From the CNR Institute of Clinical Physiology, Pisa, Italy.
Correspondence to Eugenio Picano, MD, PhD, FESC, CNR Institute of Clinical Physiology, Via Savi, 8, 56100 Pisa, Italy. E-mail picano{at}nsifc.ifc.pi.cnr.it
Methods and Results—The data bank of the large-scale,
prospective, multicenter, observational Echo Dobutamine
International Cooperative (EDIC) study was interrogated to select 314
medically treated patients (271 men; age, 58±9 years) who underwent
low-dose (
Conclusions—In medically treated patients with severe global left
ventricular dysfunction early after acute uncomplicated
myocardial infarction, the presence of myocardial viability identified
as inotropic reserve after low-dose dobutamine is
associated with a higher probability of survival. The higher the number
of segments showing improvement of function, the better the impact is
of myocardial viability on survival. The presence of inducible
ischemia in this set of patients is the best predictor of
cardiac death.
Dobutamine-Atropine Stress Echocardiography
The presence of myocardial viability was defined as an improvement in
regional function of
To quantify the amount of myocardium showing a contractile
reserve elicited by low-dose dobutamine, myocardial
viability was also assessed according to a continuous
parameter defined as
Patients were separated into three different groups according to the
stress echocardiographic results: group 1, nonviable;
group 2, viable and nonischemic; and group 3, viable and
ischemic.
Echocardiographic monitoring was performed throughout
dobutamine infusion and up to at least 5 minutes after the
end of the infusion. Two-dimensional echocardiographic
images were recorded at baseline and at the end of each
dobutamine step. For each patient, left
ventricular function was evaluated at baseline, at low dose
for the assessment of myocardial viability in dyssynergic segments, and
at peak stress.
Quality Control of Stress Echocardiographic Readings
The first criterion was tested on a videotape with 20 stress
echocardiography studies prepared in the
coordinating center (Institute of Clinical Physiology in Pisa). In all
20 studies, the readings of 2 experienced independent observers were
concordant as to presence and site of dyssynergy, and the stress
results were in full agreement with the presence and site of
coronary stenoses during coronary angiography.
The unanimous readings of the 2 observers were arbitrarily assumed to
be the "gold standard" against which to evaluate the reading of
each participating center. The reader from each center interpreted the
videotape in a blinded fashion, with no access to clinical and
angiographic data or to the interpretation given by other observers. It
was assumed a priori that the minimum threshold of concordance to
pass this part of the quality control had to be 90%.
The second criterion consisted of random sampling of 20 consecutive
studies from each contributing center. These 20 studies were examined
in a blinded fashion by an experienced
cardiologist-echocardiographist of the coordinating center,
whose reading was arbitrarily assumed to be the "gold standard." It
was assumed a priori that the minimum threshold of concordance to
pass the quality control had to be 80%. The lower concordance cutoff
compared with the first type of reading is due to the fact that this
second set of tapes was not selected on the basis of the superior
quality but randomly sampled from each center in a consecutive
fashion.
All the 11 enrolled centers met the minimum requirements of quality
control.
Follow-Up Data
Statistical Analysis
The individual effect of certain variables on event-free survival
was evaluated with the use of the Cox regression model (BMDP 2L,
Department of Biomathematics, University of California at Los Angeles,
revised 1987). The analysis was performed according to the
unmodified forward-selection stepwise procedure. In this case, the
variables were entered into the model on the basis of a computed
significance probability; accordingly, the variable that has the
most significant relation to dependent outcome is selected first for
inclusion in the model, and a solution to the functional form of the
equation is computed. At the second and subsequent steps, the set of
variables remaining at each point is evaluated, and the most
significant is included if it improves the prediction of the outcome
(dependent variable), but in this case, this probability is
conditional on the presence of the variable already selected. The
algorithm ceases to select variables when there is no further
significant improvement in the prediction of the whole model. We also
analyzed the data according to a modified stepwise procedure in
which the significant individual variables were included in the
model in the same order in which they are considered by the
cardiologist: historical and clinical data first, resting wall function
second, low dose (viability) stress echocardiographic
data third, and high-dose (ischemia) stress
echocardiographic data last.
