CHAPTER 93 Exercise Electrocardiography (Stress) Testing

Seventeen million Americans have known coronary artery disease (CAD); however, in more than half of everyone else in whom CAD will be diagnosed, the diagnosis will follow a bad outcome—namely, a myocardial infarction (MI) or sudden cardiac death. Approximately one third of all deaths (more than half a million per year) in the United States are caused by CAD, the leading cause of death in both sexes. Exercise electrocardiography (ECG) testing (EET) is not only a safe (<1 event per 10,000 properly selected patients) and cost-effective method for diagnosing CAD, it is probably the most cost-effective method to screen for and manage CAD. EET can also be used to reassure patients about the safety of exercise and to customize their exercise prescription.

For the diagnosis of CAD, although much money, time, and effort have been spent designing and applying other tests with greater sensitivity, the sensitivity of EET exceeds 90% (perhaps 95%) for significant CAD—meaning left main CAD or multivessel disease with resultant left main equivalent CAD (i.e., left ventricular [LV] dysfunction resulting from ischemia). Supporting this, several studies have examined the incremental value of exercise myocardial perfusion imaging compared with EET for diagnosis and risk stratification of CAD. In an analysis of these studies, the modest incremental benefit of imaging did not appear to justify its cost (which has been estimated at $20,550 per additional patient correctly classified). Consequently, the American College of Cardiology (ACC) and the American Heart Association (AHA) recommend a stepwise strategy for diagnosing CAD in patients with an intermediate pretest likelihood, using an EET as the initial test, and not an imaging procedure, if the patient is able to exercise, has a normal resting ECG, and is not taking digoxin* (ACC/AHA/ASNC Guidelines). (See chapter 94, Stress Echocardiography, for testing patients with an abnormal resting ECG or who are taking digoxin, and for a dobutamine echo protocol for patients unable to exercise.)

With medical management of CAD more successful than ever, primary care clinicians’ skills in managing CAD have become more important. Performing EET is one method of maximizing these skills. In fact, using the Duke Treadmill Score (DTS) or nomogram for positive tests, primary care clinicians can now risk-stratify and prognose CAD as well as their cardiologist colleagues. It should be noted that in the latest guidelines (2002, 2007) from AHA/ACC for management of stable CAD, an EET is a reasonable test for risk stratification in patients with a normal resting ECG and who are able to exercise. In part, these guidelines are based on “the simplicity, lower cost, and widespread familiarity with the performance and interpretation of the standard EET.” Also, when patients divided into risk groups using EET have been studied with imaging (Gibbons and colleagues, 1999), few patients (<5%) who have a low-risk DTS (≤1% annual cardiac mortality rate) will be identified as high risk after imaging, and thus the cost of identifying these patients again argues against routine imaging. Those patients identified as high risk (≥3% per year annual cardiac mortality) should probably be referred directly for cardiac catheterization and a possible intervention (again, see Chapter 94, Stress Echocardiography). Only those patients with an intermediate DTS (>1% and <3%) seem to benefit from an imaging study to further differentiate low-risk patients from those who might benefit from an intervention.

Performing a maximal EET provides additional information valuable for predicting prognosis, such as exercise capacity and heart rate in recovery (HRR, explained later), even if the ECG cannot be used for interpretation or predicting prognosis. From a study of 7163 patients (Diaz and colleagues, 2001) with known or suspected CAD undergoing myocardial perfusion imaging at the Cleveland Clinic and for whom a DTS could not be calculated (e.g., patient taking digoxin, resting ECG abnormalities), the independent prognostic values of exercise capacity and HRR were determined. Patients were followed for an average of 6.7 years, and, when compared with results of myocardial perfusion imaging, not only did exercise capacity and HRR provide additional prognostic information, but if exercise capacity and HRR were both abnormal, it portended a higher risk of mortality than the result from the myocardial perfusion test in nonrevascularized patients.

Primary care clinicians can also use EET to screen certain asymptomatic individuals. Such screening may be especially helpful for diabetic patients, firefighters, anyone about to undergo noncardiac surgery, high-risk patients after revascularization, patients about to undergo cardiac rehabilitation, and older individuals about to embark on a vigorous exercise program. Although the ACC/AHA are not currently recommending EET to screen all asymptomatic individuals, there is emerging evidence that this will be a future growth area for the procedure. A negative EET demonstrating good exercise capacity combined with a negative multidetector (>32-slice) computed tomography (CT) angiogram, which has a false negative rate of less than 2% for CAD, will likely be our ultimate screening test for CAD. In the meantime, with estimates that 12% of deaths in the United States are due to a lack of exercise, any method to motivate patients to exercise should be beneficial. EET can be used not only to reassure individuals of the safety of exercise, but to customize their exercise prescription. After almost every EET, patients should receive some type of customized exercise prescription based on their true maximal heart rate (MHR), their exercise (aerobic) capacity, and the test results. We now know that almost every patient benefits from an exercise program, even cardiac transplant recipients. In fact, of all the options available, exercise may be the single best method for improving endothelial function.

