Ellestad's Stress Testing Principles and Practice, 6th Edition
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Copyright © 2003 by Oxford University Press, Inc.
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Library of Congress Cataloging-in-Publication Data
Stress testing : principles and practice / Myrvin H. Ellestad ; with contributions by
Ronald H. Startt Selvester, Fred S. Mishkin, Frederick W. James. — Ed. 5.
p. ; cm.
Includes bibliographical references and index.
ISBN 0-19-515928-4
1. Heart function tests. 2. Exercise tests. 3. Stress (Physiology)
I. Ellestad, Myrvin H., 1921–
[DNLM: 1. Exercise Test — methods. 2. Stress. WG 141.5.F9 S915 2003]
RC683.5.H4 S776 2003
616.1⬘20754—dc21
2002030793
1 2 3 4 5 6 7 8 9
Printed in the United States of America
on acid-free paper
Dedicated to my lovely and loving wife, Lera.
Preface
The first edition of this book was released in 1975. When the 4th edition was pub-
lished I planned that it should be the last. As before however, new information on
exercise testing has stimulated a desire to revise the previous text and integrate our
present state of knowledge with what went before.
It is of some concern that many cardiologists and others doing exercise testing
have little interest in the newer information now available on exercise physiology.
Fortunately, there is still a significant cadre of investigators asking tough questions
and proposing unconventional ideas. There will always be many practitioners who
want to know everything they can about a technique that they are using every day.
For this group this book will be required reading.
Because of the book’s popularity the general format has not been changed but
every chapter has been revised to not only include new information but to make it
more readable. The chapter on electrocardiographic changes has been completely
reorganized to emphasize the importance of unconventional markers of ischemia,
which are rarely applied in most exercise laboratories. To emphasize important
points, take home messages are sprinkled throughout some chapters to help em-
phasize various concepts. Two new chapters provide information on exercise
echocardiography and exercise testing in congestive heart failure. Many of the fig-
ures have been redrawn for clarity.
Some of the new concepts proposed recently include the idea that ST de-
pression occurring in premature ventricular contractions (PVCs) can indicate
ischemia. It appears that horizontal ST changes during exercise may indicate
subendocardial ischemia while Downsloping ST segments represent a more severe
process that is probably most commonly seen with multivessel disease and possibly
posterior wall subepicardial dysfunction. There are a number of patterns that can
localize the area of the myocardium and the culprit stenotic vessel, a capacity that
was once the exclusive claim of nuclear scintigraphy. New concepts on the physi-
ology of ischemia are presented as well as the new information on chronotropic
incompetence.
As an example of the new format a summary of the patterns that suggest false-
positive ST depression include (1) complexes with a short PR interval, (2) com-
plexes with steep PQ slopes, (3) when there are prominent enlarged septal Q waves,
(4) when ST depression is confined to the inferior leads, especially if P waves are
large and (5) the ST segment is convex or “humped.”
It is hoped that students of the physiology of exercise induced ischemia will
find this work a valuable reference and will be stimulated by its contents to add new
ideas to this important field of cardiology.
vii
viii PREFACE
An acknowledgement of the support staff at Memorial Heart Institute and es-
pecially the diligent labor of my secretary, Carole Sweet, is in order. Without their
help this book could not have been completed.
Long Beach, California M.H.E.
Contents
Contributors xi
1. History of Stress Testing 1
2. Cardiovascular and Pulmonary Responses to Exercise 11
3. Physiology of Cardiac Ischemia 43
4. Indications 77
5. Contraindications, Risks, and Safety Precautions 85
6. Parameters to Be Measured 103
7. Stress Echocardiography 127
8. Stress Testing Protocol 135
9. Memorial Heart Institute Protocol 157
10. Stress Testing After Myocardial Infarction 169
11. Stress Testing After Surgical Intervention and
Coronary Angioplasty 179
12. ECG Patterns and Their Significance 189
13. Rhythm and Conduction Disturbances in Stress Testing 241
14. Predictive Implications 271
15. Stress Testing in Women 309
16. Exercise Testing in Congestive Heart Failure 319
17. Chest Pain and Normal Coronary Arteries 327
18. Blood Pressure Measurements During Exercise 335
19. Silent Myocardial Ischemia 353
20. Sports Medicine and Rehabilitation 367
21. Pediatric Exercise Testing 381
22. Radionuclide Techniques in Stress Testing 413
23. Metabolic Abnormalities and Drugs 481
24. Computer Technology and Exercise Testing 513
Index 535
ix
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Contributors
Frederick W. James, M.D.
