Circulation. 1995;91:1855-1860
(Circulation. 1995;91:1855-1860.)
© 1995 American Heart Association, Inc.
Evaluation of the Postinfarct Patient
Bertram Pitt, MD
From the Division of Cardiology, Department of Internal Medicine,
University of Michigan Medical Center (Ann Arbor).
Correspondence to Dr Bertram Pitt, Division of Cardiology, Department of
Internal Medicine, University of Michigan Medical Center, 1500 East Medical
Center Dr, Ann Arbor, MI 48109-0366.
Key Words: testing stress exercise infarcts mortality
 |
Introduction
|
|---|
A recent study by Moss et
al
1 in which the authors evaluated
in 966 patients
discharged from the coronary care unit, the
role of exercise ECG,
exercise
201Tl myocardial perfusion imaging,
and ambulatory
(Holter) ECG recording in detecting silent myocardial
ischemia 1 to 6
months after discharge has called into question
the prognostic
usefulness of stress testing and detection of
myocardial ischemia after
infarction. The authors noted that
the presence of ST-segment
depression on the exercise ECG failed
to predict recurrent ischemic
events. A positive exercise
201Tl
myocardial stress test
had only a borderline significant effect
in predicting ischemic events.
The difference between patients
with and those without a positive
exercise
201Tl stress test
was not, however, evident for
several years. Similarly, the
ambulatory (Holter) ECG used to detect
silent myocardial ischemia
failed to predict recurrent myocardial
infarction. The investigators,
however, did note that patients with an
exercise duration of
<6 minutes and ST-segment depression had a
relatively high,
threefold to fourfold, incidence of recurrent ischemic
events
and that those with redistribution of myocardial
201Tl on exercise
testing who also had increased lung
uptake of
201Tlsuggesting
multivessel coronary artery
disease, compromised left ventricular
function, or bothwere at
increased risk for recurrent
ischemic events. However, these high-risk
subsets comprised
<3% of the patients studied and accounted for <6%
of the
recurrent ischemic events. The authors concluded that detection
of
silent or symptomatic myocardial ischemia by noninvasive testing
in
stable patients 1 to 6 months after an acute coronary event
is not
useful in identifying patients at increased risk for
subsequent
coronary events. Exercise ECG stress testing in patients
treated with
thrombolytic therapy after infarction also has
been shown to have only
limited value in identifying patients
at risk for recurrent ischemic
events.
2 In a study of 256 consecutive
patients treated
with a thrombolytic agent after infarction,
Stevenson et
al
2 found in patients who underwent the treadmill
exercise
ECG stress test that ST-segment depression at a low
workload (<7 METs)
identified 50% to 70% of patients who
had a subsequent ischemic
event. These variables had a good
negative predictive accuracy of 81%
but a positive predictive
accuracy of only 21% to 26%. None of the
other exercise variables,
including exercise-induced angina, were
significantly associated
with recurrent ischemic events. The failure of
noninvasive testing
to predict recurrent ischemic events in these
studies has received
wide notoriety and has lead many clinicians to
advocate the
use of coronary arteriography after infarction. The case
for
routine coronary arteriography after infarction has been eloquently
made
by Kulick and Rahimtoola.
3 They suggest that of 100
patients
surviving an acute myocardial infarction, at least 85 require
coronary
arteriography and that "performance of early cardiac
catheterization
and angiography in virtually all survivors of acute
myocardial
infarction with selective use of appropriate noninvasive
tests
may provide a more efficacious means of risk assessment after
myocardial
infarction."
 |
Coronary Arteriography
|
|---|
The view that routine coronary arteriography is useful in
predicting
recurrent ischemic events has gained acceptance over the
past
few years as demonstrated by an increased use of coronary
angiography
before hospital discharge for patients with acute
myocardial
infarction.
4 5 6 In a recent
study, Hamann et
al
4 noted that
coronary arteriography was performed in
32.6% of a VA hospital
population of patients from 65 to 69 years old
and in 52% of
Medicare patients in a nonVA hospital population.
