress Nuclear Myocardial Perfusion SPECT and Myocardial Perfusion PET e378 2.2.3.4. Pharmacological Stress CMR Wall Motion/Perfusion e378 2.2.3.5. Hybrid Imaging e378 2.2.4. Diagnostic Accuracy of Anatomic Testing for the Initial Diagnosis of SIHD e379 2.2.4.1. Coronary CT Angiography e379 2.2.4.2. CAC Scoring e379 2.2.4.3. CMR Angiography e379 3. Risk Assessment e380 3.1. Clinical Assessment e380 3.1.1. Prognosis of IHD for Death or Nonfatal MI: General Considerations e380 3.1.2. Risk Assessment Using Clinical Parameters e380 3.2. Advanced Testing: Resting and Stress Noninvasive Testing e381 3.2.1.


Risk Assessment Using Clinical Parameters e380 3.2. Advanced Testing: Resting and Stress Noninvasive Testing e381 3.2.1. Resting Imaging to Assess Cardiac Structure and Function: Recommendations e381 Fihn et al Stable Ischemic Heart Disease: Full Text e355 3.2.2. Stress Testing and Advanced Imaging in Patients With Known SIHD Who Require Noninvasive Testing for Risk Assessment: Recommendations e383 3.2.2.1. Risk Assessment in Patients Able to Exercise e383 3.2.2.2. Risk Assessment in Patients Unable to Exercise e383 3.2.2.3. Risk Assessment Regardless of Patients Ability to Exercise e384 3.2.2.4. Exercise ECG e385 3.2.2.5. Exercise Echocardiography and Exercise Nuclear MPI e385 3.2.2.6. Dobutamine Stress Echocardiography and Pharmacological Stress Nuclear MPI e386 3.2.2.7. Pharmacological Stress CMR Imaging e386 3.2.2.8. Special Patient Group: Risk Assessment in Patients Who Have an Uninterpretable ECG Because of LBBB or Ventricular Pacing e386 3.2.3. Prognostic Accuracy of Anatomic Testing to Assess Risk in Patients With Known CAD e387 3.2.3.1. Coronary CT Angiography e387 3.3. Coronary Angiography e387 3.3.1. Coronary Angiography as an Initial Testing Strategy to Assess Risk: Recommendations e387 3.3.2. Coronary Angiography to Assess Risk After Initial Workup With Noninvasive Testing: Recommendations e387 4. Treatment e389 4.1. Definition of Successful Treatment e389 4.2. General Approach to Therapy e390 4.2.1. Factors That Should Not Influence Treatment Decisions e392 4.2.2. Assessing Patients Quality of Life e393 4.3. Patient Education: Recommendations e393 4.4. Guideline-Directed Medical Therapy e395 4.4.1. Risk Factor Modification: Recommendations e395 4.4.1.1. Lipid Management e395 4.4.1.2. Blood Pressure Management e397 4.4.1.3. Diabetes Management e398 4.4.1.4. Physical Activity e399 4.4.1.5. Weight Management e400 4.4.1.6. Smoking Cessation Counseling e401 4.4.1.7. Management of Psychological Factors e401 4.4.1.8. Alcohol Consumption e402 4.4.1.9. Avoiding Exposure to Air Pollution e403 4.4.2. Additional Medical Therapy to Prevent MI and Death: Recommendations e403 4.4.2.1. Antiplatelet Therapy e403 4.4.2.2. Beta-Blocker Therapy e404 Aldosterone Blocker Therapy e405 4.4.2.4.


Antiplatelet Therapy e403 4.4.2.2. Beta-Blocker Therapy e404 Aldosterone Blocker Therapy e405 4.4.2.4. Influenza Vaccination e406 4.4.2.5. Additional Therapy to Reduce Risk of MI and Death e407 4.4.3. Medical Therapy for Relief of Symptoms e408 4.4.3.1. Use of Anti-ischemic Medications: Recommendations e408 4.4.4. Alternative Therapies for Relief of Symptoms in Patients With Refractory Angina: Recommendations e411 4.4.4.1. Enhanced External Counterpulsation e412 4.4.4.2. Spinal Cord Stimulation e412 4.4.4.3. Acupuncture e413 5. CAD Revascularization e413 5.1. Heart Team Approach to Revascularization Decisions: Recommendations e413 5.2. Revascularization to Improve Survival: Recommendations e416 5.3. Revascularization to Improve Symptoms: Recommendations e417 5.4. CABG Versus Contemporaneous Medical Therapy e417 5.5. PCI Versus Medical Therapy e417 5.6. CABG Versus PCI e418 5.6.1. CABG Versus Balloon Angioplasty or BMS e418 5.6.2. CABG Versus DES e418 5.7. Left Main CAD e419 5.7.1. CABG or PCI Versus Medical Therapy for Left Main CAD e419 5.7.2. Studies Comparing PCI Versus CABG for Left Main CAD e419 5.7.3. Revascularization Considerations for Left Main CAD e419 5.8. Proximal LAD Artery Disease e420 5.9. Clinical Factors That May Influence the Choice of Revascularization e420 5.9.1. Completeness of Revascularization e420 5.9.2. LV Systolic Dysfunction e420 5.9.3. Previous CABG e421 5.9.4. Unstable Angina/Non ST-Elevation Myocardial Infarction e421 5.9.5. DAPT Compliance and Stent Thrombosis: Recommendation e421 5.10. Transmyocardial Revascularization e421 5.11. Hybrid Coronary Revascularization: Recommendations e421 5.12. Special Considerations e422 5.12.1. Women e422 5.12.2. Older Adults e423 5.12.3. Diabetes Mellitus e424 5.12.4. Obesity e425 5.12.5. Chronic Kidney Disease e425 5.12.6. HIV Infection and SIHD e426 5.12.7. Autoimmune Disorders e426 5.12.8. Socioeconomic Factors e426 5.12.9. Special Occupations e426 6. Patient Follow-Up: Monitoring of Symptoms and Antianginal Therapy e426 6.1. Clinical Evaluation, Echocardiography During Routine, Periodic Follow-Up: Recommendations e427 6.2. Follow-Up of Patients With SIHD e427 6.2.1. Focused Follow-Up Visit: Frequency e428 6.2.2.


Follow-Up of Patients With SIHD e427 6.2.1. Focused Follow-Up Visit: Frequency e428 6.2.2. Focused Follow-Up Visit: Interval History and Coexisting Conditions e428 6.2.3. Focused Follow-Up Visit: Physical Examination e429 6.2.4. Focused Follow-Up Visit: Resting 12-Lead ECG e429 6.2.5. Focused Follow-Up Visit: Laboratory Examination e429 6.3. Noninvasive Testing in Known SIHD e429 6.3.1. Follow-Up Noninvasive Testing in Patients With Known SIHD: New, Recurrent, or Worsening Symptoms Not Consistent With Unstable Angina: Recommendations e429 6.3.1.1. Patients Able to Exercise e429 6.3.1.2. Patients Unable to Exercise e430 6.3.1.3. Irrespective of Ability to Exercise e430 6.3.2. Noninvasive Testing in Known SIHD Asymptomatic (or Stable Symptoms): Recommendations e431 6.3.3. Factors Influencing the Use of Follow-Up Testing e432 6.3.4. Patient Risk and Testing e432 6.3.5. Stability of Results After Normal Stress Testing in Patients With Known SIHD e433 6.3.6. Utility of Repeat Stress Testing in Patients With Known CAD e433 6.3.7. Future Developments e434 Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e464 Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) e467 Appendix 3. Abbreviations List e470 Appendix 4. Nomogram for Estimating Year CAD Event-Free Survival e471 Preamble The medical profession should play a central role in evalu- ating the evidence related to drugs, devices, and procedures for the detection, management, and prevention of disease. When properly applied, expert analysis of available data on the benefits and risks of these therapies and procedures can improve the quality of care, optimize patient outcomes, and favorably affect costs by focusing resources on the most effective strategies. An organized and directed approach to a thorough review of evidence has resulted in the production of clinical practice guidelines that assist physicians in selecting the best management strategy for an individual patient.