Benefits of performing EET in the primary care clinician’s office include having test results immediately available, improving communication and referral patterns to cardiologists, and improving primary care clinicians’ ECG reading skills. Clinicians performing EET also naturally improve their understanding of CAD pathophysiology as well as exercise physiology. With results immediately available, patient satisfaction is usually improved and liability from failure to diagnose should be decreased. Using the DTS when there is a positive study, the patient can immediately be counseled from an outcomes or prognosis perspective. Such data allow a patient to make a truly informed decision before undergoing a major procedure, such as coronary artery bypass graft (CABG) surgery. With personalized data, the patient can weigh his or her known risks of forgoing surgery against available known risks of an intervention, with interventions reserved for those who choose to accept the risks.

For primary care clinicians covering emergency departments or urgent care centers, or those working as hospitalists, knowledge of a patient’s recent EET results may be helpful for perioperative evaluation. Management of patients with an acute chest pain syndrome is also greatly facilitated when EET is available. For many patients, after myocardial damage has been excluded by serial blood tests, resolution of the symptoms, and stabilized ECG findings, an EET may be useful for triage or early discharge. National guidelines with algorithms are available, and they have been demonstrated to be both safe and useful.

Physiology of Exercise ECG Testing

Performing exercise increases total oxygen demand and consumption, with the amount of increase depending on the size of the muscles used. In other words, the larger the muscles, the more oxygen is consumed. Oxygen demand and consumption also increase as the intensity of exercise increases. In response to increased exercise and oxygen demand, the body increases ventilation, oxygenation, cardiac output, and oxygen extraction by tissues. Unless there is moderate to severe lung disease (e.g., chronic obstructive pulmonary disease) or a process severely limiting oxygen transport or extraction (e.g., severe anemia), cardiac output is usually the factor limiting an individual’s maximal exercise capacity. In turn, the limiting factor for cardiac output in those with obstructive CAD is usually coronary blood flow. Maximal exercise capacity can therefore be limited by coronary blood flow. In fact, maximal exercise capacity is usually quantified by measuring or estimating an individual’s maximal oxygen uptake (). In other words, maximal exercise with large muscles can be used both to estimate and to evaluate limitations in coronary blood flow.

Cardiac output is calculated by multiplying the stroke volume by the heart rate; therefore, increases in either the stroke volume or the heart rate will increase the cardiac output. Increasing the stroke volume is generally a more efficient method of increasing cardiac output (i.e., requires less oxygen). However, unless the patient is taking a beta blocker, the initial physiologic response to increased demand for cardiac output is usually an increase in heart rate. (In part, this is why beta blockers work for treating angina; they block the increase in heart rate when there is a need for increased cardiac output, thereby forcing an increase in stroke volume and keeping the increased myocardial oxygen demand to a minimum.) Therefore, as intensity of exercise increases, heart rate increases up to a maximum (MHR), usually when the patient has reached maximal voluntary effort or exertion.

In normal patients there is a linear relationship between myocardial oxygen demand and heart rate. In other words, the faster the heart rate, the more oxygen the heart requires. Because the heart rate continues to increase as exercise intensity increases, so does the myocardial oxygen demand. MHR can be crudely estimated based on age (i.e., 220 − age in years ≅ MHR) or by using graphs; however, true MHR is best determined with a maximal EET. MHR is the heart rate noted when the patient is at maximal voluntary effort (voluntarily fatigued), and this number should be recorded and given to the patient at the completion of each EET when the clinician is customizing an exercise prescription.

There is also a linear relationship between myocardial oxygen demand and systolic blood pressure (SBP). In other words, the higher the SBP, the harder the heart is working (and consequently the higher the myocardial oxygen demand). Therefore, one method of quantifying the overall myocardial oxygen demand is to multiply the SBP by the heart rate; the product obtained is the double product, also known as the rate–pressure product (RPP). At any given moment the RPP is therefore an estimate of total myocardial oxygen demand; as long as the demand has not exceeded the supply, it is also a measure of total myocardial oxygen uptake or consumption. In other words, the higher the RPP, the more oxygen the heart is demanding; if supply is matching demand, the higher the capacity the heart has to deliver its own oxygen.