Every
et al
5 found that 59% of fee-for-service patients
underwent
angiography after infarction compared with 30% of patients
in
the VA system. It should be pointed out, however, that there
is no
direct evidence to support the use of routine coronary
arteriography
after infarction. In fact, a recent study comparing
the predictability
of clinical findings; of clinical findings
plus exercise stress
testing; and of clinical findings, an exercise
test, and coronary
arteriography has shown that the addition
of results from coronary
arteriography to the clinical and exercise
data did not significantly
improve the ability to predict subsequent
mortality.
7
There are, on close scrutiny, several difficulties
with the suggestion
that patients undergo routine coronary arteriography
after infarction
to detect and correct high-risk coronary lesions
in an attempt to
prevent recurrent myocardial infarction and
death. One difficulty with
the argument relates to the fact
that "angiographically
significant" coronary arterial lesions
of 50% to 80% diameter
stenosis may or may not be hemodynamically
significant.
8
If a coronary arterial lesion has

80% diameter
stenosis, it is
almost certainly hemodynamically significant,
with the exception of
those with extensive collaterals. The
failure of angiographically
estimated percent diameter stenosis
to predict hemodynamic
significance, the occurrence of myocardial
ischemia on stress testing,
or recurrent ischemic events on
follow-up after infarction is likely
related to several factors,
including the difficulty in estimating the
true extent of the
atherosclerotic lesion by angiography as well as the
variable
role of coronary vasomotor tone. Perhaps of greater importance
is
the finding by Little et al
9 and Nobuyoshi et
al
10 that angiographically
significant coronary arterial
lesions of >50% diameter stenosis
are not necessarily associated with
subsequent myocardial infarction.
In the study of Little et
al
9 of serial angiograms, it was
found that a large
proportion of recurrent myocardial infarctions
was related to lesions
of <50% diameter stenosis (minimal
lesion) on the baseline
arteriogram. Coronary arterial spasm
as demonstrated by a positive
ergonovine response at angiography
has also been identified by Fukai et
al
11 as a cause of myocardial
infarction in patients with
<50% diameter stenosis. Mechanisms
other than classic ergonovine
coronary arterial spasm are likely
to account for plaque rupture,
subsequent thrombosis, and infarction
in the majority of patients with
"minimal lesions" and subsequent
infarction. Coronary angiography
with the presumption that percutaneous
transluminal coronary
angioplasty (PTCA) or coronary artery
bypass graft surgery (CABG) of
angiographically significant
coronary lesions will prevent recurrent
myocardial infarction
may not be correct in that subsequent infarction
may be related,
as reviewed above, to rupture of an atherosclerotic
plaque in
a "minimal lesion," which would not be corrected by
current
criteria for PTCA or CABG. In fact, the CASS study could not
show
a significant reduction in myocardial infarction after
CABG.
12 In a study of patients with one-vessel coronary
artery disease
and myocardial infarction, Ogawa et al
13
reported 19 episodes
of recurrent myocardial infarction over a
follow-up period of
110 months. Only 1 of the 19 recurrent infarcts
could be attributed
to the one-vessel lesion on the original
arteriogram. Routine
coronary arteriography has not proved to be an
effective strategy
to detect recurrent ischemic events, even in
relatively young
patients. Cross et al
14 have shown that
asymptomatic patients
less than 60 years of age with a negative
exercise stress test
after infarction have an excellent prognosis
despite the presence
of multivessel disease on coronary arteriography.
Based on a
study of postinfarction patients less than 40 years old,
Negus
et al
15 also concluded that routine coronary
arteriography
was not indicated in asymptomatic patients after
infarction.
Based on a multivariate analysis of 588 patients
discharged
after myocardial infarction, Diaz et al
16 could
not show that
TIMI flow of the infarct-related vessel or the number of
diseased
vessels was a predictor of 6-month mortality. Examination of
the
infarct-related artery as to whether it is patent or occluded,
with
the assumption that a patent artery serves viable myocardial
tissue and
an occluded artery serves infarcted tissue, may also
be erroneous.
Mahmarian et al
17 found that 42% of patent
infarct-related
arteries with coronary artery stenosis severity of
>80% diameter
stenosis had no redistribution of
201Tl,
suggesting infarction,
whereas 60% of occluded infarct-related
arteries had complete
(13%) or partial (47%) redistribution,
suggesting viable myocardium.
