(Circulation. 1995;91:580.)
© 1995 American Heart Association, Inc.
Articles |
Exercise Standards
A Statement for Healthcare Professionals From the American Heart Association
The purpose of this report is to provide revised standards and guidelines for the exercise testing and training of individuals free from clinical manifestations of cardiovascular disease as well as those with known cardiovascular disease. These guidelines are intended for physicians, nurses, exercise physiologists, specialists, technologists, and other healthcare professionals involved in the regular exercise testing and training of these populations. This report is in accord with the "Statement on Exercise" published by the American Heart Association in Circulation (1992;86:340-344).
These guidelines are a revision of the 1990 standards1 of the AHA that addressed the issues of exercise testing and training. An update of background, scientific rationale, and selected references are provided, and current issues of practical importance in the clinical use of these standards are considered.
Exercise Testing
The Cardiovascular Response to Exercise
Exercise, a common
physiological stress, can elicit cardiovascular
abnormalities not present at rest and can be used to determine the
adequacy of cardiac function. Because exercise is only one of many
stresses to which humans can be exposed, it is more appropriate to call
an exercise test exactly that and not a "stress test." This is
particularly relevant considering the increased use of nonexercise
stress tests.
Types of Exercise
Three types of muscular
contraction or exercise can be applied as
a stress to the cardiovascular system: isometric (static), isotonic
(dynamic or locomotory), and resistive (a combination of isometric and
isotonic).2 3 Isometric exercise, defined as a
muscular
contraction without movement (eg, handgrip), imposes greater pressure
than volume load on the left ventricle in relation to the body’s
ability to supply oxygen. The cardiovascular response to isometric
exercise is difficult to grade. In addition, cardiac output is not
increased as much as in isotonic exercise because increased resistance
in active muscle groups limits blood flow. Isotonic exercise, defined
as muscular contraction resulting in movement, primarily provides a
volume load to the left ventricle, and the cardiovascular response is
proportional to the size of the muscle mass and the intensity of the
exercise. Resistive exercise combines both isometric and isotonic
exercise by using muscular contraction with movement, as in free weight
lifting.
Key Point: Dynamic exercise is preferred for
testing because it puts a volume stress rather than a pressure load on
the heart and because it can be graduated. However, most activities
(especially employment and leisure time activities, such as sports)
usually combine all three types of exercise in varying degrees.
Maximum Oxygen Uptake
When dynamic exercise is
begun or increased, oxygen uptake by the
lungs quickly increases. After the second minute, oxygen uptake usually
remains relatively stable (steady state) at each intensity of exercise.
During steady state, heart rate, cardiac output, blood pressure, and
pulmonary ventilation are maintained at reasonably constant
levels.2
O2max is the
greatest amount of oxygen
a person can use while performing dynamic exercise involving a large
part of total muscle mass.4
O2max represents the amount
of oxygen
transported and used in cellular metabolism. It is convenient to
express oxygen uptake in multiples of sitting, resting requirements.
The metabolic equivalent (MET) is a unit of sitting, resting oxygen
uptake (3.5 mL O2 per kilogram body weight
per minute
[mL · kg-1 · min-1]).
Rather than determining each person’s true resting oxygen uptake, a
MET is taken as this average.
O2max is
significantly related
to age, gender, exercise habits, heredity, and cardiovascular clinical
status.
Age: Maximum values of
O2max occur between the
ages of
15 and 30 years, decreasing progressively with age. At age 60, mean
O2max in men is
approximately
three fourths that at age 20. With a sedentary lifestyle, there is a
9% reduction per decade versus less than 5% per decade for an active
lifestyle.
Gender: Through age 12 to 16 years, there is no significant
difference in O2max among
children, but a decrease is observed in girls between 12 and 14 years
of age. Reduced O2max in
women
is attributed to smaller muscle mass, lower hemoglobin and blood
volume, and smaller stroke volume as compared with men.
Exercise
habits: Physical activity has an important influence on
O2max. After 3 weeks of bed
rest, there is a 25% decrease in
O2max in healthy men. In
moderately active young men,
O2max is about 12 METs,
whereas
individuals performing aerobic training such as distance running can
have a O2max as high as 18
to
24 METs (60 to 85
mL · kg-1 · min-1).
Heredity:
There is a natural variation in
O2max related to genetic
factors.
Cardiovascular clinical status:
O2max is affected by the
degree
of impairment caused by disease.
It is difficult to accurately predict
O2max from its relation to
exercise habits and age because of considerable scatter and
correlations that are generally low. Table 1
lists key
values of METs that are clinically relevant, and Table 2
depicts normal values for age. The nomogram shown in
Fig 1 expresses the concept of METs by reflecting it
in terms of that expected for age, with 100% being
normal.5
|
|
|
Maximum
O2 is equal to maximum
cardiac output times maximum arteriovenous oxygen
(aO2) difference. Since
cardiac
output is equal to the product of stroke volume and heart rate,
O2 is directly related to
heart
rate. The maximum aO2
difference during exercise has a physiological limit of 15 to 17 vol%
hence, if maximum effort is achieved,
O2max can be used to
estimate
maximum cardiac output.
Myocardial Oxygen Uptake
Myocardial oxygen uptake (MO2) is
determined by intramyocardial wall tension ([left ventricular (LV)
systolic pressure times end-diastolic volume] divided by LV wall
thickness), contractility, and heart rate. Other less important factors
include external work performed by the heart, the energy necessary for
activation, and the basal metabolism of the myocardium (Table
3).
|
Accurate measurement of MO2
requires cardiac
catheterization. MO2 can be estimated during
clinical exercise testing by the product of heart rate and systolic
blood pressure, which is called the double product or
rate-pressure product. There is a linear relation between
MO2 and coronary blood flow. During exercise
coronary blood flow increases as much as fivefold above the resting
value. A subject with obstructive coronary disease often cannot
maintain adequate coronary blood flow to supply the metabolic demands
of the myocardium during exercise and, as a consequence, myocardial
ischemia occurs. Angina pectoris usually occurs at the same double
product rather than at the same external workload. Key
Point: An important basic principle of exercise physiology is that
O2 and
MO2 have distinct determinants and
methods of measurement or estimation (Table 3
).
Although they are directly related, this relation can be altered by
training and cardioactive medications such as ß-blockers.
Response to Dynamic Exercise
The body’s
response to dynamic exercise consists of a complex
series of cardiovascular adjustments to provide active muscles with the
blood supply appropriate for their metabolic needs, to dissipate the
heat generated by active muscles, and to maintain the blood supply to
the brain and the heart.
As cardiac output increases with dynamic exercise, peripheral resistance increases in organ systems and tissues that do not function during exercise and decreases in active muscles.6 Arterial blood pressure increases only mildly; thus, flow can increase as much as fivefold. Since the denominator (flow) increases much more than the numerator (pressure) in the formula for resistance, the result is a decrease in systemic vascular resistance.
Heart Rate
Response
An increase in heart rate due to a decrease in vagal outflow
is an
immediate response of the cardiovascular system to exercise; this
increase is followed by an increase in sympathetic outflow to the heart
and systemic blood vessels. During dynamic exercise, heart rate
increases linearly with workload and
O2. During low levels of
exercise and at a constant work rate, heart rate will reach steady
state within several minutes. As workload increases, the time necessary
for the heart rate to stabilize will progressively lengthen.