Variables selected for examination were age, sex, history of
angina, previous myocardial infarction, thrombolysis,
Q-wave myocardial infarction, WMSI at rest, WMSI at viability,
dobutamine-atropine stress
echocardiography positivity, WMSI at peak
dobutamine, low-dose
Continuous variables were compared by the unpaired two-sample
t test. Proportions were compared by the
Feasibility and Tolerability of Dobutamine-Atropine
Stress Echocardiography
Stress Echocardiographic Findings
One hundred forty-eight patients (53%) had a positive
dobutamine-atropine stress
echocardiography result, and 166 had a negative
dobutamine-atropine stress
echocardiography result. The average WMSI at peak
dobutamine-atropine stress
echocardiography was 2.0±0.3.
Follow-Up Data
Cardiac-Related Death
Cardiac death occurred in 8 patients with positive and in 4 with
negative tests for myocardial ischemia (5.4% versus 2.4%,
P=0.2). In Figure 2
Spontaneous Events
Prognostic Impact of Myocardial Viability After Acute
Myocardial Infarction
In light of this evidence, one would expect myocardial viability to
carry a potential positive prognostic impact. If a segment has an
inotropic reserve after dobutamine infusion, it is likely
to recover, and left ventricular function will improve.
This should be mirrored by a longer survival, given the hyperbolic
relationship linking resting left ventricular function to
cardiac death, with better function being associated with longer
survival.10 In reality, the prognostic meaning of
viability is not always beneficial but should be put in the
larger context provided by the clinical picture (recent versus chronic
myocardial infarction), resting left ventricular function
(preserved versus severely depressed), type of treatment (medical
versus revascularization), and prognostic end point
considered (unstable angina versus cardiac death).
In the present subset analysis of the EDIC data bank, we
selected only those patients with a moderate to severe left
ventricular dysfunction (mean resting WMSI=1.9), whereas in
the previous EDIC study, unselected patients had preserved left
ventricular function (mean resting WMSI=1.5). The
beneficial effect of functional recovery on survival, if any, is
expected to be mild in patients with preserved global left
ventricular function, who are on the flat part of the
hyperbolic curve relating left ventricular function to
cardiac death, whereas it appears to be critical in patients with
severe left ventricular dysfunction, in whom even the
recovery of a limited area might imply a significantly better survival.
In fact, no patient with a high number of segments showing contractile
reserve at low-dose dobutamine experienced cardiac death
(Figure 1
Study Limitations
Dobutamine echocardiography was
performed at various intervals after the index infarction. The response
of dysfunctioning but viable myocardium to
dobutamine early after acute myocardial infarction may
differ from that at discharge. However, this relatively wide
variability reflects the lack of an established consensus on the timing
for risk stratification and the different logistical situations,
ranging from unrestricted bed availability to the pressing demand for
coronary care unit space, which can obviously influence the
timing of testing. The best time to perform stress test varies,
depending on physician preferences, patient characteristics, and local
laboratory expertise.23
Clinical Implications
Received January 26, 1998;
revision received April 21, 1998;
accepted May 3, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Prognostic Value of Myocardial Viability in Medically Treated Patients With Global Left Ventricular Dysfunction Early After an Acute Uncomplicated Myocardial Infarction
A Dobutamine Stress Echocardiographic Study
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Residual viable
myocardium identified by dobutamine stress
after myocardial infarction may act as an unstable substrate for
further events such as subsequent angina and reinfarction. However, in
patients with severe global left ventricular dysfunction,
viability might be protective rather than detrimental. The aim of this
study was to assess the impact on survival of
echocardiographically detected viability in medically
treated patients with global left ventricular dysfunction
evaluated after acute uncomplicated myocardial infarction. 
