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Overview of the management of stable angina pectoris

Author Joseph P Kannam, MD Julian M Aroesty, MD Bernard J Gersh, MB, ChB, DPhil, FRCP Section Editor Christopher P Cannon, MD Deputy Editor Gordon M Saperia, MD, FACC

Last literature review for version 16.2: mayo 31, 2008 | This topic last updated: junio 13, 2008
INTRODUCTION Angina pectoris occurs whenever myocardial oxygen demand exceeds oxygen supply; the clinical manifestation is chest discomfort caused by transient myocardial ischemia. A clinical diagnosis of angina has a 90 percent predictive accuracy for the presence of coronary heart disease (CHD). The management of stable angina involves pharmacologic intervention to prevent or minimize ischemia, reduction of risk factors for CHD and revascularization in some patients. Our recommendations for the management of stable angina are generally in accord with those made in the 2002 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of patients with chronic stable angina and the limited revisions in the 2007 ACC/AHA chronic angina focused update [1,2] . The initial diagnosis of angina, patients with angina that is refractory to conventional therapeutic approaches, and unstable angina are discussed separately. (See "Diagnostic approach to chest pain in adults" and see "New therapies for angina pectoris" and see "Overview of the management of unstable angina and acute non-ST elevation (non-Q wave) myocardial infarction"). DEFINITIONS There are two types of angina:

Stable angina, which refers to chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. Unstable angina, which is an acute coronary syndrome that encompasses a variety of clinical conditions including the new onset of chest pain, rest angina, an accelerating pattern of previously stable angina, post-myocardial infarction (MI) angina, and angina after a revascularization procedure. (See "Classification of unstable angina and non-ST elevation (non-Q wave) myocardial infarction").

GENERAL PRINCIPLES The treatment of angina is aimed at decreasing oxygen demand and/or increasing oxygen supply [3] . (See "Pathophysiology and clinical presentation of ischemic chest pain"). Myocardial oxygen demand varies with:

Heart rate Systolic blood pressure (afterload) Contractility Left ventricular (LV) wall stress, which is proportional to LV end-diastolic volume (preload) and myocardial mass

Myocardial oxygen supply is dependent upon:

Coronary blood flow Perfusion pressure

Both of these are limited in patients with critical (70 percent) coronary artery stenoses or prominent coronary vasoconstriction [3] . The subendocardium, which is most vulnerable to ischemia, receives most of its blood supply during diastole [4] ; conditions that decrease the duration of diastole, such as tachycardia, enhance the potential for subendocardium ischemia.

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In addition to severe obstructive lesions that cause stable angina, there are also nonobstructive (ie, non-flow-limiting) may remain silent, progress slowly to obstructive symptomatic lesions, or rupture, causing an acute coronary syndrome that may be manifested as unstable angina, an acute MI, or ischemic sudden death [3] . (See "The role of plaque rupture in acute coronary syndromes"). Goals of therapy The goals of the therapy of stable angina include:

Relief of symptoms Prevention or slowing of disease progression Prevention of future cardiac events, such as MI, unstable angina, or the need for revascularization Improvement in survival

These goals can be achieved with a variety of modalities including medical therapy, nonpharmacologic and lifestyle measures, percutaneous coronary intervention (PCI), and surgical revascularization with a coronary artery bypass graft (CABG). RECOMMENDATIONS FOR ANTIANGINAL THERAPY There are currently three major classes of antiischemic drugs used in the medical management of angina pectoris: nitrates (short and long acting), beta blockers, and calcium channel blockers [1] . Most commonly, a combination of these agents is used for management. Nitrates For patients with stable angina, the various nitrate preparations are useful both to treat acute episodes and to prevent new episodes and improve exercise capacity (show table 1). Nitrates, usually in the form of a sublingual preparation, are a first-line therapy for the treatment of acute anginal symptoms. While they act as venodilators, coronary vasodilators, and modest arteriolar dilators [5,6] , the primary antiischemic effect of nitrates is to decrease myocardial oxygen demand by producing systemic vasodilation more than coronary vasodilation. In patients with exertional stable angina, chronic nitrate therapy, with oral or dermal preparations, improves exercise tolerance, time to onset of angina, and STsegment depression during exercise testing. In combination with beta blockers or calcium channel blockers, nitrates produce greater antianginal and antiischemic effects. There are various preparations of nitrates available; there is no difference in efficacy among these preparations. The use of the various preparations as well as their side effects, including nitrate tolerance, is discussed elsewhere. (See "Nitrates in the management of stable angina pectoris"). Beta blockers Beta blockers relieve anginal symptoms by competitively inhibiting sympathetic stimulation of the heart, reducing both heart rate and contractility. Since beta blockers reduce the heart rate-blood pressure product during exercise, the onset of angina or the ischemic threshold during exercise is delayed or avoided. All types of beta blockers appear to be equally effective in exertional angina. Choice of agents In patients with chronic stable angina, important considerations in the choice of which beta blocker to use are ancillary properties, such as side effects, dosing interval, and cost. In general propranolol is less expensive than other beta blockers. Lower doses of the cardioselective beta blockers (such as atenolol and metoprolol) have the advantage of blocking beta-1-receptor mediated stimulation of the heart with lesser inhibition of the peripheral vasodilation and bronchodilation induced by the beta-2 receptors. As a result, a long acting cardioselective agent (atenolol or metoprolol) is preferred for the treatment of stable angina. There are no major advantages of a nonselective agent, other than the low cost of propranolol, and there are potential disadvantages in patients with certain underlying diseases such as obstructive lung disease, asthma, peripheral vascular disease, diabetes, and depression. The starting dose of atenolol is 25 mg once daily which can be increased as tolerated to a maximum of 200 mg once a day (assuming renal function is relatively normal) until the resting heart rate is 50 to 60 beats/min and does not exceed 100 beats/min with ordinary activity. The starting dose of metoprolol is 25 mg BID, which can be increased to 200 mg BID as tolerated. An extended release form of metoprolol, given once per day, can substituted once an effective dose has been established. Beta blockers are generally well tolerated and extremely effective in reducing anginal episodes and improving exercise tolerance. In addition, beta blockers are the only antianginal drugs proven to prevent reinfarction and to improve survival in patients who have sustained an MI [7] . (See "Beta blockers in the management of stable angina pectoris" and see "Beta blockers in the management of acute coronary syndrome"). In comparison to these benefits, beta blockers do not appear to improve survival or reduce the incidence of MI in patients with chronic stable angina who have never had an MI, as in trials on mild hypertension. As a result, the primary therapeutic goal with beta blockers in such patients is to reduce the frequency and