When the myocardium demands more oxygen, there are two options for supplying it: either the coronary arterial flow increases or the extraction of oxygen from the flow increases. As it turns out, increased myocardial oxygen demand during exercise is met primarily through an increase in coronary arterial flow rather than through increased oxygen extraction. This is because myocardial tissue is very efficient at extracting almost all of the available oxygen from the coronary arterial flow, even in the resting state. Therefore, coronary arterial flow is usually the limiting factor for cardiac oxygenation. This is especially true in patients with obstructive CAD.

With gradually increasing levels of exertion in the patient with obstructive CAD, a threshold is eventually reached where the heart’s supply of oxygen cannot meet the demand. At this threshold, the heart becomes ischemic, initially at the subendocardial layer. With subendocardial ischemia, the patient usually demonstrates ECG changes in the form of ST segment depression. Usually, and eventually, this is followed by chest discomfort (i.e., angina). Because in most cases the ischemia is due to a fixed lesion, patients develop these ECG changes at about the same threshold or RPP every time. If symptoms occur, they also occur at the same RPP and follow the same pattern every time. In other words, angina caused by a fixed lesion does not radiate only into the left arm one day and into the right arm another day. If ST segment depression occurs (due to ischemia) and angina is not experienced, the diagnosis is silent ischemia.

Large muscles, such as leg muscles, rapidly increase the oxygen demand with increased exertion (e.g., using a treadmill or bicycle). is the greatest amount (i.e., volume) of oxygen that a person can extract from inspired air while performing dynamic exercise. It is usually reached when the patient is in the anaerobic range. Measuring is a method of quantifying maximal exercise capacity, and varies with body weight, heredity, sex, and exercise habits. It often decreases progressively with age, but this decrease may be purely due to inadequate exercise habits. Performing aerobic exercise on a regular basis may maintain a constant for life. There is a nearly linear relationship between and the maximum cardiac output; therefore the is a measure of the functional capacity of the cardiovascular system. It can be measured directly with inspired/expired gas analysis or more easily estimated from a maximal EET. As mentioned previously, in those with CAD, may be limited by coronary blood flow. With prognosis data discussed later in this chapter, estimating is very important for predicting outcomes from a cardiovascular perspective.

Basal oxygen consumption, or 1 metabolic equivalent (1 MET), defines the amount of oxygen an average individual consumes sitting at rest, which is approximately 3.5 mL/kg/min (i.e., 1 MET = 3.5 mL/kg/min O₂). is often quantified as a multiple of the basal oxygen consumption in METs. For instance, walking 2 miles per hour (mph) on level ground requires approximately 2 METs. Walking 4 mph on level ground requires approximately 4 METs. Moderately active young men usually have a of at least 42 mL/kg/min, or 12 METs. This means they are able to consume 12 times the amount of oxygen that they consume at rest. Obviously METs can also be used as a conversion factor between types of exercise. Charts are available (Fig. 93-1) to estimate a patient’s exercise capacity or maximal METs by cross-referencing MET levels with different daily activities. This estimate may then be used to predict performance before placing a patient on a treadmill. Performing a maximal EET remains one of the more accurate methods of estimating maximal METs. An individual’s maximal METs, whether determined on a bicycle or a treadmill, has significant management and prognosis implications if the person has CAD. Even if the test is positive for CAD, achieving certain MET thresholds can be very reassuring for prognosis.

Figure 93-1 Veterans’ Administration specific activity questionnaire.

During a maximal EET, a perceived exertion scale (PES) may be helpful for monitoring the patient. The PES is similar to a pain scale; however, the patient quantifies “effort” or “exertion” instead of “pain” during testing. Originally studied and published with a scale from 5 to 20 (with 20 being the subjective maximum that an individual could work and 5 being minimal or no work at all), it has now been modified. Most clinicians in the United States use a range from 1 to 10 (Box 93-1) for the PES. Although it is a subjective measurement, in most patients the PES level is very reproducible; in other words, if they were asked to repeat the EET in 2 weeks, they would report the same PES level at the same workload and duration for both EETs. Interestingly, their heart rate is also usually very similar at a given PES. As a result, a PES target can be given to most patients to use as part of their exercise prescription. This replaces the patient’s need to check the heart rate during exercise, and anything that simplifies an exercise prescription will, it is hoped, increase the chance of adherence/compliance.

