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(Circulation. 1997;95:1402-1410.)
© 1997 American Heart Association, Inc.
Articles |
Dobutamine Stress Echocardiography for Risk Stratification After Myocardial Infarction
Presented in part at the 43rd Scientific Session of the American College of Cardiology, Atlanta, Ga, March 13–17, 1994.
From the Division of Cardiology/Hypertension, Medical College of Wisconsin (Milwaukee).
Correspondence to Kiran B. Sagar, MD, Medical College of Wisconsin, Division of Cardiology, FMLH-East, 9200 W Wisconsin Ave, Milwaukee, WI 53226.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background Because dobutamine stress echocardiography (DSE) provides assessment of left ventricular function and ischemia at a distance, the major determinants of adverse outcome after acute myocardial infarction (AMI), we undertook this study to determine the role of DSE in risk stratification after AMI.
Methods and Results A graded DSE in 5-minute stages was
performed in 214 patients (age, 57±13 years [mean±SD]) at 2 to 7
days after AMI. Coronary angiography was performed in 193 patients.
Follow-up data regarding major cardiac events were obtained through
telephone interviews and chart reviews. All patients were followed
for 
500 days or until a hard cardiac event occurred. The mean
follow-up interval was 494±182 days after AMI. Peak heart rate and
systolic blood pressure were 115±21 bpm and 135±29 mm Hg,
respectively. An adverse outcome occurred in 80 of 214 patients;
cardiac death occurred in 15, nonfatal AMI occurred in 15, sustained or
symptomatic ventricular arrhythmia occurred in 5, congestive heart
failure occurred in 14, and unstable angina occurred in 31. Significant
predictors of adverse outcome by univariate analysis were prior
myocardial infarction (P=.005), anterior infarction
(P=.006), multivessel coronary artery disease
(P<.0001), global resting left ventricular wall motion
score index (P<.0001), infarction zone nonviability based
on akinesis unresponsive to low-dose dobutamine (P<.0001),
and ischemia/infarction at a distance (P<.0001).
Furthermore, the extent of infarct zone and nonviability correlated
with the severity of the cardiac event. Multivariate analysis of
clinical, angiographic, and DSE variables revealed that the only
independent predictors of adverse outcome were
ischemia/infarction at a distance (P<.0001) and
infarction zone nonviability (P<.0001). Multivessel disease
identified through DSE was more predictive of adverse outcome than was
angiographically determined multivessel disease.
Conclusions DSE can be used to predict adverse outcomes after AMI.
Key Words: myocardial infarction • prognosis • stress • echocardiography
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Determination of prognosis after survival of AMI remains a challenging clinical task. Identification of patients at high risk for a future adverse cardiac event may guide the decision for early intervention with specific medical therapy or a revascularization procedure. Predictors of an adverse outcome after AMI include reduced left ventricular systolic function, multivessel coronary artery disease, and the presence of inducible myocardial ischemia.1 2 3 Noninvasive risk stratification after AMI has focused on exercise stress testing, but the inability to exercise and resting ECG abnormalities remain prevalent limitations. Exercise myocardial perfusion scintigraphy provides additional sensitivity for identifying coronary stenosis4 but at limited specificity and high cost. Thrombolytic therapy, with the potential to salvage myocardium at risk, has made identification of functional viability of the infarct zone and flow-limiting residual stenoses supplying the infarct zone an area of increasing interest. Moreover, clinical features, angiographic variables, and exercise stress testing do not provide direct analysis of the infarct territory. Resting, delayed, or reinjection 201Tl scintigraphy can detect and predict functional recovery, but the prognostic significance remains unknown.5 6 7
Multistage DSE offers a safe, convenient, low-cost alternative to these approaches. The response of viable but stunned myocardium to inotropic stimulation with low doses of dobutamine has been shown to correlate with functional recovery of stunned myocardial segments.8 9 Higher doses of dobutamine increase heart rate and, therefore, myocardial oxygen demand, resulting in ischemia and the appearance of wall motion abnormalities in the presence of flow-limiting coronary stenosis.10
We postulated that DSE is an effective means of risk stratification after AMI because it noninvasively identifies poor left ventricular function, multivessel coronary artery disease, and potentially viable myocardium. Therefore, the purpose of this study was to prospectively evaluate the predictive accuracy of DSE early after AMI, to identify predictors of short- and long-term prognoses and to compare the results of DSE with those of traditional clinical and angiographic variables by means of multivariate stepwise discriminant function analysis.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Selection
From November 1991 through June 1994, 214 patients underwent DSE within the first 7 days after AMI at John L. Doyne Hospital (Milwaukee, Wisc). Eligible patients gave informed consent and included those treated with and without thrombolytic therapy and those with first or recurrent AMI. AMI was documented by prolonged (>30 minutes) chest pain, elevated creatine kinase and MB fraction (>2 SDs above normal), and ECG (Q wave and non–Q wave). All patients were administered ß-blockers if there were no contraindications. An additional 130 eligible patients were excluded due to patient or physician refusal (35), referral >7 days after AMI (25), technically inadequate echocardiography (5), hemodynamic instability for >7 days (45), or sustained VT >24 hours after admission (20).