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severity of angina and to improve exercise capacity without significant side effects. (See "Choice of therapy in essential hypertension: Clinical trials", section on Beta blockers as initial therapy?). We agree with the 2007 ACC/AHA chronic angina focused update, which recommends beta blockers in all patients with stable angina who have had an ACS or who have left ventricular dysfunction, unless contraindicated [2] . Achieving adequate beta blockade The efficacy of beta blockers in relieving angina is dose-dependent. Thus, it is important to be certain that adequate beta blockade has been attained. Reasonable goals when titrating the dose include:

Resting heart rate between 50 and 60 beats/min. The target heart rate for some patients with more severe angina can be <50 beats/min, as long as the bradycardia is asymptomatic and heart block does not develop.

Patients with resting bradycardia prior to therapy can be treated with a calcium channel blocker (such as diltiazem or nifedipine), nitrates, or a drug with intrinsic sympathomimetic activity if a beta blocker is necessary. Similar considerations apply to patients with atrioventricular conduction delay.

Blunting of peak heart rate and blood pressure during exercise, which can be measured by the patient or during exercise testing, if performed. Reduction in the frequency and severity of angina and in the use of sublingual nitroglycerin.

Side effects The most frequent side effects associated with beta blockers include: bradycardia, conduction disturbances, bronchoconstriction, worsening of symptoms of peripheral vascular disease, fatigue, central nervous system side effects, and impotence. As a result, beta blockers should be used with caution in patients with obstructive airways disease or peripheral vascular disease and, initially at very low doses in patients with heart failure. (See "Major side effects of beta blockers" and see "Use of beta blockers in heart failure due to systolic dysfunction"). Beta blockers should not be used in patients with vasospastic or variant (Prinzmetal) angina. In such patients, they are ineffective and may increase the tendency to induce coronary vasospasm from unopposed alpha-receptor activity. (See "Variant angina"). Calcium channel blockers Calcium channel blockers prevent calcium entry into vascular smooth muscle cells and myocytes, which leads to coronary and peripheral vasodilatation, decreased atrioventricular (AV) conduction, and reduced contractility [8] . In patients with angina, these effects result in decreased coronary vascular resistance and increased coronary blood flow. Calcium blockers also decrease myocardial oxygen demand by reducing systemic vascular resistance and arterial pressure and a negative inotropic effect. Choice of agent The degree to which these changes occur varies with the type of calcium channel blocker given.

Verapamil is a negative inotrope that also slows sinus rate and decreases AV conduction (negative chronotrope). It is a much less potent vasodilator than the dihydropyridines. The dihydropyridines (eg, nifedipine, nicardipine, felodipine, amlodipine) have a greater selectivity for vascular smooth muscle than for the myocardium. They are potent vasodilators with less effect on contractility and AV conduction. Diltiazem is a modest negative inotropic and chronotropic agent and vasodilator and has intermediate effects between the dihydropyridines and verapamil.

If a calcium channel blocker is used, long-acting diltiazem or verapamil or a second generation dihydropyridine (amlodipine or felodipine) should be selected. Short-acting dihydropyridines, especially nifedipine, should be avoided unless used in conjunction with a beta blocker in the management of CHD because of evidence of an increase in mortality after an MI and an increase in acute MI in hypertensive patients. (See "Major side effects and safety of calcium channel blockers"). When to use All of the calcium channel blockers reduce anginal symptoms and increase exercise tolerance and exercise time before the onset of angina or ischemia, especially when used in conjunction with other antianginal agents. (See "Calcium channel blockers in the management of stable angina pectoris").

They should be used in combination with beta blockers when initial treatment with beta blockers is not successful. They may be a substitute for a beta blocker when beta blockers are contraindicated or cause side effects. Calcium channel blockers (eg, diltiazem at a dose of 240 to 360 mg per day) are effective in patients with vasospastic or variant (Prinzmetal) angina; they are the preferred agents in this setting. (See "Variant angina").

Side effects Potential side effects include symptomatic bradycardia, heart block, worsening heart failure, constipation, flushing, headache, dizziness, and pedal edema. (See "Major side effects and safety of calcium channel blockers").

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Relative effectiveness of medical therapies Beta blockers and calcium channel blockers generally have equal efficacy in the management of stable angina [1,9] . A meta-analysis was performed of 90 randomized or crossover studies comparing at least two of the classes of beta blockers, calcium channel blockers, and long-acting nitrates for efficacy and tolerability in the treatment of patients with stable angina [9] . The following observations were noted:

There were no observed differences in outcome (eg, cardiac death and MI) between beta blockers and calcium channel blockers. Too few patients received long-acting nitrates for efficacy analysis of these drugs against either of the other classes. For the variables where differences existed between beta blockers and calcium blockers (eg, episodes of angina per week and side effects), the major effect was observed with beta blockers compared to nifedipine. As an example, there were 0.31 fewer episodes of angina per week with beta blockers than with calcium channel blockers as a group and 0.63 fewer episodes per week than with nifedipine. However, as noted above, nifedipine is typically avoided now in the treatment of patients with CHD. Short-acting calcium channel blockers were also associated with a 0.44 increase in weekly angina episodes compared to beta blockers, while long-acting calcium channel blockers decreased angina frequency by 0.08 episodes per week.

Beta blockers were discontinued because of adverse reaction less often than calcium channel blockers (odds ratio 0.72). Again, this difference was most striking with nifedipine.

Despite the differences in angina frequency, there were no differences in nitroglycerin use or exercise time between beta blockers and calcium channel blockers.