Heart rate response is influenced by several factors, including age. There is a decline in mean maximum heart rate with age7 that appears to be related to neural influences. Dynamic exercise increases heart rate more than isometric or resistive exercise. An accentuated heart rate response is observed after bed rest. Other factors that influence heart rate include body position, certain physical conditions, state of health, blood volume, and environment.
Key Point: Heart rate response to maximum dynamic exercise depends on numerous factors, particularly age and health. It appears that the reduction in heart rate averages 5 to 7 beats per minute per decade.
Arterial Blood Pressure
Response
Systolic blood pressure rises with increasing dynamic work as
a
result of increasing cardiac output, whereas diastolic pressure usually
remains about the same or may be heard to zero in some normal subjects.
Normal values of maximum systolic blood pressure for men have been
defined and are directly related to age.
An inadequate rise in systolic blood pressure (less than 20 to 30 mm Hg) can result from aortic outflow obstruction, LV dysfunction, or myocardial ischemia. Changes of blood pressure reflect more than the contractile function of the LV since they also depend on peripheral resistance. Subjects who develop hypotension during exercise frequently have severe heart disease; subjects with valvular or myocardial disease can also exhibit a drop in systolic blood pressure. A drop in systolic pressure below standing rest is of great concern during the actual test or during follow-up.
After maximum exercise there is usually a decline
in systolic blood
pressure, which normally reaches resting levels in 6 minutes, then
often remains lower than preexercise levels for several hours. In some
subjects with coronary artery disease (CAD), higher levels of systolic
blood pressure exceeding peak exercise values have been observed during
the recovery phase. When exercise is terminated abruptly, some healthy
persons have precipitous drops in systolic blood pressure due to venous
pooling. Fig 2 shows the physiological response to
submaximum and maximum treadmill exercise based on tests of more than
700 apparently healthy men aged 25 to 54 years. Maximum double product
(heart rate times systolic blood pressure) ranges from a tenth
percentile value of 25 000 to a 90th percentile value of 40 000.
|
Testing Procedures
The Physician’s Role
Exercise testing should be conducted only by well-trained
personnel with a basic knowledge of exercise physiology. Only
technicians and physicians familiar with normal and abnormal responses
during exercise can recognize or prevent untoward events. Equipment,
medications, and personnel trained to provide cardiopulmonary
resuscitation (CPR) must be readily available.
Although exercise
testing is considered a safe procedure, there are
reports of acute myocardial infarctions (MIs) and deaths. Multiple
surveys confirm that up to 10 MIs or deaths or both can be expected per
10 000 tests.8 However, the relative risk of an adverse
event during an exercise test versus during usual activity of subjects
with CAD is estimated to be 60- to 100-fold. Risk is greater in the
post-MI subject and in those being evaluated for malignant ventricular
arrhythmias. A recent review summarizing eight studies of estimates of
sudden cardiac death during exercise testing revealed rates from 0.0
(four studies) to 5 per 100 000 tests.8 Table 4
lists three classes of complications secondary to
exercise tests.
|
Good clinical judgment should be foremost in deciding
indications and
contraindications for exercise testing.9 Whereas absolute
contraindications are definitive, in selected cases with relative
contraindications even submaximum testing can provide valuable
information. Table 5 lists absolute and relative
contraindications to exercise testing.
|
In any procedure with a risk of complications, the physician should be certain that the subject understands the situation and acknowledges the risks. Some physicians believe that informing subjects of possible risks may cause them to become anxious or discourage them from undergoing a test. This possibility and the fact that a signed consent form does not protect a physician from legal action have recently led to less insistence on obtaining written consent. However, if consent is not initially obtained, a physician may be held responsible for a major adverse event, even if the test is carefully performed. The argument can be made that the subject would not have undergone the procedure if he or she had been aware of the risks associated with the test. Good physician-subject communication about testing is mandatory.
Exercise testing should be performed under the supervision of a physician who is appropriately trained to conduct exercise tests. The physician should be responsible for ensuring that the exercise laboratory is properly equipped and that exercise testing personnel are appropriately trained. The degree of subject supervision needed during a test can be determined by the clinical status of the subject being tested. This determination is made by the physician or physician’s designated staff member, who asks pertinent questions about the subject’s medical history, performs a brief physical examination, and reviews the standard 12-lead ECG performed immediately before testing. The physician should interpret data derived from testing, suggest further evaluation or therapy, and help deliver effective and timely advanced CPR when necessary. The physician or senior medical professional conducting the test must be trained in advanced CPR. A defibrillator and appropriate medications should also be immediately available.
The degree of supervision can range from assigning direct monitoring of the test to a properly trained nonphysician (ie, a nurse or exercise physiologist or specialist) for testing apparently healthy younger persons (less than 40 years old) and those with stable chest pain syndromes to the physician who directly monitors the subject’s blood pressure and status throughout exercise and recovery. The latter is the ideal for testing subjects for diagnostic or prognostic purposes and is certainly a requirement for testing all subjects at increased risk for exercise-induced complications. A physician should be immediately available during all exercise tests.
Subject Preparation
Preparations for exercise testing include the following:
• The subject should be instructed not to eat or smoke for 3 hours before the test and to dress appropriately for exercise, especially with regard to footwear. No unusual physical efforts should be performed for at least 12 hours before testing.
• A brief history and physical examination should be performed to rule out contraindications to testing or to detect important clinical signs such as a cardiac murmur, gallop sounds, pulmonary bronchospasm, or rales. Subjects with a history of increasing or unstable angina or heart failure should not undergo exercise testing until their condition stabilizes. A cardiac physical examination should indicate which subjects have valvular or congenital heart disease. Because hemodynamic responses to exercise may be abnormal in such subjects, they always warrant careful monitoring, and at times they may be excluded from testing.
• When exercise testing is performed for diagnostic purposes, withdrawal of medications may be considered since some drugs interfere with exercise responses and complicate the test interpretation. There are no formal guidelines for tapering medications, but rebound phenomena may occur with discontinuance of ß-blockers. Therefore, most subjects are tested while taking their usual medications. Specific questioning is important to determine which drugs have been taken so that the physician can be aware of possible electrolyte abnormalities and other effects.
• If the reason for the exercise test is not clear, the subject should be questioned and the referring physician contacted.
• A resting 12-lead ECG should be obtained since it may differ from the resting preexercise ECG. This is essential, particularly in subjects with known heart disease, since an abnormality or a change may contraindicate testing. Recording the ECG before starting the exercise test and after hyperventilation at another time may be helpful in confirming a false-positive (or indeterminate) ECG change.
• Standing ECG and blood pressure should be recorded to determine vasoregulatory abnormalities, particularly ST depression.
• A detailed explanation of the testing procedure should be given that outlines risks and possible complications. The subject should be told how to perform the exercise test, and the testing procedure should be demonstrated.
Electrocardiographic
Recording
Skin preparation. The most critical point of
the
electrode-amplifier-recording system is the interface between electrode
and skin. Removal of the superficial layer of skin significantly lowers
its resistance, thus decreasing the signal-to-noise ratio. The areas
for electrode application are first shaved and then rubbed with
alcohol-saturated gauze. After the skin dries, it is marked with a
felt-tipped pen and rubbed with a fine sandpaper or rough material.
With these procedures, skin resistance should be reduced to 5000 
or
less.