An organized and directed approach to a thorough review of evidence has resulted in the production of clinical practice guidelines that assist physicians in selecting the best management strategy for an individual patient. Moreover, clinical practice guidelines can provide a founda- tion for other applications, such as performance measures, appropriate use criteria, and both quality improvement and clinical decision support tools. The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly produced guidelines in the area of cardiovascular disease since 1980. The ACCF/AHA Task Force on Practice Guide- lines (Task Force), charged with developing, updating, and revising practice guidelines for cardiovascular diseases and procedures, directs and oversees this effort. Writing commit- tees are charged with regularly reviewing and evaluating all available evidence to develop balanced, patient-centric rec- ommendations for clinical practice. Experts in the subject under consideration are selected by the ACCF and AHA to examine subject-specific data and write guidelines in partnership with representatives from other medical organizations and specialty groups. Writing committees are asked to perform a literature review; weigh the strength of evidence for or against particular tests, treatments, or procedures; and include estimates of expected outcomes where such data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that may influence the choice of tests or therapies are considered. When available, information from studies on cost is consid- ered, but data on efficacy and outcomes constitute the primary basis for the recommendations contained herein.


When available, information from studies on cost is consid- ered, but data on efficacy and outcomes constitute the primary basis for the recommendations contained herein. In analyzing the data and developing recommendations and supporting text, the writing committee uses evidence-based methodologies developed by the Task Force.1 The Class of Recommendation (COR) is an estimate of the size of the treatment effect, with consideration given to risks versus benefits as well as evidence and/or agreement that a given treatment or procedure is or is not useful/effective or in some situations may cause harm. The Level of Evidence (LOE) is an estimate of the certainty or precision of the treatment effect. The writing committee reviews and ranks evidence supporting each recommendation, with the weight of evi- dence ranked as LOE A, B, or C according to specific definitions that are included in Table 1. Studies are identified as observational, retrospective, prospective, or randomized as appropriate. For certain conditions for which inadequate data are available, recommendations are based on expert consen- sus and clinical experience and are ranked as LOE C. When recommendations at LOE C are supported by historical clinical data, appropriate references (including clinical re- views) are cited if available. For issues for which sparse data are available, a survey of current practice among the clini- cians on the writing committee is the basis for LOE C recommendations, and no references are cited. The schema for COR and LOE is summarized in Table 1, which also provides suggested phrases for writing recommendations Fihn et al Stable Ischemic Heart Disease: Full Text e357 within each COR. A new addition to this methodology is separation of the Class III recommendations to delineate whether the recommendation is determined to be of no benefit or is associated with harm to the patient.


A new addition to this methodology is separation of the Class III recommendations to delineate whether the recommendation is determined to be of no benefit or is associated with harm to the patient. In addition, in view of the increasing number of comparative effectiveness studies, comparator verbs and suggested phrases for writing recommendations for the comparative effectiveness of one treatment or strategy versus another have been added for COR I and IIa, LOE A or B only. In view of the advances in medical therapy across the spectrum of cardiovascular diseases, the Task Force has designated the term guideline-directed medical therapy (GDMT) to represent optimal medical therapy as defined by ACCF/AHA guideline (primarily Class I) recommended therapies. This new term, GDMT, will be used herein and throughout all future guidelines. Because the ACCF/AHA practice guidelines address pa- tient populations (and healthcare providers) residing in North America, drugs that are not currently available in North America are discussed in the text without a specific COR. For studies performed in large numbers of subjects outside North America, each writing committee reviews the potential influ- ence of different practice patterns and patient populations on the treatment effect and relevance to the ACCF/AHA target population to determine whether the findings should inform a specific recommendation. The ACCF/AHA practice guidelines are intended to assist healthcare providers in clinical decision making by describ- Table 1. Applying Classification of Recommendations and Level of Evidence A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Although randomized trials are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.


Although randomized trials are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful or effective. *Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as sex, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. For comparative effectiveness recommendations (Class I and IIa; Level of Evidence A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated. ing a range of generally acceptable approaches to the diag- nosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment about care of a particular patient must be made by the healthcare provider and patient in light of all the circumstances presented by that patient. As a result, situations may arise in which deviations from these guidelines might be appropriate. Clinical decision making should involve consid- eration of the quality and availability of expertise in the area where care is provided. When these guidelines are used as the basis for regulatory or payer decisions, the goal should be improvement in quality of care. The Task Force recognizes that situations arise in which additional data are needed to inform patient care more effectively; these areas will be identified within each respective guideline when appropriate. Prescribed courses of treatment in accordance with these recommendations are effective only if followed. Because lack of patient understanding and adherence may adversely affect outcomes, physicians and other healthcare providers should make every effort to engage the patient s active participation in prescribed medical regimens and lifestyles.


Because lack of patient understanding and adherence may adversely affect outcomes, physicians and other healthcare providers should make every effort to engage the patient s active participation in prescribed medical regimens and lifestyles. In addition, patients should be informed of the risks, benefits, and alternatives to a particular treatment and should be involved in shared decision making whenever feasible, particularly for COR IIa and IIb, for which the benefit-to-risk ratio may be lower. The Task Force makes every effort to avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the members of the writing committee. All writing committee members and peer reviewers of this guideline were required to disclose all such current health care-related relationships, including those existing 24 months (from 2005) before initiation of the writing effort. The writing committee chair may not have any relevant relationships with industry or other entities (RWI); however, RWI are permitted for the vice chair position. In December 2009, the ACCF and AHA imple- mented a new policy that requires a minimum of 50% of the writing committee to have no relevant RWI; in addition, the disclosure term was changed to 12 months before writing committee initiation. The present guideline was developed during the transition in RWI policy and occurred over an extended period of time. In the interest of transparency, we provide full information on RWI existing over the entire period of guideline development, including delineation of relationships that expired more than 24 months before the guideline was finalized. This information is included in Appendix 1. These statements are reviewed by the Task Force and all members during each conference call and meeting of the writing committee and are updated as changes occur.


These statements are reviewed by the Task Force and all members during each conference call and meeting of the writing committee and are updated as changes occur. All guideline recommendations require a confidential vote by the writing committee and must be approved by a consensus of the voting members. Members who recused themselves from voting are indicated in the list of writing committee members, and specific section recusals are noted in Appendix 1. Authors and peer reviewers RWI pertinent to this guideline are disclosed in Appendixes 1 and 2, respectively. Compre- hensive disclosure information for the Task Force is also available online at http://www.cardiosource.org/ACC/About- ACC/Who-We-Are/Leadership/Guidelines-and-Documents- Task-Forces.aspx. The work of the writing committee is supported exclusively by the ACCF, AHA, American College of Physicians (ACP), American Association for Thoracic Surgery (AATS), Preventive Cardiovascular Nurses Associ- ation (PCNA), Society for Cardiovascular Angiography and Interventions (SCAI), and Society of Thoracic Surgeons (STS), without commercial support. Writing committee members volunteered their time for this activity. The recommendations in this guideline are considered current until they are superseded by a focused update or the full-text guideline is revised. Guidelines are official policy of both the ACCF and AHA. Jeffrey L. Anderson, MD, FACC, FAHA Chair, ACCF/AHA Task Force on Practice Guidelines 1.1. Methodology and Evidence Overview The recommendations listed in this document are, whenever possible, evidence based. An extensive evidence review was conducted as the document was compiled through December 2008. Repeated literature searches were performed by the guideline development staff and writing committee members as new issues were considered. New clinical trials published in peer-reviewed journals and articles through December 2011 were also reviewed and incorporated when relevant.


New clinical trials published in peer-reviewed journals and articles through December 2011 were also reviewed and incorporated when relevant. Furthermore, because of the extended development time period for this guideline, peer review comments indicated that the sections focused on imaging technologies required addi- tional updating, which occurred during 2011. Therefore, the evidence review for the imaging sections includes published literature through December 2011. Searches were limited to studies, reviews, and other evi- dence in human subjects and that were published in English. Key search words included but were not limited to the following: accuracy, angina, asymptomatic patients, cardiac magnetic resonance (CMR), cardiac rehabilitation, chest pain, chronic angina, chronic coronary occlusions, chronic ischemic heart disease (IHD), chronic total occlusion, con- nective tissue disease, coronary artery bypass graft (CABG) versus medical therapy, coronary artery disease (CAD) and exercise, coronary calcium scanning, cardiac/coronary com- puted tomography angiography (CCTA), CMR angiography, CMR imaging, coronary stenosis, death, depression, detec- tion of CAD in symptomatic patients, diabetes, diagnosis, dobutamine stress echocardiography, echocardiography, el- derly, electrocardiogram (ECG) and chronic stable angina, emergency department, ethnic, exercise, exercise stress test- ing, follow-up testing, gender, glycemic control, hyperten- sion, intravascular ultrasound, fractional flow reserve (FFR), invasive coronary angiography, kidney disease, low-density lipoprotein (LDL) lowering, magnetic resonance imaging (MRI), medication adherence, minority groups, mortality, myocardial infarction (MI), noninvasive testing and mortal- ity, nuclear myocardial perfusion, nutrition, obesity, out- comes, patient follow-up, patient education, prognosis, prox- imal left anterior descending (LAD) disease, physical Fihn et al Stable Ischemic Heart Disease: Full Text e359 activity, reoperation, risk stratification, smoking, stable is- chemic heart disease (SIHD), stable angina and reoperation, stable angina and revascularization, stress echocardiogra- phy, radionuclide stress testing, stenting versus CABG, un- protected left main, weight reduction, and women. Appendix 3 contains a list of abbreviations used in this document.