Angina that persists with monotherapy Addition of a second drug is indicated if angina persists with monotherapy. If, for example, the patient is already taking a beta blocker, a long-acting calcium channel blocker, particularly if the patient is also hypertensive, or a long-acting nitrate can be started. The efficacy of combination therapy was illustrated in a study that randomly assigned 397 patients to four weeks of monotherapy with felodipine or metoprolol or a combination of felodipine and metoprolol [10] . Combination therapy was more effective for increasing exercise duration and better tolerated than monotherapy. Although a third class of antianginal drug can be added in patients who have limiting angina on two agents, many physicians would consider coronary angiography in such patients and revascularization if indicated. ACE inhibitors Angiotensin converting enzyme (ACE) inhibitors are not considered a usual treatment for angina pectoris. There are conflicting data regarding a possible benefit in reducing exercise-induced ischemia. A small randomized trial noted an improvement in time to 0.1 mV ST depression on treadmill testing with an ACE inhibitor [11] . In contrast, ACE inhibitors had no effect on the development of myocardial ischemia in the QUASAR trial [12] . It has also been suggested that ACE inhibitors have a specific benefit in patients at high risk for cardiovascular disease [13] . However, as described in detail elsewhere, the available evidence suggests that the attained blood pressure not the drug used is of primary importance in such patients. (See "Choice of antihypertensive drug and blood pressure goal in patients at increased risk for a cardiovascular event"). The 2007 ACC/AHA chronic angina focused update makes the following recommendations regarding the use of angiotensin inhibitors in patients with stable angina unless contraindicated [2] :

ACE inhibitors are recommended for patients with myocardial infarction, left ventricular ejection fraction (LVEF) less than 40 percent, hypertension, diabetes, or chronic kidney disease ACE inhibitors are recommended for patients with stable angina who are not lower risk as defined as those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed ACE inhibitors may be considered for lower risk patients with mildly reduced or normal LVEF in whom risk factors are well controlled and revascularization has been performed Angiotensin receptor blockers (ARBs) are recommended for patients who have hypertension, have indications for but are intolerant of ACE inhibitors, have heart failure, or have had and MI with LVEF 40 percent ARBs may be considered in combination with ACE inhibitors for heart failure due to left ventricular systolic dysfunction Aldosterone antagonists (spironolactone or eplerenone) are recommend for post MI patients without significant renal dysfunction or hyperkalemia who are already receiving therapeutic doses of an ACE inhibitor and a beta blocker, have an LVEF 40 percent and have either diabetes or heart failure (strong recommendation)

New therapies A number of new medical and invasive therapies have been evaluated for use in patients with stable angina. Only ranolazine, a fatty acid oxidation inhibitor, has been approved for clinical use and its role is evolving [14] . The absence of a proarrhythmic effect of ranolazine in the MERLIN-TIMI 36 trial has mitigated concerns of possible QT interval prolongation. We believe ranolazine can be used as an option for angina patients who have failed all other antianginal therapies. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction", section on Ranolazine). Other potential therapies include ivabradine and fasudil, and mechanical therapies such as enhanced external balloon counterpulsation, spinal cord stimulation, and transmyocardial laser revascularization. These approaches are discussed separately. (See "New therapies for angina pectoris").

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Exacerbating factors Treatment of any underlying medical conditions that might aggravate myocardial ischemia, such as hypertension, fever, tachyarrhythmias (eg, atrial fibrillation), thyrotoxicosis, anemia or polycythemia, hypoxemia, or valvular heart disease should be undertaken. Asymptomatic low grade arrhythmias are not treated routinely, but may require therapy under circumstances, such as left ventricular dysfunction. There should also be modification of activities that exacerbate angina, such as exercise in cold weather or after a meal. Summary Since beta blockers and calcium channel blockers appear to be of equivalent efficacy, the choice of one or another as initial therapy is usually based upon other factors, such as associated medical conditions (show table 2). As examples, beta blockers should, in the absence of a contraindication, be given to virtually all patients who have had a prior MI or who have stable heart failure on an ACE inhibitor. (See "Beta blockers in the management of acute coronary syndrome" and see "Use of beta blockers in heart failure due to systolic dysfunction"). Combination therapy using beta blockers and calcium blockers, with or without long acting nitrates, is often beneficial in patients who are not controlled with monotherapy. OTHER INTERVENTIONS The optimal management of stable angina requires more than antianginal medical therapy. Reducing myocardial oxygen demand and preventing both the development of symptomatic lesions and cardiovascular events are also central to long term care. Most nonpharmacologic measures relieve angina primarily by reducing myocardial oxygen demand; other measures are of importance for the treatment of risk factors associated with the development and progression of coronary artery disease and its sequelae [1,3] . (See "Secondary prevention of cardiovascular disease: Risk factor reduction"). Antiplatelet therapy In the absence of a contraindication, all patients should be treated with aspirin (81 to 325 mg/day). Patients who have a gastrointestinal bleed on low dose aspirin should, after the episode is controlled, be treated with aspirin (81 mg/day) plus a proton pump inhibitor. Clopidogrel is an alternative in patients who are allergic to aspirin. There is no role for dipyridamole. (See "Benefits of aspirin in cardiovascular disease"). Risk factor reduction Risk factor reduction should be a central component of the management of patients with stable angina. This includes treatment of hypertension, cessation of smoking, lipid lowering with a regimen that includes statin therapy, weight reduction, and glycemic control in diabetics. In addition to contributing to chronic progression of atherosclerosis, smoking and hypertension can precipitate acute coronary ischemia by increasing oxygen demands and reducing oxygen supply [15,16] . The specific goals are described elsewhere. (See "Secondary prevention of cardiovascular disease: Risk factor reduction" and see "Choice of antihypertensive drug and blood pressure goal in patients at increased risk for a cardiovascular event", section on Goal blood pressure, and see "Cardiovascular risk of smoking and benefits of smoking cessation" and see "Intensity of lipid lowering therapy in secondary prevention of coronary heart disease"). Stress reduction should also be encouraged and treatment of underlying depression and anxiety should be considered, if appropriate. The impact of these interventions in patients with chronic CHD and stable angina is unknown, although their role in patients with a prior MI is better established. (See "Psychosocial factors in coronary and cerebral vascular disease" and see "Psychosocial and other social factors in acute myocardial infarction"). Exercise program Gradual institution of a regular aerobic exercise program should be encouraged. Exercise can result in a lower oxygen requirement for a given workload, thereby improving exercise tolerance and a sense of well-being, and reducing symptoms [17-19] . An exercise program is also beneficial in the management of risk factors for CHD such as lipids, blood pressure, obesity, and diabetes mellitus. The potential efficacy of exercise training was illustrated in a trial of 101 men age 70 with class I to III angina (show table 3) and angiographic evidence of coronary disease; higher risk patients were excluded [20] . The patients were randomly assigned to PCI with stenting or an exercise training program. At 12 months, survival free of cardiac events (cardiac death, cardiac arrest, MI, stroke, revascularization, or hospitalization for worsening angina) was significantly higher with exercise training than with PCI (88 versus 70 percent). Recommendations for referral to cardiac rehabilitation programs and routine physical activity for patients with stable angina pectoris are discussed separately. (See "Components of cardiac rehabilitation and exercise prescription" and see "Exercise and fitness in the prevention of cardiovascular disease"). Optimal medical care The potential benefit of utilizing all of the interventions discussed above was evaluated in the COURAGE trial, which is discussed separately. (See "Medical versus interventional therapy in the management of stable angina pectoris", section on PCI versus medical therapy). Influenza vaccination The 2007 ACC/AHA chronic angina focused update and the 2007 Advisory Committee on Immunization Practices report recommend annual influenza vaccination for all patients with cardiovascular disease, excluding hypertension [2,21] . (See "Influenza vaccination in adults", section on Target groups for immunization). MEASUREMENT OF LV SYSTOLIC FUNCTION Most patients with chronic stable angina do not need measurement of LV systolic function. However, it may be useful in selected patients to determine optimal medical, the role of interventional or surgical therapy, or in making recommendations about activity level, rehabilitation, and work status. This assessment may be appropriate at the time of diagnosis, later in the patient's course, or both. The 2002 ACC/AHA guidelines on the management of patients with chronic stable angina strongly recommends measurement of LV systolic function in patients with the following [1] :