Thus, routine coronary arteriography
cannot be justified on
the basis of our current knowledge to reliably
predict subsequent
risk of noninfarct- or infarct-related arteries to
cause
recurrent ischemic events.
 |
Noninvasive Stress Testing
|
|---|
The suggestion that noninvasive stress testing after infarction
is
not useful must also be challenged. Moss et al
1 selected
a
low-risk group of patients by excluding patients who could
not
exercise, waiting at least 1 month after patients were discharged
from
the coronary care unit to perform stress testing, and excluding
those
who received PTCA or CABG in the early postinfarction
period. By
excluding these high-risk subsets, they ended up
with a study
population with a 1.5% annual mortality rate. By
waiting 1 month, they
excluded many high-risk patients who are
at risk during the early days
and weeks after discharge. Stress
testing should be performed before
hospital discharge to reassure
the patient and his or her family as
well as to achieve maximum
sensitivity. Many studies that had been
performed several weeks
after hospital discharge before the use of
thrombolytics are
no longer relevant because stress testing can now be
performed
safely before discharge. The use of thrombolytic therapy
after
infarction also identifies a relatively low-risk subset of
patients
for subsequent ischemic events. Thus, in the study by
Stevenson
et al,
2 mortality at 10 months after infarction
was <2%,
and only 8% of patients had a recurrent infarction. It is
therefore
not surprising that if one uses a technique such as exercise
201Tl
myocardial perfusion imaging with a sensitivity of
82% to 95%
and a specificity of 44% to 91%
18 in a
low-risk population,
there will be a high percentage of false-positive
and false-negative
results. The positive predictive accuracy of
exercise stress
testing after infarction is relatively
low
2 ; one of the reasons
may relate to the finding that
patients with obstructive coronary
artery disease and those with risk
factors for ischemic heart
disease often have diffuse or segmental
endothelial dysfunction.
19 20 21
Endothelial dysfunction of
angiographically normal coronary
arteries has been shown to result in
exercise-induced coronary
vasoconstriction.
22 Thus, the
net effect of stress testing,
whether evaluated by ECG,
201Tl, or echocardiography, is likely
the sum of ischemia,
as determined by angiographically and hemodynamically
significant
obstructive coronary artery lesions, and increased
vasomotor tone in
angiographically normal or insignificant coronary
artery lesions with
endothelial dysfunction. Many of the hemodynamically
significant
coronary arterial lesions, although exercise limiting
and responsible
for angina pectoris, may not be associated with
recurrent myocardial
infarction. Hemodynamically significant
left main coronary artery
disease and proximal left or right
coronary artery disease with >80%
diameter stenosis may,
but do not necessarily, result in a decrease in
exercise tolerance,
manifested by a decrease in METs achieved and/or a
limitation
in exercise-induced systolic blood pressure elevation as
well
as recurrent ischemic events. Angiographically significant
coronary
artery lesions of >50% but <80% diameter stenosis have
a
more variable effect on exercise tolerance and prognosis.
These
lesions, although hemodynamically significant, may remain
stable for
many years. Progression of these lesions will more
likely result in
symptomatic angina pectoris than acute infarction
or sudden coronary
death. Absence of hemodynamic significance,
increased vasomotor tone,
or both, resulting in a negative stress
test, are, however, of
prognostic importance, as demonstrated
by a relatively high negative
predictive accuracy of 80% to
89% after infarction.