Appendix 3 contains a list of abbreviations used in this document. To provide clinicians with a comprehensive set of data, the absolute risk difference and number needed to treat or harm, if they were published and their inclusion was deemed appropriate, are provided in the guideline, along with confi- dence intervals (CIs) and data related to the relative treatment effects, such as odds ratio (OR), relative risk (RR), hazard ratio, or incidence rate ratio. 1.2. Organization of the Writing Committee The writing committee was composed of physicians, cardiovas- cular interventionalists, surgeons, general internists, imagers, nurses, and pharmacists. The writing committee included repre- sentatives from the ACP, AATS, PCNA, SCAI, and STS. 1.3. Document Review and Approval This document was reviewed by 2 external reviewers nomi- nated by both the ACCF and the AHA; 2 reviewers nomi- nated by the ACP, AATS, PCNA, SCAI, and STS; and 19 content reviewers, including members of the ACCF Imaging Council, ACCF Interventional Scientific Council, and the AHA Council on Clinical Cardiology. Reviewers RWI information was collected and distributed to the writing committee and is published in this document (Appendix 2). Because extensive peer review comments resulted in substan- tial revision, the guideline was subjected to a second peer review by all official and organizational reviewers. Lastly, the imaging sections were peer reviewed separately, after an update to that evidence base. This document was approved for publication by the gov- erning bodies of the ACCF, AHA, ACP, AATS, PCNA, SCAI, and STS. 1.4. Scope of the Guideline These guidelines are intended to apply to adult patients with stable known or suspected IHD, including new-onset chest pain (ie, low-risk unstable angina [UA]), or to adult patients with stable pain syndromes (Figure 1).


Scope of the Guideline These guidelines are intended to apply to adult patients with stable known or suspected IHD, including new-onset chest pain (ie, low-risk unstable angina [UA]), or to adult patients with stable pain syndromes (Figure 1). Patients who have ischemic equivalents, such as dyspnea or arm pain with exertion, are included in the latter group. Many patients with IHD can become asymptomatic with appropriate therapy. Accordingly, the follow-up sections of this guideline pertain to patients who were previously symptomatic, including those who have undergone percutaneous coronary intervention (PCI) or CABG. This guideline also addresses the initial diagnostic ap- proach to patients who present with symptoms that suggest IHD, such as anginal-type chest pain, but who are not known to have IHD. In this circumstance, it is essential that the practitioner ascertain whether such symptoms represent the initial clinical recognition of chronic stable angina, reflecting gradual progression of obstructive CAD or an increase in supply/demand mismatch precipitated by a change in activity or concurrent illness (eg, anemia or infection), or whether they represent an acute coronary syndrome (ACS), most likely due to an unstable plaque causing acute thrombosis. For patients with newly diagnosed stable angina, this guide- line should be used. Patients with ACS have either acute myocardial infarction (AMI) or UA.


Patients with ACS have either acute myocardial infarction (AMI) or UA. For patients with AMI, the reader is referred to the ACCF/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial In- farction (STEMI).2,3 Similarly, for patients with UA that is believed to be due to an acute change in clinical status attributable to an unstable plaque or an abrupt change in supply (eg, coronary occlusion with myocardial supply through collaterals), the reader is referred to the ACCF/AHA Guidelines for the Management of Patients With Unstable Angina/non ST-Elevation Myocardial Infarction (UA/ NSTEMI).4,4a There are, however, patients with UA who can be categorized as low risk and are addressed in this guideline (Table 2). A key premise of this guideline is that once a diagnosis of IHD is established, it is necessary in most patients to assess their risk of subsequent complications, such as AMI or death. Because the approach to diagnosis of suspected IHD and the assessment of risk in a patient with known IHD are concep- tually different and are based on different literature, the writing committee constructed this guideline to address these issues separately. It is recognized, however, that a clinician might select a procedure for a patient with a moderate to high pretest likelihood of IHD to provide information for both diagnosis and risk assessment, whereas in a patient with a low likelihood of IHD, it could be sensible to select a test simply for diagnostic purposes without regard to risk assessment.


It is recognized, however, that a clinician might select a procedure for a patient with a moderate to high pretest likelihood of IHD to provide information for both diagnosis and risk assessment, whereas in a patient with a low likelihood of IHD, it could be sensible to select a test simply for diagnostic purposes without regard to risk assessment. By separating the conceptual approaches to ascertaining diagno- Asymptomatic (SIHD) Asymptomatic Persons Without Known IHD (CV Risk) Stable Angina or Low-Risk UA* (SIHD; PCI/CABG) Acute Coronary Syndromes (UA/NSTEMI; STEMI; PCI/CABG) Patients with Known IHD Noncardiac Chest Pain New Onset Chest Pain (SIHD; UA/NSTEMI; STEMI) Sudden Cardiac Death (VA-SCD) Noninvasive Testing *Features of low risk unstable angina: Age, 70 y Exertional pain lasting <20 min. Pain not rapidly accelerating Normal or unchanged ECG No elevation of cardiac markers Figure 1. Spectrum of IHD. Guidelines relevant to the spectrum of IHD are in parentheses. CABG indicates coronary artery bypass graft; CV, cardio- vascular; ECG, electrocardiogram; IHD, ischemic heart disease; PCI, percutaneous coronary inter- vention; SCD, sudden cardiac death; SIHD, stable ischemic heart disease; STEMI, ST-elevation myo- cardial infarction; UA, unstable angina; UA/NSTEMI, unstable angina/non ST-elevation myocardial infarction; and VA, ventricular arrhythmia. sis and prognosis, the goal of the writing committee is to promote the sensible application of appropriate testing rather than routine use of the most expensive or complex tests whether warranted or not. It is not the intent of the writing committee to promote unnecessary or duplicate testing, al- though in some patients this could be unavoidable. Additionally, this guideline addresses the approach to asymptomatic patients with SIHD that has been diagnosed solely on the basis of an abnormal screening study, rather than on the basis of clinical symptoms or events such as anginal symptoms or ACS.


Additionally, this guideline addresses the approach to asymptomatic patients with SIHD that has been diagnosed solely on the basis of an abnormal screening study, rather than on the basis of clinical symptoms or events such as anginal symptoms or ACS. The inclusion of such asymptom- atic patients does not constitute an endorsement of such tests for the purposes of screening but is simply an acknowledg- ment of the clinical reality that asymptomatic patients often present for evaluation after such tests have been performed. Multiple ACCF/AHA guidelines and scientific statements have discouraged the use of ambulatory monitoring, treadmill testing, stress echocardiography, stress myocardial perfusion imaging (MPI), and computed tomography (CT) scoring of coronary calcium or coronary angiography as routine screen- ing tests in asymptomatic individuals. The reader is referred to these documents for a detailed discussion of screening, which is beyond the scope of this guideline (Table 3). Patients with known IHD who were previously asymptom- atic or whose symptoms were stable can develop new or recurrent chest pain or other symptoms suggesting ACS. Just as in the case of patients with new-onset chest pain, the clinician must determine whether such recurrent or worsening pain is consistent with ACS or simply represents symptoms more consistent with chronic stable angina that do not require emergent attention. As indicated previously, patients with AMI or moderate- to high-risk UA fall outside of the scope of this guideline, whereas those with chronic stable angina or low-risk UA are addressed in the present guideline. When patients with documented IHD develop recurrent chest pain, the symptoms still could be attributable to another condition. Such patients are included in this guideline if there is sufficient suspicion that their heart disease is a likely source of symptoms to warrant cardiac evaluation.