A history of prior MI, pathologic Q waves, or symptoms or signs of heart failure.

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A systolic murmur suggesting mitral regurgitation. Complex ventricular arrhythmias.

The methodology for the measurement of LV systolic function is discussed separately. (See "Noninvasive methods for measurement of left ventricular systolic function"). EXERCISE TESTING A stress test should be performed in patients with stable angina to evaluate the efficacy of the antiischemic program and for prognostic information. (See "Stress testing to determine prognosis and management of patients with known or suspected coronary heart disease"). The choice of initial stress test, eg, exercise ECG, exercise with perfusion imaging, pharmacologic stress testing with imaging (echocardiography or myocardial perfusion scan), may be influenced the patient's resting ECG, physical ability to perform exercise, local expertise, and available technologies. A standard exercise ECG is preferred as the initial test in patients with a normal resting ECG who are able to exercise and are not taking digoxin. (See "Advantages and limitations of different stress testing modalities"). Exercise testing can identify a subset of high-risk patients who have an annual mortality of more than 3 per cent (show table 4) [22,23] . In comparison, low-risk patients, with an annual mortality below one per cent, are able to exercise into stage 3 of a Bruce protocol with a normal ECG. (See "Exercise ECG testing to determine prognosis of coronary heart disease", section on Treadmill scores). Once this information has been obtained, the therapeutic approach is determined by the individual patient characteristics. Low- and intermediate-risk patients are generally treated medically, while high-risk patients or those with angina refractory to medical therapy undergo coronary angiography and revascularization with either PCI or CABG. CORONARY ANGIOGRAPHY AND REVASCULARIZATION The 2002 ACC/AHA guidelines on the management of chronic stable angina recommended coronary angiography in selected patients (show table 5) [1] . There are two primary indications for coronary angiography followed by revascularization of appropriate lesions:

Angina that significantly interferes with a patient's lifestyle despite maximal tolerable medical therapy. This includes active patients who desired improved quality of life compared to medical therapy. Patients with high-risk criteria and selected patients with intermediate-risk criteria on noninvasive testing, regardless of anginal severity. (See "Stress testing to determine prognosis and management of patients with known or suspected coronary heart disease", section on Choice of therapy).

Although coronary angiography is the traditional gold standard for the diagnosis of coronary atherosclerosis, it is not a reliable indicator of the functional significance of a coronary stenosis [24] . However, the extent and severity of CHD and LV dysfunction identified on coronary angiography are powerful clinical predictors of prognosis and the findings are often used to guide further therapy in patients with angina pectoris [25,26] . Revascularization is performed in appropriate patients in whom angiography reveals anatomy for which revascularization has a proven benefit or in whom medical therapy has failed. (See "Medical versus interventional therapy in the management of stable angina pectoris", section on Factors that favor an interventional approach). Since the rates of MI and overall survival are generally similar, the choice between PCI and CABG is based upon anatomy and other factors such as left ventricular function and the presence or absence of diabetes. With the availability of drug-eluting stents, PCI is increasingly performed for most lesions. These issues are discussed in detail separately. (See "Bypass surgery versus percutaneous intervention in the management of stable angina pectoris: Recommendations" and see "Bypass surgery versus percutaneous intervention in the management of stable angina pectoris: Clinical trials"). CONSIDERATIONS IN THE ELDERLY Individuals over the age of 65 years represent a growing proportion of the population in developed countries; as the population ages, the frequency of both coronary heart disease (CHD) and myocardial infarction (MI) increases [27,28] . The Cardiovascular Health Study reported that the incidence of CHD in the elderly was 16.3 and 5.8 per 1000 person-years in men and women, respectively between the ages of 65 and 74; the respective values between the ages of 75 and 84 were 28.7 and 12.9 [27] . In addition, elderly patients who have CHD have more severe disease than younger subjects. The approach to the management of angina in the elderly should not differ substantially from that advocated for younger patients. However, both medical and especially interventional therapy have been underutilized in this population [29] . This occurs for several reasons:

Elderly patients with CHD often present with atypical symptoms, including exertional dyspnea. Silent myocardial ischemia is also common. The efficacy of therapies for CHD in the elderly is often unrecognized or underestimated, in part because the elderly are usually underrepresented in randomized controlled studies [30] . The presence of comorbid conditions and difficulties managing medications in the elderly also complicate care.