Electrodes and cables. Many electrodes are available for performing exercise testing. Silver plate or silver chloride crystal pellets are preferred because they have the lowest offset voltage. The electrodes should be constructed with a metal interface that is sunken, creating a column to be filled with either an electrolyte solution or a saturated sponge. When using fluid column electrodes, direct metal-to-skin contact should be avoided in order to decrease motion artifact.
Connecting cables between the electrodes and recorder should be light, flexible, and properly shielded. Most available commercial exercise cables are constructed to lessen motion artifact. Cables generally have a life span of a year or so, depending on use. They eventually become a source of both electrical interference and discontinuity and must be replaced.
Lead systems. Bipolar leads. Bipolar
lead systems were
the first to be used to detect ECG changes during exercise. The
relatively short placement time, freedom from motion artifacts, and the
ease with which noise problems can be located are factors that favor
their use. The usual positive reference is an electrode placed in the
same position as the positive reference for V5 (the fifth intercostal
space at the midclavicular line). The negative reference for V5 is
Wilson’s central terminal. Fig 3 illustrates negative
electrode placement for most bipolar lead systems. CM5 is
the most sensitive for ST segment changes. CC5 excludes the
vertical component included in CM5 and decreases the
influence of atrial repolarization (Ta), thus reducing false-positive
responses.10 Key Point: Electrode
placement affects ST segment slope and amplitude. The various
placements do not result in comparable waveforms for analysis. For
comparison of the resting 12-lead recording, arm and leg electrodes
should be moved to the wrists and ankles, with the subject in the
supine position.
|
Multiple leads. Since a standard 12-lead ECG with electrodes placed on the limbs cannot be obtained during exercise, other electrode placements have been used. Differences can be minimized by placing the arm electrodes as close to the shoulders as possible and the leg electrodes below the umbilicus and by recording the resting ECG with the subject supine. Any modification of lead placement should be recorded on the tracing.
Relative sensitivity of leads. The lateral precordial leads (V4 through V6) are capable of detecting 90% of all ST depression observed in multiple lead systems. Other reports indicate that using other leads in addition to V5 will increase the yield of abnormal responses by about 10%. However, the specificity of an abnormal response in other leads is lower. Key Point: Complete 12-lead tracings during exercise are not needed in many individuals with normal resting ECGs. However, they are necessary in subjects with arrhythmias, Q waves consistent with myocardial damage, or symptoms suggestive of coronary spasm and when evaluating severity of disease in subjects with known CAD.
Recorders. There are many good recorders designed to capture high-quality ECG data during exercise. Many use microprocessors to generate average waveforms and make ECG measurements. The physician must compare the raw analog data with computer-generated output to validate its accuracy. Computer processing is not completely reliable because of software limitations in handling noise and inadequacy of the available algorithms.
Equipment and Protocols
Fig
4 illustrates the relation of METs to stages
in the common testing protocols. Numerous devices have been used in the
past to provide dynamic exercise for testing, including steps,
escalators, and ladder mills. However, the treadmill and cycle
ergometer are now the most commonly used dynamic exercise testing
devices.
|
Cycle. Mechanical or electrically braked
cycles vary the force
to the pedaling speed (rate-independent ergometers), permitting better
power output control since it is common for uncooperative or fatigued
subjects to decrease their pedaling speed. The highest values of
O2 and heart rate are
obtained
with pedaling speeds of 50 to 80 rpm. Cycles are calibrated in
kiloponds (kp) or watts; 1 W is equivalent to approximately 6
kilopond-meters per minute (kpm/min). Since exercise on a cycle
ergometer is non–weight bearing, kiloponds or watts can be converted
to oxygen uptake in milliliters per minute. METs are obtained by
dividing O2 in milliliters
per
minute by the product of body weightx3.5.
The cycle ergometer is usually less expensive, occupies less space, and makes less noise than a treadmill. Upper body motion is usually reduced, making it easier to obtain blood pressure measurements and to record the ECG. Care must be taken to prevent isometric or resistive exercise of the arms.
There is a marked difference between the
body’s response to acute
exercise in the supine and upright positions. In healthy persons,
stroke volume and end-diastolic volume change little during supine
cycle exercise from volumes obtained at rest, whereas in the upright
position, these values increase and then plateau during mild work. In
subjects with cardiac abnormalities, LV filling pressure is more likely
to increase during exercise in the supine position than in the upright
position. When subjects with angina perform identical submaximum cycle
work in the supine and upright positions, heart rate is higher in the
supine position, maximum work performed is lower, and angina develops
at a lower double product. ST segment depression is usually greater in
the supine position because of the greater LV volume. A major
limitation to cycle ergometer testing is the discomfort and fatigue of
the quadriceps muscles. Usually leg fatigue of an inexperienced
"cyclist" causes subjects to stop before reaching a true
O2max. Thus,
O2max is 10% to 15% lower
in
cycle versus treadmill testing in those not accustomed to cycling.
Treadmill. The treadmill should have front and/or side
rails
for subjects to steady themselves; some subjects may also require the
assistance of the person administering the test. Subjects should not
tightly grasp the front or side rails since this decreases
O2 and increases exercise
time
and muscle artifact. Most subjects can walk without the aid of hand
rails, but older subjects may need such support. It is helpful if
subjects take their hands off the rails, close their fists, and place
one finger on the rails to maintain balance after they are accustomed
to walking on the treadmill. The treadmill should have both variable
speed and grade capability and must be accurately calibrated.
Protocols. Protocols for clinical exercise testing include an initial warm-up (low load), progressive uninterrupted exercise with increasing loads and an adequate duration in each level, and a recovery period. For cycle ergometry, the initial power output is usually 10 or 25 W (150 kpm/min), usually followed by increases of 25 W every 2 or 3 minutes until end points are reached. If arm ergometry is substituted for cycle ergometry, a similar protocol may be used, except that initial power output and incremental increases are lower. Two-minute stages are most popular with arm ergometry.11 12
Several different treadmill protocols are in use. The advantages of the
Bruce protocol include a seventh or final stage that cannot be
completed by most individuals as well as its use in many published
studies. Its disadvantages include large increments in work that make
estimation of O2max less
accurate. The fourth stage can be either run or walked, resulting in
different oxygen costs. Some subjects are forced to stop exercising
prematurely because of musculoskeletal discomfort or an inability to
tolerate the high workload increments. An initial zero and one-half
stages (1.7 mph at 0% and 5% grades) can be used for subjects with
compromised exercise capacities. Many exercise testing laboratories
currently use Balke-type protocols (Stanford, McHenry, and the
frequently used Naughton) with even MET level increments for stage
advances. The optimum protocol should last 6 to 12 minutes and should
be adjusted to the subject.
Exercise protocols should be individualized according to the type of subject being tested. Three-minute stages are not necessary to achieve steady state at a low workload. Performance can be estimated with the oxygen cost of maximum workload or power output achieved rather than by total treadmill time if subjects do not use hand rails, allowing comparison of performance in different protocols. A 9-minute targeted Ramp protocol that increases in small steps has many advantages, including more accurate estimates of MET level. Key Point:It is important to adjust or select the treadmill or cycle ergometer protocol to the subject being tested. The optimum protocol is 6 to 12 minutes. Exercise capacity should be reported in METs rather than minutes.