10 µg · kg-1 ·
min-1) dobutamine for the detection of
myocardial viability and high-dose dobutamine for the
detection of myocardial ischemia (40 µg ·
kg-1 · min-1 with atropine 1 mg)
performed 12±6 days after an acute uncomplicated myocardial infarction
and showing a moderate to severe resting left ventricular
dysfunction (wall motion score index [WMSI] >1.6). Patients
were followed up for 9±7 months. Low-dose dobutamine
stress echocardiography identified myocardial
viability in 130 patients (52%). Dobutamine-atropine
stress echocardiography was positive for
ischemia in 148 patients (47%) and negative in 166 patients
(53%). During the follow-up, there were 12 cardiac deaths (3.8% of
the total population). With the use of Cox proportional hazards model,
delta low-dose WMSI (the variation between rest WMSI and
low-dose WMSI) was shown to exert a protective effect by reducing
cardiac death by 0.8 for each decrease in WMSI at low-dose
dobutamine (coefficient, -0.2; hazard ratio, 0.8;
P<0.03); WMSI at peak stress was the best predictor of
cardiac death in this set of patients (hazard ratio, 14.9;
P<0.0018).
Key Words: dobutamine • echocardiography • infarction • prognosis
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
It has been
demonstrated that in patients evaluated early after a first acute
uncomplicated myocardial infarction, the presence of myocardial
viability detected by dobutamine stress
echocardiography is associated with an increased
incidence of unstable angina.1 The induction of
remote ischemia is associated with an increased incidence of
cardiac death and reinfarction, hard events that are not predicted by
the presence of myocardial viability in that group of
patients.1 The data on the prognostic meaning of
viability on survival are still uncertain, largely preliminary, and
apparently conflicting.2 3 4 5 6 7 8 9 In fact, to detect a
possibly potential beneficial effect of
echocardiographically recognized viability on survival,
we decided to select patients according to 3 predefined conditions
related to resting left ventricular function, type of
treatment, and sample size. First, patients with severely
depressed resting function should be included, because only these
patients are on the steep portion of the hyperbolic curve relating left
ventricular function to mortality.10
It is entirely possible that the survival benefit linked to functional
recovery can offset in these patients the risk of ischemic
instability associated with persisting viability in regions with
resting dysfunction. Second, only medically treated patients should be
included, with follow-up censored at
revascularization, because coronary
revascularization dramatically changes the natural
history of the disease in these patients, obscuring any direct
relationship between viability and prognosis. Third, populations of an
adequate sample size should be enrolled, because cardiac death is a
relatively rare event in these patients. Therefore, to assess the
impact of myocardial viability on survival, the data bank of the
large-scale, prospective, multicenter, observational Echo
Dobutamine International Cooperative (EDIC) study was
interrogated to select 314 medically treated patients (271 men; age,
58±9 years) who underwent low-dose dobutamine (10
µg · kg-1 ·
min-1) for the detection of myocardial viability
and high-dose dobutamine (40 µg ·
kg-1 · min-1 with
atropine 1 mg) for the detection of myocardial ischemia
performed 12±6 days after an acute uncomplicated myocardial infarction
and showing a moderate to severe resting left ventricular
dysfunction (wall motion score index [WMSI] >1.6). Patients were
followed up for 9±7 months.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Patient Selection
The initial population consisted of 1362 patients admitted to
the coronary care unit for an episode of acute myocardial
infarction. Of these, 159 were excluded for continuing myocardial
ischemia, left ventricular failure, shock, or
important cardiac arrhythmias. Of the remaining 1203, 34
patients had a technically poor acoustic window at baseline, making the
dobutamine-atropine stress
echocardiography unfeasible; 224 were excluded for
age >75 years; 58 did not undergo stress testing because of their
refusal of the test or for logistical reasons; and 71 experienced an
early reinfarction. Another 38 patients were eligible for
dobutamine-atropine stress
echocardiography but were subsequently lost to
follow-up. This patient selection has already been
published1 ; in the present selection, we also
included patients with previous chronic myocardial infarction (n=39).