Such patients are included in this guideline if there is sufficient suspicion that their heart disease is a likely source of symptoms to warrant cardiac evaluation. If the evaluation demonstrates that IHD is unlikely to cause the symptoms, the evaluation of noncardiac causes is beyond the scope of this guideline. If the evaluation demonstrates that IHD is the likely cause of their recurrent symptoms, subsequent man- agement of such patients does fall within this guideline. The approach to screening and management of asymptom- atic patients who are at risk for IHD but who are not known Table 2.


The approach to screening and management of asymptom- atic patients who are at risk for IHD but who are not known Table 2. Short-Term Risk of Death or Nonfatal MI in Patients With UA/NSTEMI Feature High Risk Intermediate Risk Low Risk No high- or intermediate-risk features are present, but patient may have any of the following: At least 1 of the following features must be present: No high-risk features are present, but patient must have 1 of the following: History Accelerating tempo of ischemic symptoms in preceding 48 h Prior MI, peripheral or cerebrovascular disease, or CABG Prior aspirin use N/A Characteristics of pain Prolonged ongoing (.20 min) rest pain Prolonged (.20 min) rest angina, now resolved, with moderate or high likelihood of CAD Rest angina (.20 min) or relieved with rest or sublingual NTG Nocturnal angina New-onset or progressive CCS Class III or IV angina in previous 2 wk without prolonged (.20 min) rest pain but with intermediate or high likelihood of CAD Increased angina frequency, severity, or duration Angina provoked at a lower threshold New-onset angina with onset 2 wk to 2 mo before presentation Clinical findings Pulmonary edema, most likely due to ischemia New or worsening mitral regurgitation murmur S3 or new/worsening rales Hypotension, bradycardia, or tachycardia Age .75 y Age .70 y N/A ECG Angina at rest with transient ST-segment changes .0.5 mm Bundle-branch block, new or presumed new Sustained ventricular tachycardia T-wave changes Pathological Q waves or resting ST-depression ,1 mm in multiple lead groups (anterior, inferior, lateral) Normal or unchanged ECG Cardiac markers Elevated cardiac TnT, TnI, or CK-MB (ie, TnT or TnI .0.1 ng/mL) Slightly elevated cardiac TnT, TnI, or CK-MB (ie, TnT .0.01 but ,0.1 ng/mL) Normal Estimation of the short-term risks of death and nonfatal cardiac ischemic events in UA or NSTEMI is a complex multivariable problem that cannot be fully specified in a table such as this.


Short-Term Risk of Death or Nonfatal MI in Patients With UA/NSTEMI Feature High Risk Intermediate Risk Low Risk No high- or intermediate-risk features are present, but patient may have any of the following: At least 1 of the following features must be present: No high-risk features are present, but patient must have 1 of the following: History Accelerating tempo of ischemic symptoms in preceding 48 h Prior MI, peripheral or cerebrovascular disease, or CABG Prior aspirin use N/A Characteristics of pain Prolonged ongoing (.20 min) rest pain Prolonged (.20 min) rest angina, now resolved, with moderate or high likelihood of CAD Rest angina (.20 min) or relieved with rest or sublingual NTG Nocturnal angina New-onset or progressive CCS Class III or IV angina in previous 2 wk without prolonged (.20 min) rest pain but with intermediate or high likelihood of CAD Increased angina frequency, severity, or duration Angina provoked at a lower threshold New-onset angina with onset 2 wk to 2 mo before presentation Clinical findings Pulmonary edema, most likely due to ischemia New or worsening mitral regurgitation murmur S3 or new/worsening rales Hypotension, bradycardia, or tachycardia Age .75 y Age .70 y N/A ECG Angina at rest with transient ST-segment changes .0.5 mm Bundle-branch block, new or presumed new Sustained ventricular tachycardia T-wave changes Pathological Q waves or resting ST-depression ,1 mm in multiple lead groups (anterior, inferior, lateral) Normal or unchanged ECG Cardiac markers Elevated cardiac TnT, TnI, or CK-MB (ie, TnT or TnI .0.1 ng/mL) Slightly elevated cardiac TnT, TnI, or CK-MB (ie, TnT .0.01 but ,0.1 ng/mL) Normal Estimation of the short-term risks of death and nonfatal cardiac ischemic events in UA or NSTEMI is a complex multivariable problem that cannot be fully specified in a table such as this. Therefore, the table is meant to offer general guidance and illustration rather than rigid algorithms.


Therefore, the table is meant to offer general guidance and illustration rather than rigid algorithms. CABG indicates coronary artery bypass graft; CAD, coronary artery disease; CCS, Canadian Cardiovascular Society; CK-MB, creatine kinase-MB fraction; ECG, electrocardiogram; MI, myocardial infarction; NTG, nitroglycerin; N/A, not available; TnI, troponin I; TnT, troponin T; and UA/NSTEMI, unstable angina/non ST-elevation myocardial infarction. Modified from Braunwald et al.6 Fihn et al Stable Ischemic Heart Disease: Full Text e361 to have IHD is also beyond the scope of this guideline, but it is addressed in the ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults. 5 Similarly, the present guideline does not apply to patients with chest pain symptoms early after revascularization by either percu- taneous techniques or CABG. Although the division between early and late symptoms is arbitrary, the writing com- mittee believed that this guideline should not be applied to patients who develop recurrent symptoms within 6 months of revascularization. Pediatric patients are beyond the scope of this guideline, because IHD is very unusual in such patients and is related primarily to the presence of coronary artery anomalies. Patients with chest pain syndromes after cardiac transplantation also are not included in this guideline. 1.5. General Approach and Overlap With Other Guidelines or Statements This guideline overlaps with numerous clinical practice guidelines published by the ACCF/AHA Task Force on Practice Guidelines; the National Heart, Lung, and Blood Institute; and the ACP (Table 3). To maintain consistency, the writing committee worked with members of other committees to harmonize recommendations and eliminate discrepancies.


To maintain consistency, the writing committee worked with members of other committees to harmonize recommendations and eliminate discrepancies. Some recommendations from earlier guidelines have been updated as warranted by new evidence or a better understand- ing of earlier evidence, whereas others that were no longer accurate or relevant or were overlapping were modified; recommendations from previous guidelines that were similar or redundant were eliminated or consolidated when possible. Most of the topics mentioned in the present guideline were addressed in the ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina Summary Article, 7 and many of the recommendations in the present guideline are consistent with those in the 2002 document. Whereas the 2002 update dealt individually with specific drugs and interventions for reducing cardiovascular risk and medical therapy of angina pectoris, the present document recommends a combination of lifestyle modifica- tions and medications that constitute GDMT. In addition, recommendations for risk reduction have been revised to reflect new evidence and are now consistent with the AHA/ ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update. 8 Also in the present guideline, recommendations and text related to revascularization are the result of extensive collaborative discussions between the PCI and CABG writing committees, as well as key members of the SIHD and UA/NSTEMI writing committees. In a major undertaking, the PCI and CABG guidelines were written concurrently with input from the STEMI guideline writing committee and additional collaboration with the SIHD guide- line writing committee, allowing greater collaboration be- tween these writing committees on revascularization strate- gies in patients with CAD (including unprotected left main PCI, multivessel disease revascularization, and hybrid proce- dures).9,10 Section 5 is included as published in both the PCI and CABG guidelines in its entirety.


In a major undertaking, the PCI and CABG guidelines were written concurrently with input from the STEMI guideline writing committee and additional collaboration with the SIHD guide- line writing committee, allowing greater collaboration be- tween these writing committees on revascularization strate- gies in patients with CAD (including unprotected left main PCI, multivessel disease revascularization, and hybrid proce- dures).9,10 Section 5 is included as published in both the PCI and CABG guidelines in its entirety. In addition to cosponsoring practice guidelines, the ACCF has sponsored appropriate use criteria (AUC) documents for imaging testing, diagnostic catheterization, and coronary revascularization since 2005.11 16 Practice guideline recom- mendations are based on evidence from clinical and obser- vational trials and expert consensus; AUCs are complemen- tary to practice guidelines and make every effort to be concordant with their recommendations. In general, the rec- ommendations in this guideline and current AUCs are con- sistent. Apparent discrepancies usually reflect differing frameworks or imaging methodologies. Moreover, where guidelines leave gaps (ie, unaddressed applications), AUCs can provide additional clinical guidance based on the best Table 3.