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Medical treatment of angina The cornerstones of medical management of chronic angina in patients of any age are aspirin (81 to 325 mg/day) and beta blockers [1] . Both are underutilized in the elderly, particularly as secondary prevention in those who have had a recent MI [31,32] . (See "Benefits of aspirin in cardiovascular disease"). All of the drugs used in younger patients for the control of anginal symptoms are appropriate for the elderly. However, the elderly may experience more side effects, particularly hypotension from nitrates and calcium channel blockers and central nervous system effects from beta blockers. Elderly patients may need to be started on lower doses initially and should be monitored carefully for side effects. Revascularization Percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) can be used to treat stable angina in the elderly but are typically performed less often, in part due to concerns about age specific risk [33] . However, decision making should make an attempt at weighing risk with potential advantages as is done in younger patients. Elderly patients undergoing a PCI are at an increased risk for a complication compared to younger patients [34-38] . The magnitude of this effect was illustrated in a report that compared 7472 octogenarians (mean age 83) and 102,236 younger patients (mean age 62) undergoing an intervention between 1994 and 1997 [37] . The octogenarians had an increased risk of death (3.8 versus 1 percent), ST elevation infarction (1.9 versus 1.3 percent), renal failure (3.2 versus 1 percent), and vascular complications (6.7 versus 3.3 percent). The long-term outcome after PCI is also less favorable in elderly patients, with a higher incidence of death from all causes, cardiac death, and angina compared to younger patients [34-36] . The increase in adverse outcomes with PTCA alone is most prominent in patients with incomplete revascularization [34,35] . The risk of bleeding requiring transfusion is higher in elderly patients undergoing PCI, whether or not they receive a glycoprotein (GP) IIb/IIIa inhibitor. This issue was examined in a series of 1392 patients 80 years of age undergoing PCI (more than two-thirds with stenting) at a single institution [39] . There were no intracranial hemorrhages. The incidence of bleeding requiring transfusion was 8.6 percent without a GP IIb/IIIa inhibitor versus 9.8 percent with such therapy (eptifibatide in 73 percent). Transfusion rates were much lower in randomized trials of younger patients such as EPISTENT (2.2 percent without versus 2.8 percent with abciximab) or ESPRIT (1 percent with or without eptifibatide). CABG is usually well tolerated in the elderly, including those over 80 years of age [40-43] . However, Medicare data comparing 24,461 CABG patients 80 years of age to those 65 to 70 years of age undergoing CABG found that the older patients had a longer hospital stay (14.3 versus 10.4 days) and higher mortality rates in-hospital (11.5 versus 4.4 percent), at one year (19.3 versus 7.9 percent), and at three years (28.8 versus 13.1 percent) [44] . As in younger subjects, the outcome of CABG is improved with the use of an arterial compared to a saphenous vein graft [45,46] . Despite the initial increase in surgical risk, elderly subjects, including octogenarians, who undergo CABG have a long-term survival rate similar to that of an agematched control population [44,47] and an improvement in quality of life similar to that in younger patients [43,48] . (See "Long-term outcome after coronary artery bypass graft surgery"). Coronary artery reoperation Elderly patients are increasingly being considered for CABG reoperation, but the outcome from a second CABG is usually not as good as with the first surgery. The short- and long-term outcome of elderly patients undergoing a second CABG was examined in a review of 739 patients 70 years of age (mean age 74 ) [49] . In-hospital mortality was 7.6 percent. Perioperative factors associated with an increased risk included emergency surgery, left main disease, and left ventricular dysfunction. Actuarial survival at 5 and 10 years was 75 and 49 percent, respectively, and cardiac-event free survival was 60 and 27 percent, respectively. Mortality was associated with comorbidities such as diabetes mellitus, left ventricular dysfunction, peripheral vascular disease, and postoperative stroke. Summary While the elderly have been underrepresented in clinical trials, there are sufficient data that medical and revascularization therapies are effective in the elderly. The decision whether to continue with optimal medical therapy or perform revascularization requires the elderly patient's understanding of the strengths and weaknesses of each approach and a respect by the health care delivery team of that patient's subsequent preferences. FOLLOW-UP Patients with chronic stable angina that is effectively managed require follow-up on a regular basis, eg, every four to six months during the first year, and every 4 to 12 months thereafter [1] . At each visit, a detailed history should be obtained and physical examination performed. In particular, it is important to establish:

A change in physical activity Any change in the frequency, severity, or pattern of angina Tolerance of and compliance with the medical program Modification of risk factors The development of new or worsened comorbid illnesses

Routine laboratory examination includes glucose, lipid profile, and hematocrit. An assessment of electrolytes and renal and thyroid function is guided by symptoms or history. An ECG should be obtained if medications are altered or if the history or physical examination have changed.

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The ACC/AHA Task Force has published recommendations for noninvasive testing and angiography during follow-up [1] . These studies are primarily indicated when there is a change in clinical status, such as a change in anginal frequency, severity, or pattern; a new MI; new or worsening heart failure; or the appearance of a new murmur suggesting significant valvular disease.

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Gibbons, RJ, Abrams, J, Chatterjee, K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina. Available at: www.acc.org/qualityandscience/clinical/statements.htm (accessed August 24, 2006). Fraker, TD Jr, Fihn, SD, Gibbons, RJ, et al. 2007 chronic angina focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 guidelines for the management of patients with chronic stable angina. J Am Coll Cardiol 2007; 50:2264. Abrams, J, Thadani, U. Therapy of stable angina pectoris: the uncomplicated patient. Circulation 2005; 112:e255. Lewis, FB, Coffman, JD, Gregg, DE. Effect of heart rate and intracoronary isoproterenol, levarterenol, and epinephrine on coronary flow and resistance. Circ Res 1961; 9:89. Kaski, JC, Plaza, LR, Meran, DO, et al. Improved coronary supply: Prevailing mechanism of action of nitrates in chronic stable angina. Am Heart J 1985; 110:238. Parker, JO. Nitrates and angina pectoris. Am J Cardiol 1993; 72:3C. Teo, KK, Yusuf, S, Furberg, CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction: An overview of results from randomized controlled trials. JAMA 1993; 270:1589. Braunwald, E. Mechanism of action of calcium-channel-blocking agents. N Engl J Med 1982; 307:1618. Heidenreich, PA, McDonald, KM, Hastie, T, et al. Meta-analysis of trials comparing-blockers, calcium antagonists, and nitrates for stable angina. JAMA 1999; 281:1927.

