ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina—Summary Article

HomeCirculationVol. 107, No. 1ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina—Summary Article Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina—Summary ArticleA Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina) Committee Members Raymond J. Gibbons, MD, FACC, FAHA, Chair, Jonathan Abrams, MD, FACC, FAHA, Kanu Chatterjee, MB, FACC, Jennifer Daley, MD, FACP, Prakash C. Deedwania, MD, FACC, FAHA, John S. Douglas, MD, FACC, T. Bruce FergusonJr, MD, Stephan D. Fihn, MD, MPH, FACP, Theodore D. FrakerJr, MD, FACC, Julius M. Gardin, MD, FACC, FAHA, Robert A. O’Rourke, MD, FACC, FAHA, Richard C. Pasternak, MD, FACC, FAHA, Sankey V. Williams, MD, MACP, Raymond J. Gibbons, Task Force Members:, MD, FACC, Chair, Joseph S. Alpert, MD, FACC, FAHA, Elliott M. Antman, MD, FACC, Vice Chair, Loren F. Hiratzka, MD, FACC, FAHA, Valentin Fuster, MD, PhD, FACC, FAHA, David P. Faxon, MD, FACC, FAHA, Gabriel Gregoratos, MD, FACC, FAHA, Alice K. Jacobs, MD, FACC, FAHA and Sidney C. SmithJr, MD, FACC, FAHA Committee Members , Raymond J. GibbonsRaymond J. Gibbons , Jonathan AbramsJonathan Abrams , Kanu ChatterjeeKanu Chatterjee , Jennifer DaleyJennifer Daley , Prakash C. DeedwaniaPrakash C. Deedwania , John S. DouglasJohn S. Douglas , T. Bruce FergusonJrT. Bruce FergusonJr , Stephan D. FihnStephan D. Fihn , Theodore D. FrakerJrTheodore D. FrakerJr , Julius M. GardinJulius M. Gardin , Robert A. O’RourkeRobert A. O’Rourke , Richard C. PasternakRichard C. Pasternak , Sankey V. WilliamsSankey V. Williams , Raymond J. GibbonsRaymond J. Gibbons , Joseph S. AlpertJoseph S. Alpert , Elliott M. AntmanElliott M. Antman , Loren F. HiratzkaLoren F. Hiratzka , Valentin FusterValentin Fuster , David P. FaxonDavid P. Faxon , Gabriel GregoratosGabriel Gregoratos , Alice K. JacobsAlice K. Jacobs and Sidney C. SmithJrSidney C. SmithJr Originally published7 Jan 2003https://doi.org/10.1161/01.CIR.0000047041.66447.29Circulation. 2003;107:149–158The Clinical Efficacy Assessment Subcommittee of the American College of Physicians–American Society of Internal Medicine acknowledges the scientific validity of this product as a background paper and as a review that captures the levels of evidence in the management of patients with chronic stable angina as of November 17, 2002.Table of ContentsI. Introduction ••II. Angiotensin Converting Enzyme (ACE) Inhibitors • •III. Treatment of Risk Factors • •A. LDL Cholesterol • •B. Non-HDL Cholesterol • •C. HDL Cholesterol • •D. Triglycerides • •E. Obesity • •F. Metabolic Syndrome • •G. Hormonal Replacement Therapy • •H. Oxidative Stress • •IV. Alternative Therapies for Chronic Stable Angina in Patients Refractory to Medical Therapy Who Are Not Candidates for Percutaneous Intervention or Revascularization • •A. Spinal Cord Stimulation • •B. Enhanced External Counterpulsation • •C. Laser Transmyocardial Revascularization • •V. Asymptomatic Patients With Known or Suspected Coronary Artery Disease • •A. Treatment of Risk Factors • •B. Revascularization • •References • •I. IntroductionThe American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or a full revision is needed. This process gives priority to areas in which major changes in text, and particularly recommendations, are merited on the basis of new understanding or evidence. Minor changes in verbiage and references are discouraged.The ACC/AHA/American College of Physicians–American Society of Internal Medicine (ACP-ASIM) Guidelines for the Management of Patients With Chronic Stable Angina, which were published in June 1999, have now been updated. The full-text guideline incorporating the updated material is available on the Internet (www.acc.org or www.americanheart.org) in both a track-changes version showing the changes in the 1999 guideline in strike-out (deleted text) and highlighting (new text) and a “clean” version that fully incorporates all the changes.This summary article describes the 4 most important areas of change reflected in the update in a format that we hope can be read and understood as a stand-alone document. Interested readers are referred to the full-length version on the Internet to completely understand the location of these changes within the full-length guideline, as well as their proper context. The full-length guideline includes some additional changes that are not reflected in this summary article. All new references appear in bold-faced type; all original references appear in normal type.Although the primary focus of this guideline is on symptomatic patients, asymptomatic patients with known or suspected coronary disease are included in this update and are described in Section V.The customary ACC/AHA classifications I, IIa, IIb, and III and the corresponding levels of evidence are used throughout the document.Class I:Conditions for