Box 93-1 Perceived Exertion Scale

0	Nothing at all
0.5	Very, very weak
1	Very weak
2	Weak
3	Moderate
4	Somewhat strong
5	Strong
6
7	Very strong
8
9
10	Very, very strong

A positive test result occurs when subendocardial ischemia causes ST segment depression on the ECG tracing. Because this is a “global” phenomenon, meaning much of the subendocardial layer is affected, it is almost always seen in more than one lead; if suspected it should be confirmed in an area of the ECG tracing where the baseline is relatively flat. True ischemia will cause ST segment depression for at least three beats in a row, and the ischemia (ST changes) usually persists or worsens during the recovery period. ST segment depression occurs because ischemia impairs the sodium/potassium adenosine triphosphatase (Na⁺/K⁺ ATPase) pump at the cellular level. Such an ST segment change can also be noted in patients taking digitalis, whose site of action is the Na⁺/K⁺ ATPase pump. When the pump is affected, there is a resultant change in the Na⁺/K⁺ intracellular gradient and a subsequent small shift in polarity. This shift in polarity is what is noted on the ECG tracing as ST segment depression.

With exercise-induced ischemia, ST segment depression becomes a global phenomenon, meaning it involves the entire subendocardium. When one area of the subendocardium becomes ischemic, there is a “fail-safe” mechanism that responds, meaning this subendocardial segment reduces its workload or shuts down before becoming permanently damaged. As a result, the remaining and surrounding subendocardium must work harder to compensate. This surrounding area subsequently becomes ischemic, and a domino effect occurs, cascading around the entire subendocardium. Consequently, ST segment depression is usually seen in multiple leads. In fact, this is such a global phenomenon that the coronary vessels involved cannot be predicted by which of the leads are demonstrating ST segment depression. (If knowledge of the coronary vessels involved or the total burden of ischemia is needed, an imaging test [myocardial perfusion or echocardiogram, see Chapter 94, Stress Echocardiography] should be added to the stress test.)

If the entire wall of the myocardium (full thickness) becomes ischemic, such as from severe CAD, ST segment elevation may be noted. It may appear very similar to that seen with a transmural/ST-elevation infarct or a ventricular aneurysm. In this situation, unless the clinician is certain that the finding is due to a ventricular aneurysm (e.g., associated with Q waves, or the clinician previously diagnosed/managed the infarct), the EET should be stopped. If either transmural ischemia or a new infarction is occurring, the potential for an arrhythmia is very high. However, transmural ischemia is rare in a community setting. In almost all positive EETs, ST segment depression is what is noted, the same as with what used to be called a subendocardial infarct. The subendocardial layer is usually the first to become ischemic because it is the “watershed” area of the heart, or the farthest from the arteries that are located in the epicardium (Figs. 93-2 and 93-3).

Figure 93-2 Normal myocardial perfusion. Note perfusion gradient is from 80 mm Hg to 5 to 10 mm Hg.

(Redrawn from Ellestad MH: Stress Testing: Principles and Practice, 4th ed. Philadelphia, FA Davis, 1996.)

Figure 93-3 Myocardial perfusion in coronary artery disease (CAD). Note perfusion gradient is only from 40 mm Hg to 30 mm Hg.

(Redrawn from Ellestad MH: Stress Testing: Principles and Practice, 4th ed. Philadelphia, FA Davis, 1996.)

Certain other conditions may also make it difficult to perfuse the subendocardial layer, even in the absence of CAD. Normally the subendocardial layer is perfused during diastole and relies on perfusing “downhill” from 80 to 90 mm Hg of diastolic blood pressure (DBP) to an area where there is only 5 to 10 mm Hg pressure (i.e., end-diastolic pressure [EDP]). Thus, the pressure gradient, or the difference between “uphill” DBP and “downhill” EDP, is 80 or 90 minus 5 or 10, which is a 75 to 85 mm Hg difference (DBP − EDP = 75 to 85). If hypertension is poorly controlled, EDP may be elevated, reaching as high as 30 to 40 mm Hg, with the resultant drop in this pressure gradient (DBP − EDP = 40 to 60). In other words, there is much less “pressure” for blood to flow “downhill.” Anything causing diastolic dysfunction, such as profound hypothyroidism or severe valvular disease, can also result in an elevated EDP, a decreased pressure gradient, and a false-positive EET result. A thickened myocardial wall, as seen in left ventricular hypertrophy, can make it physically difficult to perfuse through the wall, thereby causing subendocardial ischemia and ST segment depression, even without CAD. In addition to physical causes, other situations that can cause false-positive results include hypokalemia and other electrolyte imbalances. Inadequate potassium prevents the Na⁺/K⁺ ATPase pump from functioning correctly, resulting in ST segment changes. As mentioned previously, digitalis may also result in ST segment depression, even at physiologic doses.