Moreover, where guidelines leave gaps (ie, unaddressed applications), AUCs can provide additional clinical guidance based on the best Table 3. Associated Guidelines and Statements Document Reference(s) Organization Publication Year Guidelines Chronic Stable Angina: 2007 Focused Update (19) ACCF/AHA 2007 Valvular Heart Disease (20) ACCF/AHA 2008 Assessment of Cardiovascular Risk in Asymptomatic Adults (5) ACCF/AHA 2010 Coronary Artery Bypass Graft Surgery (9) ACCF/AHA 2011 Percutaneous Coronary Intervention (10) ACCF/AHA/SCAI 2011 Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease Statements NCEP ATP III Implications of Recent Clinical Trials (18, 24) NHLBI 2004 National Hypertension Education Program (JNC VII) (17) NHLBI 2004 Referral, Enrollment, and Delivery of Cardiac Rehabilitation/Secondary Prevention Programs at Clinical Centers and Beyond: A Presidential Advisory From the AHA ACCF indicates American College of Cardiology Foundation; AHA, American Heart Association; ATP III, Adult Treatment Panel 3; JNC VII, The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; NHLBI, National Heart, Lung and Blood Institute; and SCAI, Society for Cardiovascular Angiography and Interventions. available clinical evidence and use a prospective, expert consensus methodology.16 Specifically, AUCs provide de- tailed indications for testing and procedures to aid clinical decision making, categorizing each indication as appropriate, uncertain, or inappropriate. Thus, ACCF AUCs provide an additional means to identify candidates for testing or proce- dures as well as those for whom they would be inappropriate or for whom the optimal approach is uncertain. Inappropriate candidates are those for whom compelling evidence indicates that testing is not indicated or, in some cases, results in reduced accuracy. Uncertain indications are those with either published evidence or lack of expert consensus on testing use.


Uncertain indications are those with either published evidence or lack of expert consensus on testing use. AUCs also include relevant clinical scenarios not ad- dressed by these guidelines,11 such as the issue of testing during follow-up of patients with SIHD with stress echocar- diography,15 single-photon emission computed tomography (SPECT) MPI,12 CMR, and CCTA.13,14 These AUC docu- ments address the intervals between testing for various stress imaging indications. As with all standards documents, ongo- ing evaluation is required to update the recommendations on the value, limitations, timing, costs, and risks of imaging as an adjunct to clinical assessment during follow-up of patients with established SIHD. Review of these AUCs is beyond the scope of the present document, and the reader is referred to the most recent AUC documents to complement the guide- lines provided here. As the scientific basis of the approach to management of cardiovascular disease has rapidly expanded, the size and scope of clinical practice guidelines have grown commensu- rately to a point where they have become too unwieldy for routine use by practicing clinicians. The most current national guidelines for management of hypertension (Joint National Committee VII)17 and hyperlipidemia (Adult Treatment Panel III)18 combined comprise nearly 400 pages. Thus, the writing committee recognized that it would be unfeasible to produce a document that would be simultaneously practical and exhaustive and, therefore, has tried to create a resource that provides a comprehensive approach to management of SIHD for which the relevant evidence is succinctly summarized and referenced. The writing committee used current and credible meta-analyses, when available, instead of conducting a sys- tematic review of all primary literature. 1.6. Magnitude of the Problem IHD remains a major public health problem nationally and internationally.


Magnitude of the Problem IHD remains a major public health problem nationally and internationally. It is estimated that 1 in 3 adults in the United States (about 81 million) has some form of cardiovascular disease, including .17 million with coronary heart disease and nearly 10 million with angina pectoris.26,27 Among persons 60 to 79 years of age, approximately 25% of men and 16% of women have coronary heart disease, and these figures rise to 37% and 23% among men and women $80 years of Although the survival rate of patients with IHD has been steadily improving,28 it was still responsible for nearly 380 000 deaths in the United States during 2010, with an Although IHD is widely known to be the number 1 cause of death in men, this is also the case for women, among whom this condition accounts for 27% of deaths (compared with 22% due to cancer).30 IHD also accounts for the vast majority of the mortality and morbidity of cardiac disease. Each year, .1.5 million patients have an MI. Many more are hospital- ized for UA and for evaluation and treatment of stable chest pain syndromes. Beyond the need for hospitalization, many patients with chronic chest pain syndromes are temporarily unable to perform normal activities for hours or days and thus experience a reduced quality of life. Among patients enrolled in the BARI (Bypass Angioplasty Revascularization Investi- gation) study,31 about 30% never returned to work after coronary revascularization, and 15% to 20% of patients rated their own health as fair or poor despite revascularization.


Among patients enrolled in the BARI (Bypass Angioplasty Revascularization Investi- gation) study,31 about 30% never returned to work after coronary revascularization, and 15% to 20% of patients rated their own health as fair or poor despite revascularization. Similarly, observational studies of patients recovering from an AMI demonstrated that 1 in 5 patients, even after intensive treatment at the time of their AMI, still suffered angina 1 year later.32 These data confirm the widespread clinical impression that IHD continues to be associated with considerable patient morbidity despite the decline in cardiovascular mortality rate. Patients who have had ACS, such as AMI, remain at risk for recurrent events even if they have no, or limited, symptoms and should be considered to have SIHD. In approximately 50% of patients, angina pectoris is the initial manifestation of IHD.27 The incidence of angina rises continuously with age in women, whereas the incidence of angina in men peaks between 55 and 65 years of age before declining.27 Despite angina s clinical importance and high frequency, modern, population-based data are quite limited, and these figures likely underestimate the true prevalence of The annual rates per 1000 population of new episodes of angina for nonblack men are 28.3 for ages 65 to 74 years, 36.3 for ages 75 to 84 years, and 33.0 for age $85 years. For nonblack women in the same age groups, the rates are 14.1, 20.0, and 22.9, respectively. For black men, the rates are 22.4, 33.8, and 39.5, and for black women, the rates are 15.3, 23.6, and 35.9, respectively.30 In a study conducted in Finland, the age-standardized, annual incidence of angina was 2.03 in men Further estimates of the prevalence of chronic, symptom- atic IHD can be obtained by extrapolating from data on ACS and, more specifically, AMI.


For black men, the rates are 22.4, 33.8, and 39.5, and for black women, the rates are 15.3, 23.6, and 35.9, respectively.30 In a study conducted in Finland, the age-standardized, annual incidence of angina was 2.03 in men Further estimates of the prevalence of chronic, symptom- atic IHD can be obtained by extrapolating from data on ACS and, more specifically, AMI. About one half of patients presenting to the hospital with ACS have preceding angina.27 One current estimate is that about 50% of patients who suffer an AMI each year in the United States survive until hospi- talization.27 Two older population-based studies from Olm- sted County, MN, and Framingham, MA, examined the annual rates of MI in patients with symptoms of angina and reported similar rates of 3% to 3.5% per year.34,35 On this basis, it can be estimated that there were 30 patients with stable angina for every patient with infarction who was hospitalized, which represents 16.5 million persons with angina in the United States. However, since the data reported in these studies were collected, it is likely that the much greater use of effective medical therapies, including antiangi- nal medications and revascularization procedures, has re- duced the proportion of patients with symptomatic angina although there are still many patients whose symptoms are Fihn et al Stable Ischemic Heart Disease: Full Text e363 The costs of caring for patients with IHD are enormous, estimated at $156 billion in the United States for both direct and indirect costs in 2008. More than one half of direct costs are related to hospitalization.


More than one half of direct costs are related to hospitalization. In 2003, the Medicare program alone paid $12.2 billion for hospitalizations for IHD, includ- ing $12 321 per discharge for AMI and $11 783 per discharge for admissions for coronary atherosclerosis.39 Another major expense is for invasive procedures and related costs. In 2006 in the United States, there were 1 313 000 inpatient PCI procedures, 448 000 inpatient coronary artery bypass procedures, and 1 115 000 inpatient diagnostic cardiac catheterizations.27,40 In addition, $13 million outpa- tient visits for IHD occur in the United States annually.41 It was estimated that the costs of outpatient and emergency department visits in 2000 by patients with chronic angina were $922 million and $286 million, respectively, and pre- scriptions accounted for $291 million. Long-term care costs including skilled nursing, home health, and hospice care were $2.6 billion, which represented 30% of the total cost of care for chronic angina.42 Although the direct costs associated with SIHD are sub- stantial, they do not account for the significant indirect costs of lost workdays, reduced productivity, long-term medica- tion, and associated effects. The indirect costs have been estimated to be almost as great as the direct costs27,43 (Table 4). The magnitude of the problem can be summarized succinctly: SIHD affects many millions of Americans, with associated annual costs that are measured in tens of billions of dollars. 1.7. Organization of the Guideline The overarching framework adopted in constructing this guideline reflects the complementary goals of treating pa- tients with known SIHD, alleviating or improving symptoms, and prolonging life. This guideline is divided into 4 basic sections summarizing the approaches to diagnosis, risk as- sessment, treatment, and follow-up.