Submaximum Versus Maximum Exercise Testing
In some cases, testing is terminated when subjects reach 85% to
90% of predicted maximum heart rate for their age and level of
training. Unfortunately, there is a wide spread of maximum heart rate
around the regression line, declining with age (SD, 12 beats per
minute). Thus, the target heart rate is maximal for some subjects,
beyond the limit of others, and submaximal for still others. A test is
considered maximal when the subject appears to give a true maximum
effort (point of bodily exhaustion) or when other clinical end points
are reached. Paradoxically, when using an age-predicted heart
rate–targeted submaximum test, the most vulnerable subjects are
stressed to a relatively greater extent, whereas the less impaired are
limited by the submaximum target heart rate.
Perceived exertion. The subjective rating of the
intensity of
exertion perceived by the person exercising is generally a sound
indicator of relative fatigue. Rather than using heart rate alone to
clinically determine intensity of exercise, the 6 to 20 Borg scale of
perceived exertion13 is useful (Table 6).
Special verbal and written explanations about the rating of perceived
exertion are available for subjects. Although there is some variation
among subjects in their actual rating of fatigue, they seem to rate
consistently from test to test. Thus, the Borg scale can assist the
clinician in judging degree of fatigue reached from one test to another
or to correlate the level of fatigue during testing with that
experienced during daily activities.
|
Indications for terminating exercise testing. Indications for interruption of an exercise test have been derived from clinical experience.
Absolute indications
• Drop in systolic blood pressure (persistently below baseline) despite an increase in workload
• Increasing anginal pain
• Central nervous system symptoms (eg, ataxia, dizziness, or near syncope)
• Signs of poor perfusion (cyanosis or pallor)
• Serious arrhythmias (ie, high-grade ventricular arrhythmias such as multiform complexes, triplets, and runs)
• Technical difficulties monitoring the ECG or systolic blood pressure
• Subject’s request to stop
Relative indications
• ST or QRS changes such as excessive ST displacement, extreme junctional depression, or marked axis shift
• Fatigue, shortness of breath, wheezing, leg cramps, or claudication
• General appearance (see below)
• Less serious arrhythmias, including supraventricular tachycardias
• Development of bundle branch block that cannot be distinguished from ventricular tachycardia
Postexercise Period
Some abnormal responses occur only in recovery after exercise. If
maximum sensitivity is to be achieved with an exercise test, subjects
should be supine in the postexercise period; however, for subject
comfort, many physicians prefer the sitting position. A cooldown walk
after the test can delay or eliminate the appearance of ST segment
depression; however, the cooldown may be indicated in some subjects.
Monitoring should continue for 6 to 8 minutes after exercise or until
changes stabilize, and heart rate and ECG are close to baseline. In the
supine position, 4 to 5 minutes into recovery, approximately 85% of
subjects with abnormal responses are abnormal at this time only or in
addition to any other time. An abnormal ECG response occurring only in
the recovery period is not unusual, nor is it more likely to be
false-positive. Mechanical dysfunction and electrophysiological
abnormalities in the ischemic ventricle after exercise can persist from
minutes to hours. Monitoring of blood pressure should continue during
recovery, as abnormal responses may occur.
Interpretation
Clinical Responses
Symptoms. Ischemic chest pain induced by the exercise
test is
strongly predictive of CAD and is even more predictive with ST
depression. It is important to obtain a careful description of the pain
from the subject to ascertain that it is typical angina rather than
nonischemic chest pain.
Subject’s appearance. The subject’s general appearance is helpful in clinical assessment. A drop in skin temperature, cool and light perspiration, and peripheral cyanosis during exercise can indicate poor tissue perfusion due to inadequate cardiac output with secondary vasoconstriction. Such subjects should not be encouraged to attempt higher workloads. Neurological manifestations such as light-headedness or vertigo can also indicate inadequate cardiac output.
Physical examination. Cardiac auscultation immediately after exercise can provide information about ischemia-induced LV dysfunction. Gallop sounds or a precordial bulge can result from LV dysfunction. A new mitral regurgitant murmur suggests papillary muscle dysfunction, which may be related to transitory ischemia. It is preferable to have subjects lie supine after exercise testing and allow those who develop orthopnea to sit up. In addition, severe angina or ominous arrhythmias after exercise may be lessened by allowing the subject to sit up, since ischemia may be decreased. Key Point: Symptoms and signs of ischemia induced by exercise testing are clinically important, and their combinations influence interpretation.
Exercise
or Functional Capacity
O2max is a measure
of the
functional limit of the cardiovascular system and the best index of
exercise capacity. As previously discussed,
O2max depends on many
factors
(training, age, and gender) and is an indirect estimate of maximum
cardiac output. A decline in maximum cardiac output, which is the major
hemodynamic consequence of symptomatic CAD, usually causes a decrease
in exercise capacity. Although many subjects may stop exercising
because of anginal pain, acute reduction in LV performance resulting in
decreased stroke volume and heart rate and increasing pulmonary artery
pressure appear to be the mechanisms limiting cardiac output. In normal
women as opposed to normal men, LV ejection fraction (LVEF)
"plateaus" and may decrease with maximal
exercise.14
A mean exercise capacity of 10 METs has been observed in nonathletic middle-aged healthy men. If subjects with CAD reach 13 METs, their prognosis is good, regardless of other exercise test responses that may occur and medical or surgical treatment. Mortality is higher in subjects with an exercise capacity of 5 METs or less compared with subjects whose exercise capacities are higher.
A normal exercise capacity does not exclude severe cardiac impairment. Mechanisms proposed to explain a normal work performance in these subjects include increased peripheral oxygen extraction, preservation of systolic volume and chronotropic reserve, ability to tolerate elevated pulmonary wedge pressures without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise. Many subjects with decreased ejection fractions at rest can perform relatively normal levels of exercise, some without side effects, whereas others report increased fatigue for some time after the test. Key Point: An exercise capacity of 5 METs or less is associated with a poor prognosis in subjects less than 65 years old. An exercise capacity of 13 METs indicates a good prognosis despite abnormal exercise test responses. Resting LVEF does not correlate well with exercise capacity.
Hemodynamic Responses
Blood Pressure During Exercise
Blood pressure is dependent on cardiac output and peripheral
resistance. Systolic blood pressure at maximum exertion or at immediate
cessation of exertion is considered a clinically useful first
approximation of the heart’s inotropic capacity. An inadequate rise or
a fall in systolic blood pressure during exercise can occur. Although
some normal subjects have a transient drop in systolic blood pressure
at maximum exercise, this finding is frequently associated with severe
CAD and ischemic dysfunction of the myocardium. Exercise-induced
hypotension also identifies subjects at increased risk for ventricular
fibrillation in the exercise laboratory. Key Point: A
drop in systolic blood pressure below standing rest during exercise is
associated with increased risk in subjects with a prior MI or
myocardial ischemia.
Heart Rate During Exercise
Relatively rapid heart rate during submaximum exercise or recovery
could be due to deconditioning, a condition that decreases vascular
volume or peripheral resistance, prolonged bed rest, anemia, or
metabolic disorders. This finding is relatively frequent soon after MI
and coronary artery surgery. Relatively low heart rate at any point
during submaximum exercise could be due to exercise training, enhanced
stroke volume, or drugs. The common use of ß-blockers, which lower
heart rate, has complicated interpretation of the heart rate response
to exercise. Conditions that affect the sinus node can attenuate the
normal response of heart rate during exercise testing. Key
Point: Abnormalities of exercise capacity, systolic blood
pressure, and heart rate response to exercise can be due to either LV
dysfunction, ischemia, cardioactive drugs, or autonomic dysfunction.