which there is evidence or general agreement that a given procedure or treatment is useful and effective.Class II:Conditions for which there is conflicting evidence or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. ClassIIa:Weight of evidence/opinion is in favor of usefulness/efficacy. ClassIIb:Usefulness/efficacy is less well established by evidence/opinion.Class III:Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful.Level of Evidence A:Data derived from multiple randomized clinical trials.Level of Evidence B:Data derived from a single randomized trial or nonrandomized studies.Level of Evidence C: Consensus opinion of experts.The ACC/AHA Task Force on Practice Guidelines welcomes feedback on this update process and the format of this article. Please direct your comments to the Task Force in care of Dawn Phoubandith, American College of Cardiology, or via e-mail ([email protected]).II. Angiotensin Converting Enzyme InhibitorsNew Recommendations for Angiotensin Converting Enzyme (ACE) InhibitorsClass I1. ACE inhibitor in all patients with coronary artery disease (CAD)* who also have diabetes and/or left ventricular systolic dysfunction.(Level of Evidence: A)Class IIa1. ACE inhibitor in patients with CAD* or other vascular disease.(Level of Evidence: B)*Significant CAD by angiography or previous myocardial infarction.The results of the Heart Outcomes Prevention Evaluation (HOPE) trial now confirm that use of the ACE inhibitor ramipril (10 mg/d) reduced the incidence of cardiovascular death, myocardial infarction (MI), and stroke in patients who were at high risk for, or had, vascular disease in the absence of heart failure.1 The primary outcome in HOPE was a composite of cardiovascular death, MI, and stroke. However, the results of HOPE were so definitive that each of the components of the primary outcome by itself also showed statistical significance. Furthermore, only a small part of the benefit could be attributed to a reduction in blood pressure (−2 to −3 mm Hg).The results of HOPE were extremely impressive when one considers the magnitude of the difference between ramipril and placebo in the primary outcomes of cardiovascular death, MI, and stroke. The HOPE study was unique in that of the 9541 patients in the study, 3577 (37.5%) had diabetes. There was a very significant reduction in diabetic complications, a composite for the development of diabetic nephropathy, need for renal dialysis, and laser therapy for diabetic retinopathy, in those patients receiving ramipril. Even more fascinating was the finding that among the patients who were not designated as diabetic at the beginning of the trial, fewer were diagnosed with diabetes during the 4-year observation period if they were treated with ramipril. Before the HOPE trial, numerous clinical trials suggested that ACE inhibitor treatment may delay or prevent cardiovascular outcomes in patients with diabetes after an MI, in the presence of hypertension, and in the presence of a low ejection fraction or heart failure. Furthermore, ACE inhibitors may also prevent overt nephropathy and other microvascular outcomes in patients with type 1 or type 2 diabetes.The Microalbuminuria, Cardiovascular, and Renal Outcomes (MICRO)-HOPE study, a substudy of the HOPE study, has provided new clinical data on the cardiorenal therapeutic benefits of ACE inhibitor intervention in a broad range of middle-aged patients with diabetes mellitus who are at high risk for cardiovascular events. The risk of MI was reduced by 22% (P=0.01), stroke by 33% (P=0.0074), cardiovascular death by 37% (P=0.0001), and the combined primary outcome of these events by 25% (P=0.0004). Ramipril also lowered the risk of overt nephropathy by 24% (P=0.027).ACE inhibitors should be used in most cases as routine secondary prevention for patients with known CAD, particularly in diabetics without severe renal disease. There are 2 ongoing clinical trials evaluating the effect of 2 different ACE inhibitors in patient populations that do not include patients with diabetes mellitus. These studies will answer the question whether a vasculoprotective effect can be accomplished in a lower-risk group of patients than those enrolled in the HOPE study.III. Treatment of Risk FactorsNew/Changed Recommendations†Class IIa1. In patients with documented or suspected CAD and low-density lipoprotein (LDL) cholesterol 100 to 129 mg/dL, several therapeutic options are available:(Level of Evidence: B) a. Lifestyle and/or drug therapies to lower LDL to less than 100 mg/dL.(Level of Evidence: B) b. Weight reduction and increased physical activity in persons with the metabolic syndrome.(Level of Evidence: B) c. Institution of treatment of other lipid or nonlipid risk factors; consider use of nicotinic acid or fibric acid for elevated triglycerides or low high-density lipoprotein (HDL) cholesterol.