2
Another reason for the relatively low risk of patients in the study by
Moss et al1 is that they excluded patients who could not
exercise because of peripheral vascular disease, pulmonary disease, or
angina pectoris on minimal exertion. Patients who cannot undergo
exercise stress testing have been shown to be at high risk for
recurrent ischemic events.23 If we are to be successful in
predicting recurrent ischemic events, we will need to apply strategies
early after infarction that include those high-risk patients who were
not included in studies such as those by Moss et al1 and
Stevenson et al.2 This can be accomplished in part through
pharmacological stress testing with 201Tl or
echocardiography. Bolognese et al24 have shown that
dipyridamole echocardiography after infarction is a better predictor of
recurrent ischemic events than exercise ECG. Dipyridamole or adenosine
201Tl myocardial imaging may also be of value after
infarction.25 The extent of a 201Tl defect
may, however, be more important in regard to the prediction of
recurrent ischemic events and death than the presence or absence of
201Tl redistribution.17 Mahmarian et
al17 found that 90% of patients with an ischemic event
after infarction had
25% perfusion defect on single-photon emission
computed tomography 201Tl. The positive predictive accuracy
for an ischemic event was 30% when the perfusion defect size was
>30%. In those patients who can exercise, the duration of exercise
and other parameters reflecting exercise performance appear to be
better predictors of recurrent infarction and mortality than the
presence or absence of ST-segment depression.26 The
duration of exercise or workload achieved during exercise likely
reflects the extent of myocardial damage and/or exercise-induced
vasoconstriction. It has been previously shown, before the use of
thrombolytics, that the left ventricular ejection fraction (LVEF) after
infarction was an excellent predictor of ventricular arrhythmias and
survival.27 Studies in patients who have undergone
thrombolysis show that survival is improved for a given LVEF compared
with those who have not undergone thrombolysis.28 There
remains, however, an excellent correlation between the extent of
myocardial damage and subsequent mortality, although at a lower LVEF.
Patients with extensive myocardial damage are at risk for recurrent
ventricular arrhythmias, sudden cardiac death, and progressive heart
failure. Exercise and pharmacological stress testing are at best likely
to be only partially successful in detecting patients with recurrent
myocardial infarction and death since, as pointed out, many recurrent
infarcts occur due to rupture of "minimal" coronary artery
lesions that may not be hemodynamically significant. Hemodynamically
significant lesions, although likely to result in a positive stress
test, may not necessarily result in myocardial infarction or sudden
coronary death. The study by McHenry et al29 on Indiana
State Police illustrates the difficulty with exercise ECG stress
testing and pharmacological stress testing in predicting survival and
recurrent ischemic events. In that study, asymptomatic patients with a
positive exercise ECG stress test were followed for more than 10 years.
At the end of the follow-up period, those with a positive exercise ECG
stress test had a high incidence of subsequent ischemic events.
However, the patients usually presented with symptomatic angina
pectoris before their ischemic event. The larger number of patients
with an initially negative exercise ECG stress test had the highest
number of new myocardial infarctions and incidence of sudden coronary
death.
 |
Clinical Findings
|
|---|
It is important to point out that clinical findings independent
of
stress testing in patients after infarction may be of value
in
predicting recurrent ischemic events. For example, in a study
of 3695
patients with a first myocardial infarction, Kornowski
et
al
30 found that angina pectoris before the first
infarction;
a history of symptomatic hypertension, diabetes mellitus,
or
peripheral vascular disease; anterior location of a Q-wave first
infarction;
or evidence of heart failure on admission independently
predicted
recurrence of infarction. Patients with five or six of these
variables
had a 1-year reinfarction rate of 23% compared with 4% in
those
with none or one of these factors, 5.5% with two of these
factors,
8% with three of these factors, and 15% with four of these
factors.
In a group of 3666 patients followed for 1 year after
infarction,
Gilpin et al
31 found a history of prior
infarction, congestive
heart failure, angina pectoris, diabetes
mellitus, or nonQ-wave
infarction to be associated with recurrent
myocardial infarction.
The ability to predict recurrent myocardial
infarction is of
importance since it has been shown that recurrent
myocardial
infarction is one of the most important predictors of
subsequent
death after infarction. Efforts should therefore be directed
at
detecting those at high risk for recurrent myocardial infarction
and
preventing infarction if the natural history of these patients
is to be
altered. In the European Cooperative Study group trials
of
alteplase-placebo and alteplase-PTCA, Arnold et al
32
evaluated
factors predictive of mortality in 1043 patients surviving
myocardial
infarction and found on stepwise multivariant analysis
that
use of digitalis, diuretics, or both; a history of previous
infarction;
age >60 years; inability to perform an exercise test; and
a
<30 mm Hg exercise-induced systolic blood pressure increase
were
predictive of death after hospital discharge. The addition
of
information from the coronary angiogram did not add to the
clinical and
noninvasive test data in predicting death.
32 Other
factors,
such as QRS duration on the ECG
33 after
infarction, have also
been shown to be of importance in predicting
death.
 |
Conclusions
|
|---|
How, then, should clinician approach the postinfarction patient?