Responses in Subjects With Normal Resting ECGs
Normal responses. P wave. During exercise, P vectors
become more vertical, and P wave magnitude increases significantly in
inferior leads. There are no significant changes in P wave duration.
PR segment. The PR segment shortens and slopes downward in the inferior leads during exercise. The decreasing slope has been attributed to atrial repolarization (the Ta wave) and can cause false-positive ST depression in the inferior leads.
QRS complex. The Q wave shows very small changes from the resting values; however, it does become slightly more negative at maximum exercise. Changes in median R wave amplitude are noted near maximum effort. A sharp decrease in the R wave is observed in the lateral leads (V5) at maximum exercise and into the first minute of recovery. In the lateral and vertical leads (V5 and aVF), the S wave becomes greater in depth (more negative), showing a greater deflection at maximum exercise, and then gradually returns to resting values in recovery. As the R wave decreases in amplitude, the S wave increases in depth.
J-junction depression. The J-junction is depressed in lateral leads to a maximum depression at maximum exercise, then gradually returns toward preexercise values in recovery. A dramatic increase in J-junctional depression is observed in all leads and is greatest at 1 minute into recovery. Subjects with resting J-junction elevation may develop an isoelectric J-junction with exercise; this is a normal finding. These changes return toward pretest values later in recovery. The normal ST segment vector response both to tachycardia and exercise is a shift rightward and upward. There appears to be considerable biological variation in the degree of this shift.
T wave. A gradual decrease in T wave amplitude is observed in all leads during early exercise. At maximum exercise the T wave begins to increase, and at 1 minute into recovery the amplitude is equivalent to resting values in the lateral leads.
U wave. No significant changes are noted with exercise; however, U waves may be difficult to identify because of the close approximation of the T and P waves with the increased heart rate of exercise.
Abnormal responses. ST segment changes. The ST level is measured relative to the PR segment since the UP segment disappears during exercise. ST elevation is measured as the deviation from the baseline ST level. ST depression is measured from the isoelectric PR level since the normal response is a downward shift from early repolarization. If the baseline ST segment is depressed, the deviation from that level to the level during exercise or recovery is considered. The point for measuring the ST level is the J-junction. Points beyond this (60 or 80 milliseconds) should only be used if the ST segment slope is horizontal or downsloping. Considering ST depression that is rapidly upsloping to be abnormal increases sensitivity but decreases specificity. Many ST scores to quantify ischemia have been recommended, but none have been validated as superior to standard measurements. Exercise-induced myocardial ischemia can result in one of three ST segment manifestations on the surface ECG: depression, elevation, and normalization.
ST segment depression. ST segment depression is
the most
common manifestation of exercise-induced myocardial ischemia. It
represents subendocardial ischemia, with direction determined largely
by the placement of the heart in the chest. The standard criterion for
this abnormal response is horizontal or downsloping ST segment
depression of 0.10 mV or more for 80 milliseconds. However, as shown in
Fig 5, other criteria have been considered.
Downsloping ST segment depression is a more significant change than
horizontal depression. In the presence of baseline abnormalities,
exercise-induced ST segment depression is less specific for ischemia.
Other factors related to the probability and severity of CAD include
the amount, time of appearance, duration, and number of leads with ST
segment depression.
|
Severity of CAD is also related to the time of appearance of ischemic shifts. The lower the workload and double product at which it occurs, the worse the prognosis and the more likely the presence of multivessel disease. The persistence of ST depression in the recovery phase is also related to the severity of CAD. Key Point: The probability and severity of CAD are directly related to the amount of J-junction depression and are inversely related to the slope of ST segment (ie, the greater the depression and the downslope, the more likely and more severe the CAD).
ST segment elevation. ST elevation must be classified by whether it occurs over Q waves of an MI or in an ECG area without Q waves. The mechanisms and implications are markedly different. ST segment elevation has been more frequently observed in anterior leads (V1 and V2) with Q waves.15
ST segment elevation over Q waves of prior MI. Prior MI is the most frequent cause of ST segment elevation during exercise and appears to be related to the presence of dyskinetic areas or ventricular aneurysms. Approximately 50% of subjects with anterior MI and 15% of subjects with inferior MI exhibit this finding during exercise. Subjects with elevation usually have a lower ejection fraction than those without elevation over Q waves. These changes can result in reciprocal ST depression that simulates ischemia in other leads. ST segment elevation and depression during the same test may indicate multivessel CAD. The underlying extent of Q waves or myocardial damage actually determines the amount of ST elevation rather than independently reflecting the amount of dysfunction.
ST segment elevation without Q waves. In subjects without previous MI (absence of Q waves on the resting ECG), ST segment elevation during exercise frequently pinpoints the site of severe transient ischemia resulting from significant proximal disease or spasm. Key Point: Severe transmural ischemia is the mechanism for ST segment elevation during exercise in subjects without prior MI or diagnostic Q waves on the resting ECG. It locates the site of ischemia, in contrast to ST depression, which does not.16
In subjects with variant angina, ST segment elevation occurs during spontaneous anginal episodes, frequently at rest. During exercise, ST segment elevation has been reported in about 30% of these subjects. A reversible thallium-201 perfusion defect usually corresponds to the site of ST elevation. Many subjects with ST elevation have coexistent ST segment depression in other leads. Ventricular arrhythmias also appear to be more frequent in subjects with ST elevation.
ST segment normalization or absence of change. Another manifestation of ischemia may be normalization of or no change in the ST segment related to cancellation effects, but this is nonspecific. ECG abnormalities at rest, including T wave inversion and ST segment depression, reportedly return to normal during attacks of angina and during exercise in some subjects with ischemic heart disease, but they can also be observed in subjects with a persistent juvenile pattern on the resting ECG. This cancellation effect is rare but should be considered.
Diagnostic value of R wave changes. Many within-subject estimates of the variability of R wave amplitude changes during exercise in normal subjects have been reported. However, the average response in normal subjects is an increase in R wave amplitude during submaximum exercise, with a drop at maximum exercise. Exercise-induced changes in R wave amplitude have not improved diagnostic accuracy despite use of several lead systems, clinical subsets of subjects, and different criteria for an abnormal response. Key Point: A multitude of factors affect the R wave amplitude response to exercise, and the response does not have diagnostic significance.
T wave changes. In normal subjects, a gradual decrease in T wave amplitude is observed in all leads during early exercise. At maximum exercise the T wave begins to increase, and 1 minute into recovery amplitude is equivalent to resting values in lateral leads.
U wave changes. U wave inversion is associated with LV hypertrophy, CAD, and aortic and mitral regurgitation. These conditions are associated with abnormal LV distensibility. Exercise-induced U wave inversion in subjects with a normal resting ECG appears to be a marker of myocardial ischemia and suggests left anterior descending CAD.