(Level of Evidence: B)2. Therapy to lower non-HDL cholesterol in patients with documented or suspected CAD and triglyceride levels greater than 200 mg/dL, with a target non-HDL cholesterol level of less than 130 mg/dL.(Level of Evidence: B)3. Weight reduction in obese patients in the absence of hypertension, hyperlipidemia, or diabetes mellitus.(Level of Evidence: C)Class III1. Initiation of hormone replacement therapy (HRT) in postmenopausal women for the purpose of reducing cardiovascular risk.(Level of Evidence: A)2. Vitamin C and E supplementation.(Level of Evidence: A) 3. Coenzyme Q. (Level of Evidence: C)†The original recommendations, and particularly the 6 Class I recommendations, continue to apply.Many of the new recommendations reflect the latest recommendations of the National Cholesterol Education Program–Adult Treatment Panel III (ATP-III),2 which the writing committee strongly endorses.The results of the largest cholesterol-lowering trial yet performed, the Heart Protection Study (HPS), were published as this update was in the final stages of preparation.2a This trial included more than 20 000 men and women age 40 to 80 years with coronary disease, other vascular disease, diabetes, and/or hypertension. Patients were randomized to simvastatin 40 mg or matching placebo and were followed for a mean of five years. The primary end point, total mortality, was reduced by statin treatment by approximately 25% overall and similarly in all important prespecified subgroups, including: women, patients more than 75 years old, diabetics, and individuals with baseline LDL cholesterol of less than 100 mg per dL. Analysis of these data by all appropriate authorities, including the National Cholesterol Education project, will be necessary to clarify their implications for these guidelines.A. LDL CholesterolThe clinical trial data indicate that in patients with established coronary disease, including chronic stable angina pectoris, dietary intervention and treatment with lipid-lowering medications should not be limited to those with extreme values. The benefits of lipid-lowering therapy were evident in patients in the lowest baseline quartile of LDL cholesterol (modest elevations) in the Scandinavian Simvastatin Survival Study (4S) and in those with minimal elevation of LDL cholesterol level in the Cholesterol And Recurrent Events (CARE) study. These trials establish the benefits of aggressive lipid-lowering treatment for most patients with coronary disease, even when LDL cholesterol is within a range considered acceptable for patients in a primary prevention setting. For patients with established coronary disease, nonpharmaceutical treatment and drug treatment are warranted in the vast majority of patients. The goal of treatment is an LDL cholesterol level less than 100 mg/dL. When LDL cholesterol is 101 to 129 mg/dL, either at baseline or with LDL-lowering therapy, several therapeutic options are available:Initiate or intensify lifestyle and/or drug therapies specifically to lower LDL.Emphasize weight reduction and increased physical activity in persons with the metabolic syndrome (see below).Delay use or intensification of LDL-lowering therapies and institute treatment of other lipid or nonlipid risk factors; consider use of other lipid-modifying drugs (eg, nicotinic acid or fibric acid) if the patient has elevated triglyceride or low HDL cholesterol levels.B. Non-HDL CholesterolThe finding that elevated triglycerides are an independent risk factor for coronary heart disease (CHD) suggests that some triglyceride-rich lipoproteins are atherogenic. The latter are partially degraded very-low-density lipoproteins (VLDL), commonly called “remnant lipoproteins.” In clinical practice, non-HDL cholesterol is the most readily available measure of the total pool of atherogenic lipoproteins, including remnants. Thus, non-HDL cholesterol can be a target of cholesterol-lowering therapy. Moreover, non-HDL cholesterol is highly correlated with total apolipoprotein B (apoB)3,4; apoB is the major apolipoprotein of all atherogenic lipoproteins. Serum total apoB also has been shown to have a strong predictive power for severity of coronary atherosclerosis and CHD events.5–12 Because of the high correlation between non-HDL cholesterol and apoB levels,3,4 non-HDL cholesterol represents an acceptable surrogate marker for total apoB; the latter is not widely available for routine measurement in clinical practice. Therefore, ATP III2 identifies the sum of LDL and VLDL cholesterol (termed “non-HDL cholesterol” [total cholesterol minus HDL cholesterol]) as a secondary target of therapy in persons with high triglycerides (greater than 200 mg/dL). The goal for non-HDL cholesterol (for persons with serum triglycerides greater than or equal to 200) is 130 mg/dL; this is 30 mg/dL higher than the goal for LDL cholesterol, because the normal VLDL