Coronary Angiography
Patients were referred for coronary angiography at the
discretion of the staff cardiologist. Left heart catheterization and
selective coronary angiography were performed according to Judkin's
technique. All angiograms were interpreted without knowledge of the
clinical, echocardiographic, or follow-up data. The IRA was identified
according to the location of acute regional wall motion abnormalities
and ECG changes. The infarct artery stenosis was identified by
angiographic evidence of thrombus and plaque ulceration and/or stenosis
severity. Coronary flow was analyzed by TIMI grade.11
Percent luminal diameter stenosis was derived according to the caliper
technique, in which the diameter of the stenosis is compared with that
of the most normal-appearing region proximal to the stenosis.
Significant coronary artery stenosis was defined as 70% luminal
diameter stenosis.10 Each patient was classified as having
one-, two-, or three-vessel coronary artery disease. The decision to
perform percutaneous transluminal coronary artery or bypass surgery
before hospital discharge was made by the patient's private
cardiologist without knowledge of the study results.
DSE
DSE was performed 2 to 7 days after AMI. The patients were
studied in the fasting state. Heart rate, blood pressure, and a 12-lead
ECG were recorded at rest and during each stage of DSE. The 5-minute
stages were 5, 10, 20, 30, and 40 µg/kg per minute. Atropine (0.2 to
0.4 mg IV every 2 minutes up to 2.0 mg) was infused to achieve the
target heart rate in patients with submaximal heart rates by dobutamine
infusion alone. Images were recorded on videotape at each stage.
Digitized images were recorded at rest, low dose (5 and 10 µg/kg per
minute), and peak dose. Recovery images were recorded on videotape 6
minutes after stopping the dobutamine infusion. If significant clinical
ischemia or untoward reactions persisted during recovery,
esmolol was infused in doses of 0.1 to 0.5 mg/kg IV every 2 minutes up
to a maximum of 1.5 mg/kg until symptoms resolved. Esmolol and/or
nitroglycerin was used only during recovery for chest pain,
hypertension, or arrhythmia. The end points for peak dose were a heart
rate of 120 bpm, 40 µg/kg per minute dobutamine and 2.0 mg of
atropine, clinical ischemia, 2.0 mm of additional
ST-segment depression or elevation in at least two contiguous leads
compared with rest, severe headache, severe nausea and vomiting,
hypotension (systolic blood pressure <90 mm Hg), hypertension
(systolic blood pressure >240 mm Hg), new remote wall motion
abnormality, supraventricular tachycardia, or VT (more than four
consecutive beats).