Of the 817 patients who underwent dobutamine stress
echocardiography study, we selected those patients
with a WMSI >1.6. Therefore, from January 1, 1992, to October 1, 1994,
we studied 314 patients (43 women, 271 men; age, 58±9 years) with
clinically uncomplicated acute myocardial infarction, baseline
echocardiographic findings of satisfactory quality, and
available follow-up information. The primary rest and stress findings
in the study patients are reported in Table 1
. All patients underwent a
dobutamine-atropine stress
echocardiography after 12±6 days from an
uncomplicated acute myocardial infarction (no continuing myocardial
ischemia, left ventricular failure, shock, or
important cardiac arrhythmias).
View this table:
[in a new window]
Table 1. Patient Characteristics
After a resting ECG and echocardiogram were performed,
intravenous access was secured and dobutamine
was infused with 3-minute dose increments, starting from 5 µg
· kg-1 · min-1
and increasing to 10, 20, 30, and 40 µg ·
kg-1 · min-1 under
continuous ECG and echocardiographic monitoring. When
no end point was reached, atropine (in 4 divided doses of 0.25 mg up to
a maximum of 1 mg) was added to the continuing 40–µg ·
kg-1 · min-1
dobutamine infusion. Regional wall motion was assessed
according to the recommendations of the American Society of
Echocardiography with a 16-segment
model.11 In all studies, segmental wall motion
was semiquantitatively graded as follows: 1=normal; 2=hypokinetic,
marked reduction of endocardial motion and thickening; 3=akinetic,
virtual absence of inward motion and thickening; and 4=dyskinetic,
paradoxic wall motion away from the center of the left ventricle in
systole. WMSI was derived by dividing the sum of individual segment
scores by the number of interpretable segments.11
Test positivity was defined as the occurrence of at least 1 of the
following conditions: (1) new dyssynergy in a region with normal
resting function (ie, normokinesis becoming hypokinetic, akinetic, or
dyskinetic); (2) worsening of a resting dyssynergy (ie, a hypokinesia
becoming akinesia or dyskinesia; a resting akinesia becoming dyskinesia
was not considered a positivity criterion)12 ; and
(3) biphasic response of a resting dyssynergy (ie, a hypokinesia
showing normal function at low dose with a following deterioration at
high dose, or an akinesia becoming hypokinesia at low dose and
returning to the initial condition at high
dose).13 Test positivity was defined as
"remote" ischemia when the development of asynergy was not
directly adjacent to the infarcted area and was supposed to be related
to another vascular region.14
Nonechocardiographic diagnostic end points
were the following15 : peak atropine dose, 85% of
target heart rate, and achievement of conventional end points (such as
severe chest pain and/or diagnostic ST-segment changes).
The test was also stopped in the absence of diagnostic end
points for 1 of the following reasons: submaximal,
nondiagnostic test15 ; untolerable
symptoms; and limiting asymptomatic side effects,
consisting of hypertension (systolic blood pressure >220
mm Hg; diastolic blood pressure >120 mm Hg),
hypotension (relative or absolute; >30 mm Hg decrease in blood
pressure), supraventricular arrhythmias
(supraventricular tachycardia or atrial
fibrillation), and ventricular arrhythmias
(ventricular tachycardia; frequent,
polymorphous premature ventricular beats). 
1 grade at low-dose dobutamine (10
µg · kg-1 ·
min-1) (ie, a hypokinetic segment becoming
normal or an akinetic segment becoming hypokinetic). 
WMSI, expressing the difference
between resting WMSI and low-dose WMSI. This parameter
provides information on not only the presence but also the extent of
contractile reserve of the dysfunctioning myocardium. An
arbitrary cutoff was set at WMSI=0.25 to identify those patients
with an extensive inotropic response.