This guideline is divided into 4 basic sections summarizing the approaches to diagnosis, risk as- sessment, treatment, and follow-up. Five algorithms summa- rize the management of stable angina: diagnosis (Figure 2), risk assessment (Figure 3), GDMT (Figure 4), and revascu- larization (Figures 5 and 6). We readily acknowledge, how- ever, that in actual clinical practice, the elements comprising the 4 sections and the steps delineated in the algorithms often overlap and are not always separable. Some low-risk patients, for example, might require only clinical assessment to deter- mine that they do not need any further evaluation or treat- ment. Other patients might require only clinical assessment and further adjustment of medical therapy if their preferences and comorbidities preclude revascularization, thus obviating the necessity for risk stratification. The stress testing/angiog- raphy algorithm might be applicable for diagnostic purposes in patients with symptoms that suggest SIHD or to perform risk assessment in patients with established SIHD. 1.8. Vital Importance of Involvement by an Informed Patient: Recommendation Class I 1. Choices about diagnostic and therapeutic options should be made through a process of shared decision making involving the patient and provider, with the provider explaining information about risks, bene- fits, and costs to the patient. (Level of Evidence: C) In accordance with the principle of autonomy, the healthcare provider is obliged to solicit and respect the patient s prefer- ences about choice of therapy. Although this principle, in the setting of cardiovascular disease, has received only limited study, the concept of shared decision making increasingly is viewed as an approach that ensures that patients remain involved in key decisions.


Although this principle, in the setting of cardiovascular disease, has received only limited study, the concept of shared decision making increasingly is viewed as an approach that ensures that patients remain involved in key decisions. This approach leads to higher quality of care.44,45 To ensure that the patient is able to make the most informed decisions possible, the provider must give sufficient information about the underlying disease process, along with all relevant diagnostic and therapeutic options including anticipated outcomes, risks, and costs to the patient.46 This information should be provided in a manner that is readily comprehensible and permits the opportunity for dialog and questions. Patients should be encouraged to seek additional informa- tion from other sources, including those on the Internet, such as those maintained by the National Institutes of Health, the Centers for Disease Control and Prevention, and the ACCF/ AHA. Substantial research indicates that when informed about absolute or marginal benefit, patients often elect to postpone or forego invasive procedures. Two patients with similar pretest probabilities of IHD could prefer different approaches because of variations in personal beliefs, eco- nomic situation, or stage of life. Because of the variation in symptoms and clinical characteristics among patients, as well as their unique perceptions, expectations, and preferences, there is often no single correct approach to any given set of clinical circumstances. In assisting patients to reach an Table 4. Estimated Direct and Indirect Costs (in Billions of Dollars) of Heart Disease and Coronary Heart Disease: United Heart Disease ($ in Billions) Coronary Heart Disease ($ in Billions) Direct costs Drugs/other Home health care 8.3 2.5 Indirect costs All estimates prepared by Thomas Thom, National Heart, Lung, and Blood Institute. *Lost future earnings of persons who will die in 2010, discounted at 3%. Reproduced from Lloyd-Jones et al.27 Figure 2.


*Lost future earnings of persons who will die in 2010, discounted at 3%. Reproduced from Lloyd-Jones et al.27 Figure 2. Diagnosis of patients with suspected ischemic heart disease.* *Colors correspond to the class of recommendations in the ACCF/AHA Table 1. The algorithms do not represent a comprehensive list of recommendations (see text for all recommendations). See Table 2 for short-term risk of death or nonfatal MI in patients with UA/NSTEMI. CCTA is reasonable only for patients with inter- mediate probability of IHD. CCTA indicates computed coronary tomography angiography; CMR, cardiac magnetic resonance; ECG, electrocardiogram; Echo, echocardiography; IHD, ischemic heart disease; MI, myocardial infarction; MPI, myocardial perfusion imaging; Pharm, pharmacological; UA, unstable angina; and UA/NSTEMI, unstable angina/non ST-elevation myocardial infarction. Fihn et al Stable Ischemic Heart Disease: Full Text e365 informed decision, it is essential to elicit the breadth of their knowledge, values, preferences, and concerns. The healthcare provider has a responsibility to ensure that patients understand and consider both the upside and down- side of available options, in both the near and long terms. All previous guidelines reviewed by the writing committee have recognized the crucial role that patient preferences play in the selection of a treatment strategy.9,10,47 49 It is essential that these discussions be conducted in a location and atmosphere that permits adequate time for discussion and contemplation. Initiating a discussion about the relative merits of PCI or CABG while a patient is in the midst of a procedure, for example, is not usually consistent with these principles. In crafting a diagnostic strategy, the objective is to ascer- tain, as accurately as possible, whether the patient has IHD while minimizing the expense, discomfort, and potential harms of any tests or procedures.


In crafting a diagnostic strategy, the objective is to ascer- tain, as accurately as possible, whether the patient has IHD while minimizing the expense, discomfort, and potential harms of any tests or procedures. This includes avoiding procedures that are likely to yield false positive or false negative results or that are unnecessary or inappropriate. The objective for procedures intended to assess prognosis is similar. Treatment options should be emphasized, especially in cases where there is no substantial advantage of one strategy over others. For most patients, the goal of treatment should be to simultaneously maximize survival and to achieve prompt and complete (or nearly complete) elimination of anginal chest pain with return to normal activities in other words, a functional capacity of Canadian Cardiovascular Society (CCS) Class I angina.50 For example, for an otherwise healthy, active patient, the treatment goal is usually the complete elimination of chest pain and a return to vigorous physical activity. Conversely, an elderly patient with more severe angina and several serious coexisting medical prob- lems might be satisfied with a reduction in symptoms that permits limited activities of daily living. Patients with anat- omy that would ordinarily favor the choice of CABG could have comorbidities that make the risk of surgery unaccept- able, in which case PCI or medical therapy is a more attractive option. In counseling patients, the healthcare provider should be aware of, and help to rectify, common misperceptions. Many patients assume, for example, that opening a partially blocked artery will naturally prevent a heart attack and prolong life irrespective of other anatomic and clinical factors. When there is little expectation of an improvement in survival from revascularization, patients should be so informed.


When there is little expectation of an improvement in survival from revascularization, patients should be so informed. When evidence points to probable benefit from either revascular- ization or medical therapy, it should be quantified to the extent possible, with explicit acknowledgment of uncertain- ties, and should be discussed in the context of what treatment option is best for that particular patient. When possible, the relative time course of response to therapy should be de- scribed for therapeutic choices. Some patients might, for example, initially opt for PCI over medical therapy because relief of symptoms is typically more rapid. However, when informed of the immediate risk of complications of PCI, some Figure 3. Algorithm for risk assessment of patients with SIHD.* *Colors corre- spond to the class of recommendations in the ACCF/AHA Table 1. The algo- rithms do not represent a comprehen- sive list of recommendations (see text for all recommendations). CCTA indi- cates coronary computed tomography angiography; CMR, cardiac magnetic resonance; ECG, electrocardiogram; Echo, echocardiography; LBBB, left bundle-branch block; MPI, myocardial perfusion imaging; and Pharm, pharmacological. patients could prefer conservative therapy. Similarly, many patients choose PCI over CABG because it is less invasive and provides for quicker recovery, despite the fact that repeat revascularization procedures are performed more frequently after PCI. Patients preferences in these circumstances often are influenced by their attitudes toward risk and by the tendency to let immediate smaller benefits outweigh larger future risks, a phenomenon termed temporal discounting. 51 2. Diagnosis of SIHD 2.1. Clinical Evaluation of Patients With Chest Pain 2.1.1. Clinical Evaluation in the Initial Diagnosis of SIHD in Patients With Chest Pain: Recommendations Class I 1.