Echocardiographic images were recorded on videotape and digitally captured with a Freeland Cineview (Prism Imaging) portable acquisition system on-line with an ECG R-wave–triggered mechanism according to the previously reported protocol.12 At each stage, images were obtained in the parasternal long- and short-axis and apical four-chamber, two-chamber, long-axis, and short-axis views. DSE images were arranged in a quadscreen, with continuous loop display on a floppy disk. The DSE images were interpreted by two investigators who had no knowledge of the clinical, angiographic, or follow-up data. The videotape recordings were made available to the interpreters but were not routinely reviewed. The left ventricle was evaluated using the previously described scoring system (1, normal; 2, hypokinesis; 3, akinesis; and 4, dyskinesis) and standard 16-segment model of the American Society of Echocardiography.12 Based on the known distribution of the segments according to vascular territory, segments were subgrouped according to infarction and noninfarction zone location. The left anterior descending vascular territory consisted of the basal and mid anterior, basal and mid anterior septal, mid septal, and apical segments (a total of nine segments). The left circumflex vascular territory consisted of the basal, mid, and apical lateral segments and the basal and mid posterior segments (five segments). The right coronary vascular territory consisted of the basal, mid, and apical inferior segments, the basal septal segment, and the basal and mid posterior segments (six segments). Global WMSIs were calculated for all stages.12 Regional WMSI was used to assess global left ventricular function.13 DSE findings at low and peak dose were categorized according to infarction and noninfarction zone location. The number of hypokinetic, akinetic, and dyskinetic segments in the infarction zone were recorded at each stage. Dobutamine-responsive wall motion was defined as improved wall thickening in at least three dysfunctional infarction zone segments at low dose. Improved wall thickening at low dose was defined as a change from akinesis or dyskinesis to hypokinesis or normal wall thickening and from hypokinesis to normal wall thickening but not from dyskinesis to akinesis. An inducible wall motion abnormality was defined as worse wall motion in at least two segments at peak dose compared with rest or low dose. Worse wall motion was defined as a change from normal wall thickening to hypokinesis, akinesis, or dyskinesis and from hypokinesis to akinesis or dyskinesis but not from akinesis to dyskinesis. The criteria for ischemia were (1) a new inducible wall motion abnormality, (2) a biphasic response of a resting wall motion abnormality (improvement at low dose with worsening at peak dose), or (3) worsening of a resting wall motion abnormality at peak dose without improvement at low dose. Echocardiographic multivessel disease was defined as resting or induced wall motion abnormalities in at least two vascular territories. Wall motion in a vascular territory was considered abnormal if wall thickening was abnormal in at least two contiguous nonoverlap segments. Overlap segments were the basal posterior, mid posterior, apical inferior, and apical lateral segments. Two-vessel disease was defined as wall motion abnormalities involving (1) the inferior and lateral walls or (2) the anterior (septum, apex, or anterior) vascular territory and either the inferior or lateral walls. Three-vessel disease was defined as wall motion abnormalities involving the anterior territory and the inferior and lateral walls.
Follow-up Data/Definition of Adverse Outcome
Patients were followed for 1 year after hospital discharge.
Outcome was determined from patient interviews, hospital chart reviews,
and/or telephone interviews. Adverse outcome was defined as cardiac
death, nonfatal MI, sustained VT or ventricular fibrillation, unstable
angina, and congestive heart failure requiring hospitalization. Hard
events were defined as cardiac death, nonfatal MI, and sustained VT or
ventricular fibrillation. Only the most severe outcome was considered
an end point. Cardiac death was defined as sudden death or death
related to MI, congestive heart failure, or cardiac arrhythmias.