There
are no simple solutions to this problem at the moment, and it
is
unlikely that any of the currently available strategiesexercise
or
pharmacological stress testing, routine coronary arteriography,
or
clinical factorswill be completely successful in predicting
recurrent
ischemic events. Recurrent infarction is the most
important predictor
of subsequent death after infarction.
23 Patients with
spontaneous angina pectoris should undergo coronary
angiography and
consideration for PTCA or CABG since angina
pectoris is the most
important factor predicting recurrent infarction.
31
Patients with symptomatic ventricular arrhythmias and those
with
persistent manifest congestive heart failure may also be
considered for
coronary arteriography, pharmacological stress
testing, or both to
determine whether the arrhythmia or heart
failure is related to
significant coronary artery disease and
myocardial ischemia.
Asymptomatic individuals should undergo clinical risk stratification
after infarction. Patients with a history of prior infarction and those
with evidence of a first anterior Q-wave infarction or extensive
inferior infarction should have a resting determination of LVEF to
detect those with an LVEF of
40% who might be suitable for therapy
with an angiotensin-converting enzyme inhibitor.34
Low-risk individualssuch as those with a first Q-wave infarction,
with an LVEF of >40%, or with three or fewer of the clinical risk
factors described by Kornowski et al30 and more than 50%
of patients with a first infarctionwho are able to exercise should
undergo maximal exercise ECG testing before hospital discharge. A
maximal exercise ECG test has been found safe before hospital discharge
in low-risk patients after infarction, and maximal work capacity has
been shown to be the best exercise variable for identifying patients at
low risk for cardiac death.35 Although it could be argued
that low-risk individuals who can perform an exercise test have a low
risk of recurrent ischemic events and need not undergo formal exercise
testing, it is often reassuring for the patient and his or her family
to realize that the patient can perform moderate exercise after
discharge without risk. Although there may be some sacrifice of
sensitivity, the stress test should be performed with the patient
receiving appropriate medical therapy such as a
ß-adrenergicblocking agent.
Low-risk individuals with a negative exercise ECG test, ie, without
evidence of exercise-induced ST- segment depression or angina
pectoris, should be followed and receive appropriate medical therapy
and risk factor reduction. Those with a positive test with ST-segment
depression of <2 mm and relatively good exercise performance (
7
METs) without exercise-induced angina pectoris should also be followed
medically. The finding of ST-segment depression in this low-risk
clinical subset is likely to have a poor positive predictive accuracy,
as pointed out by Moss et al1 and Stevenson et
al.2 Patients with
2-mm exercise-induced ST-segment
depression, a relatively poor exercise performance, or exercise-induced
angina pectoris should undergo exercise 201Tl or
echocardiography. Only those with an extensive 201Tl defect
(>20% defect score)17 or large wall motion abnormality
on stress echocardiography need to be considered for coronary
angiography and possible PTCA or CABG. Fioretti et al36
and Nielsen et al35 were not able to show that
exercise-induced ischemia as demonstrated by angina pectoris,
ST-segment change, or both was associated with increased mortality in
relatively low-risk patients after myocardial infarction. Only patients
with subsequent postdischarge spontaneous or exercise-induced angina
pectoris despite optimal medical therapy and risk factor reduction
should be considered for elective coronary angiography after discharge.
The decision to perform PTCA or CABG in this group rests on the premise
that PTCA or CABG will prevent recurrent symptomatic angina pectoris
and improve the patient's quality of life, not necessarily reduce the
possibility of reinfarction or the rate of mortality.
Patients in the low-risk clinical subset as defined by Kornowski et
al30 who cannot exercise should undergo pharmacological
stress testing with 201Tl or echocardiography since they
are at increased risk for recurrent ischemic events compared to those
who can exercise.23 Only those with extensive stress
201Tl defects17 or wall motion abnormalities
on echocardiography need to be referred for angiography and considered
for PTCA or CABG.
High-risk patients, ie, those with more than three clinical risk
factors described by Kornowski et al30 or those with the
clinical risk factors identified by Arnold et al,32 and
those with an LVEF of
40% or an abnormal signal-averaged ECG with
late potentials should undergo exercise or pharmacological stress
testing with 201Tl or echocardiography. Only those with a
positive test as demonstrated by an extensive 201Tl defect,
wall motion abnormality, or exercise-induced angina pectoris should be
considered for coronary angiography and, if suitable, PTCA or CABG.