Quality control of the diagnostic
performance in the different centers was of critical importance
to acquire meaningful information in the data bank. In the enrolled
centers, the quality control was performed based on 2 criteria, each
one having to be met to fulfill the quality control
requirements.15 16
Follow-up data were obtained from at least 1 of 4 sources:
review of the patient's hospital record, personal communication
with the patient's physician and review of the patient's chart, a
telephone interview with the patient conducted by trained personnel,
and a staff physician visiting the patients at regular intervals in the
outpatient clinic.16 Events were defined as
cardiac-related deaths, nonfatal myocardial infarction, and unstable
angina. For patients who died in the hospital or at home, the cause of
death was obtained from medical records, families, and local
physicians who signed the death certificates. The definition of
cardiac-related death required documentation of significant
arrhythmias, cardiac arrest, or both or death attributable to
congestive heart failure or myocardial infarction in the absence of any
other precipitating factors. In case of death out of hospital for which
no autopsy was performed, sudden unexpected death was attributed to a
cardiac cause. Myocardial infarction was defined as a cardiac event
requiring hospital admission, with the development of new ECG changes
and cardiac enzyme level increases. Unstable angina was defined by
accelerating anginal symptoms requiring hospital readmission (no enzyme
level elevation or new wall motion dyssynergy on the resting
echocardiogram or new Q waves on the resting ECG) or progression of
symptoms requiring revascularization. Therefore,
the outcome events were hard cardiac events (defined as cardiac-related
death or nonfatal myocardial infarction) for infarction-free survival
and spontaneously occurring events (cardiac death, nonfatal myocardial
infarction, unstable angina) for spontaneous event-free survival.
Follow-up was censored at revascularization
procedures.
Values are expressed as mean±SD. WMSI (the variation between rest
and low-dose WMSI), and dobutamine time (ie, test duration
to time of echocardiographically detected
ischemia). 
2 statistic; Fisher's exact test was used
when appropriate. Kaplan-Meier life table estimates of spontaneously
occurring event-free survival were used to summarize the follow-up
experience in these patients and to clarify presentation.
Differences of survival curves were tested with the Mantel-Haenzsel
statistic. A P value <0.05 was considered statistically
significant
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
The main clinical and echocardiographic data are
reported in Table 1
.
In 28 patients, the test was submaximal for the occurrence of
limiting side effects; the test results of these patients (10.5% of
all studies) were included in the analysis. Three patients had
major adverse reactions consisting of ventricular
tachycardia.
Resting WMSI was 1.89±0.2. At the low-dose stage (10 µg
· kg-1 · min-1
of dobutamine), WMSI was 1.76±0.3 (P<0.05
versus rest). One hundred fifty-one patients (52%) showed the presence
of myocardial viability. Among these patients, 83 (54%) had a low-dose
WMSI >0.25, showing an inotropic response to low-dose
dobutamine in at least 4 segments with resting
dysfunction.
Patients were followed up for 9±7 months. During the follow-up
period, 12 patients died of cardiac-related causes, 6 had nonfatal
myocardial infarction, 21 developed unstable angina, and 87 underwent a
coronary revascularization procedure
(bypass surgery in 48 and coronary angioplasty in 39).
When cardiac-related death was considered, patients who did not
show the presence of an inotropic response at low-dose
dobutamine (no viability group) had a higher incidence of
cardiac death (9 deaths) compared with those with an inotropic response
(viability group) to low-dose dobutamine (3 deaths) (5.5%
versus 1.9%, P<0.04).When myocardial viability was
analyzed on the basis of not only its presence but also its
extent, no patients with a low-dose WMSI value >0.25 experienced
cardiac death, while cardiac death occurred in 3 (4.3% of the
viability group, P=NS versus no-viability group) of the
patients with a low-dose WMSI <0.25. In Figure 1, the cumulative survival rates in
patients with a high grade of myocardial viability (>0.25 WMSI
variation), a low grade of myocardial viability (<0.25 WMSI
variation), and no viability (P<0.04) are shown.