Nonfatal MI was defined as a hospital admission for prolonged (>20
minutes) chest pain, ECG changes, and documented myocardial injury by
cardiac isoenzymes. Sustained ventricular tachycardia (VT) >30 seconds
was diagnosed only if it was documented on a Holter recording or
telemonitoring in the hospital and required treatment. Unstable angina
was defined as chest discomfort at rest that was judged to be caused by
ischemia and that lasted 5 minutes but 
6 hours. In
addition, new or reasonably new ECG evidence of ischemia in at
least two contiguous leads (0.01 with ST-segment elevation or 0.1
mV ST depression or T-wave inversion during an episode of rest
pain).14
Statistical Analysis
Computer-driven multiple logistic regression analysis was used
to identify independent predictors of all and hard cardiac events using
the standard enter and remove criteria of the True Epistat statistical
program. Stepwise multiple logistic regression analysis ROC
analysis15 were used to determine whether DSE findings
enhanced the prediction of outcome compared with clinical and resting
echocardiographic data. First, a model containing clinical data alone
was developed (step 1). Then, resting echocardiographic data (global
WMSI) was added to the clinical model (step 2). Next, low-dose DSE data
were added to the clinical and resting echocardiographic model (step
3). Fourth, peak dose DSE data were added to the clinical, resting
echocardiographic, and low-dose DSE model (step 4). Finally, the
predictive value of the model, including clinical, resting
echocardiographic, and angiographic data, was compared with the
clinical and resting echocardiographic model (step 5). Each of these
models was used to define the predicted probability of all and hard
events for each patient. ROC curves were developed for each of these
models for all and hard events based on these probabilities using the
methods described by Hanley and McNeil16 with the Fisher
Z test. For each logistic model, a continuous curve was
constructed from the true- and false-positive rates for all possible
thresholds of all or hard event probability. The discriminant accuracy
of each logistic model was quantified in terms of the area under these
curves. The difference in area between the different models represented
the increment in prognostic power.
ROC analysis was also used to determine optimal predictive criteria for
(1) continuously distributed resting and DSE findings and (2) a DSE
model of independent predictors. Freedom from all and hard cardiac
events was plotted by the standard technique of Kaplan-Meier plots.
Mantel-Haentzel life table 
2 analysis was used to
compare differences in freedom from events.
Continuous data were expressed as mean±SD. Categorical variables were
analyzed by the 2 or Fisher's exact test.
Continuous variables within groups were analyzed by repeated-measures
ANOVA. Multigroup ANOVA was used to compare continuous data among
different groups. The Bonferroni t test was used to identify
differences in mean values. A two-tailed test value of
P<.05 was considered statistically significant.
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Results |
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Follow-up Data
Follow-up data were available for all of the 214 study patients. Fig 1
presents the outcome data. Adverse outcome
occurred in 80 patients (group 1). There were 35 hard events, including
cardiac death in 15 patients, nonfatal MI in 15, and sustained VT in 5.
Unstable angina occurred in 31 patients, and congestive heart failure
occurred in 14 patients. Life table analysis revealed that 21 events
(26%) occurred before hospital discharge, 21 (26%) between hospital
discharge and 3 months, 17 (22%) between 3 and 6 months, and 21 (26%)
>6 months after infarction. Only 4 of the hard events (11%) occurred
before hospital discharge. The remainder, 31 (89%), occurred after
discharge. Eighty-three patients underwent revascularization procedures
for anatomic but not clinical reasons before hospital discharge.
Sixty-two patients underwent percutaneous transluminal coronary
angioplasty of the infarct artery, and 21 underwent coronary artery
bypass graft surgery. One hundred thirty-one patients were treated
medically. The event rate after the performance of revascularization
therapy or initiation of medical therapy was similar (P=NS)
in the two groups (30 of 83 [36%] versus 50 of 131 [38%]).
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Patient Data
The study population was predominantly male (163) with a mean age
of 58±13 years. Infarction location was anterior in 93, inferior in
101, and lateral in 20. One hundred twenty-one patients were treated
with thrombolytic therapy, 35 had prior MI, 122 had Q-wave MI, and 41
had rales on admission. One hundred seven (50%) were treated with
ß-adrenergic antagonists for stable angina or hypertension before the
index MI. Peak CK was 2123±2028 IU/mL. The clinical data for the 80
patients with adverse outcome (group 1) were compared with the data for
the 134 patients without events (group 2). There were no differences in
age, medications, Q-wave infarction, or treatment with thrombolytic
therapy. Anterior infarction and prior MI were the only clinical
features that were more common in group 1 (P<.01 versus
group 2). In a comparison of the clinical data of the 83 electively
revascularized patients and the 131 who were treated medically,
anterior infarction was predictive of adverse outcome
(P<.05) in both groups, but prior MI was predictive only in
revascularized patients.