PTCA or CABG in those with angiographically significant lesions should
be performed to prevent recurrent angina pectoris as well as cardiac
death. Although revascularization of angiographically significant
lesions may not prevent recurrent myocardial infarction, it may make
the myocardium more able to withstand the effects of plaque rupture and
thrombosis from a minimal lesion and therefore improve survival. The
most effective strategy for reducing recurrent myocardial infarction,
and therefore mortality, should include strategies to prevent plaque
formation and rupture of minimal lesions regardless of whether
angiographically significant lesions are revascularized. There is
evidence to suggest that this can be achieved, at least in part, by
several strategies, including aspirin, Coumadin, LDL cholesterol
reduction, ß-adrenergic receptorblocking agents, and
angiotensin-converting enzyme inhibitors.37 38
This discussion is not meant to deemphasize the importance of PTCA or
CABG in symptomatic individuals and those at high risk for recurrent
myocardial infarction but rather to emphasize the importance of
"minimal" lesions and new lesion formation in recurrent
myocardial infarction and to point out the limitations of applying
exercise or pharmacological stress testing with 201Tl or
echocardiography, each of which has (although they have a 90%
sensitivity or specificity for detecting angiographically significant
coronary artery lesions and a high negative predictive accuracy)
relatively poor positive predictive accuracy for recurrent myocardial
infarction and death, especially in relatively low-risk subsets after
infarction. Future efforts should be directed at developing both
clinical and laboratory techniques for detecting patients at risk for
recurrent myocardial infarction, such as the noninvasive assessment of
endothelial dysfunction; the evaluation of cytokines, thrombotic, and
fibrinolytic factors; activation of the renin-angiotensin system; and
endothelin release. Genotyping to predict high-risk subsets in regard
to activation of the renin-angiotensin system may also be of
value.39 New understanding of the pathophysiology of
plaque rupture and thrombosis after plaque rupture holds promise for
new diagnostic and therapeutic strategies.40 41
However,
until this new understanding can be applied and validated, we need to
have a clear view of the effectiveness, limitations, and cost
implications of currently available diagnostic strategies to predict
recurrent myocardial infarction and death after infarction. The
suggested strategy outlined in the Figure
, although
imperfect, reflects my approach to the present information. Some
might agree to eliminate all stress testing in low-risk individuals who
can exercise, whereas others may believe that the exercise ECG is an
unnecessary step and that even low-risk patients should undergo
exercise 201Tl or echocardiographic stress testing. It is,
however, likely that the strategy outlined in the Figure
, or
some
modification of it, will be more cost effective and more accurate than
the strategy of performing coronary angiography in all or most patients
after infarction. There is, however, a clear need to prospectively
validate this or other proposed strategies in large-scale trials to
ensure that patients receive the most effective and cost-effective
care.

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|
Figure 1. Flow chart of proposed approach to the prediction of
ischemic events after myocardial infarction (MI). Patients with
spontaneous angina after MI should undergo early coronary angiography
for possible percutaneous transluminal coronary angioplasty (PTCA) or
coronary artery bypass graft surgery (CABG). Low-risk patients, as
defined in the text, who can exercise (Ex) should undergo exercise ECG
stress testing. Those who have ST-segment depression of 2 mm, limited
exercise tolerance of <7 METs (METS), or exercise-induced angina
pectoris should undergo exercise or pharmacological 201Tl
myocardial imaging (Tl-201) or echocardiographic (Echo) stress testing.
Those with a negative exercise ECG, ST-segment depression of <2 mm, or
an exercise tolerance of >7 METs should be followed with medical
therapy and vigorous risk factor modification. Low-risk patients who
cannot exercise and high-risk patients, as defined in the text, should
undergo exercise or pharmacological Tl-201 or Echo. Those with an
extensive Tl-201 defect, as defined in the text, or extensive wall
motion abnormality (WMA) on Echo should undergo coronary angiography
for possible PTCA or CABG if otherwise eligible. Those with a negative
test or minor Tl-201 defects or WMAs should be followed with medical
therapy and vigorous risk factor modification.
|
|
Received August 10, 1994;
revision received October 5, 1994;
accepted October 14, 1994.
 |
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