Clinical Evaluation in the Initial Diagnosis of SIHD in Patients With Chest Pain: Recommendations Class I 1. Patients with chest pain should receive a thorough history and physical examination to assess the prob- ability of IHD before additional testing.52 (Level of Evidence: C) 2. Patients who present with acute angina should be categorized as stable or unstable; patients with UA should be further categorized as being at high, moderate, or low risk.4,4a (Level of Evidence: C) The clinical examination is the key first step in evaluating a patient with chest pain and should include a detailed assess- ment of symptoms, including quality, location, severity, and duration of pain; radiation; associated symptoms; provocative factors; and alleviating factors. Adjectives often used to describe anginal pain include squeezing, grip-like, suf- focating, and heavy, but it is rarely sharp or stabbing and typically does not vary with position or respiration. On occasion the patient might demonstrate the classic Levine s sign by placing a clenched fist over the precordium to describe the pain. Many patients do not, however, describe angina as frank pain but as tightness, pressure, or discomfort. Figure 4. Algorithm for guideline-directed medical therapy for patients with SIHD.* *Colors correspond to the class of recommendations in the ACCF/AHA Table 1. The algorithms do not represent a comprehensive list of recommendations (see text for all recommenda- tions). The use of bile acid sequestrant is relatively contraindicated when triglycerides are $200 mg/dL and is contraindicated when triglycerides are $500 mg/dL. Dietary supplement niacin must not be used as a substitute for prescription niacin.


Dietary supplement niacin must not be used as a substitute for prescription niacin. ACCF indicates American College of Cardiology Foundation; ACEI, angiotensin-converting enzyme inhibitor; AHA, American Heart Association; ARB, angiotensin-receptor blocker; ASA, aspirin; ATP III, Adult Treatment Panel 3; BP, blood pressure; CCB, calcium channel blocker; CKD, chronic kidney disease; HDL-C, high-density lipoprotein cholesterol; JNC VII, Seventh Report of the Joint National Committee on Pre- vention, Detection, Evaluation, and Treatment of High Blood Pressure; LDL-C, low-density lipoprotein cholesterol; LV, left ventricular; MI, myocardial infarction; NHLBI, National Heart, Lung, and Blood Institute; and NTG, nitroglycerin. Fihn et al Stable Ischemic Heart Disease: Full Text e367 Other patients, in particular women and the elderly, can present with atypical symptoms such as nausea, vomiting, midepigastric discomfort, or sharp (atypical) chest pain. In the WISE (Women s Ischemic Syndrome Evaluation) study, 65% of women with ischemia presented with atypical Anginal pain caused by cardiac ischemia typically lasts minutes. The location is usually substernal, and pain can radiate to the neck, jaw, epigastrium, or arms. Pain above the mandible, below the epigastrium, or localized to a small area over the left lateral chest wall is rarely angina. Angina is often precipitated by exertion or emotional stress and relieved by rest. Sublingual nitroglycerin also usually relieves angina, within 30 seconds to several minutes. The history can be used to classify symptoms as typical, atypical, or noncardiac chest pain6 (Table 5). The patient presenting with angina must be categorized as having stable angina or UA.4,4a UA is defined as new onset, increasing (in frequency, intensity, or duration), or occurring at rest50 (Table 6). However, patients presenting with UA are subdivided by their short-term risk (Table 2).


However, patients presenting with UA are subdivided by their short-term risk (Table 2). Patients at high or moderate risk often have experienced rupture of coronary artery plaque and have a risk of death higher than that of patients with stable angina but not as great as that of patients with AMI. These patients should be transferred promptly to an emergency department for evalu- ation and treatment. The short-term prognosis of patients with low-risk UA, however, is comparable to those with stable angina, and their evaluation can be conducted safely and expeditiously in an outpatient setting. After thorough characterization of chest pain, the presence of risk factors for IHD55 should be determined. These include smoking, hyperlipidemia, diabetes mellitus, hypertension, obesity or metabolic syndrome, physical inactivity, and a family history of premature IHD (ie, onset in a father, brother, or son before age 55 years or a mother, sister, or daughter before age 65 years). A history of cerebrovascular or periph- eral artery disease (PAD) also increases the likelihood of IHD. 2.1.3. Physical Examination The examination is often normal or nonspecific in patients with stable angina56 but could reveal related conditions such as heart failure, valvular heart disease, or hypertrophic cardiomyopathy. An audible rub suggests pericardial or Potential revascularization procedure warranted based on assessment of coexisting cardiac and noncardiac factors and patient preferences? Perform coronary angiography Yes Heart Team concludes that anatomy and clinical factors indicate revascularization may improve survival (Table 18) Determine optimal method of revascularization based upon patient preferences, anatomy, other clinical factors, and local resources and expertise (Table 18) Yes No No Noninvasive testing suggests high-risk coronary lesion(s) from Figure 2 Continued Guideline- Directed Medical Therapy with ongoing patient education Go to Figure 4 Guideline-Directed Medical Therapy continued in all patients Figure 5.


Perform coronary angiography Yes Heart Team concludes that anatomy and clinical factors indicate revascularization may improve survival (Table 18) Determine optimal method of revascularization based upon patient preferences, anatomy, other clinical factors, and local resources and expertise (Table 18) Yes No No Noninvasive testing suggests high-risk coronary lesion(s) from Figure 2 Continued Guideline- Directed Medical Therapy with ongoing patient education Go to Figure 4 Guideline-Directed Medical Therapy continued in all patients Figure 5. Algorithm for revascularization to improve survival of patients with SIHD.* *Colors correspond to the class of recommendations in the ACCF/AHA Table 1. The algorithms do not represent a comprehensive list of recommenda- tions (see text for all recommendations). pleural disease. Evidence of vascular disease includes carotid or renal artery bruits, a diminished pedal pulse, or a palpable abdominal aneurysm. Elevated blood pressure (BP), xantho- mas, and retinal exudates point to the presence of IHD risk factors. Pain reproduced by pressure on the chest wall suggests a musculoskeletal etiology but does not eliminate the possibility of angina due to IHD. 2.1.4.1. Resting Electrocardiography to Assess Risk: Recommendation Class I 1. A resting ECG is recommended in patients without an obvious, noncardiac cause of chest pain.57 59 (Level of Evidence: B) Patients with SIHD who have the following abnormalities on a resting ECG have a worse prognosis than those with normal ECGs57 59: evidence of prior MI, especially Q waves in multiple leads or an R wave in V1 indicating a posterior infarction60; persistent ST-T-wave inversions, particularly in leads V1 to V361 64; left bundle-branch block (LBBB), bifascicular block, second- or third-degree atrioventricular Figure 6. Algorithm for revascularization to improve symptoms of patients with SIHD.* *Colors correspond to the class of recommendations in the ACCF/AHA Table 1.


* *Colors correspond to the class of recommendations in the ACCF/AHA Table 1. The algorithms do not represent a comprehensive list of recommenda- tions (see text for all recommendations). CABG indicates coronary artery bypass graft; PCI, percutaneous coronary intervention. Table 5. Clinical Classification of Chest Pain Typical angina (definite) 1) Substernal chest discomfort with a characteristic quality and duration that is 2) provoked by exertion or emotional stress and 3) relieved by rest or nitroglycerin Atypical angina (probable) Meets 2 of the above characteristics Noncardiac chest pain Meets 1 or none of the typical anginal characteristics Adapted from Braunwald et al.6 Fihn et al Stable Ischemic Heart Disease: Full Text e369 (AV) block, or ventricular tachyarrhythmia65; or left ventric- ular (LV) hypertrophy.62,66 2.1.5. Differential Diagnosis Although the symptoms of some patients might be consistent with a very high probability of IHD, in others, the etiology might be less certain, and alternative diagnoses should be considered (Table 7). However, even when angina seems likely to be related to IHD, other coexisting conditions can precipitate symptoms by inducing or exacerbating myocardial ischemia, by either increased myocardial oxygen demand or decreased myocardial oxygen supply (Table 8). When severe, these conditions can cause angina in the absence of signifi- cant anatomic coronary obstruction. Chest pain in women is less often due to IHD than in men, even when the pain is typical. Nevertheless, pain in women can be related to vascular dysfunction in the absence of epicardial CAD. Entities that cause increased oxygen demand include hyper- thermia (particularly if accompanied by volume contrac- tion),67 hyperthyroidism, and cocaine or methamphetamine abuse. Sympathomimetic toxicity, due, for example, to co- caine intoxication, not only increases myocardial oxygen demand but also induces coronary vasospasm and can cause infarction in young patients.