Hemodynamic Data
DSE was safely performed at 4.5±1.6 days after MI. The peak dose
of dobutamine was 26±10 µg/kg per minute. Atropine was used in 65
patients. Peak heart rate and systolic blood pressure were 115±21 bpm
and 135±29 mm Hg, respectively. There were no episodes of
sustained VT or MI. End points were peak heart rate in 113, angina in
15, multiple induced wall motion abnormality in 20, ST depression in 8,
ST elevation in 20, nonsustained VT in 4, severe nausea in 2, and
maximum dose in 32.
Coronary Angiography
Coronary angiography was performed in 193 (90%) of the 214
patients. Eighty-nine patients had one-vessel disease, 88 had
two-vessel disease, and 26 had three-vessel disease. The residual
stenosis of the infarct artery was 76±26%. The infarct artery was
patent in 152 (79%) and occluded in 41 (21%). The angiographic data
for group 1 and group 2 patients were compared. The only angiographic
correlates with adverse outcome were left anterior descending and
multivessel disease. In a comparison of the angiographic data for the
83 electively revascularized and the 131 medically treated patients,
left anterior descending disease and multivessel disease
(P<.05) were predictive of adverse outcome in both
groups.
DSE Data
The DSE data for the 80 patients with adverse outcomes were
compared with those for the 134 patients without events. Global WMSI of
1.88 ±0.43 (mean±SD) at rest was significantly higher
(P<.0001) than the value in the adverse outcome group
(1.55±0.28), which is indicative of a lower ejection fraction.
Low-dose dobutamine significantly reduced global WMSI, but the
magnitude of the decrease was greater (P<.05) in patients
without events (-0.11±0.13 in group 1 versus -0.19±1.5 in group 2).
The number of infarcted segments was higher (P<.0001)
(4.1±2.1 in group 1 versus 1.9±1.9 in group 2) and the number of
dobutamine-responsive segments was lower (P<.01) (1.2±1.5
in group 1 versus 2.9±2.2 in group 2) in the adverse outcome group,
indicating that nonviability of the infarct zone was highly predictive
of adverse outcome. From rest to peak dose, WMSI increased
(P<.0001) in both groups but was only worse than rest in
the adverse outcome group, which is indicative of multivessel disease
and more severe ischemia. Echocardiographic multivessel disease
was more common (P<.0001) in the adverse outcome patients
(54 of 80 [68%] versus 21 of 134 [16%] without events). Worse
wall motion of the infarct zone compared with rest was also more common
(P<.05) in the adverse outcome patients (35 of 80 [44%]
versus 38 of 134 [28%] without events).
Fig 2 compares the incidence of cardiac events according
to the extent of coronary artery disease by DSE and coronary
angiography. DSE was 66% (69 of 104) sensitive and 98% (87 of 89)
specific for multivessel coronary artery disease. Multivessel disease
indicated by DSE tended to be more predictive of cardiac events than
disease indicated with coronary angiography. Overall, DSE identified
fewer (P<.01) patients as having multivessel disease than
did angiography but, importantly, identified a similar number of
adverse outcomes. There were no hard events in the six patients with
events who had multivessel disease as identified with angiography but
had one-vessel disease as identified with DSE.
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Fig 3 shows incremental ROC analysis of clinical data
alone, clinical data plus resting echocardiogram, clinical data plus
resting echocardiogram plus dobutamine echocardiography, and clinical
data plus resting echocardiogram plus coronary angiography. DSE added
significantly to the predictive value of clinical and resting
echocardiographic data and was superior to the combination of clinical
data plus resting echocardiogram plus angiography.
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In a comparison of the echocardiographic data of the 83 revascularized patients and the 131 medically treated patients, WMSI was worse at all stages in revascularized and medically treated patients with adverse outcome. The number of akinetic segments at rest was predictive of adverse outcome only in revascularized patients (P<.01), but the number of akinetic segments at low dose was predictive of adverse outcome in both groups. Multivessel disease was more predictive (P<.01) of adverse outcome in medically treated than revascularized patients.