Professor and Chair
Department of Pediatrics
Charles R. Drew University
Los Angeles, California
Fred S. Mishkin, M.D.
Professor of Radiological Sciences
Director, Division of Nuclear Medicine
University of California, Los Angeles
Department of Radiology
Harbor-UCLA Medical Center
Torrence, California
Ronald H. Startt Selvester, M.D.
Professor Emeritus
University of Southern California School of Medicine
Director of Electrocardiography Research
Memorial Heart Institute
Long Beach Memorial Medical Center
Long Beach, California
xi
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Stress Testing
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1
History of Stress Testing
The cornerstone of modern stress testing is based on the empirical discovery
that exercise in patients with coronary disease produces ST-segment depres-
sion. This discovery might be credited to Bousfield,1 who recorded ST-
segment depression in the three standard ECG leads during a spontaneous
attack of angina in 1918; or, it might be credited to Feil and Siegel,2 who, in
1928, actually exercised patients with known angina to bring about pain and,
concurrently, the ST- and T-wave changes we now recognize as showing ev-
idence of ischemia. These researchers described the changes as being due to
a decrease in blood flow to the heart, and they published tracings showing a
return to normal after the pain had subsided and also after administration of
nitroglycerin. Feil and Siegel conducted their stress tests by having the pa-
tients do sit-ups; in selected cases, they held their hands on the patient’s chest
to increase the resistance and therefore the energy required to perform this
maneuver. Einthoven3 may have actually recognized the changes associated
with ischemia. He published a tracing in 1908 showing ST-segment depres-
sion after exercise, but did not comment on this finding. Felberbaum and
Finesilver 4 probably published the first paper describing a step test in 1927.
Using a footstool 12 inches high, they regulated the rate of stepping and mon-
itored the heart rate before and after exercise.
Master, with Oppenheimer,5 published his first paper on an exercise test
in 1929 but did not recognize the value of the ECG in the demonstration of
ischemia. He used only pulse and blood pressure to evaluate the patient’s
cardiac capacity. Master claimed Felberbaum and Finesilver’s method was
inadequate for a number of reasons. The contribution of Master must be la-
beled as being related to an exercise protocol rather than to the use of the
ECG for the evaluation of ischemia in these early years. Master also popu-
larized the idea of evaluating exercise capacity with some type of a standard
test. In 1931, Wood and Wolferth6 also described ST-segment changes with
exercise and indicated the usefulness of exercise in diagnosis, but claimed it
was too dangerous to deliberately exercise patients with coronary disease.
They claimed that the precordial lead (lead 4) was more useful in revealing
ischemic changes than were the standard leads.
In 1932, Goldhmammer and Scherf 7 reported that ST-segment depres-
sion was present in 75% of 40 patients with angina and proposed the use of
exercise to confirm the diagnosis of coronary ischemia. It is interesting to
note that the percentage of their false-negatives is similar to that of some of
the data being published at this time.
1
2 STRESS TESTING: PRINCIPLES AND PRACTICE
Katz and Landt8 confirmed Wood and Wolferth’s findings in 1935 in
terms of precordial leads but found lead 5 to be better in terms of discrimi-
nation than lead 4. They also demonstrated that the number of negative re-
sponses in patients with a history of classic angina, could be reduced by us-
ing precordial leads. They tried to standardize their exercise test by having
the subjects lift dumbbells while lying on a table. Katz and Landt also dis-
cussed the mechanism of pain and ischemia and implicated some irritative
substance related to catabolism in the myocardium. In addition, they re-
ported on the use of anoxia to bring about characteristic changes in the ST
segment. They went on to produce the same changes with intravenous
epinephrine.8
By 1938, Missal9 studied normal patients by having them run up from
three to six flights of stairs; he may have been the first to use a maximum
stress test. For convenience, Missal later elected to use Master’s 9-inch steps
to exercise his patients. He had his patients exercise to the point of pain and
emphasized the necessity of taking the recording as quickly as possible there-
after. He cited a case report in which the stress test contributed to the man-
agement of a woman with hypothyroidism and angina who had an earlier
onset of angina and ST-segment depression after taking thyroid hormone.