cholesterol level is 30 mg/dL.C. HDL CholesterolATP III has defined a low HDL cholesterol level as less than 40 mg/dL.2 Patients with established coronary disease and low HDL cholesterol are at high risk for recurrent events and should be targeted for aggressive nonpharmacological treatment (dietary modification, weight loss, and/or physical exercise). ATP III does not specify a goal for HDL raising. Although clinical trial results suggest that raising HDL will reduce risk, the evidence is insufficient to specify a goal of therapy. Furthermore, currently available drugs do not robustly raise HDL cholesterol. A low HDL level should receive clinical attention and management according to the following sequence. In all persons with low HDL cholesterol, the primary target of therapy is LDL cholesterol; ATP III guidelines for diet, exercise, and drug therapy should be followed to achieve the LDL cholesterol goal. Second, after the LDL goal has been reached, emphasis shifts to other issues. When a low HDL cholesterol level is associated with high triglycerides (200 to 499 mg/dL) secondary priority goes to achieving the non-HDL cholesterol goal, as outlined earlier. Also, if triglycerides are less than 200 mg/dL (isolated low HDL cholesterol), drugs to raise HDL (fibrates or nicotinic acid) can be considered. Nicotinic acid and fibrates usually raise HDL levels, as do 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors.D. TriglyceridesTriglyceride levels are predictive of CHD risk in a variety of observational studies and clinical settings.13 Much of the association of triglycerides with CHD risk is related to other factors, including diabetes, obesity, hypertension, high LDL cholesterol, and low HDL cholesterol.14 In addition, hypertriglyceridemia is often found in association with abnormalities in hemostatic factors.15 Recently, however, a borderline (150 to 199 mg/dL) or high (greater than 200 mg/dL) triglyceride level has been established by meta-analyses of prospective studies as an independent risk factor for CHD.2,16,17Nonpharmacological management of high triglycerides consists of weight loss, reduction in alcohol consumption for those in whom this mechanism may be causal, smoking cessation, and physical activity. Drugs that can lower triglycerides include nicotinic acid, fibrate derivatives, and, to a lesser degree, statins. It is not clear whether treatment directed at high triglyceride levels will reduce risk for initial or recurrent CHD events. Also, triglyceride measurements vary considerably for individual patients. Accordingly, the ATP III2 provides guidance for the management of elevated triglyceride levels by focusing on a combination of therapeutic lifestyle changes and by a secondary lipid target for non-HDL cholesterol.E. ObesityObesity is a common condition associated with increased risk for coronary disease and mortality.18 Obesity is defined as a body mass index (weight in kilograms divided by the square of height in meters) of 30 kg/m2, and overweight begins at 25 kg/m2.19 Obesity is associated with and contributes to other coronary disease risk factors, including high blood pressure, glucose intolerance, low HDL cholesterol, and elevated triglyceride levels. Hence, much of the increased CAD risk associated with obesity is mediated by these risk factors. Risk is particularly raised in the presence of abdominal obesity, which can be identified by a waist circumference greater than 102 cm (40 inches) in men or 88 cm (35 inches) in women.19 Because weight reduction in overweight and obese people is a method to reduce multiple other risk factors, it is an important component of secondary prevention of CHD.F. Metabolic SyndromeEvidence is accumulating that risk for future CHD events can be reduced beyond that achieved by LDL-lowering therapy by modification of a specific secondary target of therapy—the metabolic syndrome—represented by a constellation of lipid and nonlipid risk factors of metabolic origin. This syndrome is closely linked to a generalized metabolic disorder called insulin resistance in which the normal actions of insulin are impaired. Excess body fat (particularly abdominal obesity) and physical inactivity promote the development of insulin resistance, but some individuals also are genetically predisposed to insulin resistance. In a field that has been confused by nomenclature, ATP III has introduced a standard definition for the diagnosis of the metabolic syndrome, as shown in the Table. The metabolic syndrome is considered to be present when 3 or more of the characteristics are present. Characteristics Used to Define Metabolic SyndromeRisk FactorDefining LevelAbdominal obesityWaist circumference MenGreater than 103 cm (40 in) WomenGreater than 88 cm (35 in)TriglyceridesGreater than 150 mg/dLHDL cholesterol MenLess than 40 mg/dL WomenLess than 50 mg/dLBlood