Normal Clinical Responses to Exercise ECG Testing

1 A gradual increase in heart rate to MHR where MHR is estimated by the formula 220 − age (i.e., 220 − age ≅ MHR). If a heart rate of 120 beats per minute (bpm) cannot be achieved, the diagnosis of chronotropic incompetence is possible (see “Interpretation” section).

2 Return of the heart rate to resting values within the first few minutes after exercise. The rate of return of the heart rate to its resting value depends partly on the exercise conditioning effect on vagal tone (i.e., frequent exercise or “being fit” increases vagal tone). An abnormal HRR is declared when the heart rate does not decrease by at least 12 bpm in the first minute of recovery (see “Interpretation” section).

3 A gradual rise in SBP. SBP is usually the highest at maximal workload. A drop in SBP during the exercise phase of EET, especially if it drops below resting standing SBP, may indicate severe CAD. An SBP greater than 214 mm Hg is designated a systolic hypertensive response to exercise (see “Interpretation” section).

4 A return of SBP and DPB to resting values by approximately 3 minutes after exercise. Failure of return of either blood pressure to normal by 3 minutes of recovery is also a hypertensive response to exercise (see “Interpretation” section).

5 Minimal change or a decrease in DBP during exercise. During exercise, the legs produce lactic acid, one of the most potent vasodilators known. As a result, a significant amount of blood volume flows into the legs. Because of this vasodilation, and the effects of exercise on Korotkoff sounds, diastolic pressure by auscultation can decrease all the way to zero in normal individuals. An increase in DBP of more than 10 mm Hg is also designated a diastolic hypertensive response to exercise (see “Interpretation” section).

6 Most patients perceive an increase by 1 to 3 points on the PES per stage of exercise. Few ever admit to reaching a full 10 points on the scale. For many patients, PES level increases rapidly from 7 to 9 when they are near maximal effort.

Indications

Comprehensive, national guidelines are available regarding the appropriate use of EET, including special cases and situations (e.g., diabetic patients, patients in the emergency department, firefighters, before noncardiac surgery, before and after revascularization). There are three general indications for EET: diagnosing CAD (especially helpful when evaluating atypical chest pain and screening asymptomatic patients at significant risk), managing CAD, and providing data for an exercise prescription while determining exercise capacity and safety. In certain cases, several of these indications are evaluated during the same procedure. An example would be a patient who has an intermediate pretest likelihood and is found to have CAD when performing the EET. Because the diagnosis has now been made, if it is considered safe to continue the procedure, prognosis may also be determined. Exercise capacity (i.e., aerobic capacity) could be determined if the patient were allowed to complete a maximal EET; this is helpful for determining prognosis. Based on the results, an exercise prescription along with cardiac rehabilitation might be initiated. In this manner, the diagnosis, management (e.g., prognosis, cardiac rehabilitation), and exercise prescription could all be determined during the same test.

General Indications

1 Diagnosing CAD

• Patients with an intermediate (20% to 70%) pretest probability of CAD based on sex, age, and symptoms (see “Determination of Pretest Likelihood,” later; Fig. 93-4 and Table 93-1).

• Asymptomatic patients with multiple risk factors, possible myocardial ischemia on ambulatory ECG monitoring, or an abnormal coronary calcium score from electron-beam computed tomography (EBCT) scan. It should be noted that asymptomatic patients are included in the graphs and tables (see Fig. 93-4 and Table 93-1) used to determine pretest probability.

Figure 93-4 Pretest likelihood of coronary artery disease (CAD).

(Redrawn from Diamond GA, Forrester JS: Analysis of probability as an aid in the clinical diagnosis of coronary-artery disease. N Engl J Med 300:1350–1358, 1979.)

TABLE 93-1 Pretest Likelihood of Coronary Artery Disease Based on Symptoms

NOTE: For diagnosing CAD, determining pretest likelihood is important. This is explained for patients with symptoms by examples in the section “Determination of Pretest Likelihood.”

2 Managing CAD*

• Patients with known or highly probable CAD, for initial assessment or for a change in symptoms

• After MI or revascularization (especially those at high risk), for prognostic assessment, activity prescription, evaluation of medical therapy, or cardiac rehabilitation

• Demonstrating proof of ischemia before revascularization

• Consider for perioperative evaluation of patients with CAD only if results would change management

3 Determining exercise prescription data, exercise capacity, and safety

• Evaluation of exercise-related symptoms, including possible exercise-induced arrhythmias* (also see Chapter 87, Ambulatory Electrocardiography: Holter and Event Monitoring).