All 16 variables selected as significant univariate predictors of
adverse cardiac outcome were subjected to multiple logistic regression
analysis to determine the independently predictive variables for
adverse cardiac outcome. The results are outlined in Table 1. Only three variables emerged as statistically
significant predictors: ischemia/infarction at a distance,
myocardial nonviability of the infarct region, and infarct size.
Multivariate analysis was also performed separately on the 83
revascularized and the 131 medically treated patients. The only
independent predictor of adverse outcome in the 83 revascularized
patients was infarct size of at least four segments at low dose
(P<.0001), indicating nonviable myocardium. In medically
treated patients, infarct size of at least four segments
(P<.05) and ischemia/infarction at a distance were
both independent predictors of adverse outcome.
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Multivariate analysis was separately performed on 121 patients treated
with thrombolytic therapy and 93 patients treated without thrombolytic
therapy. The number of adverse events in the two groups was similar: 42
in the thrombolysis group versus 32 without thrombolysis. Infarct size
of at least four segments at low-dose dobutamine and the presence of
multivessel disease (remote ischemia at peak dose of
dobutamine) were independent predictors of adverse prognosis in both
groups. Table 2 demonstrates the clinical usefuless of
DSE in the risk stratification of patients with AMI. In high-risk
clinical subsets (resting WMSI 1.8, rales, anterior MI, or no prior
MI), DSE was able to identify low-risk patients. In both low- and
high-risk clinical subsets with large wall motion abnormalities, the
combination of nonviability (infarct size of at least four segments,
25% of the left ventricle) and echocardiographic multivessel disease
almost universally predicted cardiac events. Nonviability without
multivessel disease predicted intermediate risk. Viability (infarct
size of at least three segments, 19% of the left ventricle) regardless
of multivessel disease almost universally predicted good outcome. In
both low- and high-risk subsets with small to moderate wall motion
abnormalities, all infarction zone wall motion abnormalities were
viable (infarct size of at least three segments, 19% of the left
ventricle), so multivessel disease was the determinant of outcome. The
presence of multivessel disease strongly predicted poor outcome, but
the absence almost universally predicted good outcome.
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Fig 4A and 4B shows Kaplan-Meier life table curves of
all and hard event–free survival, respectively, on the basis of
dobutamine-responsive wall thickening of the infarct zone or functional
viability, infarct size, and remote ischemic/infarction
indicating multivessel disease. By Mantel-Haentzel
2 analysis, infarct size of at least four
segments was a strong predictor of all adverse events throughout the
500-day follow-up period after AMI. Remote ischemia/infarction
was predictive of adverse outcome throughout the follow-up period.
Infarct size and the extent of remote ischemia/infarction
predicted the severity of cardiac events. Larger infarct size (at least
five segments) was strongly predictive of hard cardiac events (Fig 4B).
Wall motion abnormalities involving the anterior and nonanterior
vascular territories (three- or two-vessel left anterior descending
coronary artery) were also strongly predictive of hard cardiac events
(Fig 4B). The absence of dobutamine-responsive wall thickening was also
predictive of adverse outcome, but it was only predictive at >3 months
after hospital discharge.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Our data show that DSE can be used to accurately identify patients at high risk for poor outcome after an AMI. It provides incremental prognostic power when adjusted for clinical and resting echocardiographic data. The extent of MI, global left ventricular function, lack of response to low-dose dobutamine, and ischemia at a distance were powerful predictors of poor outcome.