ST/HR index and slope. Although research and clinical data are available on this methodology in exercise testing, the ST/HR index is not recommended because of problems with validation. A meta-analysis revealed that positive results with this method were obtained only by centers that were also responsible for over half the published reports.17
Other Studies
Exercise
tests can be performed with radionuclear techniques to
further evaluate myocardial perfusion and function. As an example,
thallium, an isotope that behaves like potassium, is taken up by
perfused, viable myocardium when injected at maximum exercise. Imaging
performed immediately after exercise can reveal defects. If defective
areas fill in during resting scans, they are usually due to ischemia;
if such areas do not fill in, the defects can be due to scarring or
severe ischemia. Technetium can be tagged to red blood cells and can
provide an image of the LV cavity blood volume during exercise. Changes
in ejection fraction, wall motion, and ventricular volume can be
assessed.
Echocardiographic images and Doppler flow measurements can be made during and after exercise. Ejection fraction, wall motion, and valvular function can be assessed with this technique.
More recently, thallium single-photon emission computerized tomography has been used in exercise evaluation. Such evaluation should be delayed 10 to 15 minutes after exercise to avoid artifacts secondary to heart position and respiratory rate immediately after exercise.18 As further sophistication of imaging evolves, positron emission tomography will likely become a clinically applicable tool in exercise evaluation. This technique offers the opportunity to quantify regional function in the heart spanning blood flow, biochemical reaction rates, substrate fluxes, and receptors.19 Pharmacologic stress is available for subjects who are unable to exercise. Dipyridamole infusion as a coronary vasodilator causes an increase in myocardial blood flow that is altered in the presence of diseased coronary arteries.18 Adenosine infusion, which also causes vasodilation, can be used similarly to dipyridamole in pharmacological testing,18 and dobutamine, with its chronotropic and inotropic effects, can be used with thallium scintigraphy or echocardiography to delineate regional ischemia and wall motion abnormalities.18
Magnetic resonance imaging is a relatively new technology that may serve as an excellent tool for studying the effects of exercise in both the normal and failing heart. These methods are well-suited to study the myocardial effects of chronic exercise.20
Diagnostic Value of the Exercise Test
Sensitivity and
Specificity
Sensitivity and specificity define how effectively a test
separates subjects with disease from healthy individuals, ie, how well
a test diagnoses disease. Sensitivity is the percentage of those
individuals with a disease who will have abnormal tests. Specificity is
the percentage of those without the disease who will have normal test
results; specificity may be affected by drugs such as digoxin, baseline
ECG patterns, LV hypertrophy, and gender.
Sensitivity and specificity are inversely related; when sensitivity is the highest, specificity is lowest and vice versa. All tests have a range of inversely related sensitivities and specificities that can be selected by specifying a discriminate or diagnostic cut point.
The choice of a discriminate value is further complicated by the fact that some exercise test responses do not have established values that separate normal subjects from those with disease. Once a discriminate value that determines a test’s specificity and sensitivity is chosen, the population tested must be considered. If the population is skewed toward individuals with a greater severity of disease, the test will have a higher sensitivity. For instance, the exercise test has a higher sensitivity in individuals with triple-vessel disease than in those with single-vessel disease. A test can also have a lower specificity if it is used in individuals who are more likely to give false-positive results. For instance, the exercise test has a lower specificity in women and in individuals with mitral valve prolapse.
Sensitivity and specificity of exercise-induced ST segment depression can be demonstrated by comparing the results of exercise testing and coronary angiography.21 From these studies, it can be seen that the exercise test cut point of 0.1 mV horizontal or downsloping ST segment depression has approximately 84% specificity for angiographically significant CAD; ie, 84% of those without significant angiographic disease had a normal exercise test. These studies had a mean 66% sensitivity of exercise testing for significant angiographic CAD, with a range of 40% for one-vessel disease to 90% for three-vessel disease. Key Point: Sensitivity and specificity are inversely related, affected by the population tested, and determined by the choice of a cut point or discriminate value.
Relative Risk and Predictive Value
Relative risk
and predictive value help define the
diagnostic value of a test. Table 7 shows how
sensitivity, specificity, relative risk, and predictive value are
calculated.
|
Prognostic Use of the Exercise Test
Rationale
There are two principal reasons for estimating prognosis. The
first is to provide accurate answers to a subject’s questions about
the probable outcome of his or her illness. Although discussion of
prognosis is inherently delicate and probability statements can be
misunderstood, most subjects find this information useful in planning
their work, recreational activities, personal estates, and finances.
The second reason for determining prognosis is to identify subjects in
whom cardiovascular interventions might improve outcome.
Pathophysiology of CAD
The basic pathophysiological
features of CAD include arrhythmic
risk, myocardial damage (reflected by LV function), and the degree of
myocardium in jeopardy. Arrhythmic risk does not appear to be
independently predicted by exercise testing since the prognosis of
arrhythmias is closely related to LV abnormalities. (Twenty-four hour
ambulatory ECG recording provides more information about arrhythmias
except for those that are clearly related to exercise.) Exercise test
responses due to myocardial ischemia include angina, ST segment
depression, and ST segment elevation over ECG areas without Q waves.
Predicting the amount of ischemia (ie, the amount of myocardium in
jeopardy) is difficult. It is inversely related to the double product
at the onset of signs or symptoms of ischemia. Responses related to
ischemia or LV dysfunction include chronotropic incompetence, drops in
systolic blood pressure, and poor exercise capacity.
Exercise capacity correlates poorly with LV function in subjects without signs or symptoms of heart failure, nor is exercise testing helpful in identifying subjects with moderate LV dysfunction. LV dysfunction is better recognized by a history of heart failure, physical examination, resting ECG, echocardiogram, or radionuclide ventriculogram. Several subject groups have been studied to determine prognosis with exercise testing, including post-MI subjects, subjects with stable CAD (including silent ischemia), subjects after coronary artery bypass surgery (CABS), subjects after percutaneous transluminal coronary angioplasty (PTCA), and asymptomatic individuals.
Post-MI Subjects. Purpose. Table 8
lists reasons for performing an exercise test in post-MI subjects.
Exercise testing may expedite and optimize discharge from the hospital
of subjects recovering from an MI. Ventricular arrhythmias not present
at rest can be provoked during exercise. The subject’s reaction to
exercise, work capacity, and limiting factors at the time of discharge
from the hospital can be assessed. An exercise test before discharge is
important for providing guidelines for exercise at home, reassurance of
physical status, and determination of risk of complications. It also
provides a safe basis for advising the subject to resume or increase
his or her activity level and return to work. The test can demonstrate
to the subject, family, and employer the effect of MI on capacity for
physical performance. Psychologically, it may improve self-confidence
by decreasing the subject’s anxiety about daily physical activities.
The test also reassures spouses of subjects’ physical capabilities.
The response to exercise testing reassures and encourages many subjects
to increase their activities.
|
Some investigators use symptoms or sign-limited end points 2 or 3 weeks after MI. However, a submaximum limited test using predetermined end points seems more clinically appropriate. A heart rate limit of 140 beats per minute and a MET level of 7 is arbitrarily used for subjects under the age of 40 years; a heart rate limit of 130 beats per minute and a MET level of 5 is used for subjects over 40. A Borg perceived exertion level in the range of 13 to 15 can be used as a test end point, particularly for subjects receiving ß-blockers. A symptom-limited maximum test is probably most appropriate more than 3 weeks after MI, when the subject is ready to resume full activities.