pressureGreater than or equal to 130/85 mm HgFasting serum glucoseGreater than or equal to 110 mg/dLManagement of the metabolic syndrome has a 2-fold objective: (1) to reduce underlying causes (ie, obesity and physical inactivity) and (2) to treat associated nonlipid and lipid risk factors. First-line therapies for all lipid and nonlipid risk factors associated with the metabolic syndrome are weight reduction and increased physical activity, as well as appropriate control of LDL cholesterol. In patients with triglycerides greater than 200 mg/dL, a non-HDL cholesterol goal of less than 130 mg/dL is a secondary target (see the Table).G. Hormone Replacement TherapyOn the basis of epidemiological studies and prospective studies of the effects of estrogen administration on cardiac risk factors, postmenopausal estrogen replacement has been advocated for both primary and secondary prevention of CAD in women. However, the first published randomized trial of estrogen plus progestin therapy in postmenopausal women with known CAD did not show any reduction in cardiovascular events over 4 years of follow-up,20 despite an 11% lower LDL cholesterol level and a 10% higher HDL cholesterol level in those women receiving HRT. In addition, women receiving HRT had higher rates of cardiovascular events during the first 2 years, more thromboembolic events, and more gallbladder disease.20 A subsequent angiographic study also revealed no benefit from HRT.21 Another prospective randomized controlled trial with HRT in women with a history of stroke found no benefit in reducing mortality or stroke after 2.8 years.22 The Women’s Health Initiative, a randomized controlled primary prevention trial of estrogen plus progestin, found that the overall health risks of this therapy exceeded its benefits.23 Thus, current information suggests that HRT in postmenopausal women does not reduce risk for major vascular events or coronary deaths in secondary prevention. Women who are taking HRT and who have vascular disease can continue this therapy if it is being prescribed for other well-established indications and no better alternative therapies are appropriate. However, at the present time, there is no basis for adding or continuing estrogens in postmenopausal women with clinically evident CAD or cerebrovascular disease in an effort to prevent or retard progression of their underlying disease.24If a woman develops an acute CAD event while undergoing HRT, it is prudent to consider discontinuance of the HRT.24 In women who are immobilized, HRT should be discontinued, or venous thromboembolism prophylaxis should be used.24H. Oxidative StressEvidence from clinical trials is negative regarding the effects of supplementation with antioxidant vitamins. Although several small trials and in vitro data from basic research in vascular biology have suggested that vitamin C and/or E might interfere with formation of atherosclerotic lesions, 2 large randomized clinical trials have shown no benefit when vitamin E was given to post-MI patients25 or in those with vascular disease or diabetics with a high-risk CAD profile.26–28 Furthermore, a small coronary regression trial, the HDL Atherosclerosis Treatment Study (HATS), suggested an adverse effect of antioxidant vitamins on coronary atherosclerosis, clinical events, and HDL and apoA-1 metabolism.27,28 The use of vitamin E (administered with vitamin C and beta-carotene) was the subject of a large (more than 20 000 participants) trial of patients at risk for CAD and with CAD.26 Antioxidant therapy had no effect on the end points of cardiovascular death, cardiovascular events, stroke, or revascularization, considered alone or in combination. Although previous observational and epidemiological studies have suggested a benefit from dietary supplementation with antioxidants or a diet rich in antioxidants, especially vitamin E, there is currently no basis for recommending that patients take vitamin C or E supplements or other antioxidants for the express purpose of preventing or treating CAD.IV. Alternative Therapies for Chronic Stable Angina in Patients Refractory to Medical Therapy Who Are Not Candidates for Percutaneous Intervention or RevascularizationRecommendationsClass IIa 1. Surgical laser transmyocardial revascularization (TMR).(Level of Evidence: A)Class IIb 1. Enhanced external counterpulsation (EECP).(Level of Evidence: B) 2. Spinal cord stimulation (SCS).