The prognosis of patients surviving AMI has been most strongly related to left ventricular function. Left ventricular function is a more powerful determinant of prognosis than the severity of coronary artery narrowing, coronary risk factors, clinical variable, or presence of ventricular ectopic activity.2 17 18 Left ventricular function is directly related to the infarct size. Specific quantitative studies relating regional dysfunction or infarct size to prognosis as opposed to global left ventricular function are few, limited by imaging technique. Contrast ventriculography and radionuclide angiography provide only limited views and rely on opacification of the cavity. Two-dimensional echocardiography provides qualitative assessment of infarct size, and the left ventricle can be imaged in multiple planes. Assessment of systolic wall thickening may be a more accurate method for measuring the extent of infarction. Wall thickening is an evidence of viability and akinesis unresponsive to inotropic stimulation of nonviability.19 The regional myocardial function may be a better predictor of outcome in post-MI patients than the global left ventricular function. Myocardial stunning and compensatory regional hyperkinesis of noninfarcted segments early after AMI20 21 confound the measurement of infarct size by global left ventricular function. Several studies have shown that infarct size as determined by the presence of abnormal wall thickening/wall motion analysis on resting echocardiography is strongly predictive of adverse outcome. In our study, small infarcts carried a low likelihood of adverse outcome, and large infarcts carried a significantly higher risk of adverse outcome.
The accuracy of the presence of large infarcts in the prediction of outcome was significantly enhanced if the infarct zone was functionally nonviable (ie, it did not demonstrate improved wall thickening/wall motion with low-dose dobutamine). The absence of functional viability was a strong predictor of adverse outcome, by both univariate and multivariate analyses, in our study. Patients with large but viable infarcts had a similar prognosis as those with small infarcts. To date, few studies of the relation of infarct zone viability to prognosis have been published.
Brown and associates22 correlated viability, defined as reversible perfusion defects with 201Tl scintigraphy, with higher risk of cardiac events in post-MI patients.
Gibson and coworkers4 examined the prognostic significance of non–Q wave MI versus Q wave MI. They postulated that non-Q wave MI represented an incomplete infarction with substantial residual myocardial viability. In their study, non-Q wave MI carried a significantly higher risk of adverse ischemic events than did Q wave MI. These studies did not correlate defect size or severity with outcome.
The presence of myocardial viability using positron emission tomography confers an additional risk in conservatively managed patients and improves survival in revascularized patients.23 24 However, these studies were focused on chronic coronary artery disease and did not address the viability or nonviability of the acute infarct zone. The results of the present study are highly concordant with the results of the only previous outcome study in patient with AMI that addressed the issue of myocardial viability in acute infarction. The present study and the positron emission tomography study by Yoshida and Gould25 showed that the added information of myocardial viability and infarct size dramatically improved the predictive accuracy of resting left ventricular dysfunction and clinical data after AMI. In both studies, viability and small infarct size strongly predicted good outcome in patients with significant left ventricular dysfunction and large infarct size and nonviability almost universally predicted adverse outcome.
The present study demonstrates that DSE further enhances the predictive accuracy of outcome by providing data regarding the presence or absence of multivessel disease. It was especially helpful in identifying a subset of patients with nonviability and large infarct size who are at an exceedingly high risk. The presence of multivessel disease also identified the only subset of patients with small infarct size who were at high risk for adverse outcome.
Remote ischemia, as determined by wall motion abnormalities outside of the infarct zone either at rest or with high-dose dobutamine suggestive of multivessel coronary artery disease, was another strong predictor of adverse cardiac events. In our study, remote ischemia by echocardiography was more predictive of cardiac events than the angiographic identification of multivessel coronary artery disease. This probably reflects the ability of DSE to detect the functional significance of coronary stenosis. Similar results have been reported with 201Tl imaging,26 exercise echocardiography,27 28 29 and dipyridamole stress echocardiography.30 31 32 Camerieri and associates30 showed that the presence of remote ischemia was a strong predictor of adverse outcome in the early post-MI period. Iliceto and coworkers32 used transesophageal pacing for risk stratification in patients with AMI and demonstrated that remote ischemia was a strong predictor of adverse outcome.