• Graded treadmill EET is one of the best methods for determining an individual’s MHR. The exception is the elite athlete, for whom a sport-specific EET should be used.

• True MHR must be known to calculate a training heart rate range, which can be used as a guideline for aerobic training.

• An EET can also be used to estimate an individual’s , which is helpful in determining the current level of fitness or conditioning.

Specific ACC/AHA Indications

For the sake of completeness of this chapter, most of the indications for EET in adults from the ACC/AHA guidelines will be listed. Guidelines for special cases (e.g., children, EET with expired ventilatory gas analysis) may be found in the ACC/AHA reference or on the AHA website (www.americanheart.org), under “Science and Professional, Scientific Publications, Scientific Statements.” The ACC/AHA guidelines use the following classification system for indications:

Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective.

Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.

Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.

Class IIb: Usefulness/efficacy is less well established by evidence/opinion.

Class III: Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful.

Exercise ECG Testing in Diagnosis of Obstructive CAD

Class I: Adult patients (including those with complete right bundle branch block [RBBB] or less than 1 mm of resting ST segment depression) with an intermediate pretest probability of CAD based on sex, age, and symptoms (see “Determination of Pretest Likelihood,” Fig. 93-4, and Table 93-1).

Class IIa: Patients with vasospastic angina.

Class IIb: Patients with a high or low pretest probability of CAD by age, symptoms, and sex; patients with less than 1 mm of baseline ST segment depression and taking digoxin; patients with ECG criteria for LV hypertrophy (LVH) and less than 1 mm of baseline ST segment depression.

Class III: Patients with the following baseline ECG abnormalities: preexcitation syndrome (i.e., Wolff-Parkinson-White [WPW] syndrome), electronically paced ventricular rhythm, greater than 1 mm of resting ST segment depression, complete left bundle branch block (LBBB); patients with a documented MI or prior coronary angiography demonstrating significant disease and who have an established diagnosis of CAD. (Note that for diagnostic purposes, EET may not be useful. However, overall risk for individuals can be determined from obtaining if it is deemed safe to test [see following sections “Risk Assessment and Prognosis in Patients with Symptoms or a History of CAD,” “Exercise ECG Testing after Myocardial Infarction,” and “Exercise ECG Testing before and after Revascularization”].)

Risk Assessment and Prognosis in Patients with Symptoms or a History of CAD

Class I: Patients undergoing initial evaluation with suspected or known CAD. Patients with suspected or known CAD previously evaluated but now with a significant change in clinical status (specific exceptions noted in Class IIb). Low-risk patients with unstable angina (moderate or high likelihood of CAD with new-onset or progressive angina with walking) 8 to 12 hours after presentation or intermediate-risk unstable angina (prolonged [>20 minutes] or at rest angina; patients with prior MI, CABG, atherosclerotic cerebrovascular disease [ASCVD], or peripheral artery disease; aspirin use; age older than 70 years; or troponins negative or slightly elevated [<0.1 mg/mL]) 2 to 3 days after presentation; both groups of patients with unstable angina should have been free of active ischemic or heart failure symptoms.

Class IIa: Intermediate-risk patients with unstable angina who have initial cardiac markers that are normal, a repeat ECG without significant change, cardiac markers 6 to 12 hours after the onset of symptoms that are normal, and no evidence of ischemia during observation.

Class IIb: Patients with the following resting ECG abnormalities: preexcitation (i.e., WPW syndrome), electronically paced ventricular rhythm, greater than 1 mm of resting ST segment depression, complete LBBB. Patients with a stable clinical course who undergo periodic monitoring to guide treatment.

Class III: Patients with severe comorbidity likely to limit life expectancy or candidacy for revascularization. Patients with high-risk unstable angina (prolonged, ongoing >20 minutes pain at rest; pulmonary edema; new or worsening mitral regurgitant murmur; new/worsening rales; hypotension; bradycardia; tachycardia; age older than 75 years; transient ST segment changes; or elevated troponin [>0.1 mg/mL]).

Exercise ECG Testing after Myocardial Infarction

Class I: Before discharge for prognostic assessment, activity prescription, or evaluation of medical therapy (submaximal at about 4 to 7 days). Early after discharge for prognostic assessment, activity prescription, evaluation of medical therapy, and cardiac rehabilitation if the predischarge EET was not done (do a symptom-limited EET at about 14 to 21 days). Late after discharge for prognostic assessment, activity prescription, evaluation of medical therapy, and cardiac rehabilitation if the early EET was submaximal (do a symptom-limited EET at about 3 to 6 weeks).