View larger version (12K):
[in a new window]
Figure 1. Kaplan-Meier survival curves (considering only
death as an end point) in patients with absence (no viability) and
presence (viability) of myocardial viability separated, on its turn, on
the basis of the number of segments showing improvement by use of an
arbitrary cutoff value for the difference between rest WMSI and
low-dose dobutamine WMSI ( WMSI) set at 0.25. Absence of
myocardial viability is associated with greater incidence of cardiac
death (P<0.04)., the
survival rates in patients stratified according to stress
echocardiography results for ischemia are
shown; survival is worse in patients with compared with those without
inducible ischemia. In the stepwise analysis, the most
important predictor of cardiac death was WMSI at peak stress (hazard
ratio, 14.9; P<0.0018), while in the same model, low-dose
WMSI was shown to exert a protective effect on survival
(coefficient, -0.2; hazard ratio, 0.8; P<0.03) (Table 2). In Figure 3, the survival rates in patients
stratified according to low- and high-dose stress
echocardiography results are shown. The best
survival is observed in patients with echocardiographic
evidence of myocardial viability at low dobutamine dose
with no ischemia at high dobutamine dose. The worst
survival is observed in patients without
echocardiographic evidence of myocardial viability at
low-dose dobutamine dose and with inducible
ischemia at the high dose.
View larger version (10K):
[in a new window]
Figure 2. Kaplan-Meier survival curves (considering only
death as an end point) in patients with presence (DASE +) and absence
(DASE -) of myocardial ischemia. Survival is worse in patients
with inducible ischemia.
View this table:
[in a new window]
Table 2. Stepwise Predictors of Cardiac Death
View larger version (13K):
[in a new window]
Figure 3. Kaplan-Meier survival curves (considering only
death as an end point) in patients stratified according to presence or
absence of echocardiographically assessed viability and
ischemia at low and high doses of dobutamine,
respectively. Best survival is observed in patients with low-dose
viability and no inducible ischemia; worst survival, in
patients without viability and with inducible ischemia.
Viability + and viability - indicate presence or absence of
myocardial viability at low-dose dobutamine, respectively;
DASE + and DASE -, presence or absence of myocardial ischemia
at high-dose dobutamine, respectively.
Patients with positive test results had a higher incidence of
spontaneous events than those with negative test results for myocardial
ischemia, but this difference did not reach statistical
significance (14.8% versus 10.2%, P=0.635) (8
cardiac-related deaths, 3 nonfatal myocardial infarctions, and 11
repeat hospital admissions for unstable angina in patients with
positive results versus 4 cardiac deaths, 3 nonfatal myocardial
infarctions, and 10 repeat hospital admissions for unstable angina in
patients with negative test results for myocardial ischemia).
When variables were entered into the model according to an
interactive clinically realistic approach, after age, sex, and clinical
variables were considered, dobutamine stress
echocardiography still added significant prognostic
information through peak stress WMSI (global
2, 8.76; hazard ratio, 2.68; 95% CI, 0.919 to
7.925; P<0.01).
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
The results of the present study show that in medically
treated patients with moderate to severe global left
ventricular dysfunction early after acute uncomplicated
myocardial infarction, the presence and extent of myocardial viability
identified as inotropic reserve after low-dose dobutamine
are associated with a higher probability of survival. The higher the
number is of segments showing improvement of function, expressed by the
low-dose WMSI, the better the impact of myocardial viability is on
survival. In this set of patients, the presence of inducible
ischemia identified by the WMSI at peak stress strongly added
prognostic power to myocardial viability recognized by low-dose
dobutamine, identifying those patients at higher risk of
cardiac death.