No clinical features except anterior infarct location differentiated between high- and low-risk groups. There were, however, trends toward higher risk in patients with hypertension, diabetes, Q–wave MI, antecedent angina, and high-peak creatine phosphokinase. This finding may be related to the relatively shorter follow-up period for this study. Age, sex, hypertension, and other variables have been related to prognosis in other studies, but the follow-up periods have generally been significantly longer. The distribution of infarct-related coronary artery involvement seen in the TIMI phase II trial33 for the left anterior descending, left circumflex, and right coronary arteries was 43%, 13%, and 44%, respectively. In our series, these values were 42%, 19%, and 32%, respectively. Anterior infarction was a significant univariate predictor of adverse events in our study. This is consistent with the recently published 2- and 3-year follow-up reports for the TIMI II patients, in which anterior infarction carried a risk of death almost twice that of nonanterior infarction.33 DSE provides an incremental prognostic power when adjusted for clinical and resting echocardiographic data. Previously, clinical data, global left ventricular function, low-level exercise tests, and radionuclide imaging have been used for risk stratification of patients with AMI.34 All these criteria reflect the extent of MI and the presence of additional jeopardized myocardium but do not provide any information regarding the functional viability of the infarct zone. DSE can be used to detect myocardial viability and the presence of multivessel disease and to assess the extent of the infarct. Although this study does not address the cost-benefits relation of various noninvasive techniques, DSE may be the best choice. Several studies35 36 37 have used pharmacological stress echocardiography for preoperative risk assessment of patients with chronic coronary artery disease. This is the first study to focus on the significance of the viability versus nonviability of the infarct zone.
Echocardiography is being increasingly used for the assessment of prognosis after MI. Our findings may complement the recently published echocardiographic findings of the SAVE Study.38 Of 420 post-MI patients with 1-year echocardiograms, the percent area change of the left ventricle, calculated as the average of three short-axis areas or two long-axis areas, was the most powerful predictor of the 26% of patients with death, MI, or heart failure requiring hospitalization or open-label captopril therapy. Furthermore, the incidence of death or MI was higher than that of severe symptomatic heart failure in this post-MI population with asymptotic reduced left ventricular function over a 3.5-year follow-up period.39 The relative contributions of myocardial viability and left ventricular remodeling after MI to prognosis have yet to be discerned, as the processes are likely strongly interrelated.
One of the major limitations of our study was uncontrolled medical and surgical management after the index infarction. The decision for revascularization is influenced by multiple, uncontrollable patient and physician personal biases. However, in our study, the incidence of cardiac events in patients who underwent revascularization procedures without a predefined clinical end point was not significantly different from that of patients without revascularization. Also, the same predictive factors in the multivariate analysis were operative in the two groups (ie, myocardial viability and ischemia/infarction at a distance). Nevertheless, to reach conclusions regarding the effect of revascularization procedures on prognosis in this uncontrolled series would be hazardous. The effect of revascularization could also have masked a stronger relation between residual IRA ischemia and prognosis. Barilla and associates40 reported an improvement in left ventricular function after revascularization of the IRA. Similarly, medical therapy could not be standardized; however, most patients were routinely treated with antiplatelet agents, ß-blockers, and ACE inhibitors. Most patients participated in standard cardiac rehabilitation and risk-factor modification programs.
Another limitation of the study was the use of DSE at various intervals after the index infarction. The response to stress at 2 days may differ from that at 7 days. We did not observe any significant differences in the hemodynamic responses or the accuracy of DSE to detect stunned myocardium at day 2 versus day 7. In addition, recovery of stunned segments before DSE should not alter the results; in fact, it only enhances the association of viability with a favorable prognosis.
We conclude that our preliminary data suggest that DSE in survivors of AMI may provide important prognostic information that is independent of clinical or angiographic variable for the prediction of adverse outcomes after 1 year. DSE can be performed in the early post-MI period without undue complications. The presence of ischemia or infarction at a distance and functional nonviability of the infarct zone are most strongly predictive of future adverse outcome. Semiquantitative wall motion analysis with respect to MI, stunning, and viability has prognostic importance. DSE may be the study of choice for risk stratification of patients after AMI.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The authors acknowledge the technical support of David McElmurry, Tami Knight, and Paula Wyatt and the secretarial support of Diane Lawton in the preparation of the manuscript.
Received September 23, 1996; revision received November 4, 1996; accepted November 14, 1996.
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