Safety. A review of numerous subjects with predischarge and post-MI exercise tests reports few serious complications: two cases of recurrent MI and two cases of ventricular fibrillation, one fatal. These findings represent 0.05% morbidity and 0.02% mortality.22
Meta-analysis reveals that only an abnormal systolic blood pressure response or a low exercise capacity is significantly associated with poor outcome in post-MI subjects. Submaximum testing resulted in the highest proportion of positive associations and the highest risk ratios. Abnormal responses at higher workloads are not as predictive as those at lower workloads.22 Key Point: In post-MI subjects, clinical judgment identifies subjects at highest risk, and exercise-induced ST displacement is not as predictive as an abnormal systolic blood pressure response (drop of 20 mm Hg or more or flat response for duration of the test) or poor exercise capacity. However, exercise-induced ST segment depression appears to be associated with increased risk in subjects without diagnostic Q waves (ie, subendocardial MI).23
Subjects with stable CAD. Studies using exercise testing of subjects with stable CAD have attempted to predict angiographic findings, cardiac events in subjects with silent ischemia, or improved survival with CABS.
Angiographic findings. Numerous studies have been devised to predict left main or triple-vessel disease or both.24 Different criteria have been used with varying results. Predictive value refers to the percentage of those with abnormal criteria who actually have left main or triple-vessel disease.
Exertional hypotension. In most studies, exercise-induced hypotension predicts a poor prognosis, with a positive predictive value of 50% for left main or triple-vessel disease.25 Exercise-induced hypotension is also associated with cardiac complications during exercise testing, appears to be alleviated by CABS, and can occur in subjects with CAD, valvular heart disease, or cardiomyopathy. Occasionally, subjects without clinically significant heart disease will exhibit exercise-induced hypotension during exercise related to dehydration, antihypertensive therapy, or prolonged strenuous exercise. Key Point: The definition of exercise-induced hypotension is of crucial importance in evaluating the exercise test response. A drop in systolic blood pressure below preexercise values is the most ominous criterion; a drop of 20 mm Hg or more after a rise is reason to stop a test if accompanied by serious ventricular arrhythmias or ischemia.
Cardiac events in subjects with silent ischemia. In the presence of unstable angina, asymptomatic (silent) ischemia detected by ambulatory ECG (Holter) recording appears to confer an adverse prognosis. The prognostic implication of asymptomatic ischemia detected during exercise testing is controversial. Subjects with silent ischemia may be at greater risk for cardiac death because they do not have an intact "warning system." However, in three large population studies of subjects with a high prevalence of CAD who underwent exercise testing, those with ST segment depression with or without angina during testing had similar prognoses.26 Ischemia is silent in approximately 60% of subjects with ischemic ST segment depression. Silent ischemia occurring with treadmill testing does not confer an increased risk for death relative to subjects experiencing angina. Thus, therapy should not be more intense for silent ischemia than for subjects with angina and ST depression.
Exercise-induced ventricular arrhythmias. In subjects with CAD, exercise-induced ventricular arrhythmias do not usually represent an independent risk factor for subsequent mortality or coronary events. However, recent data suggest that these arrhythmias add independent prognostic information to thallium-201, ST segment, and heart rate changes,27 28 and they are associated with severe CAD and wall motion abnormalities. Exercise testing may be of considerable value in the evaluation of drug therapy for ventricular arrhythmias, particularly in subjects with CAD.
Prognostic scores. Scores
based on the coefficients from Cox
Hazzard Survival models appear to be the optimal way of estimating
cardiovascular mortality. The Duke score represented in Fig 6
as a nomogram is the best validated and has been
shown to function in a wide range of populations, including women.
|
Improved survival after CABS. One study suggests that subjects with cardiomegaly, exercise capacity of less than 5 METs, or a maximum systolic blood pressure of less than 130 mm Hg would have a better outcome if treated with surgery.29 In one surgery trial, subjects who had an exercise test response of 1.5 mm of ST segment depression showed enhanced survival with surgery. Improved survival also extended to those with baseline ST segment depression and those with claudication.30 In another trial31 the surgical benefit to mortality was greatest in subjects with 1 mm ST segment depression at less than 5 METs. There was no difference in mortality in subjects who exceeded exercise capacity of 10 METs, and in this group, the prognosis is generally quite good. Key Point: In subjects with stable CAD, studies comparing angiographic findings, cardiac events, and the differential outcome of CABS compared with medical therapy have shown the exercise test to have prognostic power. These studies indicate that subjects with marked degrees of ST segment depression (ie, greater than 2 mm, in multiple leads, and prolonged into recovery) accompanied by poor exercise capacity, exertional hypotension, ectopic ventricular contractions, angina, or all of the above are at increased risk of having triple-vessel or left main disease and a poor prognosis.
Subjects who become symptomatic after CABS. Because more than 300 000 Americans undergo CABS each year, predicting prognosis of subjects who become symptomatic after this procedure is an important issue. Several studies have evaluated graft occlusion and recurrence of symptoms; however, exercise-induced ST depression does not predict prognosis after CABS. An exercise capacity of 9 METs or more indicates a good prognosis, regardless of other responses.32
Subjects who have undergone PTCA. More than 250 000 PTCAs are performed annually,33 with an expected angiographic restenosis rate of 30% to 40%34 within the subsequent first 6 months. Several studies have assessed the value of exercise testing in the detection of restenosis and/or in the prediction of adverse cardiac events after PTCA.34 35 36 37 38 39 40 41 Interpretation of these studies is limited because of their variability in subject populations and study design, with regard to the number of vessels diseased, the adequacy of revascularization after PTCA, the timing of the exercise test, and the definition of restenosis. Several general conclusions, however, can be drawn from these studies. Exercise electrocardiography early after PTCA is more often positive for an ischemic response among subjects with multivessel coronary disease and those who have incomplete revascularization.35 36 37 The sensitivity of exercise electrocardiography in the detection of angiographic restenosis has been reported to range widely, from 24% to 60%.38 39 40 Moreover, among asymptomatic subjects with single vessel CAD, the detection of restenosis and the utility of the exercise test to predict subsequent cardiac events is particularly low.36 38 39
In summary, the sensitivity, specificity, and predictive value of exercise testing after PTCA is sufficiently low to preclude its routine use as a screening test for restenosis and the assessment of subsequent prognosis, particularly in asymptomatic subjects. Such testing appears to have the highest yield among symptomatic subjects with multivessel coronary disease and in those with incomplete revascularization. As such, exercise testing after PTCA, if done, should be performed and interpreted with regard to the timing of the test after PTCA, assessment of clinical symptoms, and assessment of coronary anatomy at the time of PTCA.
High risk coronary profile. Exercise testing in subjects with coronary risk factors such as hypercholesterolemia and high blood pressure may be beneficial, particularly if there are symptoms suggesting CAD. The detection of myocardial ischemia or other abnormal end points can lead to further diagnostic studies and appropriate management strategies.
Apparently healthy individuals. Silent ischemia induced by exercise testing in apparently healthy men is not as predictive of a poor outcome as once thought. Use of the exercise test for screening is even more misleading than previously appreciated because of the higher false-positive rate. Approximately 19 of 20 abnormal ST responses will be false-positives. Earlier superior results can be explained by inclusion of angina pectoris as an end point, which could be caused by cardiac concerns resulting from an abnormal exercise test.42 43 Key Point: The nonselective use of exercise testing for screening apparently healthy individuals should be discouraged because of the poor predictive value of minimum (1 mm) ST segment depression. Unfortunately, this abnormal response may lead to psychological and vocational disability as well as unnecessary medical expense and risk. In these individuals, the test is helpful for motivational purposes and for designating exercise prescriptions. Only combinations of other abnormal responses and at least 2 mm or more ST depression should be considered predictors of increased risk of cardiovascular events in asymptomatic men.