Class IIa: After discharge for activity counseling or exercise training as part of cardiac rehabilitation in patients who have undergone coronary revascularization.

Class IIb: Patients with preexcitation syndrome (i.e., WPW syndrome), electronically paced ventricular rhythm, greater than 1 mm of resting ST segment depression, complete LBBB, digoxin therapy, LVH. Periodic monitoring in patients who continue to participate in exercise training or cardiac rehabilitation.

Class III: Patients with severe comorbidity likely to limit life expectancy or candidacy for revascularization. At any time after MI if there is uncompensated congestive heart failure (CHF), cardiac arrhythmia, or noncardiac conditions that limit the patient’s ability to exercise.

Exercise ECG Testing in Asymptomatic Patients without Known CAD

Class I: None.

Class IIa: Evaluation of asymptomatic persons with diabetes mellitus who plan to start vigorous exercise.

Class IIb: Evaluation of patients with multiple risk factors as a guide to risk reduction therapy. Evaluation of asymptomatic men older than 45 years of age and women older than 55 years of age planning to start vigorous exercise (especially if physically inactive), or involved in occupations in which impairment might affect public safety, or at high risk for CAD because of other diseases (e.g., peripheral vascular disease, chronic renal failure).

Class III: Routine screening of asymptomatic men or women.

NOTE: The class IIb indication evokes controversy because of the increased risk of false-positive results. However, with good clinical judgment or consultation of a table (e.g., Fig. 93-4, Table 93-1), the clinician may determine that the patient has a pretest likelihood as high as 15% to 20%, making the patient a reasonable candidate for EET.

Exercise ECG Testing for Valvular Heart Disease

Class I: In chronic aortic regurgitation, assessment of functional capacity and symptomatic responses in patients with a history of equivocal symptoms.

Class IIa: In chronic aortic regurgitation, evaluation of symptoms and functional capacity before participation in athletic activities. For prognostic assessment before aortic valve replacement in asymptomatic or minimally symptomatic patients with LV dysfunction.

Class IIb: Evaluation of exercise capacity in patients with valvular heart disease.

Class III: Diagnosis of CAD in patients with moderate to severe valvular disease or with baseline ECG abnormalities (preexcitation, electronically paced ventricular rhythm, >1 mm ST segment depression, complete LBBB).

Exercise ECG Testing before and after Revascularization

Class I: Demonstration of proof of ischemia before revascularization. Evaluation of patients with recurrent symptoms suggesting ischemia after revascularization.

Class IIa: After discharge for activity counseling or exercise training as part of cardiac rehabilitation in patients who have undergone coronary revascularization.

Class IIb: Detection of restenosis in selected, high-risk (multivessel CAD, proximal left anterior descending CAD, family history of sudden cardiac death, diabetes, hazardous occupations, suboptimal results from the revascularization, saphenous vein graft,* CHF*) asymptomatic patients within the first 12 months after percutaneous coronary intervention (PCI). Periodic monitoring of selected, high-risk asymptomatic patients for restenosis, graft occlusion, or disease progression.

Class III: Localization of ischemia for determining site of intervention. Routine, periodic monitoring of asymptomatic patients after PCI or coronary artery bypass grafting without specific indications.

Exercise ECG Testing for Investigation of Heart Rhythm Disorders

Class I: Identification of appropriate settings in patients with rate-adaptive pacemakers.

Class IIa: Evaluation of patients with known or suspected exercise-induced arrhythmias. Evaluation of medical, surgical, or ablative therapy in patients with exercise-induced arrhythmias (including atrial fibrillation).

Class IIb: Investigation of isolated ventricular ectopic beats in middle-aged patients without other evidence of CAD. Investigation of prolonged first-degree atrioventricular block or type I second-degree Wenckebach, LBBB, RBBB, or isolated ectopic beats in young patients considering participation in competitive sports.

Class III: Investigation of isolated ectopic beats in young patients.

Noninvasive Stress Testing before Noncardiac Surgery

Class IIa: Noninvasive stress testing of patients with three or more clinical risk factors (e.g, CAD, CHF, ASCVD, diabetes mellitus, renal insufficiency) and poor functional capacity (<4 METs or cannot walk up a flight of stairs) who require high-risk (often >5% risk of serious complications) surgery (e.g., vascular, defined as aortic or other major vascular, peripheral vascular surgery) is reasonable if it will change management.