Missal also described the use of the Master’s test in evaluating increases in
exercise tolerance after nitroglycerin.
In 1940, Riseman and colleagues10 published an excellent review of the
use of anoxia in the evaluation of ischemia. They compared exercise with the
anoxemia test and suggested that the latter was more specific because fewer
negative test results occurred in patients believed to have coronary disease.
They also described for the first time the use of continuous monitoring and
thus discovered that ST-segment depression usually appeared before the on-
set of pain and persisted for a time after the pain subsided. Riseman and col-
leagues demonstrated the protective effects of oxygen breathing and de-
scribed the presence of mild ST-segment depression (1.0 mm or less) in
normal subjects as contrasted with 2.0- to 7.0-mm depression in some of their
patients. In spite of all this information, these researchers concluded that the
exercise test was of little practical value because of its poor discrimination be-
tween normal and abnormal subjects.
In 1941, 12 years after his original paper on an exercise test, Master, in
collaboration with Jaffe,11 proposed for the first time that an ECG could be
taken before and after his exercise tolerance test to detect coronary insuffi-
ciency. In the same year, Liebow and Feil12 reported that digitalis caused ST-
segment depression and would confuse the diagnosis of ischemia in the ex-
ercise ECG. They also suggested the possibility of the drug’s reducing
coronary flow.
Johnson and associates,13 working at the Harvard Fatigue Laboratory,
developed the Harvard Step Test, which was similar in many ways to the
original Master’s test. It was used widely in athletic circles to measure fit-
HISTORY OF STRESS TESTING 3
ness, and a form of it (the Pack Test) was used for military purposes. A vari-
ation of this called the Schneider was also popular in evaluating military
personnel. These tests used pulse counts during recovery and provided an
index of physical fitness, a technique that was to be carried forward in the
indexes of fitness and aerobic power for a number of years. Brouha and
Heath14 also used this methodology to evaluate the cardiovascular re-
sponse to various occupations and emphasized the influence of environ-
mental factors such as room temperature. In 1949, Hellerstein and Katz15
performed their classic studies describing the direction of the vector asso-
ciated with subendocardial injury in various areas of the right and left ven-
tricle. They also used direct-current electrograms and established that ST
depression is primarily a diastolic injury current manifested during the TQ
interval.
By 1949, Hecht16 was reporting his experience with the anoxemia test
and claiming 90% sensitivity in coronary disease. He emphasized the im-
portant fact that pain is an unreliable end-point and accompanies ischemia
in only 50% of the cases. He also pointed out that ST-segment changes asso-
ciated with anoxemia may not be present if previous myocardial necrosis has
occurred. Since then, Castellanet and colleagues17 have confirmed that in-
farction tends to mask the ECG expression of ischemia.
In 1950, Wood and associates18 at the National Heart Hospital in Lon-
don described their experience with an effort test. They had patients run up
84 steps adjacent to their laboratory and also claimed that it was necessary to
push the patients to the maximum level of their capacity. Wood and associ-
ates established several points that still have validity:
1. The amount of work performed should not be fixed, but adjusted to
the patient’s capacity.
2. The more strenuous work (resulting in a heart rate greater than 90
beats per minute) would produce a higher percentage of positive
tests in patients with known coronary disease than if the heart rate
were not accelerated above this level.
3. The reliability of the test (in effect, a maximum stress test) was 88%
overall compared with 39% in the Master’s test.
Wood and colleagues, as Hecht before them, definitely recommended the use
of the stress test to uncover latent myocardial ischemia, to determine the
severity of the disease, and to evaluate therapy.
In 1951, Hellerstein and colleagues19 used stress testing as a method of
evaluating the work capacity of cardiac patients and began to amplify the
work pioneered by Brouha. They deserve credit for demonstrating to em-
ployers that their cardiac employees might safely return to work. Thus, the
continuing interest in the oxygen cost of various activities and in the analy-
sis of ischemia at various workloads planted the seed that flowered into our
present cardiac rehabilitation program.