There is substantial evidence to support the use of exercise testing as the first noninvasive step after the history, physical examination, and resting ECG in prognostic evaluation of subjects with CAD. Exercise testing accomplishes both purposes of prognostic testing: it provides information about the subject’s status and is helpful when making recommendations for optimum management. Some studies show that the value of exercise testing for risk stratification is enhanced by the addition of radionuclide imaging, particularly with submaximum testing after an uncomplicated MI. Exercise test results enhance selection of subjects who should undergo further evaluation such as coronary angiography. Since the exercise test can be performed in the physician’s office and provides valuable information about activity levels, response to therapy, and disability, it is the reasonable first choice for prognostic assessment. Because of its widespread use, the exercise test can have an enormous impact on the cost-effective delivery of cardiovascular care.
Other Uses of the Exercise Test
Assessment of Valvular
Heart Disease
Exercise testing has been used in subjects with valvular
heart
disease to quantify disability, to reproduce exercise-induced symptoms,
and to evaluate responses to medical and surgical
interventions.44 The exercise test has also been used to
identify concurrent CAD, but there is a high prevalence of
false-positive responses (ST depression not due to ischemia) because of
frequent baseline ECG abnormalities and LV hypertrophy. Some physicians
use exercise testing to determine when surgery is indicated. Exercise
testing has been used most frequently in subjects with aortic
stenosis.
Aortic stenosis. Effort syncope in subjects with aortic stenosis45 46 is an important and well-appreciated symptom. Most guidelines for exercise testing list moderate to severe aortic stenosis as a relative contraindication for testing because of concern about syncope and cardiac arrest. Four proposed mechanisms for exercise-induced syncope in subjects with aortic stenosis include carotid hyperactivity, LV failure, arrhythmia, and LV baroreceptor stimulation. Exercise testing is relatively safe in both the pediatric and adult subject when performed appropriately. Attention should focus on the subject’s symptoms, minute-by-minute response of blood pressure, slowing heart rate, and ventricular and atrial arrhythmias. In the presence of an abnormal blood pressure response, the subject with aortic stenosis should take at least a 2-minute cooldown walk at a lower stage of exertion to avoid acute LV volume overload, which may occur when the subject lies down.
Exercise plays an important role in the objective assessment of symptoms, hemodynamic response, and functional capacity. Whether ST segment depression indicates significant CAD remains unclear. The benefits of surgery and baseline impairment can be quantified by performing an exercise test before and after the operation. Exercise testing offers the opportunity to objectively evaluate disparities between history and clinical findings, eg, in the elderly asymptomatic subject with physical and/or Doppler findings of severe aortic stenosis. Echocardiographic studies are often inadequate in such subjects, particularly in smokers. When Doppler echocardiography reveals a significant gradient in the asymptomatic subject with normal exercise capacity, progress should be monitored until symptoms develop. Surgery appears to be indicated in subjects with an inadequate systolic blood pressure response to exercise or a fall in systolic blood pressure from the resting value when symptoms occur.
Aortic regurgitation. Subjects with aortic
regurgitation47 usually maintain a normal exercise
capacity for a longer time than those with aortic stenosis. Volume
workload of the myocardium requires less oxygen than pressure work.
During exercise, the decreases in diastolic duration and regurgitation
volume favor forward output. As the myocardium fails, heart rate tends
to slow, and ejection fraction and stroke volume decrease. There is an
increase in ventricular diameter and metabolic requirements. Exercise
testing is useful for monitoring subjects with aortic regurgitation,
using onset of ST segment depression, a reduction of heart rate
response to each workload, and decrease in peak
O2 as markers for worsening
LV
function.
Mitral stenosis. Subjects with mitral stenosis48 may show either a normal or excessive increase in heart rate during exercise. Since stroke volume cannot be increased, the normal rise of cardiac output is attenuated and may eventually fall during exercise, frequently accompanied by exercise-induced hypotension. A rise in pulmonary resistance results in increases in myocardial oxygen demands. In subjects with mitral stenosis, chest pain and ST segment depression during exercise may occur as a consequence of reduction in coronary perfusion or because of pulmonary hypertension. ST depression is attributed to a decrease in coronary perfusion as a consequence of a fall in cardiac output and increased myocardial oxygen demand secondary to right ventricular overload. Shortening of diastole associated with tachycardia and increased pulmonary blood flow during exercise increases effects of preexistent mitral stenosis and may cause pulmonary congestion.
Mitral regurgitation. Subjects with mild to moderate mitral regurgitation49 maintain normal cardiac output during exercise. Blood pressure, heart rate, and ECG responses are usually normal. When mitral regurgitation occurs suddenly during exercise as a result of ischemic papillary muscle dysfunction, a flat response in systolic blood pressure can occur. Subjects with severe mitral regurgitation usually show a decreased cardiac output and limited exercise capacity. ST segment depression is infrequent in these subjects since there is no significant increase in myocardial oxygen consumption with mitral regurgitation. However, a hypotensive response can develop, and arrhythmias frequently occur.
Mitral valve prolapse. Several mechanisms have been suggested to explain ST depression in subjects with mitral valve prolapse,50 including regional ischemia of the papillary muscle, abnormalities of the coronary arteries, compression of the anterior descending artery, coronary spasm, and primary cardiomyopathy. Angiography and scintigraphy studies in these subjects have been normal. ECG changes can be normalized by propranolol or other nonselective ß-blockers, which will improve the specificity of the exercise test.
Evaluation of an Exercise Program
An
exercise test is often used to evaluate the safety of an
exercise training program and is useful in formulating an exercise
prescription. In general, a sedentary individual who at the age of 40
years decides to enter an exercise program of a higher intensity than
walking at 50% to 60% of maximum heart rate reserve should undergo an
exercise test. Testing should also be recommended for younger
individuals with coronary risk factors or a strong family history of
CAD. Because of the wide scatter of maximum heart rate when plotted
against age, determining an individual’s maximum heart rate during
exercise in order to assign a target for training is preferable to
giving a predicted value. It is advantageous in certain individuals to
objectively evaluate the response to exercise in a monitored setting
before an exercise program is begun. An exercise test can be used in
adult exercise or cardiac rehabilitation programs to safely advance an
individual to a higher intensity of effort. Test-demonstrated
improvement in exercise capacity can also be an effective incentive to
continue the program and encourage risk factor modification. (Further
information may be found in the section titled "Exercise
Training.")
Functional Classification of Disability
Exercise testing is used to determine the degree of
disability of subjects with various forms of heart disease. Subjects
who exaggerate their symptoms or who have a psychological impairment
can often be identified. Exercise testing is a more accurate measure of
the degree of cardiac impairment than a physician’s assessment of
exercise capacity. O2max is
the
best noninvasive measurement of the exercise capacity of the
cardiovascular system. Inability to reach 5 METs (below 18
mL · kg-1 · min-1) without
signs or
symptoms is a criterion of disability used by the Social
Security Ad