The meaning of myocardial viability early after an acute
myocardial infarction is still unclear. A large body of evidence
collected on selected patient populations shows that the presence of
myocardial viability, recognized by low-dose dobutamine,
might exert a protective effect owing to the potential recovery of
stunned myocardial regions17 18 19 and
antiremodeling effect on left ventricular
volumes.20 Carlos et al9
performed dobutamine from 2 to 7 days after myocardial
infarction, showing that in patients with severe resting dysfunction,
myocardial viability is associated with a better survival, at least in
populations largely submitted to revascularization
procedures. ), whereas those without myocardial viability or with moderate
low-dose improvement had a worse outcome. According to the data
presented, the "paradox" of the impact of viability on
prognosis in patients evaluated early after an acute myocardial
infarction can be solved if one takes into account that viability can
be both "good" (associated with better outcome) and "bad"
(associated with worse outcome), depending on the patient under study
and the outcome end point considered.21 In
patients with good ventricles, viability is basically neutral on
survival and is associated with a higher ischemic instability
("viability is bad for good ventricles"). In patients with
depressed resting function, the presence of myocardial viability
recognized by low-dose dobutamine stress
echocardiography is associated with a better
survival. When only survival is considered, myocardial viability is
good for bad ventricles: the more the viability, the better the
prognostic benefit.
A limitation of this study is the low number of events (only 12
deaths), which may determine instability of results by
multivariate analysis. However, the literature
is inflated by studies in which the assessment of the outcome is based
on soft events, which are of questionable clinical significance. We had
to recruit 314 patients by strict selection criteria to obtain
meaningful statistical sample size in a relatively
homogeneous patient cohort. We identified myocardial
viability through the inotropic response to low-dose
dobutamine. This is a generally accepted clinical approach,
but it certainly is less than ideal for several reasons. First,
myocardial viability may be present in the absence of an inotropic
response, especially in patients with
ß-blockers,21 which totaled 11% of our
population. Second, an inotropic stress such as dobutamine
can induce an improvement in an asynergic region even in the absence of
significant viability; this may occur in transmural or horizontal
tethering, for instance, in subendocardial
infarctions.22 However, our intention was not to
establish the pathophysiological meaning of the
dobutamine-induced improvement but rather to assess the
hard prognostic impact of a response frequently found in stress
echocardiography practice—but of uncertain meaning
as yet. We included in the present study only patients with
depressed left ventricular function, defined as
a resting WMSI >1.6. Within the study population, we defined the
extent of myocardial viability on the basis of a variation in WMSI
>0.25. In both cases, we considered in a binary fashion a continuous
variable somewhat artificially introducing threshold criteria in a
parameter continuously describing resting function and
inotropic response. However, these same criteria were previously used
by our and other groups to define a depressed resting function and a
"significant" viability response.18 20 In
addition, a 0.25 value corresponds on average to 4 segments showing
viability, which is equivalent to 25% of the ventricle. Other studies
with PET scanning have demonstrated that >20% of the ventricle needs
to show evidence of viability for ventricular function to
improve after
revascularization.3 4 The
fact that a cutoff value of 0.25 worked well in differentiating
patients with low versus high risk of death agrees nicely with the
results of PET studies.
In the prognostic algorithm of risk stratification after
myocardial infarction with pharmacological stress
echocardiography, the detection of myocardial
ischemia plays a fundamental role, identifying those patients
at higher risk of hard cardiac events in the first year after the acute
event. WMSI at peak stress was the best predictor of cardiac death;
this is consistent with a large body of evidence collected both
on a multicenter basis and in single institutions, with exercise,
dipyridamole, or dobutamine
stress.23 24 25 26 27 28 The present data provide new
information on the risk stratification of patients early after an acute
myocardial infarction. On the basis of the available data, the place of
myocardial viability in this prognostic stratification of patients
recovering after an acute myocardial is strictly linked to the
underlying resting function. As shown in a previous report from
EDIC,1 in patients with preserved left
ventricular function, myocardial viability predicts softer
end points (mainly unstable angina) with no capability to predict
cardiac death. In patients with severely depressed left
ventricular function, myocardial viability significantly
reduces the mortality rate. However, even in these patients, the
beneficial prognostic impact of myocardial viability on survival is
outperformed by the negative impact of extent and severity of induced
ischemia as assessed through peak WMSI. The more practically
relevant implication of these data emphasizes the pivotal role of the
quest for myocardial ischemia in risk stratification of the
patients recovering from acute myocardial infarction.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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