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10. Emanuelsson, H, Egstrup, K, Nikus, K, et al, for the TRAFFIC Study Group. Antianginal efficacy of the combination of felodipine-metoprolol 10/100 mg compared with each drug alone in patients with stable effort-induced angina pectoris: A multicenter parallel group study. Am Heart J 1999; 137:854. 11. van den Heuvel AF, Dunselman, PH, Kingma, T, et al. Reduction of exercise-induced myocardial ischemia during add-on treatment with the angiotensin-converting enzyme inhibitor enalapril in patients with normal left ventricular function and optimal beta blockade. J Am Coll Cardiol 2001; 37:470. 12. Pepine, CJ, Rouleau, JL, Annis, K, et al. Effects of angiotensin-converting enzyme inhibition on transient ischemia: the Quinapril Anti-Ischemia and Symptoms of Angina Reduction (QUASAR) trial. J Am Coll Cardiol 2003; 42:2049. 13. Yusuf, S, Sleight, P, Pogue, J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000; 342:145. 14. Chaitman, BR. Ranolazine for the treatment of chronic angina and potential use in other cardiovascular conditions. Circulation 2006; 113:2462. 15. Winniford, MD, Jansen, DE, Reynolds, GA, et al. Cigarette smoking-induced coronary vasoconstriction in atherosclerotic coronary artery disease and prevention by calcium antagonists and nitroglycerin. Am J Cardiol 1987; 59:203. 16. Winniford, MD, Wheelan, KR, Kremers, MS, et al. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: Evidence for adrenergically mediated alterations in coronary artery tone. Circulation 1986; 73:662. 17. Thompson, PD. Exercise prescription and proscription for patients with coronary artery disease. Circulation 2005; 112:2354. 18. Dressendorfer, RH, Smith, JL, Amsterdam, EA, Mason, DT. Reduction of submaximal exercise myocardial oxygen demand post-walk training program in coronary patients due to improved physical work efficiency. Am Heart J 1982; 103:358. 19. Barnard, RJ, MacAlphin, R, Kattus, AA, Buckber, GD. Effect of training on myocardial oxygen supply/demand balance. Circulation 1977; 56:289. 20. Hambrecht, R, Walther, C, Mobius-Winkler, S, et al. Percutaneous coronary angioplasty compared with exercise training in patients with stable coronary artery disease: a randomized trial. Circulation 2004; 109:1371. 21. Fiore, AE, Shay, DK, Haber, P, et al. Prevention and control of influenza. Recommendations of the Advisory Committee on Immunization Practices (ACIP), 2007. MMWR Recomm Rep 2007; 56:1. 22. Weiner, DA, Ryan, TJ, McCabe, CH, et al. Prognostic importance of a clinical profile and exercise test in medically treated patients with coronary artery disease. J Am Coll Cardiol 1984; 3:772. 23. Mark, DB, Hlatky, MA, Harrell, FE Jr, et al. Exercise treadmill score for predicting prognosis in coronary artery disease. Ann Intern Med 1987; 106:793. 24. White, CW, Wright, CB, Doty, DB, et al. Does visual interpretation of the coronaryarteriogram predict the physiologic importance of a coronary stenosis? N Engl J Med 1984; 310:819.