Sympathomimetic toxicity, due, for example, to co- caine intoxication, not only increases myocardial oxygen demand but also induces coronary vasospasm and can cause infarction in young patients. Long-term cocaine use can cause premature development of IHD.68,69 Severe uncontrolled hypertension increases LV wall tension, leading to increased myocardial oxygen demand and decreased subendocardial perfusion. Hypertrophic cardiomyopathy and aortic stenosis can induce even more severe LV hypertrophy and resultant wall tension. Ventricular or supraventricular tachycardias are another cause of increased myocardial oxygen demand, but when paroxysmal these are difficult to diagnose. Anemia is the prototype for conditions that limit myocar- dial oxygen supply. Cardiac output rises when the hemoglo- bin drops to ,9 g/dL, and ST-T-wave changes (depression or inversion) can occur at levels ,7 g/dL. Hypoxemia resulting from pulmonary disease (eg, pneu- monia, asthma, chronic obstructive pulmonary disease, pul- monary hypertension, interstitial fibrosis, or obstructive sleep apnea) can also precipitate angina. Polycythemia, leukemia, thrombocytosis, and hypergammaglobulinemia are associated with increased blood viscosity that can decrease coronary artery blood flow and precipitate angina, even in patients without significant coronary stenoses. 2.1.6. Developing the Probability Estimate When the clinical evaluation is complete, the practitioner must determine whether the probability of IHD is sufficient to recommend further testing, which is often a standard exercise test. When the probability of disease is ,5%, further testing is usually not warranted because the likelihood of a false- positive test (ie, positive test in the absence of obstructive CAD) is actually higher than that of a true positive. On the other hand, when the exercise test is negative in a patient who has a very high likelihood of IHD on the basis of the history, there is a substantial chance that in reality the result is falsely negative.


On the other hand, when the exercise test is negative in a patient who has a very high likelihood of IHD on the basis of the history, there is a substantial chance that in reality the result is falsely negative. Thus, further testing is most useful in patients in whom the cause of chest pain is truly uncertain (ie, the probability of IHD is between 20% and 70%). It is necessary to note, however, that these probabilities relate solely to the presence of obstructive CAD and do not pertain to ischemia due to microvascular disease or other causes. They also do not reflect the likelihood that a nonobstructing plaque could become unstable and cause ischemia. A landmark study52 showed how information about the type of pain and age and sex of the patient can provide a reasonable estimate of the likelihood of IHD. For instance, a 64-year-old man with typical angina has a 94% likelihood of having significant coronary stenosis. A 32-year-old woman with nonanginal chest pain has a 1% chance of coronary stenosis.70 72 Other clinical characteristics that improved the accuracy of prediction include active or recent smoking, Q-wave or ST-T-wave changes on the ECG, hyperlipidemia (defined at the time of study as a total cholesterol level .250 mg/dL), and diabetes mellitus (defined at that time as a fasting glucose level .140 mg/dL). Of these characteristics, Table 6.


A 32-year-old woman with nonanginal chest pain has a 1% chance of coronary stenosis.70 72 Other clinical characteristics that improved the accuracy of prediction include active or recent smoking, Q-wave or ST-T-wave changes on the ECG, hyperlipidemia (defined at the time of study as a total cholesterol level .250 mg/dL), and diabetes mellitus (defined at that time as a fasting glucose level .140 mg/dL). Of these characteristics, Table 6. Three Principal Presentations of UA Rest angina Angina occurring at rest and usually prolonged .20 min, occurring within 1 wk of presentation New-onset angina Angina of at least CCS Class III severity with onset within 2 mo of initial presentation Increasing angina Previously diagnosed angina that is distinctly more frequent, longer in duration, or lower in threshold (ie, increased by $1 CCS class within 2 mo of initial presentation to at least CCS Class III severity) CCS indicates Canadian Cardiovascular Society. Reproduced from Braunwald.50 Table 7. Alternative Diagnoses to Angina for Patients With Chest Pain Nonischemic Cardiovascular Pulmonary Gastrointestinal Chest Wall Psychiatric Aortic dissection Pulmonary embolism Esophageal Esophagitis Spasm Reflux Costochondritis Fibrositis Rib fracture Sternoclavicular arthritis Herpes zoster (before the rash) Anxiety disorders Hyperventilation Panic disorder Primary anxiety Pericarditis Pneumothorax Pneumonia Pleuritis Biliary Colic Cholecystitis Choledocholithiasis Cholangitis Peptic ulcer Pancreatitis Affective disorders (ie, depression) Somatiform disorders Thought disorders (ie, fixed delusions) Reproduced from Gibbons et al.7 diabetes mellitus had the greatest influence on increasing the probability of IHD. The presence of hypertension or a family history of premature IHD did not provide additional predic- tive accuracy. The results of the aforementioned landmark study subsequently were replicated with data from CASS (Coronary Artery Surgery Study)73 and were within 5% of the original estimates for 23 of 24 patient groupings.


The results of the aforementioned landmark study subsequently were replicated with data from CASS (Coronary Artery Surgery Study)73 and were within 5% of the original estimates for 23 of 24 patient groupings. The single major exception was the category of adults who were #50 years of age with atypical angina, for whom the CASS estimate was 17% higher. On the basis of this high degree of concordance, the data from these studies were merged in the 2002 Chronic Stable Angina guideline7,52,73 (Table 9). Additional validation studies were conducted with data from the Duke Databank for Cardiovascular Disease, which also incorporated electrocardiographic findings (Q waves or ST-T changes) and information about risk factors (smoking, diabetes mellitus, hyperlipidemia).71 Table 10 presents the Duke data for mid-decade patients (35, 45, 55, and 65 years of age). Two probabilities are given. The first is for a low-risk patient with no risk factors and a normal ECG. The second is for a high-risk patient who smokes and has diabetes mellitus and hyperlipidemia but has a normal ECG. A key contribu- tion of the Duke Databank is the value of incorporating data about risk factors into the probability estimate. A limitation of these predictive models, however, is that because they were developed with data from patients referred to university medical centers, they tended to overestimate the likelihood of IHD in patients at lower risk. It is possible to correct this referral (or ascertainment) bias by using the overall prevalence of IHD in the primary-care population,72 although these adjustments are themselves subject to error if the prevalence estimates are flawed. An additional limitation of these models is that they were derived from populations of patients #70 years of age.


An additional limitation of these models is that they were derived from populations of patients #70 years of age. Yet another drawback is that they perform less well in women, in part because the prevalence of obstructive CAD is lower in women than in men. As shown in Table 9, the Diamond- Forrester model substantially overestimates the likelihood of CAD compared with the prevalence observed in the WISE After integrating data from the clinical evaluation, model predictions, and other relevant factors to develop a probabil- ity estimate, the clinician must then engage the patient in a process of shared decision making, as noted in Section 1.8, to determine whether further testing is warranted. 2.2. Noninvasive Testing for Diagnosis of IHD 2.2.1. Approach to the Selection of Diagnostic Tests to Diagnose SIHD Functional or stress testing to detect inducible ischemia has been the gold standard and is the most common noninva- sive test used to diagnose SIHD. All functional tests are designed to provoke cardiac ischemia by using exercise or pharmacological stress agents either to increase myocardial work and oxygen demand or to induce vasodilation-elicited heterogeneity in induced coronary flow. These techniques Table 8. Conditions Provoking or Exacerbating Ischemia Increased Oxygen Demand Decreased Oxygen Supply Noncardiac Noncardiac Hyperthermia Hyperthyroidism Sympathomimetic toxicity (ie, cocaine use) Hypertension Anxiety Arteriovenous fistulae Anemia Hypoxemia Pneumonia Asthma Chronic obstructive pulmonary disease Pulmonary hypertension Interstitial pulmonary fibrosis Obstructive sleep apnea Sickle cell disease Sympathomimetic toxicity (ie, cocaine use, pheochromocytoma) Hyperviscosity Polycythemia Leukemia Thrombocytosis Hypergammaglobulinemia Cardiac Cardiac Hypertrophic cardiomyopathy Aortic stenosis Dilated cardiomyopathy Tachycardia Ventricular Supraventricular Aortic stenosis Hypertrophic cardiomyopathy Significant coronary obstruction Microvascular disease Modified from Gibbons et al.7 Table 9.