(Level of Evidence: B)Evidence has emerged regarding the relative efficacy, or lack thereof, of a number of techniques for the management of refractory chronic angina pectoris. These techniques should only be used in patients who cannot be managed adequately by medical therapy and who are not candidates for revascularization (interventional and/or surgical).A. Spinal Cord StimulationSince approximately 1987, SCS has been proposed as a method for providing analgesia for patients with chronic angina pectoris refractory to medical, catheter interventional, or surgical therapy. The efficacy of SCS depends on the accurate placement of the stimulating electrode in the dorsal epidural space, usually at the C7-T1 level. A review of the literature has revealed 2 small randomized clinical trials involving implanted spinal cord stimulators, 1 of which directly tested its efficacy. One report studied the efficacy of SCS in 13 treated patients versus 12 control subjects, both groups with chronic intractable angina pectoris studied for 6 weeks.29 Another small randomized trial involved 24 patients with refractory angina.30 Nine other studies, either retrospective31–33 or prospective29,34–38 cohort studies, were identified in the literature. Although the results of these studies appear promising, there is still a paucity of data on the intermediate- and long-term benefit of these devices.B. Enhanced External CounterpulsationAnother nonpharmacological technique that has been described for treatment of patients with chronic stable angina is known as EECP. EECP was evaluated in a randomized, placebo-controlled multicenter trial to determine its safety and efficacy.39 Patients (n=139) with chronic stable angina, documented CAD, and a positive exercise treadmill test were randomly assigned to receive EECP (35 hours of active counterpulsation) or inactive EECP over a 4- to 7-week period. The authors concluded that EECP decreased angina frequency (P<0.05) and improved time to exercise-induced ischemia (P=0.01). Two multicenter registry studies that included 978 patients from 43 centers40 and 2289 patients from more than 100 centers41 evaluated the safety and effectiveness of EECP in treating chronic stable angina. These studies found the treatment to be generally well tolerated and efficacious; anginal symptoms were improved in approximately 75% to 80% of patients. However, additional clinical trial data are necessary before this technology can be recommended definitively.C. Laser TMRAnother emerging technique that has been studied for the treatment of more severe chronic stable angina refractory to medical or other therapies is laser TMR. This technique has either been performed in the operating room (with a carbon dioxide or holmium:YAG laser) or by a percutaneous approach with a specialized (holmium:YAG laser) catheter. Eight prospective randomized clinical trials have been performed, 2 with the percutaneous technique and the other 6 with an epicardial surgical technique.42–48 The goal in both approaches is to create a series of transmural endomyocardial channels to improve myocardial revascularization. Percutaneous TMR technology has not been approved by the Food and Drug Administration and should therefore be considered an experimental therapy.The surgical TMR technique has generally been associated with improvement in symptoms in patients with chronic stable angina. The mechanism for improvement in anginal symptoms is still controversial. Possible mechanisms for this improvement include increased myocardial perfusion, denervation of the myocardium, stimulation of angiogenesis, or perhaps some other unknown mechanism.49–51 There are conflicting data regarding improvement in exercise capacity.43,44,47 Despite the apparent benefit in decreasing anginal symptoms, no definite benefit has been demonstrated in terms of increasing myocardial perfusion.43,46,47There are currently no published studies to document the long-term efficacy of surgical TMR. Nonetheless, this technique appears to provide symptomatic relief for end-stage chronic angina in the short term. Additional follow-up studies are necessary to evaluate procedural efficacy in patients who have undergone surgical laser TMR alone, as well as coronary bypass surgery plus TMR.V. Asymptomatic Patients With Known or Suspected CADAt the direction of the Task Force, this update outlines the approach to asymptomatic patients with known or suspected CAD on the basis of a history and/or electrocardiographic (ECG) evidence of previous MI, coronary angiography, or an abnormal noninvasive test. The inclusion of asymptomatic patients with abnormal noninvasive tests does not constitute an endorsement of such tests for the purposes of screening but simply acknowledges the clinical reality that such patients often present for evaluation after such tests have been performed. Multiple ACC/AHA guidelines and scientific statements have discouraged the use of ambulatory monitoring, treadmill testing, stress echocardiography, stress myocardial perfusion imaging, and electron-beam computed tomography (EBCT) as routine screening tests in asymptomatic individuals.The full-text guideline includes many subsections on asymptomatic patients, which appear at the end of the appropriate sections for symptomatic patients. They are integra