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25. Ringqvist, I, Fisher, LD, Mock, M, Davis, KB. Prognostic value of angiographic indices of coronary artery disease from the Coronary Artery Surgery Study (CASS). J Clin Invest 1983; 71:1854. 26. Emond, M, Mock, MB, Davis, KB, et al. Long-term survival of medically treated patients in the Coronary Artery Surgery Study (CASS) Registry. Circulation 1994; 90:2645. 27. Psaty, BM, Furberg, CD, Kuller, LH, et al. Traditional risk factors and subclinical disease measures as predictors of first myocardial infarction in older adults. Arch Intern Med 1999; 159:1339. 28. Goldberg, RJ, McCormick, D, Gurwitz, JH, et al. Age-related trends in short- and long-term survival after acute myocardial infarction: A 20-year population-based perspective (1975-1995). Am J Cardiol 1998; 82:1311. 29. Williams, MA, Fleg, JL, Ades, PA, et al. Secondary prevention of coronary heart disease in the elderly (with emphasis on patients 75 years of age): an American Heart Association scientific statement from the Council on Clinical Cardiology Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention. Circulation 2002; 105:1735. 30. Lee, PY, Alexander, KP, Hammill, BG, et al. Representation of elderly persons and women in published randomized trials of acute coronary syndromes. JAMA 2001; 286:708. 31. Krumholz, H, Radford, MJ, Ellerback, EF, et al. Aspirin for secondary prevention after acute myocardial infarction in the elderly: prescribed use and outcomes. Ann Intern Med 1996; 124:292. 32. Soumerai, SB, McLauglin, TJ, Spiegleman, D, et al. Adverse outcomes of underuse of beta-blockers in elderly survivors of acute myocardial infarction. JAMA 1997; 277:115. 33. Bearden, D, Allman, R, McDonald, R, et al. Age, race, and gender variation in the utilization of coronary artery bypass surgery and angioplasty in SHEP. SHEP Cooperative Research Group. Systolic Hypertension in the Elderly Program. J Am Geriatr Soc 1994; 42:1143. 34. ten Berg, JM, Voors, AA, Suttorp, MJ, et al. Long-term results after successful percutaneous coronary angioplasty in patients over 75 years of age. Am J Cardiol 1996; 77:690. 35. Tan, KH, Sulke, N, Taub, N, et al. Percutaneous transluminal coronary angioplasty in patients 70 years old or older: 12 years'experience. Br Heart J 1995; 74:310. 36. Thompson, RC, Holmes, DR, Gersh, BJ, et al. Predicting early and intermediate-term outcome of coronary angioplasty in the elderly. Circulation 1993; 88:1579. 37. Batchelor, WB, Anstrom, KJ, Muhlbaier, LH, et al. Contemporary outcome trends in the elderly undergoing percutaneous coronary interventions: results in 7,472 octogenarians. National Cardiovascular Network Collaboration. J Am Coll Cardiol 2000; 36:723. 38. Thompson, RC, Holmes, DR, Grill, DE, et al. Changing outcome of angioplasty in the elderly. J Am Coll Cardiol 1996; 27:8. 39. Sadeghi, HM, Grines, CL, Chandra, HR, et al. Percutaneous coronary interventions in octogenarians. glycoprotein IIb/IIIa receptor inhibitors'safety profile. J Am Coll Cardiol 2003; 42:428. 40. Williams, DB, Carrillo, RG, Traad, EA, et al. Determinants of operative mortality in octogenarians undergoing coronary bypass. Ann Thorac Surg 1995; 60:1038. 41. Kolh, P, Kerzmann, A, Lahaye, L, et al. Cardiac surgery in octogenarians. Peri-operative outcome and long-term results. Eur Heart J 2001; 22:1235. 42. Rosengart, TK, Finnin, EB, Kim, DY, et al. Open heart surgery in the elderly: results from a consecutive series of 100 patients aged 85 years or older. Am J Med 2002; 112:143. 43. Conaway, DG, House, J, Bandt, K, et al. The elderly: health status benefits and recovery of function one year after coronary artery bypass surgery. J Am Coll Cardiol 2003; 42:1421. 44. Peterson, ED, Cowper, PA, Jollis, JG, et al. Outcomes of coronary artery bypass graft surgery in 24,461 patients aged 80 years or older. Circulation 1995; 92:II85. 45. He, GW, Achuff, TE, Ryan, WH, et al. Determinants of operative mortality in elderly patients undergoing coronary artery bypass grafting. Emphasis on the influence of internal mammary artery grafting on mortality and morbidity. J Thorac Cardiovasc Surg 1994; 108:73. 46. Galbut, DL, Traad, EA, Dorman, MJ, et al. Coronary bypass grafting in the elderly>Single versus bilateral internal mammary artery grafts. J Thorac Cardiovasc Surg 1993; 106:128. 47. Canver, CC, Nichols, RD, Cooler, SD, et al. Influence of increasing age on long-term survival after coronary artery bypass grafting. Ann Thorac Surg 1996; 62:1123. 48. Heijmeriks, JA, Pourrier,S, Dassen, P, et al. Comparison of quality of life after coronary and/or valvular cardiac surgery in patients 75 years of age with younger patients. Am J Cardiol 1999; 83:1129. 49. Yamamuro, M, Lytle, BW, Sapp, SK, et al. Risk factors and outcomes after coronary reoperation in 739 elderly patients. Ann Thorac Surg 2000; 69:464.

GRAPHICS Common nitrate preparations used in the treatment of stable angina Route of Onset of action, Preparation administration minutes Nitroglycerin Sublingual tablet 2-5 Sublingual spray 2-5

Duration of action 15-30 min 15-30 min

Dose 0.15-0.9 mg 0.4 mg

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Ointment Transdermal Oral sustained release Intravenous Isosorbide dinitrate Sublingual Oral Spray Chewable Oral slow release Intravenous Oral Oral Sublingual Sublingual Oral 2-5 30 30 2-5 2-5 30 2-5 2-5 30 2-5 30 30-60 2-5 2-5 30 Up to 7 hours 8-14 hours 4-8 hours During infusion tolerance in 7-8 hrs Up to 60 min Up to 8 hours 2-3 min 2-2.5 hours Up to 8 hours During infusion tolerance in 7-8 hrs 12-24 hours 12 hours Not known Not known Not known 2 percent, 15x15 cm (7.5 to 40 mg) 0.2-0.8 mg/hour q 12 hours 2.5-13 mg 5-200 g/min 2.5-15 mg 5-80 mg BID or TID 1.25 mg/day 5 mg 40 mg OD or BID 1.25-5 mg/hour 20-40 mg BID 60-240 mg/day 30-120 mg once daily 10 mg as needed 5-10 mg as needed 10-30 mg TID

Isosorbide mononitrate, extended release Isosorbide mononitrate, extended release Pentaerythroid tetranitrate Eyrthritol tetranitrate

ACC/AHA/ACP guidelines: recommended drug therapy (calcium antagonist vs. beta-blocker) in patients with angina and associated conditions Condition Recommended treatment (and alternative) Avoid Medical conditions Systemic hypertension Beta-blockers (calcium antagonists) Migraine or vascular headaches Beta-blockers (verapamil or diltiazem) Asthma or chronic obstructive pulmonary disease Verapamil or diltiazem Beta-blockers with bronchospasm Hyperthyroidism Beta-blockers Raynaud's syndrome Long-acting slow-release calcium antagonists Beta-blockers Insulin-dependent diabetes mellitus Beta-blockers (particularly if prior myocardial infarction) or long-acting slow-release calcium antagonists Non-insulin-dependent diabetes mellitus Beta blockers or long-acting slow-release calcium antagonists Depression Long-acting slow-release calcium antagonists Beta-blockers Mild peripheral vascular disease Beta-blockers or calcium antagonists Severe peripheral vascular disease with rest Calcium antagonists Beta-blockers ischemia Cardiac arrhythmias and conduction abnormalities Sinus bradycardia Long-acting slow-release calcium antagonist that do not decrease heart Beta-blockers, diltiazem, rate verapamil Sinus tachycardia (not due to heart failure) Beta-blockers Supraventricular tachycardia Verapamil, diltiazem, or beta-blockers Atrioventricular block Long-acting slow-release calcium antagonists that do not slow A-V Beta-blockers, diltiazem, conduction verapamil Rapid atrial fibrillation (with digitalis) Verapamil, diltiazem, or beta-blockers Ventricular arrhythmias Beta blockers Left ventricular dysfunction Congestive heart failure Mild (LVEF 40 percent) Beta-blockers Moderate to severe (LVEF <40 percent) Amlodipine or felodipine (nitrates) Verapamil, diltiazem Left-sided valvular heart disease Mild aortic stenosis Beta-blockers Aortic insufficiency Long-acting slow-release dihydropyridines Mitral regurgitation Long-acting slow-release dihydropyridines Mitral stenosis Beta-blockers Hypertrophic cardiomyopathy Beta-blockers, non-dihydropyridine calcium antagonist Nitrates, dihydropyridine calcium antagonists