Class IIb: Noninvasive stress testing may be considered for patients with at least one to two clinical risk factors and poor functional capacity (<4 METs) who require intermediate-risk (1% to 5% risk of serious complications) noncardiac surgery (e.g., intraperitoneal; intrathoracic; carotid or aortic stent; carotid endarterectomy; head and neck, orthopedic, or prostate surgery) if it will change management. Noninvasive stress testing may be considered for patients with at least one to two clinical risk factors and good functional capacity (≥4 METs) who are undergoing high-risk/vascular surgery.

Class III: Noninvasive testing is not useful for patients with no clinical risk factors undergoing intermediate-risk or low-risk (<1% risk of serious complications) noncardiac surgery (e.g., endoscopic, superficial, cataract, breast, ambulatory).

Indications for Diabetic Patients

Because of a disproportionate burden of CAD in diabetic patients, the American Diabetes Association (ADA) has developed indications for cardiac testing in diabetic patients. They include the following:

1 Patients with typical or atypical cardiac symptoms

2 Patients with an abnormal resting ECG, especially if suggestive of ischemia or infarction

The ADA has recognized additional risk factors for obstructive CAD in diabetic patients, including renal disease (40% risk of coronary event in 5 years), evidence of other atherosclerotic disease (90% of their deaths are due to CAD), cardiovascular autonomic neuropathy (e.g., tachycardia, bradycardia, orthostatic hypotension, inadequate heart rate acceleration with exertion), older age, and female sex.

Indications in the Emergency Department

Patient has or had chest pain and fulfills the following requirements:

1 Two sets of negative cardiac markers from each of two different types of assays (troponin, myoglobin, or creatinine kinase MB) at 4-hour intervals.

2 Pre-exercise 12-lead ECG shows no significant changes compared with original ECG at the time of presentation to the emergency department.

3 Absence of baseline (resting) ECG abnormalities that would preclude accurate assessment of the EET.

4 From admission to the time that results are available from the second set of cardiac markers, the patient has become asymptomatic, has had lessening of chest pain symptoms, or has had persistent atypical symptoms.

5 Absence of ischemic chest pain at the time of EET.

Indications for Firefighters

The following guidelines were recommended by the National Fire Protection Association (NFPA) in 2000:

1 At age 40 years, periodic treadmill testing should be performed. The frequency should increase with age, but at a minimum the test should be done every 2 years.

2 At age 35 years, periodic treadmill testing should be performed for individuals with one or more coronary risk factors (premature family history [younger than age 55 years], hypertension, diabetes mellitus, cigarette smoking, and hypercholesterolemia [total cholesterol >240 or high-density lipoprotein <35]).

Indications before Noncardiac Surgery

Half of serious complications related to noncardiac surgery are cardiovascular. Although older patients have the highest risk of a cardiovascular complication with surgery, they also make up the largest group of patients undergoing surgery. Consequently, as the population ages, the cardiovascular risk of surgery will increase. Guidelines are available for screening patients before noncardiac surgery, and the ACC/AHA guidelines have been studied from an outcomes perspective. Box 93-2 provides some shortcuts for determining need for noninvasive testing. Patients about to undergo low-risk surgery (<1% risk; e.g., endoscopic, superficial, cataract, breast, ambulatory surgery) or with at least a fair functional/exercise capacity do not need further testing. If the patient has undergone revascularization (PCI or CABG) within the past 5 years or a thorough evaluation of the coronary arteries (e.g., EET, stress imaging) within the past 2 years, and there has not been a change in symptoms suggestive of ischemia, then according to ACC/AHA guidelines no further testing is necessary. Conversely, if high-risk (often >5% risk of serious complications) vascular surgery is planned and the patient has three or more clinical risk factors (i.e., CAD, CHF, ASCVD, diabetes, or renal insufficiency [creatinine ≥2 mg/dL]), noninvasive testing is reasonable if the results will change the management. It should be kept in mind that the goal of perioperative cardiac assessment is to detect the patient who would benefit from revascularization anyway, not just to get him or her through surgery. (See also Chapter 230, Preoperative Evaluation.)

Box 93-2 Shortcuts to Determine Indicators for Noninvasive Testing before Noncardiac Surgery

From Fleisher LA, Beckman JA, Brown KA, et al: ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: Executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Circulation 116:1971–1996, 2007.

No testing necessary if “Yes” to any of these four questions:

1 Is this low-risk surgery (e.g., endoscopic, superficial, cataract, breast, ambulatory surgery)?

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