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NOTE: These guidelines were published before the specific survival benefits of beta blockers were proven in patients with systolic heart failure. Thus, current practice may differ from these guidelines in this and other areas. Reproduced with permission from: ACC/AHA/ACP Guidelines for the Management of Patients with Chronic Stable Angina. J Am Coll Cardiol 1999; 33:2092. Copyright 1999 American College of Cardiology. Comparison of three methods of assessing cardiovascular disability New York Heart Association functional Canadian Cardiovascular Society functional Class classification classification I Patients with cardiac disease but without Ordinary physical activity, such as walking and climbing resulting limitations of physical activity. stairs, does not cause angina. Angina with strenuous or Ordinary physical activity does not cause rapid prolonged exertion at work or recreation. undue fatigue, palpitation, dyspnea, or anginal pain. II Patients with cardiac disease resulting in slight limitation of physical activity.They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain. Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or when under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions. Marked limitation of ordinary physical activity. Walking one to two blocks on the level and climbing more than one flight in normal conditions.

III

Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain.

IV

Patient with cardiac disease resulting in Inability to carry on any physical activity without discomfort inability to carry on any physical activity - anginal syndrome may be present at rest. without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.

Specific activity scale Patients can perform to completion any activity requiring 7 metabolic equivalents, eg, can carry 24 lb up eight steps; do outdoor work (shovel snow, spade soil); do recreational activities (skiing, basketball, squash, handball, jog/walk 5 mph). Patients can perform to completion any activity requiring 5 metabolic equivalents, e.g., have sexual intercourse without stopping, garden, rake, weed, roller skate, dance fox trot, walk at 4 mph on level ground, but cannot and do not perform to completion activities requiring 7 metabolic equivalents. Patients can perform to completion any activity requiring 2 metabolic equivalents, eg, shower without stopping, strip and make bed, clean windows, walk 2.5 mph, bowl, play golf, dress without stopping, but cannot and do not perform to completion any activities requiring > 5 metabolic equivalents. Patients cannot or do not perform to completion activities requiring > 2 metabolic equivalents. Cannot carry out activities listed above (Specific activity scale III).

Noninvasive risk stratification in patients with suspected ischemic chest pain High risk (greater than 3 percent annual mortality rate) 1. Severe resting left ventricular dysfunction (LVEF <35 percent) 2. High-risk treadmill score (score -11) 3. Severe exercise left ventricular dysfunction (exercise LVEF <35 percent) 4. Stress-induced large perfusion defect (particularly if anterior) 5. Stress-induced multiple perfusion defects of moderate size 6. Large, fixed perfusion defect with LV dilation or increased lung uptake (thallium-201) 7. Stress-induced moderate perfusion defect with LV dilation or increased lung uptake (thallium-201) 8. Echocardiographic wall motion abnormality (involving greater than two segments) developing at low dose of dobutamine ( 10 mg/kg/min) or at a low heart rate (<120 beats/min) 9. Stress echocardiographic evidence of extensive ischemia Intermediate risk (1 percent to 3 percent annual mortality rate) 1. Mild/moderate resting left ventricular dysfunction (LVEF = 35 percent to 49 percent) 2. Intermediate-risk treadmill score (-11 < score <5) 3. Stress-induced moderate perfusion defect without LV dilation OR increased lung intake (thallium-201) 4. Limited stress echocardiographic ischemia with a wall motion abnormality only at higher doses of dobutamine involving less than or equal to two segments Low risk (less than 1 percent annual mortality rate) 1. Low-risk treadmill score (score 5) 2. Normal or small myocardial perfusion defect at rest or with stress* 3. Normal stress echocardiographic wall motion or no change of limited resting wall motion abnormalities during stress* * Although the published data are limited, patients with these findings will probably not be at low risk in the presence of either a high-risk treadmill score or severe resting left ventricular dysfunction (LVEF < 35 percent). Reproduced with permission from: ACC/AHA/ACP Guidelines for the Management of Patients with Chronic Stable Angina. J Am Coll Cardiol 1999; 33:2092. Copyright 1999 American College of Cardiology. ACC/AHA guideline summary: Coronary angiography for risk stratification in patients with chronic stable angina

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Class I - There is evidence and/or general agreement that coronary angiography should be performed to risk stratify patients with chronic stable angina in the following settings Disabling anginal symptoms (Canadian Cardiovascular Society [CCS] classes III and IV) despite medical therapy. High-risk criteria on noninvasive testing independent of the severity of angina. Survivors of sudden cardiac death or serious ventricular arrhythmia. Symptoms and signs of heart failure. Clinical features that suggest that the patient has a high likelihood of severe coronary artery disease. Class IIa - The evidence or opinion is in favor of performing coronary angiography to risk stratify patients with chronic stable angina in the following settings Left ventricular ejection fraction less than 45 percent, CCS class I or II angina, and evidence, on noninvasive testing, of ischemia that does not meet high-risk criteria. Noninvasive testing does not reveal adequate prognostic information. Class IIb - The evidence or opinion is less well established for performing coronary angiography to risk stratify patients with chronic stable angina in the following settings Left ventricular ejection fraction greater than 45 percent, CCS class I or II angina, and evidence, on noninvasive testing, of ischemia that does not meet highrisk criteria. CCS class III or IV angina that improves to class I or II with medical therapy. CCS class I or II angina but unacceptable side effects to adequate medical therapy. Class III - There is evidence and/or general agreement that coronary angiography should not be performed to risk stratify patients with chronic stable angina in the following settings CCS class I or II angina that responds to medical therapy and, on noninvasive testing, shows no evidence of ischemia. Patient preference to avoid revascularization. Data from Gibbons, RJ, Abrams, J, Chatterjee, K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a 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). Circulation 2003; 107:149. 2008 UpToDate, Inc. All rights reserved.

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